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ABOMASAL EMPTYING DEFECT (AED) IN SHEEP
BASICS DEFINITION
Abomasal emptying defect (AED) is a syndrome of adult Suffolk sheep characterized by chronic, progressive weight loss and abomasal dilatation in the absence of mechanical obstruction.
PATHOPHYS IOLOGY

The pathogenic mechanism for AED is unclear.
The AED syndrome shares some characteristics of a human syndrome, chronic idiopathic intestinal pseudo-obstruction that affects children and adults. Affected individuals clinically appear to have a partial or complete gastric obstruction, but none is present.
Morphologic investigations of human patients indicate degenerative changes in the smooth muscle or the tunica muscularis and/or neurons of the enteric plexus.
SYSTEMS AFFECTED
Gastrointestinal
GENETICS
Little information is available regarding genetic predisposition. A pedigree analysis performed on a flock in which 11 of 92 Suffolks were affected failed to show a hereditary pattern.
INCIDENCE/PREVALENCE
Unknown
GEOGRAPHIC DISTRIBUTION
None
SIGNALMENT
Species
Sheep
Breed Predilection
Suffolk is the predominant breed. The condition has also been reported in the Hampshire, Dorset, and Texel breeds. Mean Age and Range Adults that are at least 2 years of age.
Predominant Sex
This condition affects both males and females.
SIGNS
Historical Findings
This condition usually occurs sporadically, affecting a single individual. Usually, affected flock management is excellent with the animals appearing healthy and in good body condition, except for the affected individual.
The owners may report loss of weight in the individual, despite efforts to provide extra nutrition, anthelmintic treatment, and individual attention. Also, owners will report that animals appear “bloated” despite inappetence.
PHYSICALFINDINGS
Most typically body temperature is within normal limits unless there is concurrent disease present. Pulse and respiration rates may be normal to increased. Fecal consistency is usually normal, but fecal volume is often decreased.
Careful examination of the abdomen is important and particular attention should be paid to the following:
Abdominal conformation-may be normal; bilateral, asymmetrical abdominal distention may be observed (distension high in the left paralumbar fossa and low on the right side when the animal is viewed from behind); unilateral distension may be present (low on the right ventrolateral aspect of the abdomen).
Rumen contractions-may be normal, increased, or decreased. Rumen hyperactivity is very dramatic to visually observe in AED sheep because the left paralumbar fossa appears to be in constant motion, reflective of the almost constant rumen activity.
Abdominal ballottement-Most AED sheep are in varying stages of cachexia and their abdominal wall feels “thin” or lacks tone due to muscle wasting. The gastrointestinal organs also may lack tone or give the impression of being fluid filled. In some instances, the caudal border of the abomasum may be outlined as it extends beyond the last rib on the ventrolateral aspect of the abdomen. The distended abomasum usually feels fluid filled rather than the doughy or firm consistency that is often associated with abomasal impaction in cattle.
RISK FACTORS
Unknown
DIAGNOSIS DIFFERENTIALDIAGNOSIS
Differential diagnosis for chronic weight loss in adult sheep includes caseous lymphadenitis or other chronic infection, Johne’s disease, malnutrition, dental problems, parasitism, and rarely neoplasia.
The historical and physical findings, as described above, are fairly specific to AED.
CBC/BIOCHEMISTRY/URINALYS IS
Hematological and serum chemistry analysis are usually normal.
The typical metabolic alkalosis with hypochloremia and hypokalemia associated with proximal gastrointestinal obstruction (e.g., displaced abomasum in cattle) is not consistently noted with AED.
Elevations in liver enzymes (SGOT/AST, SDH, GGT) may be noted; however, this can be misleading chemical data.
Increased intra-abdominal pressure from a greatly distended abomasum may lead to secondary liver congestion and ischemia. This pressure can precipitate hepatic leakage of liver enzymes.
Urinalysis is usually unremarkable.
OTHER LABORATORY TESTS
An elevated rumen chloride concentration is probably the most useful test in supporting a diagnosis of AED.
Normal rumen chloride in sheep is = 15 mEq/L. Most often affected sheep will have at least a twofold increase. Rumen fluid samples are obtained most easily by percutaneous aspiration of the rumen from a site in the ventrolateral aspect of the left paralumbar fossa.
IMAGING
Abdominal radiology may be helpful; however, unless the animal can be positioned for an oblique abdominal radiographic view, results will be difficult to interpret.
Abdominal ultrasonography may be more useful than radiography in imaging the abomasum. A 3 to 5 MHz linear or sector scanner can provide adequate images of the abomasum. When placed on the lower right abdomen, the normal abomasum will not extend beyond the last rib. An animal’s abomasum with AED will usually appear two to four times normal size.
DIAGNOSTIC PROCEDURES
N/A
PATHOLOGIC FINDINGS
Gross necropsy finding: abomasum that is greatly distended with a patent pylorus.
Abomasal contents are usually liquid but may be dry. Histopathologic changes in the abomasum include smooth-muscle degeneration, vacuolation, and varying degrees of necrosis. Degenerative changes have been reported in the celiacomesenteric ganglia.
TREATMENT
GENERALCONSIDERATIONS
The prognosis for recovery when intensive treatment is initiated is variable and dependant upon the duration of the abomasal dysfunction and distention. Medical therapy alone using various cathartics and laxatives and surgical therapy (abomasotomy) have had limited success.
In animals that are good surgical candidates, abomasotomy followed by metoclopramide and supportive fluid therapy has provided some success.
SURGICALCONSIDERATIONS
An abomasotomy is best performed under general anesthesia, although an anesthetic approach using a local line block can be used. The animal is placed in left-lateral recumbency and a right paracostal approach provides excellent access to the abomasum. Subsequently the abomasum is opened and its contents removed, and the organ is flushed and closed in a routine manner. Therapy with metoclopramide should be used as an adjunct to the surgery (see Medications section below). Also, fluid replacement and electrolyte correction therapy is critical to survival and success.
MEDICATIONS DRUGS OF CHOICE
Metoclopramide (0.1 mg/kg, q 8 hrs, SQ) as an adjunct to abomasotomy has been reported to improve abomasal motility in selected cases. This medication should not be used if a gastrointestinal obstruction is suspected.
CONTRAINDICATIONS
Neostigmine should not be used in affected animals.
Appropriate milk and meat withdrawal times must be followed for all compounds administered to food-producing animals.
FOLLOW-UP PATIENT MONITORING
If intensive therapy is undertaken, the animal should be observed for attitude, appetite, volume of fecal production, and abdominal conformation. Positive signs of improvement following abomasotomy and during metoclopramide therapy may include improvement in attitude and an increased interest in eating.
Fecal production should increase and abdominal distention should decrease if abomasal motility has returned.
PREVENTION/AVOIDANCE
Because the underlying cause of this condition is unknown, no recommendations can be made.
POSSIBLE COMPLICATIONS
Complications related to abomasotomy: surgical dehiscence of the abomasal incision (especially if the abomasal wall has undergone degenerative changes) and dehiscence of the abdominal incision may occur (more likely to occur in a debilitated patient).
Once the condition is recognized, if treatment is declined, euthanasia should be offered as a humane resolution.
EXPECTED COURSE AND PROGNOSIS
The earlier the condition is recognized and treated, the better the prognosis; however, for long-term recovery, the prognosis is guarded.
In certain circumstances such as a ram completing a breeding season, or a late gestation ewe completing her pregnancy, a fair to good prognosis may be offered if intensive treatment is provided early.
MISCELLANEOUS ASSOCIATED CONDITIONS
Other concurrent conditions may occur with this disease. Pneumonia and other organ failures are viewed as secondary to any chronic debilitating diseases.
AGE-RELATED FACTORS
N/A
ZOONOTIC POTENTIAL
None
PREGNANCY
In spite of treatment, pregnant animals may abort. Pregnant animals (especially mid to late term) represent an increased surgical risk.
RUMINANT SPECIES AFFECTED
The condition has been reported in sheep only; however, the author has observed a similar syndrome in a geriatric crossbred dairy-type goat.
BIOSECURITY
N/A
PRODUCTION MANAGEMENT
This is usually observed in a single animal from a well-managed flock.
SYNONYMS
Abomasal dilatation and emptying defect Abomasal impaction
Acquired dysautonomia Functional pyloric stenosis Ovine abomasal enlargement SEE ALSO
N/A
ABBREVIATIONS
AED = abomasal emptying defect AST = aspartate transaminase GGT = gamma-glutamyltransferase SDH = succinate dehydrogenase
SGOT = serum glutamic oxaloacetic transaminase
Suggested Reading
Kopcha, M. 1988. Abomasal dilatation and emptying defect in a ewe. J Am Vet Med Assoc 192:783-84.
Pruden, S. J., McAllister, M. M., Schultheiss, P. C., et al. 2004. Abomasal emptying defect of sheep may be an acquired form of dysautonomia Vet Pathol. 41:164-69.
Ruegg, P. L., George, L. W., East, N. E. 1988. Abomasal dilatation and emptying defect in a flock of Suffolk ewes. J Am Vet Med Assoc 193:1534-36.
Author: Michelle Kopcha

ABOMASAL IMPACTION
BASICS OVERVIEW

Blockage of fluid and ingesta from the abomasum through the pylorus by feed, sand, gravel, or neurological deficit.
Pyloric obstruction from improper placement of percutaneous fixation of left-sided abomasum (“roll and toggle”) can result in abomasal impaction.
Signs can be acute or chronic and are characterized by loss of appetite, decreased or scant feces, distension of the abomasum, weakness, dehydration, metabolic alkalosis, and apparent abdominal pain.
Found in cattle and sometimes sheep. Usually isolated cases but also may have low morbidity associated with low- quality forages. High mortality.
Abomasal emptying defect (AED) is a disease syndrome that primarily affects Suffolk sheep and is characterized by distension and impaction of the abomasum.
PATHOPHYS IOLOGY
Physical blockage of the outflow from the abomasum to the duodenum occurs. This may be due to the packing of straw or poor-quality roughages, sand, or gravel in the abomasum.
Damage to branches of the vagus nerve from reticuloperitonitis or lymphoma can decrease the emptying ability of the abomasum. Failure of fluid to move from the abomasum to the intestines results in dehydration and starvation.
Sequestration of hydrochloric acid in the abomasum can result in metabolic alkalosis.
In sheep, no histologic lesion has been consistently associated with AED. There is no known etiology. In one study, histologic examination of celiacomesenteric ganglia from affected sheep revealed scattered chromatolytic or necrotic neurons, without inflammation. Chromatolytic neurons were observed more frequently in AED-affected sheep than in healthy Suffolk sheep. Neuronal necrosis was not observed in any of the healthy sheep. Neuronal lesions of AED resemble dysautonomic diseases of humans and other animals.
SYSTEMS AFFECTED
Gastrointestinal
GENETICS
N/A
INCIDENCE/PREVALENCE
Very low morbidity
GEOGRAPHIC DISTRIBUTION
Worldwide; seen more commonly where low-quality roughages or low-energy diets are fed.
Epidemiology
Feeding chopped straw or low-quality forages has been associated with abomasal impaction. Excessive intake of such feeds in attempts to meet energy needs appears to predispose cattle.
Feeding cattle on sand or gravel or including excessive dirt or gravel from feed storage areas into mixed feed.
Late-gestation animals appear more frequently affected.
SIGNALMENT
Species Affected Bovine, ovine Breed Predilections Suffolk sheep
Mean Age and Range
N/A
Predominant Sex
Commonly seen affecting pregnant females.
SIGNS
Anorexia, weight loss, scant feces, dehydration, distension of the abomasum, decrease in rumen motility, recumbency
Metabolic alkalosis in chronic cases
In sheep, clinical signs consisted of chronic anorexia and weight loss. Also, laboratory analysis failed to show the hypochloremic, hypokalemic, metabolic alkalosis commonly found in cattle. Rumen chloride concentrations in sheep indicated reflux of abomasal contents into the rumen.
GENERALCOMMENTS
Reported most often in beef cattle fed low-energy, chopped forage diets in cold weather. Seen sporadically in dairy cattle.
HISTORICALFINDINGS
Cattle on poor pasture or fed chopped, low-quality forages with low dietary energy, especially in cold weather. Cattle eating on sand or gravel or excessive gravel from the feed storage area in the feed
Pica
PHYSICALEXAMINATION FINDINGS
Anorexia, depression, decreased rumen contractions. Distension of the abomasum may be determined by palpation or ballottement of the lower-right flank. Eventually, the animal has scant feces and becomes dehydrated.
CAUSES
Physical blockage of the abomasum by low-quality chopped forages, sand or gravel, or “roll and toggle” sutures inadvertently placed in or near the pylorus.
Damage to the vagus nerve
RISK FACTORS
Cattle on low-energy diets being fed chopped forages, or fed on sand or gravel
Certain lines of Suffolk sheep may be afflicted more than others.
DIAGNOSIS DIFFERENTIALDIAGNOSIS
Abomasal volvulus or torsion, reticuloperitonitis, lymphoma
CBC/BIOCHEMISTRY/URINALYS IS
CBC usually normal
Hypochloremic, hypokalemic metabolic alkalosis may be present in chronic cases.
In sheep with AED, laboratory analyses failed to show the hypochloremic, hypokalemic, metabolic alkalosis commonly found in cattle. Rumen chloride concentrations in sheep indicated reflux of abomasal contents into the rumen.
OTHER LABORATORY TESTS
N/A
IMAGING
N/A
OTHER DIAGNOSTIC PROCEDURES
Laparotomy
GROSS AND HISTOPATHOLOGIC FINDINGS
Confirmation from laparotomy
TREATMENT
Surgical correction by abomasotomy; possible softening of impacted material by per os mineral oil once daily for 2 to 4 days.
Inpatient Versus Outpatient
Inpatient treatment may include correction of metabolic alkalosis.
CLIENT EDUCATION
Feed cattle to energy requirements, especially cattle in cold weather. Do not feed chopped poor-quality forages with low- energy diets. Feed cattle on surfaces other than sand or gravel.
MEDICATIONS DRUGS OF CHOICE
Balanced electrolytes IV for 1 to 3 days to correct metabolic alkalosis.
CONTRAINDICATIONS
N/A
PRECAUTIONS
Lactated Ringer’s solution should be used cautiously due to the possibility of metabolic alkalosis.
POSSIBLE INTERACTIONS
N/A
ALTERNATIVE DRUGS
N/A
FOLLOW-UP PATIENT MONITORING
Pain or suffering, fecal output, hydration status, electrolyte balance
PREVENTION/AVOIDANCE
Feed energy balance feeds with long fiber length. Avoid feeding on sand or gravel.
POSSIBLE COMPLICATIONS
Abomasal rupture and peritonitis
EXPECTED COURSE AND PROGNOSIS
Grave prognosis; death from dehydration, metabolic alkalosis, or peritonitis
MISCELLANEOUS PREVENTION
Feed good-quality, long forage with adequate energy supplementation. Avoid feeding on sand or gravel.
ASSOCIATED CONDITIONS
Reticuloperitonitis, lymphoma, displaced abomasum
AGE-RELATED FACTORS
More common in pregnant animals
ZOONOTIC POTENTIAL
N/A
PREGNANCY
Pregnancy predisposes due to increased energy needs and the possible effect of size and weight of the gravid uterus on abdominal organs
SYNONYMS
Abomasal emptying defect (AED) in Suffolk sheep
SEE ALSO
Abomasal emptying defect
Displaced abomasum, volvulus, or torsion Fluid therapy
Lymphoma Reticuloperitonitis ABBREVIATIONS
AED = abomasal emptying defect CBC = complete blood count
IV = intravenous
Suggested Reading
Belknap, E. B., Navarre, C. B. 2000, March. Differentiation of gastrointestinal diseases in adult cattle. In: The veterinary clinics of north america, food animal practice, diagnosis of diseases of the digestive tract, ed. R. G. Helman., vol. 16, no. 1. Philadelphia: W. B. Saunders.
Kline, E. E., Meyer, J. R., Nelson, D. R., Memon, M. A. 1983, Aug 20. Abomasal impaction in sheep. Vet Rec. 113(8): 177-79.
Pruden, S. J., McAllister, M. M., Schultheiss, P. C., O’Toole, D., Christensen, D. E. 2004, Mar. Abomasal emptying defect of sheep may be an acquired form of dysautonomia. Vet Pathol. 41(2):164-69.
Radostits, O. M., Gay, C. C., Blood, D. C., Hinchcliff, K. W., eds. 2000. Veterinary medicine: a textbook of diseases of cattle, sheep, pigs, goats and horses. 9th ed. London: W. B. Saunders.
Rings, D. M., Welker, F. H., Hull, B. L., Kersting, K. W., Hoffsis, G. F. 1984, Dec 15. Abomasal emptying defect in Suffolk sheep. J Am Vet Med Assoc. 185(12): 1520-22.
Ruegg, P. L., George, L. W., East, N. E. 1988, Dec 15. Abomasal dilatation and emptying defect in a flock of Suffolk ewes. J Am Vet Med Assoc. 193(12): 1534-36.
Author: James P. Reynolds

ABOMASAL ULCERS
BASICS DEFINITION

Damage to the abomasal mucosa continuing from erosion through complete perforation. Often subclinical but may be clinical.
Classified as type I (nonperforating ulcers), type II (nonperforating with severe blood loss), type III (perforating with localized peritonitis), and type IV (perforating with diffuse peritonitis).
Clinical signs associated with abdominal pain, blood loss, and peritonitis. Causes are not known, but may be associated with stress. Not associated with particular abomasal bacterial infections.
PATHOPHYS IOLOGY
Injuries to the protective mucosal layer allow acid and pepsin to diffuse into the mucosa.
Type I nonperforating ulcers have incomplete penetration, little local reaction, and minimal bleeding.
Type II bleeding ulcers erode into a major blood vessel in the submucosa. There may be distension of the abomasum and reflux of abomasal contents into the rumen. There is usually melena.
Type III ulcers completely perforate the wall with leakage of fluid and local peritonitis. Adhesions form to viscera localizing the peritonitis.
Type IV ulcers perforate completely and the subsequent fluid leakage is not contained by adhesions, resulting in generalized peritonitis.
SYSTEMS AFFECTED
Gastrointestinal
GENETICS
N/A
INCIDENCE/PREVALENCE
Low, less than 1 or 2%. May be higher in some types of calf-raising systems.
GEOGRAPHIC DISTRIBUTION
N/A
Epidemiology
Has been associated with physical irritation from straw in veal calves and high-grain diets in feedlot cattle
May be related to postpartum conditions in dairy cattle; not definitively associated with bacteria such as clostridia, salmonella, or helicobacter
No association with hairballs in veal calves
SIGNALMENT
Species Affected
Bovine
Breed Predilections
N/A
Mean Age and Range Occurs in calves and adults Predominant Sex
N/A
SIGNS
Anorexia, depression, pyrexia, abdominal pain, abdominal distension, melena, blanched mucous membranes. Peracute death common in adult cattle but not calves.
GENERALCOMMENTS
N/A
HISTORICALFINDINGS
Changes in feeding, such as transition from milk to solid feed in calves or high roughage prepartum to high concentrate postpartum diets may be involved.
PHYSICALEXAMINATION FINDINGS
Melena or occult blood in feces; possible distension of abomasum detected by ballottement of ventral right abdomen; blanched mucous membranes (pallor) in cases with severe blood loss; painful abdomen
Peritoneal emphysema may be detected during rectal exam.
CAUSES
Unknown in many cases, but can be related to feeds that irritate the abomasal mucosa, such as straw or almond hulls
RISK FACTORS
Sudden transition from milk diet to dry feed in calves, straw feeding in milk-fed calves, possibly high-concentrate diets
DIAGNOSIS DIFFERENTIALDIAGNOSIS
Lymphoma, left displaced abomasum, abomasal volvulus or torsion, duodenal ulcers, hemorrhagic bowel syndrome
CBC/BIOCHEMISTRY/URINALYS IS
Acute hemorrhagic anemia in cases of severe gastric hemorrhage
OTHER LABORATORY TESTS
Abdominocentesis may identify abomasal fluid in abdomen in some cases. Testing for occult blood in feces may detect blood in feces before melena is seen.
IMAGING
Ultrasonography may show free fluid in abdomen.
OTHER DIAGNOSTIC PROCEDURES
Exploratory surgery
GROSS AND HISTOPATHOLOGIC FINDINGS
Ulcers are most commonly found along the greater curvature and usually in the fundic area. Ulcers can be a few millimeters to several centimeters in size. They are often filled with debris or clotted blood. Perforating ulcers are usually adhered to the omentum.
Cattle with type IV ulcers have abomasal fluid in the abdominal cavity and may have fibrinous peritonitis.
TREATMENT
Usually unrewarding. Antacids may protect the abomasal mucosa.
Transfusions may be beneficial if bleeding stops or is controlled.
Surgical correction of perforated ulcers for valuable cattle
Inpatient Versus Outpatient
The opportunity for successful surgical correction and adequate transfusion is greater in clinic than on farm.
CLIENT EDUCATION
Gradual introduction of dry feed to calves is preferred to abrupt exposure to dry feed during the milk-fed period.
MEDICATIONS DRUGS OF CHOICE
Antacids such as magnesium oxide (500 g/400 kg body weight daily for 2 to 4 days) has been suggested.
Per os kaolin and pectin mixture (2 to 3 liters twice daily to mature cattle) has been suggested.
CONTRAINDICATIONS
NSAIDs that interfere with the production of prostaglandin E series via the arachadonic acid cascade are not recommended because the prostaglandins are important to the protective coating of the abomasal mucosa.
PRECAUTIONS
N/A
POSSIBLE INTERACTIONS
N/A
ALTERNATE DRUGS
N/A
FOLLOW-UP PATIENT MONITORING
CBC, anemia, pain
PREVENTION/AVOIDANCE
Gradually introduce dry feed to calves
POSSIBLE COMPLICATIONS
Peritonitis
EXPECTED COURSE AND PROGNOSIS
Recovery for type I and type III ulcers; death from type II if severe hemorrhage; death from type IV
MISCELLANEOUS PREVENTION
Avoid rapid change from liquid to dry feed in calves, avoid excessive concentrate diets in feedlot or dairy cattle.
ASSOCIATED CONDITIONS
Lymphoma
AGE-RELATED FACTORS
Affects all ages
ZOONOTIC POTENTIAL
N/A
PREGNANCY
N/A
SYNONYMS
N/A
SEE ALSO
Abomasal volvulus or torsion Duodenal ulcers
Hemorrhagic bowel syndrome
Left displaced abomasum Lymphoma ABBREVIATIONS
NSAIDs = nonsteroidal anti-inflammatory drugs
Suggested Reading
Braun, U., Bretscher, R., Gerber, D. 1991. Bleeding abomasal ulcers in dairy cows. Veterinary Record 129(13): 279-84.
Jelinski, M. D., Ribble, C. S., Campbell, J. R., Janzen, E. D. 1996. Investigating the relationship between abomasal hairballs and perforating abomasal ulcers in unweaned calves. Canadian Veterinarian Journal 37(1): 23-26.
Jelinski, M. D., Ribble, C. S., Chirino-Trejo, M., Clark, E. G., Janzen, E. D. 1995. The relationship between the presence of Helicobacter pylori, Clostridia perfringens type A, Campylobacter spp., or fungi and fatal abomasal ulcers in unweaned beef calves. Canadian Veterinarian Journal 36(6): 379-82.
Palmer, J. E., Whitlock, R. H. 1983. Bleeding abomasal ulcers in adult dairy cows. Journal of the American Medical Association 183(4): 448-51.
Palmer, J. E., Whitlock, R. H. 1984. Perforated abomasal ulcers in adult dairy cows. Journal of the American Medical Association 184(2): 171-74.
Radostits, O. M., Gay, C. C., Blood, D. C., Hinchcliff, K. W., eds. 2000. Veterinary medicine: a textbook of diseases of cattle, sheep, pigs, goats and horses. 9th ed. London: W. B. Saunders.
Author: James P. Reynolds

ABORTION
BASICS DEFINITION
Loss of the fetus from 60 days to term. Prior to 60 days is considered embryonic mortality.
PATHOPHYS IOLOGY

Camelids rely primarily on the corpus luteum for production of progesterone and maintenance of pregnancy for the entire gestation.
Maintenance of the corpus luteum requires normal pregnancy recognition and establishment of placentation.
Abortion is caused by any factor that acts directly or indirectly on the corpus luteum to cause luteolysis:
Treatment with prostaglandin F2 alpha
Inflammatory or febrile affection
Endotoxemia
Stress such as heat stress, transport
Debilitating diseases
Abortion can be caused by factors that compromise fetal viability or placental integrity:
Placentitis
Placental insufficiency (endometrial fibrosis, uterine capacity in maiden females, twining)
Direct insult to the fetus (mechanical or infectious)
Fetal malformation/abnormal pregnancy
Hormonal insufficiency or unbalance
SYSTEMS AFFECTED
Reproductive-potentially all systems may be affected depending on the condition.
GENETICS
N/A
INCIDENCE/PREVALENCE
Pregnancy loss ranges from 2% to 17%.
Losses of up to 60% may be experienced in some leptospirosis outbreaks.
Loss of 40-50% has been reported in maiden females under some management systems.
GEOGRAPHIC DISTRIBUTION
Potentially worldwide depending on camelid species and environment
SIGNALMENT
Species
Potentially all camelid species
Breed Predilections
N/A
Mean Age and Range
N/A Predominant Sex Female
SIGNS
Historical Findings
Return to receptivity after confirmation of pregnancy
Bloody or mucopurulent vaginal discharge
Protrusion of the placenta or fetus
Premature development of the mammary gland and lactation
PHYSICALEXAMINATION FINDINGS
History
A complete history should be taken from each aborting case and include the following:

Age of the aborting animal
Breeding technique
Individual cases vs. outbreak
Reproductive history
Stage of pregnancy
Treatments and vaccination in the last 2 weeks
Animal movement in the last month
Feeding management
Layout of the facilities, proximity to stagnant waters, runoffs from dairy or swine operations
Contact with wildlife, feral cats
Clinical Examination of the Dam
Body condition score Physical examination (TPR) Demeanor
Transabdominal ultrasound Vaginal examination
Uterine biopsy may be indicated in some cases.
Serology
Samples should be taken from: Fetus (cardiac blood)
Aborting dam (paired samples) at abortion and 2 to 3 weeks later At-risk females in face of an outbreak
Bacteriology
Samples should be taken from: Fetus-stomach content, fetal fluids Dam-vaginal discharge, uterine swab Placenta
Necropsy/Histopathology

Fetal necropsy
Measurement of the crown-rump length
External evaluation of the fetus for developmental abnormalities or lesions Internal evaluation of the fetus
Samples from liver, brain, spleen, kidney, stomach and lungs should be submitted fresh or fixed
Placenta
External examination of the chorionic surface for signs suggesting insufficient development or lack of villi Examination for signs of placentitis
Examination for developmental abnormalities or lesions of the umbilical cord
Hormone Assays
In habitual aborters, progesterone determination during pregnancy may be indicative of possible luteal insufficiency. Pregnant females with progesterone levels below 2 ng/ml should be considered suspicious. However, some females may be able to carry to term even if progesterone level is between 1.5 and 2 ng/ml.
CAUSES AND RISK FACTORS
DIAGNOSIS DIFFERENTIALDIAGNOSIS
Infectious Causes of Abortion
Brucellosis (B. meletensis in alpacas and llamas, B. abortus in camels) Listeriosis
Chlamydiosis Toxoplasmosis Leptospirosis Trypanosomiasis (in camels)
Hemorrhagic disease (Bacillus cereus, in camels)
Noninfectious Causes of Abortion
Administration of PGF2-alpha Trauma: Breeding during pregnancy Administration of corticosteroids (last trimester of pregnancy particularly, even topical corticosteroids may cause abortion) Progesterone insufficiency Hormonal imbalances, adrenal gland dysfunction particularly in fiber-producing animals Some vaccines (Some vaccines have been associated with abortion) Nutritional deficiencies Toxic plants anecdotal; no precise information
CBC/BIOCHEMISTRY/URINALYS IS
May be indicated depending on disease condition
OTHER LABORATORY TESTS
See diagnosis above.
IMAGING
Ultrasound may be a helpful adjunct. OTHER DIAGNOSTIC PROCEDURES PATHOLOGIC FINDINGS
TREATMENT
Abortion due to luteal insufficiency Requires progesterone supplementation
Anecdotal reports of successful maintenance of pregnancy by administration of progestogens in oil (150 mg to 500 mg every week or every other week until 2 weeks before due date), Norgestomet implants weekly or biweekly
The author’s observation is that natural progesterone (50 to 100 mg daily or long acting 500 to 1000 mg every week) is the most helpful in these cases if they can be diagnosed accurately. Fetal viability should be monitored regularly if these treatments are implemented.
Placental insufficiency
Early diagnosis and termination of twins
Early diagnosis and treatment of uterine infection
Early diagnosis of uterine fibrosis (uterine biopsy) and sexual rest
Adequate breeding management of young females (should be at least 15 months old and 65% of adult weight)
Drug induced
Avoid use in animals that may be pregnant:
Prostaglandin F2 alpha or analogues, ecbolics, corticosteroids, multivalent clostridial vaccines Cautious use in animals that may be pregnant: Anesthetics, organophosphates
ACTIVITY
N/A
DIET
N/A
CLIENT EDUCATION
N/A
MEDICATIONS
N/A
DRUGS OF CHOICE
N/A
CONTRAINDICATIONS
Appropriate milk and meat withdrawal times must be followed for all compounds administered to food-producing animals.
PREVENTION/AVOIDANCE
Observe strict hygiene in breeding management and during parturition.
Setup guideline for biosecurity-quarantine new animals; during movement of animals between shows and ranch, visiting animals for breeding.
Vaccination for leptospirosis (four times a year in high risk areas)
POSSIBLE COMPLICATIONS
N/A
EXPECTED COURSE AND PROGNOSIS
See specific disease/condition.
MISCELLANEOUS ASSOCIATED CONDITIONS
N/A
AGE-RELATED FACTORS
N/A
ZOONOTIC POTENTIAL
Brucellosis (B. meletensis in alpacas and llamas, B. abortus in camels)
BIOSECURITY
Set up guideline for biosecurity-quarantine new animals; during movement of animals between shows and ranch, visiting animals for breeding.
PRODUCTION MANAGEMENT
N/A
SYNONYMS
N/A
SEE ALSO
Brucellosis (B. meletensis in alpacas and llamas, B. abortus in camels) Chlamydiosis
Hemorrhagic disease (Bacillus cereus, in camels) Leptospirosis
Listeriosis
Nutritional deficiencies
Toxic plants anecdotal no precise information Toxoplasmosis
Trypanosomiasis (in camels)
ABBREVIATIONS
PGF2-alpha = prostaglandin F2 alpha
TPR = temperature, pulse, and respiration
Suggested Reading
Gidlewski, T., Cheville, N. F., Rhyan, J. C., Miller, L. D., Gilsdorf, M. J. 2000, Jan. Experimental Brucella abortus
induced abortion in a llama: pathologic effects. Vet Pathol. 37(1):77-82.
Gilsdorf, M. J., Thoen, C. O., Temple, R. M., Gidlewski, T., Ewalt, D., Martin, B., Henneger, S. B. 2001, July. Experimental exposure of llamas (Lama glama) to Brucella abortus: humoral antibody response. Vet Microbiol. 3. 81(1):85-91.
Johnson, L. W. 1993. Abortion in llamas. Veterinary Clinics of North America Food Animal 10(2): 541-44. McLaughlin, B. G., Greer, S. C., Singh, S. 1993, Jan. Listerial abortion in a llama. J Vet Diagn Invest. 5(1):105-6.
Smith, B. B., Timm, K. I., Reed, P. J., Christensen, M. 2000, Aug. Use of cloprostenol as an abortifacient in the llama (Lama glama). Theriogenology 54(3): 497-505.
Tibary, A., Anouassi, A. Reproductive disorders in the female camelidae. In: Theriogenology in Camelidae: anatomy, physiology, pathology and artificial breeding, pp. 355-57. Actes Edition, Institut Agronomique et Veterinaire Hassan II, Morocco.
Author: Ahmed Tibary

ABORTION: BACTERIAL
BASICS OVERVIEW

Many species of bacteria may cause septicemia and/or localized lesions in adult cattle with a subsequent abortion. These agents usually cause sporadic abortions.
The route of infection is usually hematogenous rather than ascending as interruption of the cervical seal occurs less often in cows than in mares. Often, cows may be predisposed to abortion by these bacteria by some immunosuppressive condition such as bovine virus diarrhea (BVD).
Two categories of bacterial abortion: (1) ubiquitous environmental organisms: A. pyogenes, E. coli, Bacillus spp.,
Streptococcus spp.; (2) abortion secondary to specific disease: Pasteurella spp., Salmonella spp., Haemophilus somnus
SYSTEMS AFFECTED
Reproductive
GENETICS
N/A
INCIDENCE/PREVALENCE
Cattle
In a 10-year survey, specimens from 8995 bovine abortions and stillbirths were evaluated for bacteria. Bacteria were determined to be the cause of 1299 (14.49%) of the presenting abortion cases.
The five bacteria most commonly associated with bovine abortion or stillbirth were Actinomyces pyogenes, 378 (4.22%); Bacillus spp., 321 (3.58%); Listeria spp., 121 (1.35%); Escherichia coli, 98 (1.09%); and Leptospira interrogans, 79 (0.88%). Twelve other genera of bacteria were associated with > or = 10 abortions or stillbirths, and 12 more species were associated with < or = 10 abortions or stillbirths.
The diagnostic success for determining the cause of abortions may be low (25%-40%).
Sheep
In a similar 10-year study, 1799 accessions of ovine abortions and stillbirths were evaluated for bacteria. Etiologic diagnoses were made in 786 (44%) of the submitted cases.
Infectious agents were found responsible in 702 accessions (39%), and noninfectious causes were involved in 84 (5%). No diagnosis was made in 998 accessions (56%).
Together, Toxoplasma gondii, Campylobacter spp., and Chlamydia psittaci caused approximately 25% of all abortions and stillbirths examined.
Goats
In an 8-year study of 217 caprine abortions, infectious agents as the cause were found in 37% of the cases: bacterial agents were identified in 30.5%, viral agents in 2%, fungal agents in 0.5%, and protozoal agents in 4% of the cases submitted.
The most common causes of abortions were Chlamydia psittaci and Coxiella burnetii infection, which accounted for 23% of all goat abortions. Mineral deficiencies were observed in 4%, fetal anomalies accounted for 3%, and leukoencephalomalacia of the brain (probable oxygen deprivation) accounted for 3% of the submissions. No diagnosis was made in 112 of the 211 submissions (53%). No lesions were noted in 104 of the submissions (49%).
GEOGRAPHIC DISTRIBUTION
Worldwide depending on environment
Epidemiology
In a study of 58,048 pregnancies from 111 herds, the respective abortion density, proportion of aborted cows, and abortions per confirmed pregnancy were 4.2%, 5.9%, and 10.2%. Heifers had the lowest, and cows of second parity the greatest risk of fetal death. The greatest risk of fetal death was observed in the first, and the lowest in the second trimesters of pregnancy. Respective proportions of aborted cows with and without a previous abortion were 17.5% and 5.9%. Odds of aborting after twinning in multiparous cows in this study were 1.3 times greater than for those having a single calf. Risk of abortion in the autumn and early winter was greater than that in the summer months.
SIGNALMENT
Species
All ruminant species Breed Predilections N/A
Mean Age and Range
N/A Predominant Sex Female
DIAGNOSIS
See under specific microbial cause below.
TREATMENT
See under specific microbial cause below.
MEDICATIONS
See under specific microbial cause below.
CONTRAINDICATIONS
Appropriate milk and meat withdrawal times must be followed for all compounds administered to food-producing animals.
FOLLOW-UP
See under specific microbial cause below.
MISCELLANEOUS
Common microbial causes of abortion:
Arcanobacteriosis
Arcanobacterium pyogenes (A. pyogenes, formerly Actinomyces or Corynebacterium) is the bacterium most frequently isolated from bovine abortions.
It is a common inhabitant of the nasal, conjunctival, vaginal, and preputial mucosa of normal animals. The organism may reach the uterus by a hematogenous route, resulting in sporadic abortions.
Diagnosis
Culture of the organism from fetal tissue and placenta Prevention and Treatment
None
Brucellosis
Once considered the most important abortion disease of cattle, brucellosis has been nearly eradicated in North America, with the exception being some small local areas.
Brucella abortus in cattle and B. melitensis in sheep and goats are gram-negative, intracellular coccobacilli able to survive in phagocytes.
Pathogenesis
The agent is transmitted by oral route. Aborted material contains large numbers of Brucella spp. organisms and contaminates the environment. Following ingestion, the organism locates in chorioallantois and results in fetal septicemia and abortion.
Clinical Signs
Abortion occurring after the fifth month of gestation
Thick, leathery placentitis, necrosis of the cotyledon
• Cows may have retained placenta and metritis. Diagnosis
Culture of the organism from fetal tissue and uterine fluids
• Infected animals identified by serology Control
Vaccination of calves between 4 and 12 months of age
This is a reportable disease in most of North America; herds with positive testing animals are quarantined and an eradication program enforced.
Zoonosis
Human infection occurs from handling infected tissue and ingesting infected milk.
Campylobacteriosis
Bovine campylobacteriosis is primarily a venereal disease resulting in early embryonic death, repeat breeders, an extended breeding season, a high percentage of open cows at the end of the breeding season, and an extended calving season. It causes occasional abortions, usually in midgestation.
The primary cause of reproductive wastage is C. fetus ssp. venerealis. It infects the prepuce of bulls, and is transmitted to cows during breeding.
Bulls may remain infected for life or recover spontaneously. The organism survives in frozen semen if not properly treated with antibiotics.
C. fetus ssp. fetus, an inhabitant of the intestine, will occasionally spread to the uterus via a hematogenous route, resulting in abortion in cows. It is a more common cause of abortion in sheep.
C. jejuni rarely causes bovine abortion but does so in sheep. Abortion due to Campylobacter spp. occurs between 4 and 8 months gestation.
Diagnosis
Culture the organism from the prepuce of infected bulls and the anterior vagina of infected cows.
Virgin heifer mating test: culture cervicovaginal mucus 18 to 30 days postcoitus.
• Culture the organism from aborted fetal tissues, abomasal contents, and placental fluids. Treatment
Bulls-preputial lavage with antibiotics Prevention
Proper vaccination program
Proper herd management
Implement an artificial insemination program
Chlamydia
Chlamydia are obligate, intracellular organisms that multiply in the cytoplasm of eukaryotic cells.
Chlamydia psittaci is associated with reproductive wastage in cattle, sheep, and goats. In cattle it causes sporadic, late- term abortion and stillborn or weak-born calves.
Pathogenesis
Transmission is by ingestion or inhalation of contaminated material.
Persistent intestinal colonization results in sporadic placental infection.
• Possible venereal transmission Diagnosis
Necrotizing placentitis
Identification of the organism in fetal liver or placenta
• Paired serum samples show a rising titer Treatment
Antibiotics (tetracycline) Zoonosis
Organisms are shed from the reproductive tract of infected animals. Pregnant women are susceptible to infection.
Epizootic Bovine Abortion (Foothills Abortion)
EBA is limited to the foothills region of central California, coinciding with the range of the tick vector Ornithodorus coriaceus, the Pajahuello tick. The cause appears to be a spirochete-like agent.
Abortion occurs in naïve cows in late gestation.
The abortion rate may be 30% to 80% in susceptible cows.
• Native cows from enzootic areas do not abort. Treatment and Control
Chlortetracycline (2-5 g/day in feed) will reduce the abortion rate.
Exposure of susceptible animals to the tick before breeding
Fall calving to avoid exposure of pregnant cows to the tick
Haemophilosis
The importance of Haemophilus somnus as a cause of abortion and infertility is controversial. It is a normal inhabitant of the male and female reproductive tract but may be a minor cause of pregnancy loss.
Pure culture of H. somnus, in the absence of other organisms, may indicate this diagnosis.
Treatment with antibiotics will reduce infection and a vaccination program may be beneficial.
Leptospirosis
Leptospires are motile, helical spirochetes. Infection occurs by penetration of the nasal, ocular, genital, or intestinal mucosa. The organism can survive outside the host in moist, warm environments with a neutral to slightly basic pH.
Direct transmission occurs by contact with infected urine, infected tissue, and fluids following abortion and sexual transmission.
• Indirect transmission occurs from contact with a contaminated environment. Pathogenesis
Leptospires localize in the proximal renal tubules and reproductive tract of cows and bulls.
• Organisms are shed in the urine and intermittent leptospiruria may persist for the lifetime of the animal. Clinical Signs
May include hemolytic anemia, hemoglobinuria, hepatorenal disease, abortion, and photosensitization.
Abortion occurs 4 to 12 weeks following infection.
Abortion due to L. interrogans serovar hardjo occurs throughout gestation due to serovar pomona usually in the last trimester.
Diagnosis
Isolation of leptospires from fetal tissue such as kidney, urine, thoracic fluid, and aqueous humor. The organism does not survive well in the autolyzed fetus.
Culture of the organism from cow’s urine
Immunofluorescent staining of fetal kidney
• Serologic testing Control
Vaccination programs
• Environmental cleanup, control population of wild animals and rodents that contaminate the environment Treatment
Antibiotics (oxytetracycline or streptomycin) Zoonosis
An important zoonotic potential
Listeriosis
Listeria monocytogenes causes encephalitis, abortion, and neonatal septicemia.
Infected cows often have fever and anorexia prior to aborting, with postparturient complications including retained placenta, pyometra septicemia, and occasionally death. Central nervous system signs seldom occur simultaneous with abortions.
Organism ubiquitous in soil, vegetation, water, feces.
Exposure often from spoiled silage
More common in winter
Usually sporadic, occasionally in outbreak form
• Organism has a predilection for fetoplacental tissues resulting in placentitis and fetal septicemia. Abortion
Usually last trimester
• Fetus autolyzed when expelled Diagnosis
Culture of organism from fetal tissues and stomach contents, placenta, uterine fluids
• Culture from feces of infected animals Control
Avoid feeding spoiled silage and other contaminated feed
• Aborted tissues source of contamination to herd mates Zoonosis
Important zoonotic potential, especially in pregnant women
Neosporosis
Neosporosis is caused by the protozoan Neosporum caninum. It has worldwide distribution. Dogs are identified as the intermediate host.
• Abortion usually occurs during the second trimester but may occur throughout gestation. Clinical Signs
Infected cows show no clinical signs.
• Infected calves may be born prematurely and exhibit neurological signs. Pathophysiology
The route of infection is vertical transmission with congenital infection occurring in 80% of seropositive cows.
Seropositive cows are more likely to abort than seronegative herd mates.
• Repeat abortions occur following recrudescence of latent infections or following a new infection. Diagnosis
Observation of characteristic histological lesions or identification of the parasite in fetal tissue, especially brain, heart, liver, and skeletal muscle
Fetal serology if abortion occurs after 5 months gestation
• Serologic testing of cows Control and Prevention
Prevention of postnatal transmission, possibly feed contamination by feces of infected dogs
Removal of seropositive cows from the herd
Embryo transfer to break the vertical transmission cycle
A vaccine is available.
Trichomoniasis
Trichomoniasis is a venereal disease caused by the protozoan Tritrichomonas foetus. Infection is demonstrated as early embryonic death, repeat breeders, an extended breeding season, a high percentage of open cows at the end of the breeding season, and an extended calving season.
• It causes occasional abortions, usually in the first half of gestation. Diagnosis
Bulls-identification and culture of the organism from preputial smegma
Cows-identification and culture of the organism from cervicovaginal mucus and uterine contents in pyometra cases
Virgin heifer mating test-culture cervicovaginal mucus 12 to 19 days postcoitus
• Culture the organism from aborted fetal tissues and fluids. Prevention
Proper vaccination program
Proper herd management
Implementation of artificial insemination program
Ureaplasmosis
Ureaplasma diversum is a normal inhabitant of the reproductive tract of cows and bulls. In clinical conditions, it may result in granular vulvitis in cows.
If artificial insemination does not include a guarded, double rod technique, the organism may be carried into the uterus, resulting in early embryonic death or abortion. Abortion is usually sporadic.
Diagnosis
Culture of the organism from fetal tissue Treatment and Control
Proper insemination technique
Postbreeding infusion of tetracycline
ASSOCIATED CONDITIONS
N/A
AGE-RELATED FACTORS
Heifers had the lowest risk, and cows of second parity the greatest risk of fetal death.
ZOONOTIC POTENTIAL
Brucellosis, chlamydiosis, listeriosis, leptospirosis, and Coxiella burnetii are all potential zoonotic agents.
PREGNANCY
The greatest risk of fetal death was observed in the first, and the lowest in the second trimesters of pregnancy.
RUMINANT SPECIES AFFECTED
Potentially, all ruminant species are affected.
BIOSECURITY
N/A
PRODUCTION MANAGEMENT
N/A
SYNONYMS
N/A
SEE ALSO
Diagnostic testing
Reproductive pharmacology
Serology
• Specific abortive disease agents ABBREVIATIONS
BVD = bovine viral diarrhea
EBA = epizootic bovine abortion
Suggested Reading
Alexander, A. V., Walker, R. L., Johnson, B. J., Charlton, B. R., Woods, L. W. 1992, Mar 1. Bovine abortions attributable to
Listeria ivanovii: four cases (1988-1990). J Am Vet Med Assoc. 200(5):711-14.
Barr, B. C., Anderson, M. L. 1993, Jul. Infectious diseases causing bovine abortion and fetal loss. Vet Clin North Am Food Anim Pract. 9(2):343-68.
Dubey, J. P., Lindsay, D. S. 1993, Dec. Neosporosis. Parasitol Today 9(12):452-58. Ellis, W. A. 1994, Nov. Leptospirosis as a cause of reproductive failure. Vet Clin North Am Food Anim Pract. 10(3):463-78.
Hassig, M., Lubsen, J. 1998, Sep. Relationship between abortions and seroprevalences to selected infectious agents in dairy cows. Zentralbl Veterinarmed B. 45(7):435-41.
Kirkbride, C. A. 1993, Jul. Diagnoses in 1,784 ovine abortions and stillbirths. JVet Diagn Invest. 5(3):398-402.
Kirkbride, C. A. 1993. Bacterial agents detected in a 10 year study of bovine abortions and stillbirths. J. Vet Diagn Invest. 5:63-68.
Mickelsen, W. D., Evermann, J. F. 1994, Mar. In utero infections responsible for abortion, stillbirth, and birth of weak calves in beef cows. Vet Clin North Am Food Anim Pract. 10(1):1-14.
Moeller, R. B., Jr. 2001, May. Causes of caprine abortion: diagnostic assessment of 211 cases (1991-1998). J Vet Diagn Invest. 13(3):265-70.
Seguin, B., Troedsson, M. 2002. Diseases of the reproductive system. In: Large animal internal medicine, ed. B. P. Smith. St. Louis: Mosby.
Smyth, J. A., Fitzpatrick, D. A., Ellis, W. A. 1999, Nov 6. Stillbirth/perinatal weak calf syndrome: a study of calves infected with Leptospira. Vet Rec. 145(19):539-42.
Authors: Walter Johnson and Alex Estrada

ABORTION: FARMED CERVIDAE
BASICS DEFINITION
Loss of a fetus
Further Definitions

Calf-cervid less than 1 year of age
Hind-adult female cervid
Stag-adult male cervid
PATHOPHYS IOLOGY
The fetus may die due to a genetic or congenital abnormality.
Infectious organisms may invade the fetus and lead to fetal death.
Abnormalities or infections of the placenta or uterus may lead to placental separation, fetal death, and reabsorption or expulsion.
Trauma, toxins, infections, malnutrition, metabolic disease, drugs, or other stress incurred by the hind may lead to fetal stress and abortion. Abnormalities of the hind’s reproductive or endocrine system may lead to abortion.
SYSTEMS AFFECTED
Reproductive; other systems may be involved depending upon the underlying etiology of the abortion. The clinician may need to monitor other body systems for complications secondary to abortion.
GENETICS
N/A
INCIDENCE/PREVALANCE
The incidence of embryonic mortality in farmed deer is relatively low. Insufficient data available for other species.
GEOGRAPHIC DISTRIBUTION
N/A
SIGNALMENT
Species
Depends upon underlying cause. Some cervids are more susceptible to infectious disease than others. When red deer hinds (Cervus elaphus) are crossbred with wapiti stags, there is a greater risk for dystocia and subsequent fetal death.
Mean Age and Range
First calving wapiti (Cervus elaphus) are more likely to deliver nonviable calves than are adults. Also, 2-year-old elk, fallow (Dama dama), and red deer have lower calving rates than mature animals.
Predominant Sex Female only SIGNS
HISTORICALFINDINGS
May be none evident, especially if the fetus is reabsorbed early in gestation
Estrus detected on a hind previously diagnosed as pregnant
Failure to produce an offspring (missed due date)
Restlessness, solitude-seeking behavior, pacing, abdominal straining, and other signs of imminent parturition
Discovery of expulsed fetus
PHYSICALEXAMINATION FINDINGS
May be none-fetal resorption early in gestation may have no visible signs. Hinds that were previously diagnosed as pregnant will later be found to be nonpregnant. If rectal palpation is done (in wapiti), the previously pregnant horn will cease to be enlarged. There will no longer be a fetal membrane slip.
Late-term abortions in cervids living in large enclosures or parks may occur unobserved as the female usually eats the placenta and the dead fetus is consumed by predators.
When clinical signs are present, they include:
Bloody or purulent vaginal discharge
Visibly expulsed fetus and/or placenta
Premature udder development and dripping
If abortion is due to systemic disease, may see other nonspecific signs of illness such as depression, dehydration, pyrexia, anorexia, and weight loss.
Brucellosis-induced abortion in female reindeer (Rangifer tarandus) is characterized by a retained placenta and metritis.
CAUSES
Degenerative
Anatomic/Congenital
Congenital abnormalities may lead to fetal death.
Metabolic
Febrile or severely stressed animals may abort.
Nutritional
Inadequate nutrition-may cause a fetus to die or be born underweight and nonviable
Iodine deficiency-may be caused by insufficient dietary intake, or be secondary to excessive calcium in the diet, overingestion of toxic plants such as Brassica spp., gross bacterial contamination of the feed, continuous intake of feeds containing cyanogenetic glucosides (i.e., white clover), or due to ingestion of canola (rapeseed and canola meal). An iodine deficiency can lead to goiter, prolonged gestation, and an increased incidence of stillbirth.
Infectious
Bacterial
Brucella abortus
Brucella suis type 4-most common cause of abortion in reindeer and caribou
Leptospirosis-serovars found in North American cervids include L. pomona,
L. grippotyphosa, L. canicola, and L. pyogenes. Leptospira pomona is believed to cause abortions in free-ranging white-tailed deer (Odocoileus virginianus) and red deer.
Experimental infections in white-tailed deer have produced abortions, anorexia, fever, and death.
Listeriosis-the septicemic form causes placentitis and endometritis leading to abortion in late-term pregnancy as well as the birth of weak, full-term young.
Fungal
Incidence of fungal infections in farmed wapiti and red deer is rare. However, fungal infections can cause abortions in other ruminant species. Therefore, it should not be excluded.
Parasitic
Toxoplasmosis-wapiti and red deer appear to be less susceptible to toxoplasmosis than other cervidae species.
Viral
Bluetongue (orbivirus)-abortion and congenital deformities have been seen in white-tailed deer, but bluetongue has not been reported to cause serious clinical disease in wapiti or red deer.
Bovine viral diarrhea virus-BVDV has not been reported as a clinical entity in wapiti or red deer, but virus has been isolated from red, fallow, and roe deer. Serological evidence of infection has been demonstrated in mule (Odocoileus hemionus), white-tailed deer, fallow deer, moose (Alces alces), and a Chinese water deer (Hydroptes inermis). Almost all of the reported BVD-related cervid cases involve a free-ranging animal, which makes it difficult to find aborted fetuses. Experimentally, BVDV isolated from a dead deer did cause stillborn fawns and mummified fetuses when injected into pregnant penned deer.
Traumatic
Congenital abnormalities, fetal oversize, or abnormalities of presentation at time of parturition may lead to dystocia and subsequent fetal death.
Toxic
Locoweed causes abortions in sheep and cattle and may be a problem for cervidae as well.
Drugs
Prostaglandin F2 alpha has been used to induce abortion in wapiti but is probably ineffective if given less than 10 days after breeding. Prostaglandins also can cause luteolysis in reindeer.
RISK FACTORS
Febrile or severely stressed animals may abort. The most common stressors for cervidae are severe weather, inadequate nutrition, recent capture or transport, and concurrent disease. It would also be wise to avoid the use of products that are known abortifacients in other ruminant species.
DIAGNOSIS DIFFERENTIALDIAGNOSIS
Other causes of vaginal discharge
Normal term parturition
Vaginitis
Pyometra
Metritis
Uterine trauma or hemorrhage
Uterine or vaginal neoplasia
Other reasons for failure to deliver on due date
Infertility (animal never became pregnant)
Incorrect due date
Other causes of abdominal straining/discomfort such as colic
CBC/BIOCHEMISTRY/URINALYS IS
May be normal. It may also indicate systemic disease.
OTHER LABORATORY TESTS
Maternal Pregnancy Specific Protein B (PSPB)
Bovine pregnancy specific protein B antibody cross reacts with caribou, red, fallow, and white-tailed deer PSPB. Hence, the PSPB radioimmunoassay developed for domestic cattle can be used for pregnancy monitoring in some cervids. It is as effective as ultrasound in diagnosing the pregnant hind. In red and fallow deer, PSPB is present by 33 days after conception. It is nondetectable in open hinds.
Serum Progesterone Levels (P4)
Serum progesterone concentrations rise during pregnancy, but they also rise during the estrus cycle. Serial measurements can be done during the breeding season to determine if an animal is pregnant or in estrus. Otherwise, one can wait until the breeding season is over. A decrease in P4 levels in a previously pregnant animal suggests early embryonic loss.
Fecal Progesterone Levels
Reserved for use in free-ranging populations. This can be used for detecting pregnancy in elk during mid to late gestation. Several factors may influence fecal P4 excretion and therefore make this test less reliable.
Urinary PDG (pregnanediol-3alpha-glucuronide)
The simultaneous evaluation of urinary PdG and urinary estrogen conjugates was effective for estimating and tracking pregnancy stage in Pere David’s deer. PdG excretions decreased to nadir concentrations between 1 and 2 weeks before abortion in the two hinds that aborted.
Paired Serology
To test for infectious disease
Testing Procedures for Specific Diseases
Bacterial
Brucellosis-There are five serological tests available: complement fixation, tube agglutination, rapid card, buffered plate, and ELISA.
Leptospirosis
Paired serology
Dark field microscopy of the urine or aqueous humor on dead deer
ELISA test may become available.
Listeriosis-Serological tests, but high number of false negatives occur
Viral
Bluetongue serological tests include ELISA, immunodiffusion, radioimmunoassay, hemolysis-in-gel assay, and a genetic probe for detection of bluetongue viral DNA in fluids and tissues.
Bovine viral diarrhea virus
Virus isolation from blood or nasal secretions
IFA or immunohistochemistry
ELISA
Paired serology (VN)
Protozoal: Toxoplasmosis
Sabin-Feldman dye test (DT)
Hemagglutination test (HA), may not be reliable for red deer.
Direct agglutination
IMAGING
Transrectal Ultrasound
Most practical method for diagnosing pregnancy in farmed deer
Restraint in a crush is preferable, but manual restraint may work for some animals and handlers. In wapiti and red deer, the best time for pregnancy diagnosis is between 35 and 60 days gestation. This technique can be used as early as 33-35 days gestation in fallow deer.
Transabdominal Ultrasonography To evaluate the fetus later in gestation Radiographs
May be more practical for the smaller cervidae species
DIAGNOSTIC PROCEDURES
Bacterial culture and histological examination of the fetal, placental fluid and placental tissues. It may be difficult to obtain the placenta as the female usually ingests it. Also, secondary bacterial overgrowth is likely to occur prior to sample collection.
Bacterial
Brucellosis
Bacterial isolation of Brucella spp. provides the only definitive diagnosis of this disease (caution: zoonotic risk, so wear gloves).
If index of suspicion is high, owner may elect to sacrifice the mother for culture of her major body lymph nodes and organs.
Listeriosis-isolation of Listeria spp.
Leptospirosis-can be isolated from urine or kidney cultures. If the hind has any swollen joints, these should also be cultured.
Fungal
Specific diagnosis may require culture of the organism.
PATHOLOGIC FINDINGS
Depends upon etiology
Bacterial
Brucellosis-necrotizing placentitis characterized by a thickened placenta covered with a purulent exudate
Listeriosis-in animals that abort, placentitis and endometritis occur.
Fungal
Gross pathology reveals discreet granulomas and raised circular areas on affected organs. Histopathology shows pyogenic inflammatory reaction, fungal hyphae.
TREATMENT APPROPRIATE HEALTH CARE
Depends upon underlying etiology-see specific disease chapter.
None may be warranted
Make appropriate changes in husbandry if condition was related to poor handling, sanitation, or malnutrition.
NURSING CARE
Supportive
ACTIVITY
N/A
DIET
If abortion was due to listeriosis or mycotoxins, make appropriate changes to silage feeding practices.
CLIENT EDUCATION
See Biosecurity and Production Management below.
SURGICALCONSIDERATIONS
Reserved for dystocias when all else has failed
MEDICATIONS DRUGS OF CHOICE
Dependent upon underlying cause
Antibiotics may be warranted for specific bacterial diseases, metritis, toxemia, and so on.
CONTRAINDICATIONS
Appropriate milk and meat withdrawal times must be followed for all compounds administered to food-producing animals.
PRECAUTIONS
N/A
POSSIBLE INTERACTIONS
N/A
ALTERNATIVE DRUGS
N/A
FOLLOW-UP PATIENT MONITORING
Depends upon cause
PREVENTION/AVOIDANCE
Establish a good nutritional and preventative health program.
Brucellosis
A test and removal program is ideal for intensively managed deer farms. It may not be possible in game or wildlife parks to round up all animals in the herd at one time for testing. In the United States, vaccination is used in cattle under strict regulations, but it is not used in deer. There is a vaccination program in place for reindeer in Alaska. The program uses a killed, homologous vaccine in adjuvant, which provides protection for up to 4 years. Unfortunately, current testing methods cannot differentiate between vaccinated and infected animals. As such, special permission from the state veterinarian is required. A newer vaccine, strain RB51, is in use for bovidae. This vaccine does not cross-react with the test. Its efficacy in cervid species has yet to be determined. So far, experimental studies have shown that this vaccine failed to prevent abortion in elk. The best way to prevent brucellosis is to allow the introduction of only nonvaccinated, blood-test negative animals from known brucellosis-free herds.
Leptospirosis
Vaccine is available although its usage in cervidae species is extralabel in the United States.
Bluetongue
Use parasite control to decrease the number of arthropod vectors (e.g., Culicoides spp. or gnats). Vaccine is available for use in deer in affected areas, but its use would be extralabel in the United States. In endemic areas, young may obtain up to 3 months’ protection from colostral antibodies.
BVDV
Isolation of virus from nasal swabs is evidence that deer via direct contact can transmit BVDV. Therefore, fencing of adequate height and double fencing are recommended in order to prevent direct contact and disease transmission between captive and wild cervids.
POSSIBLE COMPLICATIONS
Decreased fertility
EXPECTED COURSE AND PROGNOSIS
Dependent upon underlying cause
MISCELLANEOUS ASSOCIATED CONDITIONS
Dystocia, reproduction management
AGE-RELATED FACTORS
In farmed deer herds-young females that are underweight for their age should not be subjected to the risks of pregnancy.
ZOONOTIC POTENTIAL
Brucellosis, toxoplasmosis, leptospirosis, listeriosis
PREGNANCY
N/A
RUMINANT SPECIES AFFECTED
Cervidae: wapiti (Cervus elaphus), fallow deer (Dama dama)
BIOSECURITY
Newly acquired animals should always be quarantined for a minimum of 30 days before allowing entry into the herd.
Preshipment testing for infectious diseases is advisable. Avoid purchasing animals from regions where brucellosis is endemic.
Double fences may be warranted to prevent direct contact with wildlife species.
Keeping cats and wild animals out of feed storage areas and animal enclosures will help lower the risks of infection with toxoplasmosis and leptospirosis. See specific chapters for additional measures.
PRODUCTION MANAGEMENT
In farmed animals, it is important to monitor age, weight, and previous reproductive performance of hinds within a herd in order to maximize reproductive performance and overall production capability.
Good nutrition management is mandatory. Young females that are small for their age should not be bred. If more than one animal aborts, testing of the herd for infectious diseases is advisable. Stress reduction also plays a major role in lowering the risk for disease and abortion.
Habituating animals to gates and chutes makes handling during physical exams and other routine procedures less stressful on the animals. Avoid shipping animals during insect/vector season. Last, gross and histopathologic examination should always be performed on all dead fetuses and animals whenever possible.
SYNONYMS
N/A
SEE ALSO
Brucellosis
Dystocia
ABBREVIATIONS
BVDV = bovine viral diarrhea virus
DT = Sabin-Feldman dye test
ELISA = enzyme-linked immunosorbent assay
HA = hemagglutination test
IFA = immunofluorescence antibody
PDG = pregnanediol-3alpha-glucuronide
PSPB = pregnancy specific protein B
VN = virus neutralization test
Suggested Reading
Bingham, C. M., Wilson, P. R., Dives, A. S. 1990. Real time ultrasonography for pregnancy diagnosis and estimation of fetal age in farmed red deer. Vet Rec. 126(5): 102-6.
Cook, R. C., Garrot, R. A., Irwin, L. L., Monfort, S. L. 2002. Effects of diet and body condition on fecal progestagens (P4) for detecting pregnancy in elk (Cervus elaphus) during mid to late gestation. J Wildl Dis. 38(3): 558-65.
Dieterich, R. A., Morton, J. K. 1990. Reindeer health aide manual. 2nd ed. Agricultural and Forestry Experiment Station and Cooperative Extension Service, University of Alaska Fairbanks and U.S. Dept. of Agriculture Cooperating. AFES Misc. Pub. 90-4 CES 100H-00046.
Kreeger, T. J., Cook, W. E., Edwards, W. H., Elzer, P. H., Olsen, S. C. 2002. Brucella abortus strain RB51 vaccination in elk. II. Failure of high dosage to prevent abortion. J Wildl Dis. 38(1): 27-31.
Rowell, J. E., Russell, D. E., White, R. G., Sasser, R. G. 1998. Estrous synchronization and early pregnancy. Rangifer
2000;Special Issue (12).
Van Campen, H., Ridpath, J., Williams, E., Cavender, J., Edwards, J., Smith, S., Sawyer, H. 2001. Isolation of bovine viral diarrhea virus from a free-ranging mule deer in Wyoming. J Wildl Dis. 37(2): 306-11.
Author: Melissa Weisman

ABORTION: SHEEP AND GOATS
BASICS DEFINITION

Fetal loss, fetal wastage: loss of conceptus at anytime during pregnancy
Most commonly observed in the last 2 months of pregnancy
PATHOPHYS IOLOGY
Abortion results from
Fetal death from invasion by microorganisms
Fetal expulsion subsequent to placental disease, insufficiency
Fetal expulsion following maternal compromise
Premature parturition
Fetal reabsorption, maceration, autolysis
Can be caused by a variety of infectious and noninfectious agents.
Infectious causes of abortion are the most economically significant.
Most common infectious causes are Chlamydia psittaci, Toxoplasma gondii, and Campylobacter spp., which may represent up to one-third of all cases of abortions.
Chlamydiosis is more common in goats.
Campylobacter is less common in goats in North America.
SYSTEMS AFFECTED
Reproductive
Others depending on the etiology
GENETICS
Angora goat may be a habitual aborter.
INCIDENCE/PREVALENCE
Should be less than 5% on a flock basis (less than 2% ideal)
Abortion storms may occur in the case of specific infectious diseases.
GEOGRAPHIC DISTRIBUTION
Worldwide
Some diseases processes may be regional (presence of vector).
SIGNALMENT
Nonspecific
SIGNS
Early pregnancy loss may not be detected.
Clinical signs in the aborting female vary depending on the cause.
Complications depend on cause (deterioration of health, retained placenta, metritis).
Clinical Signs in Dam
Bluetongue: febrile, swollen tongue, ear, or face; lameness; ulcerative lesions on mouth
Akabane virus disease
Campylobacteriosis: aborting goats may show diarrhea.
Chlamydia: pneumonia, keratoconjunctivitis, epididymitis, and polyarthritis; anorexia, fever, bloody vaginal discharge 2 to 3 days before abortion
Brucellosis:B. melitensis in goats causes abortion, weak kids, and mastitis. B. ovis in sheep is rarely a cause of abortion but is responsible for poor reproductive performance and in the ram contagious epididymitis.
Aborting goats may experience fever, depression, weight loss, mastitis, and lameness.
Leptospirosis: anorexia, fever, marked jaundice, hemoglobinuria, anemia, neurological signs, abortion, occasionally may be fatal
Salmonellosis: abortion, retained placenta, metritis, and various systemic signs (fever, depression, diarrhea). Mostly in overcrowded flocks
Toxoplasmosis: generally none, immunocompromised females may present a neurologic form of the disease.
Leptospirosis: septicemia, fever, decreased appetite, reduced milk production, abortion, and meningoencephalitis
Mycoplasmosis (goats): mastitis, arthritis, keratoconjunctivitis, vulvovaginitis, and abortion in the last third of pregnancy
HISTORICALFINDINGS
Introduction of new animals
Vaginal discharges
Premature udder development
Presence of fetuses
Premature/stillbirths
Increased congenital abnormalities
PHYSICALEXAMINATION FINDINGS
Vaginal edema
Vaginal discharge
Anorexia
Other signs in flock
CAUSES
Viruses
Bacteria
Rickettsia
Protozoa
Fungi
Toxins
RISK FACTORS
Lack of biosecurity measures
Vector population
Overcrowding
DIAGNOSIS
Brucellosis
Isolation: best samples are vaginal discharges and milk, stomach contents.
Indirect diagnosis: complement fixation, agglutination and precipitation tests may help identify carrier animals.
Chlamydiosis (Enzootic Abortion)
C. psittaci, gram-negative intracellular organism
Abortion and other signs
Aborting females become immune
Females infected after 100 days of pregnancy may not abort.
Diagnosis
Generalized placentitis, abortion in the last month of pregnancy, high incidence in newly infected flocks
Demonstrations of characteristic inclusion bodies on smear from cotyledons, vaginal discharge, fetal stomach content
Culture from vaginal discharge, placenta, and fetal tissue
Serology: paired samples from dam and fetal serum
ELISA or Indirect Inclusion Fluorescence Antibody tests (IIFA)
Toxoplasmosis
Goats more susceptible than sheep
Diagnosis
Cotyledons are gray-white to yellow and present small, 1-3 mm focal area of necrosis and calcification. Intercotyledonary areas are generally normal. Macroscopic lesions: 2-3 mm necrotic foci on cotyledons, intercotyledonary allantochorion are generally normal. Fetus may be mummified or decomposed; chalky white necrotic brain lesions
Samples: placenta, fetal brain, fetal fluids, maternal blood, precolostral blood
Isolation from cotyledons, brain and fetal fluids, tissues (shipped packed in ice)
Histopathology: fixed cotyledons, fetal brain
Serology: presence of antibodies in fetal fluids or precolostral serum is the preferred diagnostic technique and indicate transplacental infection.
Q Fever (Coxiella burnetti)
Placentitis, placental necrosis, thickening of the intercotyledonary areas, abortion, and stillbirth
Isolation: placenta, vaginal discharges, fetal stomach content
Demonstration of organism by Ziehl-Neelsen staining
Complement fixation: need samples from several animals
Fluorescent antibody test may be used to identify organism in frozen section of placenta.
Campylobacteriosis
Campylobacter jejuni and C. fetus; most prevalent in sheep, rare in goats
Gram-negative microaerophilic rods
Symptoms
Abortion, stillbirths, and weak lambs, retained fetal membranes
Placentitis, placental edema
Fetus: hepatomegaly, hemorrhagic liver, necrotic foci of 1-3 cm
Fetal subcutaneous edema, serosanguineous fluid in abdominal and thoracic cavity
Fetus: bronchopneumonia
Isolation and Identification
Samples: placenta and vaginal discharges, frozen fetal stomach content (-20°C)
Transport medium required
Isolation from placenta, vaginal discharge, fetal stomach contents
Histopathology: necrotic areas of the chorionic villi, arterioles, and thrombosis of the hilus of the placentomes
Salmonellosis
Salmonella abortus-ovis, S. typhinurium, S. Dublin, S. Montevideo, S. arizonae
Direct diagnosis: culture from fetal tissues taken aseptically may be preserved at -20°C; placenta and uterine discharges
Indirect diagnosis: seroagglutination
Listeriosis (Listeria monocytogenes)
Gram-positive, non-acid-fast facultative microaerophilic organisms. L. monocytogenes affects sheep and goats;L. ivanovii
affects sheep only.
Direct diagnosis: placenta, fetal liver and spleen, fetal stomach content, vaginal discharge within 48 hours of abortion. Samples may be refrigerated if not cultured immediately.
Indirect diagnosis: histopathology on placenta, fetal liver and spleen microabscesses (white pinpoint spots), and necrosis and macrophages and neutrophils infiltration. Gram stain reveals numerous gram-positive rods.
Leptospirosis
Sheep and goats are generally less susceptible to leptospirosis than other species. Goats are more susceptible than sheep.
Sheep: mostly L. hardjo sometime L. pomona, L. ballum, and L. bratislava; late-term abortion, stillbirths, and ill-thrift lambs
Affected flocks are mostly reared indoors
Agalactia
Goat: L. icterohaemorrhagiae, L. pomona, L. grippotyphosa
Clinical signs in case of acute infection
Direct diagnosis: fetal tissue, fetal fluids, and placenta
Isolation is difficult
Demonstration by dark-filed microscopy, immunofluorescence and silver stain
Indirect diagnosis: serology-macroscopic agglutination test
Border Disease
Goats are fairly resistant.
Virus isolation (buffy coat) and antigen demonstration-heparinized blood from dam or hairy shaker lambs, fetal tissue (thyroid, kidney, spleen, cerebellum, placenta), hairy shakers (thyroid, kidney, spleen, cerebellum, intestine, lymph nodes)
Histopathology: cerebellum, spinal cord
Serology: flood from dam and hairy shakers
Clinical: small cotyledon with focal necrosis, hairy shakers,
Bluetongue
Viral isolation: blood, semen, fetal brain and spleen unlikely cause of abortion in goats
Akabane Disease
Fetal malformation, positive antibody titer in live-born and aborted fetuses
Cache Valley Virus
Congenital abnormalities
Detection of antibodies in fetal fluids or precolostral serum
Mycoplasmosis
Mycoplasma abortions (M. mycoides, M. agalactia) are significant in goats.
Diagnosis: culture and serotyping of the isolate from milk, fetal fluids, and placenta
Noninfectious Causes of Abortion
Genetic (goat) may be a habitual aborter
Angora goats with fine mohair
Abortion at 100 days
Adrenal dysfunction
Energy protein deficiency
Phenothiazine and levamisole in the last 2 months of pregnancy; corticosteroids in late gestation
Prostaglandin F 2 alpha or analogues (goats)
Plants that accumulate nitrates
CBC/BIOCHEMISTRY/URINALYS IS
May be indicated if aborting dam is clinically sick
OTHER LABORATORY TESTS
Sampling is critical for the proper diagnosis of abortion.
Placenta
Ideal for the isolation of most abortion-causing agents
Ideal for identification using specific staining techniques on histological section or impression smears
For isolation: need five or six cotyledons and section of intercotyledonary spaces both from healthy appearing and diseased areas
If needed, this tissue may be rinsed with sterile saline.
For isolation: need a transport medium (i.e., viruses; Campylobacter: FBP/glycerol; Leptospirosis 100 ml extender with 1% BSA)
For histopathology: 0.5 cm section of tissue in 10% formalin 1:10
For bacteriology: impression smears
Vaginal discharges
Collect in sterile manner
Vaginal/uterine swabs
Use of specific transport medium is preferred if a specific germ is suspected.
Fetal tissues
Tissue samples from all fetal organs (spleen, liver, kidneys, brain, lymph nodes, spinal cord) should be taken in an aseptic manner immediately after abortion or death.
Handle in the same manner as for placenta.
Fetal fluids
If fetus is not autolyzed
Stomach content
Peritoneal/thoracic fluids
Blood from the cardiac cavity
Milk-Samples of milk are taken from both glands using aseptic techniques (clean the mammary gland, disinfect teats, and eliminate the first two jets).
Blood
For isolation: immediately after/during abortion
For serology: paired samples immediately after abortion and 2 to 3 weeks later
In case of an outbreak, blood should be collected from aborting females as well as from lambs/kids before colostral intake.
IMAGING
N/A
OTHER DIAGNOSTIC PROCEDURES
N/A
PATHOLOGIC FINDINGS
Abortion Associated with Deformities
Bluetongue: hydranencephaly
Akabane disease: arthrogryposis (dystocia), hydranencephaly, and mummification
Cache Valley: arthrogryposis, brachygnathia, hydranencephaly, microencephaly, spinal cord hypoplasia, and mummification
Border disease: cerebellar hypoplasia, hydranencephaly, brachygnathia, arthrogryposis. dark pigmentation of the fleece, hairy shaker
Toxic plants: lupine, skunk cabbage, locoweed, and Sudan grass
Iodine, copper, manganese deficiency
Assessing Disease Risk
Toxoplasmosis-cat population
Leptospirosis
Rodent population
Humid hot environment
Proximity to dairy and swine operation
Salmonellosis
Source of infection: bird, cattle, wildlife
Predisposing condition: overcrowding, shipping, climatic changes
Chlamydia
Infection transmission: placenta, fetal fluids
Pigeon/sparrows are reservoirs, ticks or insects may play a role.
Vaginal discharge in goat up to 2 weeks before abortion
Reservoir: young maiden females
Listeria
Organisms grow in poorly fermented silage.
Can survive in soil and feces for extended period of time
Bluetongue: Culicoides gnat (cattle may be a reservoir)
Akabane virus diseases: gnats and mosquito population
Cache Valley virus: mosquitoes
Test Accuracy
Diagnosis of a specific cause of abortion can be very challenging.
Even if all samples are submitted adequately, the exact etiology will remain undiagnosed in half of the sporadic cases.
Diagnosis of the cause of an outbreak is more rewarding.
Most labs will run an abortion panel based on serology, histopathology, and culture tests described above.
TREATMENT
Treatment potential
Campylobacter: penicillin or streptomycin or tetracycline in feed
Chlamydia: tetracycline, tylosin
Leptospirosis: tetracycline
Toxoplasmosis: decoquinate, monensin
Leptospirosis: tetracycline
Mycoplasma: tetracycline and tylosin
CLIENT EDUCATION
Establish good preventative program
Biosecurity measures
Vaccination
Good nutritional programs
Consider every case of abortion as a possible outbreak.
Act quickly and help collect appropriate samples to be examined by a veterinarian.
MEDICATIONS
Daily tetracycline treatment of the flock may help with some of the abortion-causing diseases.
DRUGS OF CHOICE
N/A
CONTRAINDICATIONS
N/A
PRECAUTIONS
Appropriate milk and meat withdrawal times must be followed for all compounds administered.
POSSIBLE INTERACTIONS
N/A
ALTERNATIVE DRUGS
N/A
FOLLOW-UP PREVENTION/AVOIDANCE
General prevention program for abortion
Quarantine new animals (4-6 weeks)
Nutrition
Vaccination: chlamydia, campylobacter (2 months and last month of pregnancy)
Feed chlortetracycline (200-400 mg/head/day), monensin (15 mg/head/day) during gestation
Keep feed, pasture, and water source free from contamination by runoff particularly from cattle and hogs.
Control rat, bird, cat population.
Act quickly on any abortion and assume it is an outbreak; submit complete samples.
Separate prepartum from postpartum females.
Keep good lambing/kidding facilities.
Reduce stress due to poor nutrition, unsanitary environment, crowded conditions.
Vaccination
Bluetongue: questionable
Akabane virus: effective
Cache Valley: effective
Campylobacter: helpful
Chlamydia: helpful
Q fever: autogenous vaccines in conjunction with chlortetracycline may help.
B. ovis: poor efficacy of killed vaccine
B. melentensis: live attenuated good when permitted
Salmonellosis: autogenous vaccine may be helpful
Toxoplasmosis: may be helpful
POSSIBLE COMPLICATIONS
Dystocia, retained placenta, metritis, mastitis, male infertility (brucellosis, chlamydiosis), female infertility
EXPECTED COURSE AND PROGNOSIS
Depends on cause
MISCELLANEOUS ASSOCIATED CONDITIONS
N/A
AGE-RELATED FACTORS
N/A
ZOONOTIC POTENTIAL
Campylobacter jejuni (aborted fetus, stomach content, fetal membranes)
C. psittaci (fetal membranes, vaginal discharges)
Q fever (influenza-like symptoms, myalgia, endocarditis)
Brucellosis (B. melentensis), Malta fever, undulating fever, joint pain
Leptospirosis
Toxoplasmosis (milk, fetal membranes)
Listeriosis: aborted fetuses
PREGNANCY
N/A
RUMINANT SPECIES AFFECTED
Sheep/goat
BIOSECURITY
PRODUCTION MANAGEMENT SYNONYMS
Specific disease condition
SEE ALSO
Specific disease condition
ABBREVIATIONS
EED = early embryonic loss
ELISA = enzyme-linked immunosorbent assay
FA = fluorescent antibody
RFM = retained fetal membrane
IIFA = indirect inclusion fluorescence antibody
Suggested Reading
Kikbride, C. A. 1993. Diagnosis in 1784 ovine abortions and stillbirths. J Vet Diagnon Invest. 5: 398.
Menzies, P. I., Miller, R. 1986. Abortion in sheep: diagnosis and control. In:Current therapy in theriogenology, ed. R. S. Youngquist. 2nd ed. Philadelphia: Saunders.
Mobini, S. 2003. Investigation of abortion in sheep and goat. Proceedings Annual Meeting of the Society for Theriogenology, pp. 291-303.
Mobini, S., Heath, A., Pugh, D. 2002. Theriogenology in sheep and goats. In: Sheep and goat medicine, ed. D. Pugh. Philadelphia: Saunders.
Author: Ahmed Tibary

ABORTION: VIRAL, FUNGAL, AND NUTRITIONAL
BASICS OVERVIEW

Abortion is the expulsion of the fetus prior to the end of the normal gestation period. Besides bacterial etiology, viral, fungal, parasitic, and nutritional causes are not uncommon.
Abortions may occur near normal delivery time and it is difficult to determine whether the dam has aborted or whether a premature birth has occurred.
Diagnostic success rates for abortions of only 25%-30% attained by diagnostic laboratories are common.
Abortion frequently results from an event that occurred weeks or even months prior to the event, making diagnosis difficult in many cases.
Fungal abortions are normally sporadic, and occur from 4 months to term.
The incidence of fungal abortions in temperate climates is highest in the winter months. Severe infection of the placenta, characterized by a leathery thickening of the areas in between the cotyledons, is a common finding.
Toxic, pharmacologic, and genetic factors causing fetal death and/or abortion are many times not discernible in the specimens available for examination.
SYSTEMS AFFECTED
Reproductive
GENETICS
N/A
INCIDENCE/PREVALENCE
Viral
In a 10-year South Dakota abortion survey, viruses were associated with 10.58% of samples. Bovine herpesvirus-1 (IBR) was detected in 5.41%, and bovine viral diarrhea virus (BVDV) was detected in 4.54% of diagnostic submissions. Bovine herpesvirus-4 was isolated from 0.52%; parvovirus, enterovirus, adenovirus, parainfluenza virus, and pseudorabies virus were isolated in much smaller numbers. Malignant lymphoid neoplasia abortion was assumed to have been caused by the bovine leukosis virus.
Mycotic
In one study, mycotic infection was diagnosed in 6.8% of 6858 cases of bovine abortion and stillbirth examined during a 9- year period. Aspergilli were associated with approximately 5% of all abortion cases and 71% of 446 cases that were cultured for fungi and diagnosed as mycotic abortion. Aspergillus fumigatus was the most frequent isolate (62%), followed by A. terreus (6.7%), Emericella (Aspergillus) nidulans (3.0%), A. flavus (2.9%), and E. rugulosus (less than 1.0%). Zygomycetes (Absidia, Mortierella, Rhizomucor, Rhizopus) accounted for 21% of the cases. Pseudallescheria boydii and yeasts (Candida, Torulopsis) were each identified in 2% of the cases. Fungi that uncommonly cause infection accounted for 2% of the cases and included Curvularia geniculata, Exophilia jeanselmei, Hendersonula toruloidea, Lecythosphora hoffmannii, Talaromyces flavus var. flavus (Penicillium vermiculatus), T. (Penicillium) thermophilus, and Wangiella dermatitidis. About 10% of the mycotic cases were mixed fungal infections involving A. fumigatus (87%), A. flavus (12.5%), or E. nidulans (12.5%) coexisting with Absidia corymbifera (72%), Rhizomucor pusillus (4.3%), or Rhizopus arrhizus (4.3%). In each mixed infection, both septate and nonseptate hyphae were observed in placental tissues.
GEOGRAPHIC DISTRIBUTION
Worldwide, depending on species, agent, and environment
Epidemiology
In an Israeli study of 58,048 pregnancies from 111 herds, the respective abortion density, proportion of aborted cows, and abortions per confirmed pregnancy were 4.2%, 5.9%, and 10.2%. Among parities, heifers had the lowest risk, and cows of second parity the greatest risk of fetal death. The greatest risk of fetal death was observed in the first trimester, and the lowest in the second trimester of pregnancy. Respective proportions of aborted cows with and without a previous abortion were 17.5% and 5.9%. The potential of aborting after twinning in multiparous cows was found to be 1.3% greater than for those having a single calf. Risk of abortion was greater in the autumn and early winter than in the summer months.
SIGNALMENT
Species
All ruminant species Breed Predilections N/A
Mean Age and Range Breeding-age females Predominant Sex Female
DIAGNOSIS
See also under specific cause of abortion below.
DIFFERENTIALDIAGNOSIS
Nonbacterial
Bovine Abortion
Bluetongue
Bovine viral diarrhea virus (BVD)-mucosal disease
Drug induced
Fetal abnormalities
Infectious bovine rhinotracheitis (IBR)
Iodine deficiency
Malnutrition
Maternal stress
Mycotic abortions
Placenta abnormalities
Q fever
Twinning
Vitamin A deficiency
Ovine Abortion
Border disease (bovine viral diarrhea-BVD)
Copper deficiency
Maternal stress
Mycotic
Nutritional deficiency/excess
Parasitic
Selenium toxicity
Starvation
Toxic plant ingestion
Caprine Abortion, Early
Drug induced/iatrogenic (diazepam, xylazine, Acepromazine)
Nutrition
Progesterone deficiency
Caprine Abortion, Late
Akabane
Bovine viral diarrhea (BVD)
Caprine herpesvirus
Copper deficiency
Corticosteroid administration
Foot-and-mouth disease
Malnutrition
Selenium deficiency
Stress
Toxic plant ingestion
Vitamin A deficiency
TREATMENT MEDICATIONS CONTRAINDICATIONS
Appropriate milk and meat withdrawal times must be followed for all compounds administered to food-producing animals.
FOLLOW-UP MISCELLANEOUS
Bovine Virus Diarrhea
Caused by bovine virus diarrhea virus (BVDV)
Clinical Conditions
Subclinical BVD-Most common form of infection
Acute BVD-Generally mild with low mortality
Persistently Infected (PI) Cattle-PI calves are infected in utero and are immunotolerant to the noncytopathic virus
Mucosal Disease-PI calves become super-infected with a second, cytopathic biotype of BVDV resulting in a condition of low morbidity but high mortality
Abortions
Fetal infection may result in either PI calves or abortion.
Abortion rates are higher in BVDV type II infections.
Infections near conception result in early embryonic death and infertility.
Infections between 42 and 125 days gestation with noncytopathic biotypes result in PI calves, fetal death causing abortion or mummification, or congenital defects.
Infection between 125 and 170 days gestation results in a lower incidence of abortion and congenital defects. Calves may have an antibody titer to BVDV.
Infection after 170 days gestation has little effect on the fetus.
Diagnosis
Good history relative to the health of the herd
Virus isolation and antibody detection from herd mates
Lesions in aborted fetus compatible with BVDV infection, virus isolation, and fetal antibody detection.
Abortions prior to 4 months’ gestation will have characteristic lesions and virus while those aborted after 4 months may have congenital defects, fetal antibodies, or virus.
Calves born with congenital defects may have precolostral antibodies.
PI calves will have no titer (except from colostrum) and may be identified by virus isolation
Prevention and Control
Impeccable herd management
Identification and removal of PI animals
Proper vaccination program
Herpesviral Abortion
In cattle, the alpha-herpesviruses, bovine herpesvirus-1 (infectious bovine rhinotracheitis virus), and bovine herpesvirus- 5 (bovine encephalitis virus), and a gamma-herpesvirus, bovine herpesvirus-4, have all been implicated as causes of abortion.
Caprine herpesvirus-1 causes abortion or neonatal deaths in goats.
Infectious Bovine Rhinotracheitis Virus (Bovine Herpesvirus 1)
IBRV or BHV1 is the most frequently diagnosed viral abortion disease. In addition to abortion it causes rhinotracheitis, conjunctivitis, pustular vulvovaginitis, balanoposthitis, and enteritis.
Herpesvirus may produce latent infection, localizing in the trigeminal and sacral ganglion, resulting in a source of persistent infection following stress.
Transmission is by direct contact to respiratory, conjunctival, or genital mucous membranes. It may be spread in the semen of carrier bulls.
Abortions
Most abortions occur in the second half of pregnancy.
May occur 2 weeks to 4 months after infection; typically occurs about 20 to 45 days after infection.
Abortion rate may be sporadic or in storms, depending upon the susceptibility of the herd.
Vaccination of pregnant cattle with MLV may cause abortion.
Infertility
Infection near the time of breeding, from infected semen or other exposure routes, may cause endometritis and oophoritis, resulting in temporary infertility or early embryonic death.
Diagnosis
The entire fetus and placenta should be submitted for postmortem.
Fetus usually autolyzed, obscuring gross lesions.
Microscopic lesions include intranuclear inclusions of liver, lung, thymus, or adrenal gland.
Diagnosis is confirmed by virus isolation or antibody determination in fetal tissue, with cotyledons being the preferred tissue in severely autolyzed fetuses.
Maternal antibody titer is of limited use as the abortion may occur several months following exposure and the nature of the virus is ubiquitous.
Prevention and Control
Impeccable herd management
Proper vaccination programs
Use of semen from IBR-negative bulls
Bluetongue Virus
BTV rarely causes abortion in cattle and sheep.
Infection is transmitted by the insect Culicoides spp. Infection may result in early embryonic death, abortion, mummification, or cerebral malformation. It is shed in the semen of viremic bulls.
Although the virus is widespread throughout the world, it is not considered a major cause of bovine abortion.
Mycotic Abortions
The fungi responsible for mycotic abortion in cattle include Aspergillus, Absidia, Mucor, Rhizopus, Candida, and
Mortierella, with Aspergillus fumigatus being the most common.
Abortions are sporadic, of low incidence, and usually occur in late gestation.
Fungi seen in silver-impregnated sections of tissues could be placed into three categories designated Aspergillus, Phycomycete, and Atypical.
Gross or microscopic examination or cultures of the placenta are valuable diagnostically but examination of the fetus is seldom of value as infection in most instances does not involve fetal tissues.
Fertility following fungal abortion was apparently unimpaired.
Diagnosis
A thick, leathery placentitis
The fetus may be emaciated, with ringwormlike lesions on the skin.
Identification of fungal hyphae in fetal tissues and placenta
Pathophysiology
Route of infection is hematogenous spread from the respiratory or gastrointestinal tracts.
Source of infection is often moldy feed.
Control
Reduction of exposure to fungal agents by proper stable environment and reduced consumption of spoiled feeds
Abortion Due to Nutritional Causes
Several poisonous plants, including poison hemlock and locoweed, may cause sporadic abortion but more commonly cause a variety of congenital defects.
Nutritional deficiencies have been implicated in embryo loss however a direct cause-and-effect relationship is difficult to establish. Beta-carotene, vitamin A, iodine, selenium, phosphorus, and copper deficiencies have been implicated.
Usually, nutritional deficiencies will demonstrate primarily as reproductive problems other than abortion.
Pine Needle Poisoning
Consumption of needles from ponderosa pine trees can cause abortion in the third trimester. Isocupressic and imbricatoloic acids have been identified as the probable abortifacient agent.
Ingestion of pine needles causes a progressive reduction in uterine blood flow resulting in abortion or premature parturition within 3 days, although occasionally within 3 weeks. The problem may be prevented by providing an alternative feed source.
Nitrate Poisoning
Ruminants are susceptible to nitrate poisoning because of the nitrate-reducing potential of rumen microbes.
Plants that accumulate high levels of nitrates include Sudan grass, oats, wheat, corn, pigweed, and Johnson grass.
Heavy fertilization and cool growing conditions are conducive to nitrate accumulation. The ingested nitrates are converted to nitrites, which converts hemoglobin to methemoglobin. Methemoglobin is unable to carry oxygen, resulting in a hypoxic state. The hypoxemia may result in fetal death and abortion, or a stress-induced increase in fetal cortisol resulting in induction of parturition.
Severe methemoglobinemia may cause death of the cow.
Treatment is methylene blue IV.
Sweet Clover Hay
Moldy sweet clover hay will produce toxic levels of the anticoagulant dicoumarol. Ingestion of toxic levels will cause pregnancy loss as well as death of adult animals.
Removal of the moldy feed from the diet will prevent or terminate the loss.
ASSOCIATED CONDITIONS
Infertility and return to estrus
Infection near the time of breeding, from infected semen or other exposure routes, may cause endometritis and oophoritis, resulting in temporary infertility or early embryonic death.
AGE-RELATED FACTORS
Among parities, heifers have the lowest risk, and cows of second parity the greatest risk of fetal death.
ZOONOTIC POTENTIAL
Mycotic agents can be zoonotic.
PREGNANCY
Abortions may occur near normal delivery time and it is difficult to determine whether the dam has aborted or whether a premature birth has occurred.
Abortion frequently results from an event that occurred weeks or even months prior to the event making diagnosis difficult in many cases.
The greatest risk of fetal death is observed in the first trimester, and the lowest in the second trimester of pregnancy.
RUMINANT SPECIES AFFECTED
Potentially, all ruminant species are affected.
BIOSECURITY
Test and isolate prior to herd/flock introduction.
Impeccable herd management
PRODUCTION MANAGEMENT
Vaccination is an important tool in disease prevention.
Impeccable herd management
SYNONYMS
N/A
SEE ALSO
Bluetongue
Bovine viral diarrhea
Infectious bovine rhinotracheitis Locoweed
Mycotic infections Nitrate toxicity Pine needle toxicity Poison hemlock Sweet clover ABBREVIATIONS
BHV = bovine herpes virus BTV = blue tongue virus BVD = bovine viral diarrhea
BVDV = bovine viral diarrhea virus IBR = infectious bovine rhinotracheitis MLV = modified live vaccine Suggested Reading
Johnson, C. T., Lupson, G. R., Lawrence, K. E. 1994, Mar 12. The bovine placentome in bacterial and mycotic abortions. Vet Rec. 134(11):263-66.
Kirkbride, C. A. 1992, Oct. Viral agents and associated lesions detected in a 10-year study of bovine abortions and stillbirths. J Vet Diagn Invest. 4(4):374-79.
Knudtson, W. U., Kirkbride, C. A. 1992, Apr. Fungi associated with bovine abortion in the northern plains states (USA). J Vet Diagn Invest. 4(2):181-85.
Markusfeld-Nir, O. 1997, Aug. Epidemiology of bovine abortions in Israeli dairy herds. Prev Vet Med. 31(3-4):245-55. McCausland, I. P., Slee, K. J., Hirst, F. S. 1987, May. Mycotic abortion in cattle. Aust Vet J. 64(5):129-32.
Reuter, R., Bowden, M., Ellis, T., Carman, H. 1987, Mar. Abortion, stillbirth and ill thrift in cattle associated with mucosal disease virus. Aust Vet J. 64(3):92-93.
Seguin, B., Troedsson, M. 2002. Diseases of the reproductive system. In:Large animal internal medicine, ed. B. P. Smith. St. Louis: Mosby.
Smith, K. C. 1997, May. Herpesviral abortion in domestic animals. Vet J. 153(3):253-68.
Authors: Walter Johnson and Alex Estrada

ACIDOSIS
BASICS OVERVIEW

Rumen acidosis is a pathological condition that can be acute (i.e., leading to death) or chronic (i.e., leading to short-term or long-term production inefficiencies and illnesses).
Acidosis results from consumption of excessive amounts of readily fermentable carbohydrates (RFC) and, therefore, it can be a major problem for ruminants on high-concentrate diets (e.g., feedlot cattle).
Rumen pH of 5.6 and 5.2 are used as benchmarks for chronic and acute acidosis, respectively.
In the feedlot, acidosis occurs during adaptation of animals to high-concentrate diets and also in animals adapted to these diets due to engorgement of large amounts of RFC.
Acidosis occurs in grazing animals when large amounts of high-starch supplements are fed.
In dairy cows, the incidence of acidosis is highest during the first month postcalving. This is due to adaptation to high- concentrate diets containing more RFC than the cows are accustomed to utilizing during the dry period. It is important to note that the cow’s body is also unable to handle acid loads during early lactation.
Sources of RFC include immature/rapidly growing forages (i.e., high in intracellular carbohydrates), tubers/root crops (i.e., high in sugars), and cereal grains (i.e., high in starch).
Cereal grains are considered the most important source of RFC in animals with acute or chronic acidosis.
Cereal grains vary in their rate of ruminal starch fermentation (e.g., wheat is more fermentable than corn or milo, therefore, ruminants will be more susceptible to acidosis when fed wheat than corn).
Sheep appear to be more susceptible to acidosis than cattle.
Acidosis is of high economic significance because a large number of cattle and sheep are finished on high-concentrate diets.
The economic losses include death and/or performance of animals at much less than their genetic potential.
Many animals on high-concentrate diets experience chronic acidosis for extended periods of time without the condition being detected.
PATHOPHYSIOLOGY
When the amount of RFC is increased abruptly, rapid rumen fermentation occurs and large amounts of volatile fatty acids (VFA; mainly acetate, propionate, and butyrate) are produced.
These acids are continuously absorbed through the rumen wall without significant negative effects on the rumen environment. However, when large amounts of RFC are consumed, production of VFA is increased, and the rumen pH is decreased due to their accumulation.
The decreased rumen pH causes significant changes in the ruminal microbial population, especially a rapid increase in numbers of the amylolytic or sugar-utilizing bacteria such as Streptococcus bovis.
Under low pH conditions, lactate-producing bacteria (e.g., Lactobacillus spp.) also grow faster, increase in number, and produce increasing amounts of D- and L-lactate.
Ruminants can utilize L-lactate, as it is an intermediary metabolite. They can also use D-lactate.
In rumen environments not experiencing significant pH reductions, the lactate produced is absorbed in the rumen and small intestine or is immediately metabolized by lactate-utilizing bacterial species (e.g., Megasphaera elsdenii, Propionibacterium shermanii, and Selenomonas ruminantium). Thus, lactate either is not found in the rumen fluid or is detected at very low concentrations (< 5 F M).
When large amounts of lactate are produced, the rumen ability to utilize it is exceeded and, as a result, it accumulates (up to 40 F M as is the case in severe acidosis) and causes significant reductions in rumen pH.
Under these low pH conditions, lactate-producing bacterial species outnumber lactate-utilizing species, the number of S. bovis is decreased, and the number of Lactobacillus species is increased.
The ability of lactate to decrease pH more drastically than a similar amount of other fermentation acids (e.g., acetate) is due to its lower pK (i.e., the point of maximum buffering) value (i.e., 3.8 vs. 4.8). It is important to note that total acid (VFA and lactate) load is responsible for acidosis and this acid load causes several ruminal and systemic effects.
SYSTEMS AFFECTED
Gastrointestinal, metabolic, musculoskeletal
GENETICS
N/A
INCIDENCE/PREVALENCE
N/A
GEOGRAPHIC DISTRIBUTION
Worldwide
SIGNALMENT
Species
Potentially all ruminant species
Breed Predilections
N/A
Mean Age and Range
N/A Predominant Sex N/A
SIGNS HISTORICALFINDINGS
Marked reduction or cessation of feed intake (anorexia)
Diarrhea or loose feces
Lethargy
Laminitis or founder
Vomiting
Decreased rate of body weight gain
Distressed appearance
Polioencephalomalacia (cerebrocorticonecrosis). The thiamine deficiency is triggered by thiaminases produced by rumen bacteria under low pH conditions.
Cessation of rumen motility
In acute acidosis, dehydration occurs in response to the increase in ruminal osmotic pressure and the decrease in extracellular volume. The consequences of dehydration include decreased cardiac output, decreased peripheral perfusion, decreased renal blood flow, shock, and death.
Symptoms detected in dead or slaughtered animals include rumenitis, inflammation of the small intestinal tissues, and high incidence of abscessed livers.
Rumen Effects
A significant increase in numbers of amylolytic, sugar-utilizing, and lactate-producing bacterial species
A continuous decrease in rumen pH to 6 and 5.2, which are lethal to major microbial populations such as the rumen protozoa and cellulolytic bacterial species, respectively.
A decrease in the rumen motility and fermentation
An increase in the rumen osmotic pressure (> 300 mOsm) due to accumulation of solutes such as VFA, lactate, glucose, and minerals
When the rumen osmotic pressure exceeds that of the blood, a rapid influx of water from the blood occurs to neutralize the rumen osmotic pressure. This action results in significant rumen wall damage (i.e., swelling of the papillae and stripping of epithelium patches).
The rumen microbes responsible for liver abscess (e.g., Fusobacterium necrophorum) can freely cross the damaged rumen wall and enter the blood.
An increase in absorption of lactate
In subclinical cases of acidosis (e.g., dairy cows in early lactation), the rumen pH drops daily to < 5.5 for a given period of time. This has negative effects on fermentation and the subsequent utilization of nutrients by dairy cows.
Systemic Effects
An increase in blood lactate concentration
A decrease in blood bicarbonate concentration
A decrease in blood pH below 7.35 (i.e., a life-threatening situation)
A decrease in urine pH
A decrease in blood concentration of minerals (e.g., calcium) and electrolytes
An increase in blood histamine concentration
An increase in blood osmolality due to loss of water to the rumen
An increase in concentration of blood components (e.g., increased packed cell volume)
Uncontrolled elevation of blood pressure
Inflammation of the small intestine
Coma and death (e.g., the sudden death in feedlots)
Promoting Factors
Mismanagement of feeding RFC sources such as cereal grains
Cold weather promotes consumption of large amounts of feed and, therefore, it may dispose feedlot cattle to acidosis.
TREATMENT
Chronic Cases
Increasing bicarbonate input from the diet and/or through salivation by increasing forage levels in the diet, especially long hay to stimulate rumination. Dietary or salivary bicarbonates increase pH and stimulate lactate utilization in the rumen.
Increasing water intake causes dilution of rumen contents and reduction in rumen osmolality. This prevents water influx from the blood and helps maintain blood osmolality.
Supplementation of B vitamins (i.e., B 12and thiamin) that are involved in VFA metabolism to decrease their blood levels
Drenching with electrolytes
Acute Cases
Evacuating the rumen after a stab incision in the paralumbar fossa area
Use of antibiotics such as oral dosing of chlortetracycline and water
Inoculation with rumen fluid from healthy animals
Removing the RFC source from the diet
Feeding good-quality forages
Intravenous infusion of bicarbonate buffer to eliminate acidity but not to induce alkalosis
Intravenous infusion of electrolytes
Intravenous infusion of saline solution
MEDICATIONS CONTRAINDICATIONS
Appropriate milk and meat withdrawal times must be followed for all compounds administered to food-producing animals.
FOLLOW-UP PREVENTION/AVOIDANCE
Gradual adaptation of animals to high-concentrate diets. A 4-week adaptation period was found to provide an opportunity to induce a gradual change and stabilization of a final ruminal microbial population that can handle the increased amounts of lactate produced when high-RFC diets are fed.
Dietary inclusion of roughages (e.g., long forages or by-products containing fiber) at 10% to 15% of dry matter to enhance rumination and to increase salivation. The buffering capacity of ruminant saliva can help in reducing the negative effects of fermentation acids.
Dietary exclusion of cereal grains that promote acidosis such as wheat
Dietary exclusion of fermented feeds (e.g., silages) that are known to increase the acid load in the rumen
Management and close monitoring of feeding processed grains such as steam-flaked corn. The gelatinization of starch during steam flaking increases its rate of fermentation.
Modulating starch intake by restricting feeding (e.g., 90% of ad libitum intake) to eliminate excessive consumption of starch
Restricting feeding after working cattle or during weather change
Fat supplementation at levels up to 6% of the diet
Feeding high-protein diets to increase production of rumen ammonia (i.e., alkaline) and to decrease rumen acidity
Dietary inclusion of sodium bicarbonate at 1% or 2% of dry matter to increase the buffering capacity of the rumen and to ameliorate the acidic conditions during early feeding of high RFC levels.
Allowing access to fresh feed and water at all times. Animals will eat smaller meals more often.
Using feed additives with rumen effects such as the ionophores monensin and lasalocid. These additives alter rumen fermentation and allow adaptation to high-starch diets by inhibiting lactate-producing bacterial species and stimulating lactate-utilizing species. The actions of these ionophores are achieved by their interference with the normal transport of ions across bacterial cell membranes.
Using feed additives with systemic effects such as the antibiotics chlortetracycline, tylosin, and virginiamycin to decrease the incidence of abscessed livers.
Close monitoring of daily intake of diets containing high RFC levels
MISCELLANEOUS ASSOCIATED CONDITIONS
Diarrhea, lethargy, laminitis, decreased rate of body weight gain
Polioencephalomalacia
Cessation of rumen motility
Dehydration, decreased cardiac output, decreased peripheral perfusion, decreased renal blood flow, shock, and death
AGE-RELATED FACTORS
N/A
ZOONOTIC POTENTIAL
N/A
PREGNANCY
N/A
RUMINANT SPECIES AFFECTED
All ruminant species are affected.
BIOSECURITY
N/A

PRODUCTION MANAGEMENT

Dietary inclusion of roughages
Gradual adaptation of animals to high-concentrate diets
Dietary exclusion of cereal grains that promote acidosis such as wheat
Restricting feeding after working cattle or during weather change
Dietary inclusion of sodium bicarbonate at 1% or 2% of dry matter to increase the buffering capacity of the rumen
Allowing access to fresh feed and water at all times
SYNONYMS
Grain overload
SEE ALSO
Nutrition section Polioencephalomalacia
Rumen dysfunction: alkalosis, transfaunation Rumen fluid analysis
ABBREVIATIONS
RFC = readily fermentable carbohydrates VFA = volatile fatty acids
Suggested Reading
Crichlow, E. C., Chaplin, R. K. 1985. Ruminal lactic acidosis: Relationship of forestomach motility to nondissociated volatile fatty acid levels. Am J Vet Res. 46:1908-11.
Huntington, G. B. 1988. Acidosis. In:The ruminant animal: digestive physiology and nutrition, ed. D. C. Church. Englewood Cliffs, NJ: Prentice Hall.
Newbold, C. J., Wallace, R. J. 1988. Effects of the ionophores monensin and tetronasin on simulated development of ruminal lactic acidosis in vitro. Appl Environ Microbiol. 54:2981-85.
Nocek, J. E. 1997. Bovine acidosis: implications on laminitis. J Dairy Sci. 80:1005-28.
Owens, F. N., Secrist, D. S., Hill, W. J., Gill, D. R. 1998. Acidosis in cattle: a review. J Anim Sci. 76:275-86.
Author: Hussein S. Hussein

ACTINOBACILLOSIS
BASICS DEFINITION
Actinobacillosis is caused by Actinobacillus ligniersii infection of the soft tissues, usually in the tongue.
PATHOPHYS IOLOGY

Actinobacillus ligniersii is a gram-negative rod, which normally inhabits the mouth and rumen of domestic ruminants, and is also found on plant awns.
Mucosal lesions anywhere on the body, typically in the mouth, can be invaded by these bacteria, causing a localized lesion. Bacteria can also spread to different parts of the body via lymphatic drainage.
A typical site of bacterial invasion is through small ulcers in the sulcus lingualis at the base of the tongue, leading to hard, painful, diffuse lesions of the tongue interfering with prehension of food, hence the synonym “wooden tongue.” The bacteria initially cause an acute diffuse myositis of the muscles of the tongue, followed by development of granules and fibrosis.
SYSTEMS AFFECTED
Alimentary, musculoskeletal
GENETICS
N/A
INCIDENCE/PREVALENCE
Seen in up to 3% of cattle tongues at slaughter
GEOGRAPHIC DISTRIBUTION
Worldwide
SIGNALMENT
Species
Mainly cattle and sheep, occasionally goats
Breed Predilections
N/A
Mean Age and Range
All ages Predominant Sex N/A
SIGNS HISTORICALFINDINGS
Abrasive feeds and crowded conditions in a herd outbreak; lesions outside the oral cavity may be associated with previous wounds or needle punctures.
PHYSICALEXAM FINDINGS
Hard diffuse nodular swellings typically of the tongue in cattle and of the lips in sheep
CAUSES AND RISK FACTORS
Caused by infection of soft tissues by Actinobacillus ligniersii; abrasive feeds and crowded conditions may facilitate spread in a herd outbreak. DIAGNOSIS DIFFERENTIALDIAGNOSIS
Dental disease
Oral foreign bodies and generalized lesions
Pharyngeal trauma
Contagious ecthyma and caseous lymphadenitis in sheep
CBC/BIOCHEMISTRY/URINALYS IS
Chronic inflammatory profile
OTHER LABORATORY TESTS
Biopsy/histopathology and culture of lesions
Microscopic examination of pus compressed between two glass slides shows “sulfur granule” or clublike rosette appearance with a central mass of bacteria.
IMAGING
N/A
OTHER DIAGNOSTIC PROCEDURES
N/A
PATHOLOGIC FINDINGS
Firm, pale, gritty granulomatous abscesses with multifocal necrotic foci containing mononuclear cells, neutrophils, eosinophils, and plant fibers
TREATMENT ACTIVITY
N/A
DIET
Use of a soft feed will aid prehension during treatment.
CLIENT EDUCATION
See Diet above.
MEDICATIONS
Sodium iodide
Daily organic iodides orally in severe cases
DRUGS OF CHOICE
Sodium iodide 70 mg/kg IV as 10-20% solution; give once, repeat at least once at 7-10-day intervals.
CONTRAINDICATIONS
Use sodium iodide with caution in pregnant cattle; see Precautions below.
Appropriate milk and meat withdrawal times must be followed for all compounds administered to food-producing animals.
PRECAUTIONS
Anecdotal reports of association with abortion in cattle at high doses of sodium iodide
POSSIBLE INTERACTIONS
N/A
ALTERNATIVE DRUGS
Penicillin, tetracycline, ceftiofur FOLLOW-UP
May need surgical debulking of lesions in severe cases.
PATIENT MONITORING
If signs of iodism seen (dandruff, excessive lacrimation, inappetence, coughing, diarrhea), halt therapy until signs disappear.
PREVENTION/AVOIDANCE
Reduce access to abrasive feed and pastures with hard penetrating plant awns or thistles.
POSSIBLE COMPLICATIONS
Anecdotal reports of association with abortion in cattle at high doses of sodium iodide
EXPECTED COURSE AND PROGNOSIS
Good prognosis if only the tongue is involved.
Fair prognosis if atypical sites are involved.
MISCELLANEOUS ASSOCIATED CONDITIONS
N/A
AGE-RELATED FACTORS
N/A
ZOONOTIC POTENTIAL
Bite wounds from ruminants can contain Actinobacillus ligniersii, but rarely result in actinobacillosis.
PREGNANCY
See Precautions above.
RUMINANT SPECIES AFFECTED
Mainly cattle and sheep, rare in goats
BIOSECURITY
N/A
PRODUCTION MANAGEMENT
N/A
SYNONYMS
Wooden tongue
SEE ALSO
Caseous lymphadenitis Contagious ecthyma Dental disease
Oral foreign bodies Pharyngeal trauma ABBREVIATIONS
IV = intravenous
Suggested Reading
Pugh, D. G., ed. 2002. Sheep and goat medicine. Philadelphia: W. B. Saunders.
Radostits, O. M., Gay, C. C., Blood, D. C., Hinchcliff, K. W., eds. 2000. Veterinary medicine. 9th ed. London: W. B. Saunders.
Smith, B. P., ed. 2002. Large animal internal medicine, 3rd ed. St. Louis: Mosby.

Author: David McKenzie

ACTINOMYCOSIS: LUMPY JAW
BASICS OVERVIEW
Common, sporadic, chronic granulomatous osteomyelitis of cattle caused by non-spore-forming, filamentous, gram-positive, anaerobic bacterium Actinomyces bovis
PATHOPHYS IOLOGY

Actinomyces
normal members of oral microbiota in cattle
same order as Mycobacterium
low virulence
only cause disease when mucosal barriers are compromised
gram-positive, branching/filamentous, nonencapsulated bacteria
Trauma to oral mucosa from rough feed or foreign objects or dental alveoli permits entrance of Actinomyces into buccal tissues.
Grows in anaerobic conditions associated with devitalized tissue, lack of phagocyte delivery.
In mandible and maxillae, initially, painless, hard, immovable swellings. In weeks or months, swelling frequently develops along lower edge of bone and in intermandibular space.
Abscess/granuloma formation, necrotic foci (mycetoma)
Masses open through sinus tracts, lesions may become painful.
Discharge of viscous, sticky, “honey- or whey-like,” odorless, yellowish pus from openings.
Pus contains sandlike, firm, yellowish granules, which do not contain sulfur. The granule contains microcolonies of
Actinomyces in an eosinophilic, amorphous matrix made of calcium phosphate/antigen-antibody complexes.
Occasional involvement of soft tissues, especially of esophageal groove with spread to lower esophagus, anterior wall of reticulum, may cause peritonitis.
Rare hematogenous spread to other organs
Local lymph nodes usually not involved
Teeth may loosen.
Swelling may cause dyspnea.
Trauma to digestive tract could introduce Actinomyces into regions below oral cavity.
SYSTEMS AFFECTED
Musculoskeletal; rare hematogenous spread to other organs; oral cavity
GENETICS
N/A
GEOGRAPHIC DISTRIBUTION
Worldwide
INCIDENCE/PREVALENCE
Common, sporadic
SIGNALMENT
Species
Cattle; potentially all ruminant species
Breed Predilections
N/A
Mean Age and Range
Young cattle with erupting teeth, commonly
Predominant Sex
N/A
SIGNS HISTORICALFINDINGS
Hard, immovable swellings of maxillae/mandible
Draining fistulous tracts-yellowish, sticky, odorless pus
Misaligned teeth, difficulty masticating
Weight loss, periodic diarrhea, chronic bloat
Dyspnea
Less frequently partial tracheal obstruction, orchitis, brain/lung abscesses
CAUSES AND RISK FACTORS
Eruption of teeth in young cattle
Rough feeds containing awns, foreign objects
Procedures causing oral lacerations
SIGNALMENT
Young cattle, erupting teeth
Cattle fed awn-containing feeds or subjected to oral trauma
Source of Infections
Endogenous infections; oral microbiota
If noninfected cattle present with oral lacerations, Actinomyces may be spread from infected animals to noninfected animals via contaminated draining pus.
Normally not contagious
Transmission
Endogenous; oral lacerations permit entry into devitalized buccal tissues and subsequent spread
DIAGNOSIS
Palpation of hard, immovable masses
Draining tracts, odorless, sticky, yellowish pus with hard, small yellowish-white granules
Microscopic exam of pus: mix with saline; crush granules between two glass slides; use Gram’s stain. Rosettes of thin, filamentous, branching gram-positive rods seen at periphery of granule. May appear irregularly stained, “beaded.” May be misidentified as fungi.
Fastidious, slow-growing bacterium. Culture anaerobically 10-14 days or more.
DIFFERENTIALDIAGNOSIS
Cheek abscess, causes other than Actinomyces (movable, located in soft tissue)
Impacted feed/foreign bodies between cheek and teeth
Chronic peritonitis, causes other than Actinomyces
Mandibular lymphosarcoma CBC/BIOCHEMISTRY/URINALYS IS
N/A
OTHER LABORATORY TESTS
Culture and sensitivity of the lesion is indicated.
Microscopic exam of purulent debris: mix sample with saline and crush granules between glass slides; use Gram’s stain.
IMAGING
Radiographs should reveal changes consistent with osteomyelitis of the affected mandible.
TREATMENT
Difficult to treat
Surgical debridement/drainage. Pack wound with streptomycin or tincture of iodine soaked gauze.
DRUG(S) OF CHOICE
Streptomycin, penicillin, sulfonamides
Iodine therapy: (See Precautions below.) Some animals become distressed (restlessness, dyspnea, tachycardia). Stop when signs of iodism occur (lacrimation, anorexia, cough, scaling skin lesions). Subcutaneous iodine causes severe irritation and immediate swelling. Potassium iodine as drench. Sodium iodine IV as 10% solution.
Isoniazid as adjunct to antibiotic/iodine therapy
CONTRAINDICATIONS
Appropriate milk and meat withdrawal times must be followed for all compounds administered to food-producing animals.
PRECAUTIONS
Caution: abortion has followed iodine therapy in some animals.
POSSIBLE INTERACTIONS
N/A
ALTERNATIVE DRUGS
N/A
FOLLOW-UP PREVENTION
Avoid feeds/procedures that could cause oral lacerations.
Monitor young cattle for swelling of mandible especially following tooth eruptions.
Isolate cattle with discharging lesions
No vaccine
MISCELLANEOUS ASSOCIATED CONDITIONS
N/A
AGE-RELATED FACTORS
Young cattle with erupting teeth
ZOONOTIC POTENTIAL
No cattle-human transmission
PREGNANCY
N/A
RUMINANT SPECIES AFFECTED
Cattle; potentially all ruminant species
BIOSECURITY
N/A
PRODUCTION MANAGEMENT
N/A
SYNONYMS
Actinostreptothricosis Cervicofacial actinomycosis Lumpy jaw
Ray fungus disease
SEE ALSO
Cheek abscess, causes other than Actinomyces (movable, located in soft tissue) Impacted feed/foreign bodies between cheek and teeth
Chronic peritonitis, causes other than Actinomyces
ABBREVIATIONS
IV = intravenous
Suggested Reading
Bertone, A. L., Rebhun, W. C. 1984, Jul 15. Tracheal actinomycosis in a cow. J Am Vet Med Assoc. 185(2): 221-22.
Radostits, O. M., Gay, C. C., Blood, D. C., Hinchcliff, K. W., eds. 2000. Actinomycosis. In:Veterinary medicine. 9th ed. Philadelphia: W. B. Saunders.
Seifi, H. A., Saifzadeh, S., Farshid, A. A., Rad, M., Farrokhi, F. 2003, May. Mandibular pyogranulomatous osteomyelitis in a Sannen goat. J Vet Med A Physiol Pathol Clin Med. 50(4): 219-21.
Smith, B. P. 2002. Actinomycosis (lumpy jaw). In:Large animal internal medicine. 3rd ed. St. Louis: Mosby.
Strohl, W. A., Harriet, R., Fisher, B. D., eds. 2001. Lippincott’s illustrated reviews: microbiology. Philadelphia: Lippincott, Williams and Wilkins.
Watts, T. C., Olson, S. M., Rhodes, C. S. 1974, Feb. Letter: Use of isoniazid in cattle. Can Vet J. 15(2): 28.
Watts, T. C., Olson, S. M., Rhodes, C. S. 1973, Sep. Treatment of bovine actinomycosis with isoniazid. Can Vet J. 14(9): 223-24.
Author: Karen Carberry-Goh

ACUTE COLIC-ABDOMINAL PAIN
BASICS DEFINITION

Acute colic is abdominal pain of < 48 hours duration.
Once pain has exceeded 48 hours duration, it is considered chronic.
PATHOPHYS IOLOGY
The gastrointestinal tract is the source of most acute abdominal pain, but any abdominal organ can be involved.
Gastrointestinal pain can result from distension, displacement, torsion/volvulus, obstruction, smooth muscle spasm, and mesenteric tension, and may involve hypermotility, hypomotility, ischemia, and inflammation.
Urinary tract pain can result from obstruction, inflammation, infection.
Reproductive pain can result from parturition, abortion, dystocia, uterine torsion, inflammation, infection, or tumor.
Peritoneal pain results from inflammation, infection, and penetrating metallic foreign bodies.
Other abdominal organs are less likely sources of pain, but should be considered if the source of the pain cannot be identified.
Gastrointestinal lesions can be strangulating or nonstrangulating.
Strangulating lesions are by definition associated with reduced blood supply, which can result in necrosis.
Nonstrangulating lesions result in less circulatory disturbance and as a result are not usually associated with necrosis unless chronic.
Any interference with gastrointestinal function can result in endotoxemia due to the large volume of natural gastrointestinal flora.
Lesions originating in one system or organ can eventually result in other organs being affected.
SYSTEMS AFFECTED
Gastrointestinal
Urinary
Reproductive
Cardiovascular
Respiratory, if abdominal distension is severe
GENETICS
N/A
INCIDENCE/PREVALENCE
N/A
GEOGRAPHIC DISTRIBUTION
Worldwide distribution
SIGNALMENT
All ages and sexes can be affected.
Certain etiologies may be more common for specific groups.
SIGNS
Abdominal pain may be mild to severe.
Early signs may be subtle and easily missed, progressing in severity.
Cause is often obvious from a careful physical examination including rectal examination.
Ruminants are often stoic animals, bearing much pain without overt signs of colic as seen in the horse.
The veterinarian should be familiar with the location of the gastrointestinal components in cattle, and with associated areas of tympany (pings), which indicate a gas-fluid interface under pressure.
Sometimes diagnosis is made by presumption in early stages, based on a particular signalment and a few clinical symptoms.
Mild colic-slight depression, reduced interest in feed, slight reduction in manure output, restlessness
Moderate colic-reduced interest in feed, reduced manure output, restlessness, stretching abdomen (sawhorse stance), teeth grinding, posturing to urinate or defecate without producing much
Severe colic-kicking at belly, recumbency (esp. lateral recumbency), severe depression, vocalization, straining to urinate or defecate, severe restlessness (getting up and down repeatedly), extended head and neck, rolling (very rare in ruminants)
PHYSICALEXAM FINDINGS
Depression
Increased heart and respiratory rates
Abdominal distension
Change in body temperature above or below normal
Reduced gastrointestinal sounds
Gastrointestinal hypermotility
The presence of pings in the abdomen
Lack of urine or feces
Discharge of uterine fluids
Palpably distended or displaced viscus on rectal exam
Grainy or constricted rectal palpation (peritonitis)
Vomiting (rare)
Dry prepuce (with urinary obstruction)
CAUSES
Forestomachs
Ruminal acidosis (grain overload), vagal indigestion, traumatic reticuloperitonitis, omasal impaction, ruminal fermentation (calves), bloat (gas or frothy)
Abomasum
Ulcers, impaction, left displacement (LDA), right displacement (RDA), right abomasal volvulus (RAV), right omasal- abomasal volvulus (ROAV), abomasal rupture, vagal indigestion, abomasal stricture
Small intestine
Enteritis, ileus, impaction, stricture, entrapment, segmental torsion, jejunal flange torsion, jejunal hemorrhage syndrome, intussusception, adhesions, fat necrosis, tumor, hernia (inguinal, umbilical, diaphragmatic)
Large intestine
Colitis, impaction, cecal tympany, displacement, torsion, volvulus, adhesions, fat necrosis, tumor, intussusception, atresia coli
Reproductive
Dystocia, parturition, abortion, tumor, peri-uterine abscess, testicular torsion, testicular trauma, penile/preputial trauma, vaginal prolapse, seminal vesiculitis, inguinal hernia
Urinary
Urolithiasis, cystitis, nephrolith, pyoureter, pyelonephritis
Other
Hernia, torsion of root of mesentery, peritonitis, hepatic inflammation, hepatitis, cholelith
RISK FACTORS
Dietary change(s)
Lack of access to water
Pregnancy
Stress
Recent parturition
DIAGNOSIS DIFFERENTIALDIAGNOSIS
Many diseases can cause signs resembling abdominal pain, including choke, rabies, tetanus, myositis, hypocalcemia, septicemia, and obesity
CBC/CHEMISTRY/URINALYS IS
Increased WBC count with peritonitis or other inflammation
Increased PCV and TP with dehydration
Decreased Cl, K, Na with most intestinal obstructive lesions in adult cattle
Increased fibrinogen in inflammatory conditions
Metabolic alkalosis in most gastrointestinal obstructive lesions in adult cattle
Acidosis with grain overload or severe, long-standing obstructions
Azotemia with urinary obstruction or severe dehydration
Urinalysis shows increased WBC, RBC, bacteria, crystals in urinary tract
OTHER LAB TESTS
Abdominocentesis
Increased WBC, TP, turbidity
Serosanguineous color indicative of obstruction
Foul smell indicative of GI rupture or enterocentesis
Plant material indicative of rupture or enterocentesis
Urine smell with uroabdomen
Volume increased with pregnancy, inflammation
Can be hard to obtain fluid in ruminants-try the flank region
Rumen Fluid Analysis
Decreased protozoal activity with poor rumen function or obstruction
Decreased pH with acidosis and abomasal reflux
Increased Cl with abomasal reflux
Abnormal color or smell with acidosis, ruminal fermentation, rumenitis
IMAGING
Ultrasound
May be helpful in examination of urinary and reproductive tract
Can identify fluid pockets in abdomen
New publications suggest use transabdominal to detect abnormalities of the GI tract
Radiographs and contrast radiology
Not usually useful in adult ruminants due to size
May be useful in examination of the urinary tract
DIAGNOSTIC PROCEDURES
Liptak test: Transabdominal paracentesis of a viscus on the left side of the adult cow to differentiate a LDA from rumen. Low pH = abomasum, high pH = rumen
Laparotomy: Often used as diagnostic procedure in cows. The problem can be identified and repaired in many cases by flank laparotomy.
Laparoscopy: Can be used as diagnostic procedure, but most abdominal problems require laparotomy to repair.
TREATMENT
APPROPRIATE HEALTH CARE
Colic should be considered an emergency and diagnosis and treatment initiated immediately.
Affected animals should not be fed until the cause is determined.
Often the organ system involved is readily obvious following physical exam and the choice of medical treatment vs. surgery quickly made.
Indications for immediate surgical treatment include severe abdominal pain, severe abdominal distension, HR >80 bpm, presence of pings, abnormal abdominocentesis, urinary obstruction, uterine torsion nonresponsive to rolling or manipulation, fetal oversize causing dystocia, confirmed gastrointestinal torsion, displacement, or obstruction.
Surgical approach to the abdomen in adult bovines is made in a standing position by right flank laparotomy. If the desired lesion is located on the left side, a left flank approach can be made, but there can be limited exploration of the right side of the cow from this approach. In exploratory surgeries, the right flank is almost always chosen.
• In small ruminants, flank or middling approach can be used. Acute colic-abdominal pain
NURSING CARE
IV fluids will be necessary in most cases. As alkalosis is present in most adult cattle with GI problems, a neutral or acidifying fluid is recommended. In cattle with grain overload, and any other animals with confirmed acidosis, an alkalinizing fluid and/or bicarbonate are recommended.
IV fluids should be supplemented to correct any electrolyte abnormalities.
Oral fluids may be administered in certain cases, such as impaction, in order to provide a large volume of fluids to the GI tract.
The use of oral fluids combined with hypertonic saline (1 ml/kg/min) has gained some favor as being cheaper than IV fluids, with similar effectiveness in restoring vascular volume.
Caution should be used in supplementing calcium to endotoxemic cows, as endotoxin sensitizes the heart to potentially fatal arrhythmias.
Animals with severe rumen bloat will require immediate ororuminal intubation to relieve the pressure.
ACTIVITY
N/A
DIET
During the colic episode, feed should be withheld.
Following resolution of the condition, refeeding should begin slowly to avoid recurrence or complications.
CLIENT EDUCATION
None
SURGICALCONSIDERATIONS
None
MEDICATIONS DRUGS OF CHOICE
Analgesics
Flunixin meglumine: 1.1-2.2 mg/kg IV q24h or divided q12h
Ketoprofen: 2 mg/kg IM q24h
Phenylbutazone: 4 mg/kg IV or PO q24h
The use of phenylbutazone is illegal in dairy animals and highly discouraged in all food animals.
Butorphanol: 0.02-0.04 mg/kg IV Laxatives
Mineral oil: 10 ml/kg given by ororuminal tube
Magnesium oxide: 0.5-1 kg for adult cow given by ororuminal tube
Dactyl sodium succinate: 10-30 mg/kg of 10% solution given by ororuminal tube
Antibloat Agents
Mineral oil: 10 ml/kg given by ororuminal tube
Poloxalene: 30-60 mL per animal (can be repeated) by ororuminal tube
Detergent soap can be used in emergency.
Prokinetics
None are truly effective for promoting forestomach motility.
Metoclopramide 0.1 mg/kg SQ q6-12h may provide some abomasal stimulation.
Bethanechol: 0.07 mg/kg SQ q8h may provide some cecal stimulation.
Antibiotics
Necessary in infective conditions or following surgery
Transfaunation
4-8 L of fresh rumen juice for repopulation of rumen microbes
Probiotic gels and yeast can be used for substitute.
Endotoxemia
Flunixin meglumine: 0.25-1.1 mg/kg IV q6-12h
CONTRAINDICATIONS
Prokinetic drugs should not be used if obstruction present.
Appropriate milk and meat withdrawal times must be followed for all compounds administered to food-producing animals.
PRECAUTIONS
Prolonged use of NSAIDs can cause ulceration of abomasum and renal damage.
Use of butorphanol or xylazine for pain control will cause ileus.
FOLLOW-UP PATIENT MONITORING
Once stable, refeeding should begin slowly and the animal monitored for passage of manure.
If the urinary tract was involved, urination must be monitored.
Patient should be monitored for recurrence of signs of abdominal pain or distension, or deteriorating cardiovascular status.
PREVENTION/AVOIDANCE
Avoid sudden feed changes.
Ensure access to water in all weather and temperatures.
Investigate signs of abdominal pain or distension early.
Investigate cows not calving by their due date.
POSSIBLE COMPLICATIONS
Peritonitis
Adhesions
Shock
Endotoxemia
Gastrointestinal or bladder rupture
Fetal loss
EXPECTED COURSE AND PROGNOSIS
Varies with the condition
MISCELLANEOUS
ASSOCIATED CONDITIONS
N/A
AGE-RELATED FACTORS
Young animals more likely to have intussusception.
Old animals more likely to have tumor, fat necrosis.
Pregnant animals have indigestion of pregnancy/pseudo-obstruction.
Peripartum animals predisposed to LDA, RDA < RAV, ROAV, abomasal ulcers
Animals < 18 months more likely to have urolithiasis
ZOONOTIC POTENTIAL
N/A
PREGNANCY
Late gestation cows most likely to have indigestion of pregnancy/pseudo-obstruction, uterine torsion
Parturition/abortion can resemble GI pain.
RUMINANT SPECIES AFFECTED
All
BIOSECURITY
N/A
PRODUCTION MANAGEMENT
N/A
SYNONYMS
Acute abdominal pain Bloat
Colic
SEE ALSO
Individual diseases/diagnoses
ABBREVIATIONS
GI = gastrointestinal HR = heart rate
IM = intramuscular IV = intravenous
LDA = left displacement
NSAID = nonsteroidal anti-inflammatory drug PCV = packed cell volume
RAV = right abomasal volvulus RDA = right displacement
ROAV= right omasal-abomasal volvulus SQ = subcutaneous
TP = total protein WBC = white blood cell Suggested Reading
Bickers, R. J., Templer, A., Cebra, C. K., Kaneps, A. J. 2000, Feb 1. Diagnosis and treatment of torsion of the spiral colon in an alpaca. J Am Vet Med Assoc. 216(3): 380-82.
Braun, U., Eicher, R., Hausammann, K. 1989, Sep 2. Clinical findings in cattle with dilatation and torsion of the caecum.
Vet Rec. 125(10): 265-67.
Cable, C. S., Rebhun, W. C., Fortier, L. A. 1997, Oct 1. Cholelithiasis and cholecystitis in a dairy cow. J Am Vet Med Assoc. 211(7): 899-900.
Cebra, C. K., Cebra, M. L., Garry, F. B., Johnson, L. W. 1997, Sep 1. Surgical and nonsurgical correction of uterine torsion in New World camelids: 20 cases (1990-1996). J Am Vet Med Assoc. 211(5): 600-602.
Farrow, C. S. 1999, Jul. Reticular foreign bodies. Causative or coincidence?Vet Clin North Am Food Anim Pract. 15(2): 397-408.
Wikse, S. E., Craig, T. M., Hutcheson, D. P. 1991, Mar. Nutritional and dietary interrelationships with diseases of grazing beef cattle. Vet Clin North Am Food Anim Pract. 7(1): 143-52.
Author: Jennifer M. Ivany Ewoldt

ACUTE RENAL FAILURE
BASICS OVERVIEW

Acute renal failure (ARF) is caused by decline of renal function over a period of hours to days.
This rapid onset of renal failure may result from prerenal, intrinsic renal, or postrenal causes.
Intrinsic renal problems are usually due to ischemic or toxic insults resulting from injury, disease, or certain therapeutic agents.
The kidneys are particularly susceptible to toxic injury.
PATHOPHYS IOLOGY
The kidneys receive approximately 20% of cardiac output, which exposes them to a high proportion of toxicants present in the blood.
The surface area of the large glomerular capillaries allows for a significant area of cells in the proximal tubules and ascending loop of Henle makes them particularly susceptible to intoxication.
Tubular epithelial cell resorption of toxins may cause excessive accumulation of toxins intracellularly.
Tubule-concentrating ability may result in increased levels of toxicants in the distal portion of the nephron.
SIGNALMENT
All ruminants are susceptible to ARF if primary predisposing factors are present.
SIGNS
Signs of acute renal failure are nonspecific in ruminants and may not be indicative of urinary dysfunction.
Depending on the underlying cause, anuria, oliguria, or polyuria may be observed.
Affected animals may present with depression, poor appetite, diarrhea, epistaxis.
Saliva may have a strong ammonia odor.
Severe cases develop muscular weakness and even recumbency due to electrolyte and acid-base abnormalities.
Rectal palpation may not be remarkable although occasionally renal enlargement or perirenal edema may be detected.
CAUSES AND RISK FACTORS
Risk of ARF is enhanced by dehydration, fever, sepsis, vasculitis, hypotension, electrolyte abnormalities, hypoalbuminemia, and exposure to nephrotoxic agents.
Nephrotoxic agents include certain metals, antimicrobials, NSAIDs, toxic plants, hemoglobin, myoglobin, calcium oxalate, as well as other toxins.
DIAGNOSIS DIFFERENTIALDIAGNOSIS
Development of a differential list is difficult due to the nonspecific clinical signs in cases of ARF and because of the variety of primary disease conditions that may predispose ruminants to ARF.
Differentials include those diseases causing epistaxis (coagulopathies and pulmonary abscesses), diarrhea, and recumbency.
CBC/BIOCHEMISTRY/URINALYS IS
Increased BUN and creatinine
Isosthenuria on urinalysis indicates azotemia of renal origin.
Proteinuria, hematuria, and granular casts may be present on UA.
Metabolic alkalosis, hypochloremia, and hypocalcemia are common findings in ruminants with ARF.
Hyponatremia, hyperphosphatemia, hypermagnesemia may also be seen.
OTHER LABORATORY TESTS
Fractional excretion of sodium may be evaluated but the test should be compared to a normal animal (e.g., herd mate) of similar age, physiologic state, and nutritional status.
Imaging
Ultrasonographic evaluation may reveal enlargement of one or both kidneys or presence of perirenal edema.
DIAGNOSTIC PROCEDURES
Renal biopsy may provide diagnostic as well as prognostic information in cases of ARF.
PATHOLOGIC FINDINGS
Gross and microscopic findings depend on the initial cause of renal failure (ischemic, infectious, or toxic).
TREATMENT
In cases of toxic nephrosis, the animal should be removed from the source of the toxin.
If ARF is due to use of a nephrotoxic drug, treatment should be discontinued.
Focus of treatment should be on IV fluid therapy for correction of acid-base and electrolyte abnormalities and encouragement of diuresis.
Isotonic, sodium-containing fluids with added calcium and potassium, as indicated, should be utilized.
Oral fluid therapy may be used if IV administration is impractical.
IV or oral fluids should be administered at a rate of one-and-a-half to two times the adult maintenance rate of 60 ml/kg/day to encourage diuresis.
Monitor hydration and plasma protein to avoid overhydration and edema formation.
Once the animal begins to urinate, IV fluids should be maintained until the serum creatinine has returned to normal.
Supportive care, which may be necessary for 2-3 weeks, includes rumen transfaunation and nutritional support.
MEDICATIONS DRUGS OF CHOICE
If fluid therapy does not promote diuresis, furosemide (1 mg/kg IV or IM, every 2-3 hours) may be beneficial.
If anuria or oliguria persists, a dopamine drip (3-7 mcg/kg/min IV) should be considered.
CONTRAINDICATIONS
With repeated use of furosemide, the patient’s serum sodium and potassium must be monitored carefully.
Drug withdrawal times need to be determined and maintained in food-producing animals.
FOLLOW-UP
N/A
MISCELLANEOUS
ARF due to ischemic episodes generally results in a grave prognosis.
Renal failure due to toxic causes may have a more favorable prognosis with early intervention and aggressive fluid therapy.
SEE ALSO
Diarrhea Epistaxis (coagulopathies and pulmonary abscesses) Recumbency
ABBREVIATIONS
ARF = acute renal failure BUN = blood urea nitrogen IM = intramuscular
IV = intravenous
NSAIDs = nonsteroidal anti-inflammatory drugs
Suggested Reading
Anderson, D. E., Constable, P. D., Yvorchuk, K. E., Anderson, N. V., St-Jean, G., Rock, L. 1994, May-Jun. Hyperlipemia and ketonuria in an alpaca and a llama. JVet Intern Med. 8(3):207-11.
Pugh, D. G. 2002. Sheep and goat medicine. Philadelphia: W. B. Saunders.
Schlumbohm, C., Harmeyer, J. 2004 Feb. Hyperketonemia impairs glucose metabolism in pregnant and nonpregnant ewes. J Dairy Sci. 87(2):350-58.
Author: M. S. Gill

AESCULUS (BUCKEYE) TOXICOSIS
BASICS OVERVIEW

Aesculus is a toxic tree or shrub that may produce neurotoxicity in cattle or sheep. The tree is commonly observed in the eastern United States and in Europe in wooded areas or fencerows.
Leaves are opposite palmately compound and consist of 5-7 leaflets.
Fruit is a leathery capsule with or without spines (depending on species).
Nuts are chocolate in color with a tan scar.
Bark, leaves, and especially fruit are toxic, containing the glycosides aesculin and fraxin and neurotoxic saponins.
SIGNALMENT
Affects ruminant animals of all ages although cattle seem more often affected
SIGNS
Onset of signs may be 12-16 hours after consuming buckeye.
In calves, 0.5% body weight of nuts has produced poisoning.
Initial signs in ruminants are staggering, weakness, muscle twitching, and an incoordinated gait.
Recumbency may occur in severe cases followed by coma and death.
Death is rare.
CAUSES AND RISK FACTORS
Toxicosis may occur in the spring when young foliage is abundant.
Toxicosis often occurs in the fall from ingestion of the nuts.
Animals seldom eat the nuts if ample good-quality forage is available.
DIAGNOSIS DIFFERENTIALDIAGNOSIS
Other causes of CNS signs in cattle include hypomagnesemia, polio, Claviceps paspali, lead, arsenic, Clostridium botulinum
type D, and insecticide poisonings.
CBC/BIOCHEMISTRY/URINALYS IS
Blood glucose may be high.
Glucosuria and proteinuria may be present in severe cases.
OTHER LABORATORY TESTS
N/A
IMAGING
N/A
DIAGNOSTIC PROCEDURES
N/A
PATHOLOGIC FINDINGS
No specific lesions are observed.
TREATMENT
No specific treatment
MEDICATIONS DRUGS OF CHOICE
Laxatives-mineral oil: 1/2-1 gallon for adult cow
Activated charcoal-1/2-1 pound for adult cow
IV calcium gluconate-500 ml/for adult cow
IV 50% dextrose-500 ml/for adult cow
If cases are found are found soon enough, stimulants and purgatives are indicated.
CONTRAINDICATIONS
Appropriate milk and meat withdrawal times must be followed for all compounds administered to food-producing animals.
Steroids should not be used in pregnant animals.
FOLLOW-UP PATIENT MONITORING
N/A
PREVENTION/AVOIDANCE
Provide ample good quality forage so that animals are not forced to ingest buckeye.
Remove buckeye trees in areas where cattle graze.
POSSIBLE COMPLICATIONS
N/A
EXPECTED COURSE AND PROGNOSIS
Mild cases of buckeye toxicosis respond without treatment if the source of the toxin is removed.
More severe cases respond quickly following treatment and may be normal in 12-24 hours.
Prognosis is poor for recumbent animals.
MISCELLANEOUS ASSOCIATED CONDITIONS
Initial signs in ruminants are staggering, weakness, muscle twitching, and an incoordinated gait.
Recumbency may occur in severe cases followed by coma and death.
Death is rare.
AGE-RELATED FACTOR
In calves, 0.5% body weight of nuts has produced poisoning.
ZOONOTIC POTENTIAL
N/A
PREGNANCY
N/A
RUMINANT SPECIES AFFECTED
Cattle, sheep; potentially all ruminant species
BIOSECURITY
N/A
PRODUCTION MANAGEMENT
N/A
SEE ALSO
Arsenic
Claviceps paspali Clostridium botulinum type D Hypomagnesemia
Insecticide poisonings Lead Polioencephalomalacia ABBREVIATIONS
CNS = central nervous system
Suggested Reading
Burrows, G. E., Tyrl, R. S. 2001. Toxic plants of North America. Ames: Iowa State University Press.
Hulbert, L. C., Oehme, F. W. 1968. Plants poisonous to livestock. Manhattan: Kansas State University Printing Service.
Knight, A. P., Walter, R. G. 2001. A guide to plant poisoning of animals in North America. Jackson, WY: Teton New Media.
Author: Larry A. Kerr

AGRICULTURAL CHEMICAL TOXICITIES
BASICS OVERVIEW
This chapter focuses on the ingestion, inhalation, and/or topical exposure to agricultural chemical compounds resulting in morbidity and/or mortality. Compounds include the following:

Chlorinated hydrocarbons-a group of insecticides that incorporate a chlorine molecule and are also known as organochlorines. They are mostly known for their environmental persistence and bioaccumulation (concentration levels of compound increase in animals higher up in the food chain).
Herbicides-compounds used for weed control. Many are selective against specific plants or types of plants.
Fungicides-compounds used to treat or prevent fungal infections in plants or animals
Polybrominated biphenyls (PBBs)-chemicals that were primarily used in industry as fire retardants in the 1970s
Dinitro compounds-herbicides that are highly toxic to all animals
The mechanism of action in animals of most of these agricultural chemicals is unknown.
Many of these chemicals, especially the herbicides, are frequently used in most agricultural crop enterprises today.
Their widespread use can create opportunity for exposure.
Toxicity typically occurs through oral or dermal exposure.
The currently available fungicides appear to be some of the safest chemicals discussed here due to their inefficient digestive absorption as well as their low toxicity in mammals.
Aerosol exposure to fungicides can cause irritation to the eyes and respiratory tract.
Most of the highly toxic and environmentally persistent compounds are no longer available in the United States today, but can be found worldwide.
Many of these compounds (especially many of the chlorinated hydrocarbons and all PBBs) are still present worldwide due to their previous extensive use and potential for bioaccumulation.
Acute toxicities due to accidental exposures are the most common presentation.
This exposure can occur either through contaminated feeds, access to stored chemicals or treated seeds for planting, or sometimes through exposure to fields or pastures recently treated with these chemicals.
Fields treated with chemicals many times require livestock access to be limited for some period of time; always read and follow label directions.
Acute toxicities will usually show up in the first 24 hours postexposure (ranging from a few hours up to a day or more).
Systemic absorption will usually result in these compounds ending up in particular areas, especially the liver, brain, kidney, fat, and milk.
Transplacental transmission can occur with some chemicals (especially the chlorinated hydrocarbons).
Most toxicities will result in minimal or nonspecific manifestations.
Carbamates are a type of herbicide with cholinesterase-inhibiting properties similar to organophosphates.
Cerebral and spinal cord congestion are probably the most common presentation along with pulmonary congestion.
Congestion of kidneys, liver, and spinal cord can also be seen.
Liver injury can be common, especially with chronic exposure.
SYSTEMS AFFECTED
Systems affected vary with the different class of chemicals as well as a particular chemical within a class.
Cardiovascular-methemoglobinemia (chlorate herbicides), cardiac arrest
Endocrine/metabolic-pyrexia
Gastrointestinal-anorexia, excess salivation, decreased rumen motility, bloat, digestive irritation and abdominal pain (especially some herbicides), diarrhea
Hepatobiliary-congestion, hepatic lipidosis or amyloidosis
Herd health-decreased milk production (PBBs), tainted milk (chlorinated hydrocarbons and PBBs), chronic poor performance
Musculoskeletal-incoordination, recumbency, anorexia, extended hoof growth (PBBs)
Nervous-stimulation or depression, ataxia, apprehension, hypersensitivity, muscle fasciculation, seizures, coma, death
Ophthalmic-irritation (aerosol exposure), nystagmus
Renal/urologic-congestion, nephritis (PBBs)
Reproductive-early embryonic death (PBBs); cross placental barrier (chlorinated hydrocarbons)
Respiratory-tachypnea, dyspnea, congestion
Skin-alopecia (PBBs)
GENETICS
None
INCIDENCE/PREVALENCE
Rare
GEOGRAPHIC DISTRIBUTION
Widespread use of many of these chemicals in today’s agriculture.
Many chlorinated hydrocarbons and all PBBs have been banned from use in many countries.
SIGNALMENT
Species
Susceptibility among compounds varies between ruminant species.
Breed Predilections
None
Mean Age and Range
None Predominant Sex None
SIGNS
Clinical signs or death are commonly seen within 24 hours of an acute exposure.
HISTORICALFINDINGS
Whole herd or a large percentage of the herd will usually be affected.
Individual clinical signs may differ, but there usually will be a common system affected.
Severe signs, including death, will be more common in the very young or old.
Usually a new feed batch or pasture recently treated can be identified.
Chronic exposures can be very difficult to identify.
PHYSICALEXAMINATION FINDINGS
Elevated temperatures can be recorded due to seizuring or other excessive muscle movement.
PATHOPHYS IOLOGY
Exposure to significant amounts of these chemicals
Toxicity levels vary for each compound as well as for the species involved.
RISK FACTORS
Improper storage or labeling of chemicals
Proper disposal of chemicals should have been followed especially for those products with bioaccumulation capabilities (chlorinated hydrocarbons, PBBs).
Age of animals-very young or very old are at higher risk.
Preexisting health and nutritional status
Amount of exposure and time before first identified
Dependent on chemical used, concentration, and formulation
DIAGNOSIS
History of possible exposure to chemicals directly to affected animal or to area/pasture where they were applied is suggestive.
DIFFERENTIALDIAGNOSIS
Neurologic signs-rabies, polioencephalomalacia, nervous ketosis, nervous coccidiosis, infectious thromboembolic meningoencephalitis, lead as well as other poisonings
Digestive signs-poisonous plants, coccidiosis, grain overload, frothy or gas bloat
Respiratory signs-infectious respiratory complex, nitrate toxicity (chlorate herbicides), bloat, acidosis, or other poisonings
CBC/BIOCHEMISTRY/URINALYS IS
Increased SGOT (PBBs)
Mostly unremarkable CBC and panels
Urine can be analyzed in some instances for chemicals or their by-products.
OTHER LABORATORY TESTS
Chromatography or other specialized tests can be run on frozen samples of brain, liver, kidney, fat, stomach contents, and suspected samples. These tests cannot be run on formalin-fixed tissues.
Normal workup to rule out the more common infectious agents
IMAGING
N/A
DIAGNOSTIC PROCEDURES
Fat biopsies, urine, and milk samples sometimes can be used to determine possible exposure.
PATHOLOGIC FINDINGS
Usually unremarkable
Many times will have pulmonary, renal, hepatic, or brain and spinal congestion
Petechial hemorrhages or blanching of the gastrointestinal tract
Cardiac parenchymal petechial hemorrhages suggestive of sudden death
TREATMENT APPROPRIATE HEALTH CARE
Immediate removal of possible contaminated source
Barbiturates, chloral hydrate, or diazepam for convulsing animals
Activated charcoal (900 g/adult cow)
Mineral oil drench
For chloral hydrate herbicide poisoning and methemoglobinemia, use a 2%-4% solution of methylene blue at 10 mg/kg IV.
Appropriate milk and meat withdrawal times must be followed for all compounds administered to food-producing animals.
NURSING CARE
Supportive care including IV fluids may be helpful.
ACTIVITY
Restrict activity and minimize stimulation.
DIET
Roughage diet may be needed if rumen motility was affected.
CLIENT EDUCATION
Proper storage and disposal of chemicals as directed by labels
Limit access of livestock to treated areas if indicated by label
SURGICALCONSIDERATIONS
N/A
MEDICATIONS DRUGS OF CHOICE
N/A
CONTRAINDICATIONS
Do not use corn oil or other type of digestible oil in drenching. These oils can increase the absorption of some chemicals. Only use mineral oil.
POSSIBLE INTERACTIONS
N/A
ALTERNATIVE DRUGS
N/A
FOLLOW-UP PATIENT MONITORING
Seizuring animals usually will do so only for the first 24 hours.
Animal/milk testing may be needed to determine amount of contamination and expected time needed to clear their system based on half-life of chemical.
PREVENTION/AVOIDANCE
Proper storage and disposal of all chemicals on farm
Proper labeling of all chemicals
Do not store chemicals next to feedstuffs.
POSSIBLE COMPLICATIONS
Some animals may not recover.
Some animals and/or their products (milk) may never be able to enter the human food chain.
EXPECTED COURSE AND PROGNOSIS
Highly variable
Severity of signs at any one point in time is not indicative of prognosis; must be able to monitor the progress before a better prognosis can be made.
Poor future performance is possible.
MISCELLANEOUS ASSOCIATED CONDITIONS
N/A
AGE-RELATED FACTORS
N/A
ZOONOTIC POTENTIAL
There is potential for agricultural chemical exposure to animals from milk and meat of poisoned animals.
In some states, there are restrictions on movement or marketing of cattle poisoned with agricultural chemicals.
The veterinarian should consult the local diagnostic laboratory or department of public health for questions specific to their practice area.
PREGNANCY
Early embryonic deaths have been attributed to PBBs.
RUMINANT SPECIES AFFECTED
All ruminant species are susceptible to toxicosis.
BIOSECURITY
N/A
PRODUCTION MANAGEMENT
Proper storage and disposal of all chemicals on farm
Proper labeling of all chemicals
Do not store chemicals next to feedstuffs.
SYNONYMS
Chlorinated hydrocarbons are also known as organochlorines.
SEE ALSO
FARAD
Specific toxicity chapters Toxicology: herd outbreaks ABBREVIATIONS
FARAD = Food Animal Residue Avoidance Databank IV = intravenous
PBBs = polybrominated biphenyls
SGOT = serum glutamic oxaloacetic transaminase
Suggested Reading
Campagnolo, E. R., Kasten, S., Banerjee, M. 2002, Oct. Accidental ammonia exposure to county fair show livestock due to contaminated drinking water. Vet Hum Toxicol. 44(5): 282-85.
Coppock, R. W., Mostrom, M. S., Khan, A. A., Semalulu, S. S. 1995, Dec. Toxicology of oil field pollutants in cattle: a review. Vet Hum Toxicol. 37(6): 569-76.
Galey, F. D. 2000, Nov. Diagnostic toxicology for the food animal practitioner. Vet Clin North Am Food Anim Pract. 16(3): 409-21.
Hoff, B., Boermans, H. J., Baird, J. D. 1998, Jan. Retrospective study of toxic metal analyses requested at a veterinary diagnostic toxicology laboratory in Ontario (1990-1995). Can Vet J. 39(1): 39-43.
Reigart, J. R., Roberts, J. R. 1999. Recognition and management of pesticide poisonings. 5th ed. Washington, DC: U.S. Environmental Protection Agency. Also available online http://www.epa.gov/pesticides/safety/healthcare.
Smith, R. A. 2000, Nov. Toxicology. Vet Clin North Am Food Anim Pract. 16(3): 545-57.
Villar, D., Schwartz, K. J., Carson, T. L., Kinker, J. A., Barker, J. 2003, Mar. Acute poisoning of cattle by fertilizer- contaminated water. Vet Hum Toxicol. 45(2): 88-90.
Author: Alejandro Ramirez

AKABANE
BASICS DEFINITION
Akabane, also known as congenital arthrogryposis-hydranencephaly syndrome, is a viral disease of ruminants that has the potential for serious economic losses. It results in abortions, stillbirths, premature births, and deformities of the fetus or newborn with no clinical signs in the dam during pregnancy.

The Akabane virus is an arbovirus (transmitted by arthropods) in the family Bunyaviridae, genus Orthobunyavirus.
The single-stranded RNA virus causes intrauterine infection of the fetus in pregnant cattle, sheep, and goats. After invading the endothelium of the placenta, the virus replicates in the trophoblastic cells and the fetus itself, resulting in death or deformities of the fetus or newborn.
Akabane is similar to Cache Valley virus, which is found in the United States.
The vector for Akabane virus has not been proven, however epidemiological evidence suggests that mosquitoes and gnats spread the virus.
Akabane virus has been isolated from a number of mosquito species (Aedes, Culex, Anopheles) as well as Culicoides
species (biting midges).
Direct contact, infected tissues, exudates, body fluids, or fomites do not transmit Akabane.
Ruminants do not appear to become long-term carriers of this virus.
SYSTEMS AFFECTED
Reproductive-arthrogryposishydranencephaly syndrome, abortions, stillbirths
Musculoskeletal-arthrogryposis (persistent flexion of joints)
Neurological-hydranencephaly (absence of the cerebral hemisphere tissue, which becomes occupied by cerebrospinal fluid)
GENETICS
N/A
INCIDENCE/PREVALENCE
Incidence for Akabane and the potential for epizootics is correlated with climatic factors, a distinct seasonal pattern (warm, moist summer and autumn months), the geographic distribution of competent vectors, and the availability of susceptible ruminant populations.
In endemic areas, most animals are immune to Akabane virus by the time they reach sexual maturity.
Surveys indicate that more then 80% of adult cattle in an endemic area are seropositive for the virus. However, following years of drought or times of reduced vector populations, native livestock may not be exposed prior to breeding age and therefore become susceptible.
Data from Japanese and Australian outbreaks suggest that the virus subsequently may invade the fetus in approximately 30-40% of infected pregnant cows.
GEOGRAPHIC DISTRIBUTION
Akabane is a foreign animal disease in the United States. It is, however, common in the tropics and subtropics. It is considered endemic in northern Australia, Japan, Israel, and Korea. Occasional outbreaks have occurred in southern Australia, Asia, the Middle East, and South Africa, when conditions are favorable for virus transmission.
Outbreaks typically occur in areas where naïve and susceptible animals are located and when environmental conditions are favorable for the disease.
Most epizootics occur at the northern and southern periphery of the endemic band or to susceptible animals introduced into endemic areas.
Outbreaks usually occur in late winter, indicating that the peak of virus activity and fetal infections occurs during the previous late summer and early autumn periods.
SIGNALMENT
Species
Disease from Akabane virus only occurs in cattle, sheep and goats; however, antibodies to the virus have been found in horses, buffalo, deer, camels, dogs, monkeys, and most recently pigs.
Breed Predilections
N/A
Mean Age and Range
The disease primarily affects fetal or newborn cattle, sheep, and goats.
Adult animals do not typically show any sign of the disease. However, there has recently been documentation of five adult cattle in Korea that have developed neurological signs (encephalomyelitis) due to the virus.
Predominant Sex
N/A
SIGNS GENERALCOMMENTS
Adult ruminants with Akabane infection are typically asymptomatic.
Viremia usually occurs 1-6 days after infection and lasts for 1-9 days. Only during this limited time are viral titers sufficient for potential vectors.
Long-term carriers of the disease are not believed to occur.
HISTORICALFINDINGS
Cases will most likely be noted in naïve pregnant animals that have been introduced into an endemic area or have had exposure to competent vectors.
PHYSICALEXAMINATION FINDINGS
Congenital abnormalities of the fetus or newborn are the hallmark of this disease. Effects on the young vary depending on the stage of gestation reached at the time of infection.
When infected late in the first trimester, animals are usually born bright and alert but are unable to stand, are ataxic, and may have one or more paralyzed limbs.
Muscle atrophy, limb rotation, exophthalmos (protruding eyes), and abnormal vocalization may also occur.
Animals infected during the second trimester have arthrogryposis at birth; most cannot stand. The joints are rigid and fixed in flexion and muscles are severely atrophied.
Torticollis, scoliosis, and kyphosis may also be seen.
When infected late in pregnancy, animals can usually stand and walk, but have behavioral abnormalities, such as slow or absent suckle reflex, depression, dullness, periodic hyperexcitablility, incoordination, and blindness.
Skull deformities can be common.
Dystocia at parturition may occur due to the deformities of the fetus.
CAUSES
Akabane virus is transmitted by arthropods (biting midges, mosquitoes) and the virus affects the developing fetus in ruminants.
Outbreaks are typically related to seasonal conditions that enhance the vectors.
RISK FACTORS
The major risk factor for Akabane is exposure of pregnant ruminants (particularly naïve animals) to potential vectors in endemic areas.
DIAGNOSIS
A presumptive diagnosis of Akabane disease can be made on the basis of clinical and postmortem examination. Diagnosis is typically confirmed by serology.
DIFFERENTIALDIAGNOSIS
Cache Valley virus
Bluetongue
Bovine viral diarrhea
Border disease
Wesselsbron virus
Nutritional, genetic, or toxic causes of abortion and/or fetal deformities
CBC/BIOCHEMISTRY/URINALYS IS
N/A
OTHER LABORATORY TESTS
Virus isolation should be done but is rarely successful unless the fetus and placenta were aborted before the fetus developed an immune response.
Specimens to collect include the placenta, fetal muscle, cerebrospinal fluid, and fetal nervous tissue.
Serology may be performed on fetal or precolostral serum and the serum from the dam.
Histopathology of the spleen, liver, lung, kidney, heart, lymph nodes, affected muscle, spinal cord, and brain can also be done.
IMAGING
N/A
DIAGNOSTIC PROCEDURES
N/A
PATHOLOGIC FINDINGS
Arthrogryposis and hydranencephaly are the most commonly noted lesions.
Most of the affected joints are ankylosed and cannot be straightened.
Other neurological lesions may include hydrocephalus, agenesis of the brain, microencephaly, proencephaly, and cerebellar cavitation.
Additionally, fibrinous leptomeningitis or ependymitis, spinal cord agenesis or hypoplasia, torticollis, scoliosis, brachygnathism, cataracts, ophthalmia (severe inflammation of the eye), hypoplastic skeletal muscles and lungs, or fibrinous polyarticular synovitis may be seen.
TREATMENT APPROPRIATE HEALTH CARE
There is no effective treatment for Akabane virus.
Most affected neonates die or must be euthanized soon after being born.
Animals with mild symptoms may gradually become more mobile, but most die by 6 months.
Subsequent pregnancies of the infected dam will not be affected.
NURSING CARE
N/A
ACTIVITY
N/A
DIET
N/A
CLIENT EDUCATION
In endemic areas, advise clients of the risks to newly introduced animals, especially during late summer and autumn months.
SURGICALCONSIDERATIONS
N/A
MEDICATIONS DRUGS OF CHOICE
N/A
CONTRAINDICATIONS
N/A
PRECAUTIONS
N/A
POSSIBLE INTERACTIONS
N/A
ALTERNATIVE DRUGS
N/A
FOLLOW-UP PATIENT MONITORING
N/A
PREVENTION/AVOIDANCE
Prevention of Akabane disease includes vector control measures and vaccination. Akabane virus does not appear to be transmitted between animals, except by arthropod vectors.
Prevention efforts should include elimination of vector breeding sites, and repellants or screened housing for pregnant animals.
Avoid breeding ruminants during the prime transmission season (late summer and autumn).
An inactivated and an attenuated vaccine have been developed and used in Japan. An effective killed vaccine has been developed but not marketed in Australia. The vaccines must be used prior to exposure to the infected vectors. A vaccine is not currently available in the United States.
POSSIBLE COMPLICATIONS
N/A
EXPECTED COURSE AND PROGNOSIS
Most affected neonates die or must be euthanized soon after being born. Subsequent pregnancies of the infected dam will not be affected.
MISCELLANEOUS ASSOCIATED CONDITIONS
N/A
AGE-RELATED FACTORS
Akabane affects fetal or newborn cattle, sheep, and goats.
ZOONOTIC POTENTIAL
There is no evidence that humans can be infected by Akabane virus.
PREGNANCY
Effects of Akabane virus are dependent on the stage of pregnancy when infected. However, most affected neonates die or must be euthanized soon after birth despite the time of infection.
RUMINANT SPECIES AFFECTED
Cattle, sheep, and goats
BIOSECURITY
Suspected cases or outbreaks of Akabane outside of its endemic area (see geographical distribution), should immediately be reported to the proper governmental veterinary authorities (e.g., state or federal veterinarian).
PRODUCTION MANAGEMENT
In endemic areas, avoid introducing naïve pregnant animal in summer and autumn.
Implement vector control measures to reduce the potential transmission of the virus.
Consider vaccination protocols prior to breeding.
SYNONYMS
Acorn calves
Congenital arthrogryposis-hydranencephaly (A-H) syndrome Congenital bovine epizootic A-H syndrome
Curly calf disease Curly lamb disease Dummy calf disease Silly calves
SEE ALSO
Arthrogryposis Bluetongue Border disease
Bovine viral diarrhea Cache Valley virus
Nutritional, genetic, or toxic causes of abortion and/or fetal deformities Wesselsbron virus
ABBREVIATIONS
A-H = arthrogryposis-hydranencephaly
Suggested Reading
Charles, J. A. 1994. Akabane virus. Vet Clin North Am Food Anim Pract. 10(3): 525-46. Foreign Animal Disease Gray Book. Akabane.
Accessed at http://www.vet.uga.edu/vpp/gray book/FAD/AKA.htm.
Kirkland, P. D. 2002. Akabane and bovine ephemeral fever virus infections. Vet Clin North Am Food Anim Pract. 18:501-14.
Author: Glenda Dvorak

ALOPECIA
DEFINITION

Alopecia means partial or complete loss of hairs in an area where hairs are normally found.
The terms “hair loss” and “alopecia” are often used interchangeably.
The term “hypotrichosis” is a more accurate term for congenital or hereditary hair loss or alopecia because it refers to less than an expected amount of hair.
PATHOPHYS IOLOGY
There are two major etiologies of alopecia or hair loss:congenital or hereditary and acquired.
Acquired hair loss is the result of any disease that causes direct damage to the hair follicle or skin (e.g., dermatophytosis) or indirect damage (e.g., pruritus).
Acquired hair loss may or may not be permanent depending upon the amount of follicular damage.
Congenital alopecia may or may not be hereditary and it is caused by the lack of the development of hair follicles. These changes are permanent.
Congenital alopecia is usually evident shortly after birth.
Hereditary alopecia may be evident shortly after birth or may develop as the animal ages.
SYSTEMS AFFECTED
Skin
GENETICS
Hereditary and/or congenital alopecia are rare and several syndromes have been described (see Alopecia Table 1).
INCIDENCE/PREVALENCE
Acquired alopecia is a common skin disease in ruminants.
Hereditary and/or congenital alopecia is rare.
GEOGRAPHIC DISTRIBUTION
N/A
SIGNALMENT
Congenital and/or hereditary alopecia may or may not be sex linked (Table 1).
Congenital and/or hereditary alopecia is usually evident at birth or shortly thereafter (Table 1).
The signalment of inflammatory causes of hair loss reflect those of the underlying disease.
SIGNS
Alopecia may be focal, multifocal, symmetrical, or generalized.
Alopecia may develop acutely or gradually depending upon the cause.
Hyperpigmentation, lichenification, erythema, and pruritus are common findings in acquired alopecia.
Acquired alopecia may also be complicated by bacterial infections and/or seborrhea.
Congenital, hereditary, and endocrine alopecia is noninflammatory unless complicated by secondary infections or damage to the skin.
CAUSES
Diseases that destroy or damage hairs/hair follicles include bacterial skin diseases, dermatophytosis, demodicosis, severe inflammatory diseases, trauma, burns, frostbite, poisonings, and parasites.
Diseases that slow hair growth include poor nutrition and protein deficiencies.
Pregnancy, lactation, severe illness, and/or fever can cause a temporary alopecia characterized by large amounts of shedding within a few days.
Anagen defluxion occurs as a result of acute damage/cessation of growth in a growing hair shaft characterized by sudden massive hair loss.
Telogen defluxion occurs as a result of stressful situations (fever, illness, shock, anesthesia, surgery, etc.) that cause cessation of anagen hairs and synchrony of hair follicles into telogen and loss of hairs 1-2 months post event.
Any disease that causes pruritus (parasites, allergies, neoplasia) may result in hair loss.
Friction can cause local hair loss.
Alopecia areata is a rare disease that can cause focal noninflammatory alopecia in cattle.
Follicular dysplasia can present as focal, regional, or diffuse adult onset slowly progressive noninflammatory hair loss.
RISK FACTORS
Calves, kids, and lambs that develop severe illness and/or fevers are at risk for anagen defluxion.
Animals undergoing stressful situations are at risk for development of telogen defluxion.
Overcrowding, poor nutrition, and poor management may predispose animals to diseases associated with acquired hair loss.
DIAGNOSIS DIFFERENTIALDIAGNOSIS
Focal, regional, or generalized hair loss in a neonate-congenital or hereditary hair loss
Focal inflammatory alopecia: dermatophytosis, dermatophilosis, demodicosis, parasitic diseases, and staphylococcal folliculitis
Focal noninflammatory hair loss: alopecia areata
Generalized acute alopecia-telogen or anagen defluxion
Excessive generalized hair loss in spring-abnormal spring shed
Patchy hair loss in individual animals that have normal skin-abnormal shedding
Adult onset slowly progressive alopeciafollicular dysplasia
CBC/BIOCHEMISTRY/URINALYS IS
Routine laboratory tests are not usually very helpful in the diagnosis of alopecia.
OTHER LABORATORY TESTS
N/A
IMAGING
N/A
DIAGNOSTIC PROCEDURES
Skin scrapings to look for mites
Flea combings to look for macroscopic parasites (lice, keds, fleas)
Fungal culture for dermatophytosis
Skin biopsy can help differentiate between acquired and congenital/hereditary causes of alopecia.
Skin biopsy is the most cost effective diagnostic test.
Hair trichogram for differentiation of anagen versus telogen defluxion
PATHOLOGICAL FINDINGS
Anagen defluxion hairs have irregular and dysplastic hair shafts, hairs break easily.
Telogen defluxion hairs have a normal, uniform shaft diameter, clubbed nonpigmented root lacking a root sheath.
Small or absent hair follicles with little or no inflammatory changes are present in skin biopsies from congenital and hereditary alopecia.
Inflammatory changes characterize acquired alopecia; special stains may identify infectious agents (e.g., dermatophytes).
Atrophic, distorted hair follicles with melanin clumping are seen in follicular dysplasia.
TREATMENT
Depends upon underlying cause
No treatment for congenital or hereditary hair loss
Successful treatment depends upon the underlying cause and diagnosis.
MISCELLANEOUS ASSOCIATED CONDITIONS
N/A
AGE-RELATED FACTORS
N/A
ZOONOTIC POTENTIAL
Some causes of acquired alopecia are of zoonotic importance.
PREGNANCY
N/A
RUMINANT SPECIES AFFECTED
Cattle, goats, sheep, llamas, camels; potentially all species
BIOSECURITY
Highly contagious parasitic diseases may require quarantine of specific animals or herds.
PRODUCTION MANAGEMENT
Acquired causes of hair loss can cause decreased milk, meat, or reproduction depending upon the cause.
Congenital and/or hereditary alopecia compromise the health of the animal because of the lack of normal protection.
SYNONYMS
Hair loss, hypotrichosis
SEE ALSO
Camelid dermatology Dairy goat dermatology
Dermatologic pharmacology Dermatophilosis Hypothyroidism
Mange
ABBREVIATIONS
N/A
Suggested Reading
Drogemuller, C., Kuiper, H., Peters, M., Guionaud, S., Distl, O., Leeb, T. 2002. Congenital hypotrichosis with anodontia in cattle: a genetic, clinical and histological analysis. Veterinary Dermatology 13:307-13.
Howard, J. L., Smith, R. A. 1999. Skin diseases. In:Current veterinary therapy 4: food animal practice. Philadelphia: W.
B. Saunders.
Martin, W. B., Aitken, I. D., eds. Skin diseases. In:Diseases of sheep. 3rd ed. Edinburgh: Blackwell Science. Rebhun, W. C. 1995. Skin diseases. In: Diseases of dairy cattle. Baltimore: Williams and Wilkins.
Scott, D. W. 1988. Congenital and hereditary diseases. In:Large animal dermatology. Philadelphia: W. B. Saunders.
Steffen, D. J. 1993. Congenital skin abnormalities. Veterinary Clinics of North America Food Animal Practice 9(1): 105- 14.
Authors: Karen A. Moriello and Susan D. Semrad
Table 1 Summary of Congenital and/or Hereditary Types of Hypotrichosis
Source: Adapted from Scott, 1988.

ANALYTICAL TESTING
BASICS OVERVIEW

Energy status, protein values, liver function, macromineral levels, micromineral levels, vitamin status of domestic livestock and wild ruminants are important in the animals’ ability to maintain a healthy immune system.
Measuring serum levels as a diagnostic/prognostic indicator of health is a crucial tool in maintaining healthy animal populations.
SYSTEMS AFFECTED
Potentially all systems can be affected.
GENETICS
N/A
INCIDENCE/PREVALENCE
N/A
GEOGRAPHIC DISTRIBUTION
N/A
SIGNALMENT
Species
All ruminant species Breed Predilections N/A
Mean Age and Range
N/A Predominant Sex N/A
DIAGNOSIS
CBC/BIOCHEMISTRY/URINALYS IS OTHER LABORATORY TESTS
Energy Status
Energy balance is by far one of the most critical nutritional factors in animal health, lactation, and reproductive performance. Traditionally we have monitored changes in energy balance via body weight and condition changes over time. This procedure, however, may not be a sensitive enough tool when dealing with the transition cow.
NEFA-Nonesterified fatty acids
Serum NEFA concentration is directly associated with adipose tissue catabolism of triglycerides and is a measure of energy balance.
Feeding of dietary fats can slightly elevate serum NEFA, but not significantly to alter interpretation of energy balance.
Serum or plasma concentrations range from < 0.1 to 2.5 mEq/L (<0.1-2.5 mmol/L).
Concentrations are higher prior to a major feeding bout and reduce significantly following feeding. There is less significant variation in total mixed ration fed farms.
Reasonably stable in serum or plasma, but concentration greatly affected by hemolysis (lowers value)
BHB-ß-hydroxybutyrate
One of three ketone bodies generated by partial oxidation of fatty acids
Can be elevated due to dietary sources (dietary ketosis), primarily poorly fermented silages high in butyric acid; butyric acid converted to BHB by rumen epithelium
Serum or plasma concentrations range from < 1 mg/dL (0.1 mmol/L) to > 40 mg/dL (0.38 mmol/L)

Subclinical ketosis:> 14.5 mg/dL (1.4 mmol/L)
Clinical ketosis:> 26 mg/dL (2.5 mmol/L)

Greatest blood concentrations found 3-5 hours after feeding
Very stable analyte, but hemolysis may artificially elevate value
EXPECTED VALUES FOR METABOLIC PROFILING: Serum or plasma concentrations for NEFA and BHB in the periparturient dairy cow should remain below the concentrations shown (Table 1). Higher values are suggestive of potential energy balance problems.
Protein
There is no single measurable analyte that directly reflects protein status. As a result, a combination of metabolite parameters needs to be utilized, including serum or plasma UN, Cr, total protein, albumin, and Ck.
Serum or Plasma UN
UN reflects dietary protein status and balance relative to rumen and animal needs and is intertwined with available dietary fermentable carbohydrate. Insufficient dietary protein or excessive fermentable carbohydrate relative to degradable protein will result in lower UN concentrations. Likewise, excessive dietary protein or insufficient fermentable carbohydrate results in high UN concentrations.
Cr is used to assess renal function and its impact on UN values.
Concentrations can range from near 0 to over 30 mg/dL (0 to 21.4 mmol/L) and vary with feeding. Highest values occur between 3 and 5 hours after a meal.
Very stable metabolite, not affected by hemolysis
EXPECTED VALUES FOR METABOLIC PROFILING

Dry cows should maintain a mean serum or plasma UN concentration between 10 and 12 mg/dL (7.14-8.57 mmol/L).
Fresh cows should maintain a mean serum or plasma UN concentration between 12 and 14 mg/dL (8.57-10 mmol/L).
Individual values below 8 mg/dL and above 16 mg/dL are of concern and should be investigated.

Total protein
Concentration reflects dietary protein status, but due to half-life of protein molecules is not extremely sensitive to dietary changes.
Confounded by changes in gamma globulin in response to inflammatory conditions.
EXPECTED VALUES FOR METABOLIC PROFILING

Early dry cows: 6.5-8.3 g/dL
Close-up dry cows: 5.8-7.7 g/dL
Fresh cows: 6.1-8.8 g/dL
Values below 6 g/dL and above 9.5 g/dL should be investigated.

Albumin
Albumin has a relatively short half-life compared to other blood proteins and can reflect protein deficiency problems over a period of a month or two.
Physiologic concentrations range from 3.2 to 4.5 g/dL
Dehydration and protein-losing disease processes can confound interpretation of results.
Stable metabolite, even with hemolysis.
EXPECTED VALUES FOR METABOLIC PROFILING

Early dry cows: 3.5-4.0 g/dL
Close-up dry cows: 3.3-3.8 g/dL
Fresh cows: 3.5-4.2 g/dL
Close-up dry and fresh cows with albumin concentration < 3.25 g/dL and < 3.5 g/dL, respectively, are at greater risk for periparturient disease problems.

Ck (Creatine kinase)
Released from muscle when it is catabolized or injured
Due to a tremendous range in values, provides little diagnostic value unless coupled with other parameters
Concentrations between 400 and 1000 IU/L might suggest muscle breakdown and possible protein deficiency if coupled with corresponding changes in UN and albumin. Liver Function
Liver Function
Enzyme activities (GGT, AST, SDH) and total bilirubin concentrations
Elevations in any of these parameters suggest some insult has occurred to the liver but are not specific to liver.
SDH is liver specific for ruminants, but elevations cannot be directly attributed to fat infiltration of the liver.
Bilirubin values are most specific to bile flow problems than overt hepatocyte damage.
Enzyme activities have a wide potential range in values and need to be interpreted in conjunction with other measures of liver function.
Most enzymes are sensitive to freezing and thawing. Hemolysis will lower GGT, but increase AST activities.
EXPECTED VALUES FOR METABOLIC PROFILING

AST: Dry cows: 46-83 U/L; fresh cows: 61-103 U/L
GGT: Dry cows: 18-38 U/L; fresh cows: 20-49 U/L
SDH: 6.4-58.5 U/L
Total bilirubin: 0.1-0.3 mg/dL (1.71-5.13 mol/L)
Enzyme activities exceeding the above ranges would be of concern and liver function should be further evaluated.

Total cholesterol
Associated with various lipoprotein molecules in blood; provides an indicator for very low density lipoprotein (VLDL) production (fat export) by the liver
Serum or plasma concentrations are elevated with dietary fat feeding, which may confound interpretation.
Physiologic concentrations vary from < 70 up to 300 mg/dL (<2.0 up to 8.7 mmol/L) with lowest values observed around the time of calving.
Very stable metabolite, but artificially increased with hemolysis
EXPECTED VALUES FOR METABOLIC PROFILING

Early dry cows:> 80 mg/dL (>2.28 mmol/L)
Close-up dry cows:> 75 mg/dL (>2.14 mmol/L)
Fresh cows:> 100 mg/dL (>2.86 mmol/L)
Liver’s capacity to export fat is of concern whenever fresh cow cholesterol concentrations are less than close-up dry cows.

NEFA: Cholesterol ratio
The liver takes up NEFA in direct relationship with their concentration in blood. Once in the liver, NEFA can either be partially metabolized to ketone bodies or they can be used to synthesize triglycerides.
High NEFA associated with low cholesterol is suggestive of a situation where fat will accumulate in hepatocytes, inducing fatty liver condition.
Ratio is calculated on a molar ratio (mmol NEFA/mmol cholesterol).

mEq/L NEFA x 1 = mmol/L NEFA
mg/dL cholesterol x 0.02856 = mmol/L cholesterol

EXPECTED VALUES FOR METABOLIC PROFILING

Calculated ratio ranges from 0.01 to
0.2 for healthy cows with increasing values from early dry to fresh period.
Close-up dry cows with ratios > 0.2 are at greater risk for experiencing one or more periparturient disease problems.
Fresh cows with ratios > 0.3 are at greater risk for having postpartum disease problems.
Macrominerals

Macrominerals Ca, P, K, Mg, Na, Cl, and S are of extreme interest as to their status relative to their role in milk fever, alert downer cows, and weak cow syndrome.
Most of these minerals are tightly regulated in the body through a variety of homeostatic processes.
Blood concentrations of macrominerals are not reflective at all of dietary status when the homeostatic system is properly functioning.
Phosphorus, K, Mg, and S are those macrominerals in which blood concentrations are somewhat sensitive to dietary intake.
Macromineral concentrations need to be carefully interpreted in light of whether or not the homeostatic system is in proper operation.
Mineral concentrations are very stable, but can be altered by prolonged exposure to the clot (serum sample) or hemolysis (P, Mg, K artificially elevated).
EXPECTED VALUES FOR METABOLIC PROFILING (Table 2)
Microminerals
Microminerals are of interest relative to their role in modulating immune function as well as other important metabolic roles.
Cu, Fe, Se, and Zn are routinely assayed in blood as their concentrations are within detectable limits with current analytical diagnostics.
Blood or serum micromineral concentrations are buffered from acute changes as a result of dietary problems through mobilization of storage minerals, usually from the liver; thus blood concentrations may not adequately reflect nutritional status.
Liver trace mineral status may be a better indicator of dietary adequacy, whereas measurement of a mineral-specific enzyme activity better reflects presence of overt clinical deficiency disease compared to blood concentrations.
Many trace mineral concentrations in blood are influenced by disease. Bacterial infections induce sequestering of iron and zinc and elevation of copper, thus confounding interpretation of blood mineral status.
Physiologic state and age influence blood and liver micromineral concentrations and must be accounted for in interpretation of concentrations.
Minerals are very stable in blood, serum, or plasma, but hemolysis can greatly distort serum Se and Zn concentrations.
EXPECTED VALUES FOR METABOLIC PROFILING (ADULT VALUES ONLY) (Table 3)
Vitamins
Vitamins A and E are of greatest potential interest for metabolic profiling relative to their role in immune function and association with mastitis, metritis, and retained placenta.
Vitamin analyses are affected by hemolysis and are prone to oxidation (direct sunlight). Samples should be iced following collection and remain chilled or frozen until analysis.
Age and physiologic state influence serum and liver vitamin concentrations and reference values need to be adjusted accordingly.
Vitamin A (total retinol)
Concentration of total retinol can be measured in serum (plasma) or liver tissue.
Serum concentration is less indicative of dietary status and can be influenced by Zn and protein status as they impact retinol-binding protein availability.
Serum concentration declines during late gestation.
Liver vitamin A concentration reflects the storage pool and is sensitive to dietary status.
Both serum and liver concentrations are diagnostic for disease problems.
EXPECTED VALUES FOR METABOLIC PROFILING (ADULTS ONLY)
Sample
Adequate Range
Deficient
Serum
225-500 µg/mL (0.79-1.74 µmol/L)
<150 µg/mL (<0.52 µmol/L)
Liver
300-1100 µg/g dry weight
<40 µg/g dry weight
Vitamin E (a-tocopherol)
Concentration of a-tocopherol can be measured in either serum (plasma) or liver tissue.
Serum concentrations generally reflect dietary intake, but are influenced by variations in blood lipoprotein content.
Serum concentrations decline in late gestation.
Relating serum vitamin E to total cholesterol concentration reduces variation as vitamin E is carried on blood lipoproteins.
Vitamin E to cholesterol ratio is calculated on a molar basis (µmol vitamin E/µmol cholesterol) and is unitless.
Liver vitamin E concentration is reflective of the storage pool and reflects nutritional status.
Both serum and liver vitamin E concentrations are diagnostic for disease problems.
EXPECTED VALUES FOR METABOLIC PROFILING (ADULTS ONLY) (Table 5)
INTERPRETATION
A complete understanding of underlying metabolic and physiologic mechanisms controlling blood metabolite concentrations is necessary to properly interpret metabolic profiles and their application.
Unlike the interpretation of individual cow clinical chemistry profiles, interpretation of metabolic profiles requires appreciation of statistical probabilities and acceptable level of risk.
Table 5
Sample
Adequate Range
Deficient
Serum
3-10 g/mL
<3.0 g/mL
Vitamin E: Cholesterol ratio
2.5-6.0
<1.5
Liver
20-40 µg/g dry weight
<10 µg/g dry weight
Reference values for each metabolite need to be refined to minimize inherent variability due to effects of age, physiologic state, production level, and other cow-specific factors on analyte concentration and improve sensitivity of analyte to environmental (i.e., nutritional) influences.
REFERENCE VALUES
Interpretation of metabolic profiles requires some standard reference values for comparison.
Analyte reference values should represent the population mean and variation from a defined population of animals clinically evaluated to be free of disease and other health problems.
Each population mean needs to be statistically analyzed for a normal population distribution.
Median values should be used in place of means for metabolites not showing a normal distribution.
Abnormal metabolite values are defined as those outside of the predefined normal reference range.
At present, few laboratories have specialized blood analyte reference criteria that are adjusted for age, physiologic state, and time relative to calving effects.
Research is currently under way to develop appropriate metabolic profiling reference criteria.
Until more specific criteria are developed, use of current reference ranges adjusted to a 1 or 1.3 standard deviation have been used for interpretation.
ASSESSMENT
Metabolic profile results must be correlated with animal and dietary evaluations.
Mean comparison to reference range
Individual samples within groupings

Mean values and standard deviation for all analytes are calculated for each sampled individual within a defined group.
Means and associated statistical variation are compared to reference range.
Sampled populations where 10-25% of individuals are outside the reference range might be considered to be subclinical. If more than 40% are outside the range, then there is a greater risk of clinical disease.

Pooled samples within groupings

Pooled analyte values are compared to reference range mean or median.
Pooled values should be within a 0.5 standard deviations of reference mean to be considered normal.
As pooled values deviate further from the reference mean, potential for subclinical and clinical disease will increase.
More research is needed to better define pooled sample interpretation.

Comparison across groups
Besides comparing individual group means to reference ranges, tracking metabolite concentrations across physiologic groups within a herd may provide useful information.
This assuming there have not been any major feed changes within group rations over a period of time.
This process is useful in evaluation of transition cow problems. Compare analyte values across early dry, close-up dry, and fresh cow groups.
Changes in group means are correlated with observed clinical signs, body condition changes, and ration evaluations to come up with some interpretation and recommendations.
Mean comparison within groups over time
Statistical process control-statistical method used by industry to track quality control in manufacturing
Same concepts can be applied to repeated measures of analytes within a defined group over time.
Determine overall mean and statistical variation within and between time periods.
Track means graphically identifying individual tests outside of control limits or three or more consecutive means above or below overall average.
Proportion comparison within groups
Compare individual samples to analyte reference value.
Identify all individuals that have values exceeding or below defined threshold value.
Determine proportion of individuals with abnormal values.
With increasing proportion of individuals with abnormal values, there is an increasing risk of subclinical to clinical disease problems.
MISCELLANEOUS ASSOCIATED CONDITIONS
N/A
AGE-RELATED FACTORS
N/A
ZOONOTIC POTENTIAL
N/A
PREGNANCY
N/A
RUMINANT SPECIES AFFECTED
All ruminant species are affected
BIOSECURITY
N/A
PRODUCTION MANAGEMENT
N/A
SEE ALSO
Bovine blood chemistry
Differential diagnosis: philosophy of test usage Fatty liver
Ketosis
Rumen dysfunction: acidosis
ABBREVIATIONS
AST = aspartate aminotransferase BHB =ß-hydroxybutyrate
Ck = creatine kinase Cr = creatinine
GGT =?-glutamyltransferase NEFA = nonesterified fatty acids SDH = sorbitol dehydrogenase UN = urea nitrogen
Suggested Reading
Herdt, T. H. 2000. Variability characteristics and test selection in herd-level nutritional and metabolic profile testing. Vet Clinics NA: Food Anim Pract. 16(2): 387-403.
Herdt, T. H., Dart, B., Neuder, L. 2001. Will large dairy herds lead to the revival of metabolic profile testing? AABP Proceedings 34:27-34.
Herdt, T. H., Rumbeiha, W., Braselton, W. E. 2000. The use of blood analyses to evaluate mineral status in livestock. Vet Clinics NA: Food Anim Pract. 16(3): 423-44.
Oetzel, G. R. 2003. Herd-based biologic testing for metabolic disorders. Available at: http://www.vetmed.wisc.edu/dms/fapm/fapmtools/2nutr/herdtest.pdf, Accessed August 16, 2004.
Van Saun, R. J. 1997. Nutritional profiles: A new approach for dairy herds. Bov Pract. 31(2): 43-50.
Van Saun, R. J., Wustenberg, M. 1997. Metabolic profiling to evaluate nutritional and disease status. Bov Pract. 31(2): 37-42.
Author: Robert J. Van Saun

ANAPHYLAXIS
BASICS DEFINITION

An anaphylactic reaction is a pathological immune response that occurs following exposure of a sensitized animal to a specific antigen. This exposure results in urticaria, pruritus, and angioedema, followed by vascular collapse, shock and often life-threatening respiratory distress.
Anaphylaxis has now been included under type I (immediate) hypersensitivity.
PATHOPHYS IOLOGY
Anaphylaxis is an acute systemic manifestation of the interaction of an antigen (allergen) binding to IgE antibodies, which are bound to mast cells and basophils. This binding of antigens to cell-bound IgE antibodies triggers the release of chemical substances from the mast cells and basophils.
The major biologically active mediators produced by mast cells and basophils include histamine, leukotrienes, the eosinophilic chemotactic factor, platelet-activating factor, kinins, serotonins, and proteolytic enzymes. These chemicals directly affect both the vascular system, causing vasodilatation and increased vascular permeability, and smooth muscles, causing contraction of the bronchi and respiratory distress.
SYSTEMS AFFECTED
Cardiovascular, pulmonary, urinary, gastrointestinal, integument
GENETICS
There have been reports of higher incidence in certain lines and breeds of cattle.
INCIDENCE/PREVALANCE
Sporadic, dependent on exposure to inciting antigen
GEOGRAPHIC DISTRIBUTION
N/A
SIGNALMENT
Bovine, ovine; also reported in many other species of ruminants
SIGNS
Sudden, severe dyspnea, muscle tremors, anxiety, occurs within a few to 10-15 minutes following exposure to the antigen; Muscle tremor may be severe and temperature may rise to 105°F
History of injection in the previous hour
Occasionally profuse salivation, mild bloat, diarrhea, urticaria, angioneurotic edema, and rhinitis
Laminitis rarely occurs in ruminants.
PHYSICALEXAMINATION FINDINGS
Auscultation of the chest-vesicular murmur, crackling if edema is present, and emphysema in the later stages if dyspnea was severe
CAUSES
Common agents causing anaphylaxis include blood transfusions, vaccines, horse sera, insect bites, heterologous enzymes and hormones, and certain drugs, such as penicillin and lidocaine.
Milk allergy occurs occasionally in cows. This can happen when there is increased intramammary pressure to a point that normally sequestered milk components, notably casein, gain access to the circulation; these “foreign” proteins induce a type I hypersensitivity.
RISK FACTORS
Previous exposure to antigens (i.e., previous treatment with blood or blood products or vaccines)
DIAGNOSIS DIFFERENTIALDIAGNOSIS
Acute Bloat
A history of introduction to new forage and/or concentrate diet. Obvious distention of the rumen occurs suddenly, and the left flank may be so distended that the paralumbar fossa protrudes above the vertebral column; the entire abdomen is enlarged. Dyspnea and grunting are marked and are accompanied by mouth breathing, protrusion of the tongue, and extension of the head.
Acute Bronchopneumonia
A history of recent episodes of stress (i.e., weaning, transport, vaccination) within the last 2-7 days. Clinical signs of bacterial bronchopneumonia are often preceded by a viral infection of the respiratory tract. With the onset of secondary bacterial pneumonia, the severity of clinical signs increases and is characterized by depression and toxemia. There will be fever (104-106°F); serous to mucopurulent nasal discharge; moist cough; a rapid, shallow respiratory rate and dyspnea. Auscultation of the lung field reveals increased bronchial sounds, crackles, and wheezes. In severe cases, pleurisy may develop, which is characterized by an irregular breathing pattern and grunting on expiration.
CBC/BIOCHEMSTRY/URINALYS IS
Increase in PCV, high plasma K+, neutropenia
OTHER LABORATORY TESTS
N/A
IMAGING
N/A
DIAGNOSTIC PROCEDURES
N/A
PATHOLOGIC FINDINGS
Lungs-severe pulmonary edema in calves and lambs; pulmonary edema and emphysema without blood engorgement
TREATMENT APPROPRIATE HEALTH CARE
Ancillary support of blood pressure (IV fluids) and respiration may be necessary.
In dairy cattle that have been recently dried off, recovery usually is prompt once the gland is emptied.
ACTIVITY
N/A
DIET
N/A
CLIENT EDUCATION
Clients may be instructed to have epinephrine on hand so it can be administered as soon as signs are noted.
SURGICALCONSIDERATIONS
N/A
MEDICATIONS DRUGS OF CHOICE
Anaphylactic shock is treated with an IV injection of epinephrine.
Corticosteroids potentiate the effects of epinephrine and may be given following the administration of epinephrine.
Antihistamines have no effect once signs are present.
CONTRAINDICATIONS
N/A
PRECAUTIONS
When treating food-producing animals, drug withdrawal times must be determined and maintained.
POSSIBLE INTERACTIONS
N/A
ALTERNATIVE DRUGS
N/A
FOLLOW-UP PATIENT MONITORING
Animals need to have their respiratory system monitored for the next 24 hours to detect any emphysema.
PREVENTION/AVOIDANCE
Discuss the situation associated with the onset with the producer. Certain products may need to be avoided.
POSSIBLE COMPLICATIONS
Emphysema may result from severe dyspnea and violent muscle spasms.
EXPECTED COURSE AND PROGNOSIS
Animals treated promptly usually return to normal within 12 to 24 hrs.
MISCELLANEOUS ASSOCIATED CONDITIONS
N/A
AGE-RELATED FACTORS
N/A
ZOONOTIC POTENTIAL
N/A
PREGNANCY
Following anaphylaxis, animals may spontaneously abort.
RUMINANT SPECIES AFFECTED
Bovine, ovine, other ruminants
BIOSECURITY
N/A
PRODUCTION MANAGEMENT
N/A
SYNONYMS
Type 1 hypersensitivity
SEE ALSO
Acute bloat
Acute bronchopneumonia
ABBREVIATIONS
IgE = immunoglobulin E IV = intravenous
PCV = packed cell volume
Suggested Reading
Gershwin, L. J. 2001. Immunoglobulin E-mediated hypersensitivity in food-producing animals. Vet Clin North Am Large Anim Pract. 17(3): 599-619.
Meeusen, E. N. 1999, Aug 1. Immunology of helminth infections, with special reference to immunopathology. Vet Parasitol. 84(3-4):259-73.
Ruby, K. W., Griffith, R. W., Gershwin, L. J., Kaeberle, M. L. 2000, Oct 20. Haemophilus somnus-induced IgE in calves vaccinated with commercial monovalent H. somnus bacterins. Vet Microbiol. 76(4):373-83.
Ruby, K. W., Griffith, R. W., Kaeberle, M. L. 2002, Jan 25. Histamine production by Haemophilus somnus. Comp Immunol Microbiol Infect Dis. (1):13-20.
Schultz, K. T. 1982, Nov 15. Type I and type IV hypersensitivity in animals. J Am Vet Med Assoc. 181(10):1083-87.

ANAPLASMOSIS
BASICS OVERVIEW

Anaplasmosis is a hemoparasitic disease with a worldwide distribution, most common in tropical and subtropical areas.
Upon infection, Anaplasma organisms double in number every 24 hours for the first several days.
PATHOPHYS IOLOGY
Infected red blood cells are destroyed by the reticuloendothelial system (spleen) leading to extravascular hemolysis and anemia.
SYSTEMS AFFECTED
Hemolymphatic
GENETICS
N/A
INCIDENCE/PREVALENCE
Unknown
GEOGRAPHIC DISTRIBUTION
Worldwide distribution
SIGNALMENT
Species
Primarily cattle but also sheep, goats, and many wild ruminants
Breed Predilections
N/A
Mean Age and Range
Cattle under 6 months of age generally show no clinical signs.
In cattle from 6 months to 3 years of age, signs are progressively more severe.
Mature cattle (over 3 years of age) are the most susceptible to severe clinical manifestations of the disease. Mortality in this age group can be as high as 50% in naïve herds.
Predominant Sex
N/A
SINGS
In the early stages of the disease, cattle may appear lethargic, be anorexic, have decreased milk production, and develop fever.
Pale or icteric mucous membranes will be present.
Other signs include depressed rumination, constipation with dark brown mucous-covered feces, dry muzzle, and weight loss.
Hemoglobinemia and hemoglobinuria are not seen with anaplasmosis.
Infected cattle subsequently develop varying degrees of anemia, which can be fatal if untreated.
Cattle exhibiting signs of anaplasmosis should be handled with caution.
Cerebral anoxia can cause aggressiveness.
Severe anemia coupled with stress may precipitate sudden death.
If anemia is severe, abortions may occur due to fetal anoxia.
If animals survive the initial infection, they generally become carriers, maintaining a low level of infection without overt clinical signs.
CAUSES AND RISK FACTORS
Three species of Anaplasma have been identified.
Anaplasma marginale is the most common cause of disease in cattle.
Anaplasma centrale can cause mild disease in cattle.
Anaplasma ovis causes mild disease in sheep.
There is some cross-protection between species.
Other species of Anaplasma are suspected but have not been definitely identified in ruminants.
Strains of the organism vary in pathogenicity.
The disease is spread biologically and mechanically.
Biological transmission occurs with Dermacentor spp. ticks.
Mechanical transmission occurs with tabanid flies and blood-contaminated instruments (such as needles, tattooers, dehorners, and castrating equipment).
Transmission is highest during heavy tick and fly seasons.
Moving naïve adults into an endemic area or carrier animals into a nonendemic area often results in outbreaks of the disease.
Black-tailed deer are effective reservoirs of A. marginale and complicate control of the disease in some areas. White-tailed deer are uncommon reservoirs.
DIAGNOSIS DIFFERENTIALDIAGNOSES
Babesiosis-presence of hemoglobinuria, identify typical piriform organisms on Giemsa-stained blood smear
Leptospirosis-elevated titers, identification of organism in urine by dark-field microscopy
Bacillary hemoglobinuria or Clostridium novyi infection-presence of hemoglobinuria, liver enzyme elevation; identify organisms on impression smear of liver on freshly dead specimen
Hepatotoxic plants, for example: Senecio spp., Crotalaria spp., Lantana camara-evidence of plant ingestion, marked elevation of liver enzymes, histopathology of liver
Severe intestinal parasitism-fecal examination
Copper toxicity, most commonly in sheep-methemoglobinemia, hemoglobinuria, elevated serum, liver and kidney copper concentrations, elevated renal and hepatic enzymes
CBC/BIOCHEMISTRY/URINALYS IS
Blood collected from animals showing clinical signs will appear thin and watery.
The packed cell volume will be severely decreased (less than 30%).
A regenerative response will appear leading to anisocytosis, basophilic stippling, poikilocytosis, polychromatophilia, and reticulocytosis.
A blood smear stained with Wright’s, new methylene blue, or Giemsa stain will definitively diagnose Anaplasma organisms. The organisms will appear darkly stained on red blood cells. A. marginale is typically at the periphery of the cell and A. centrale is at the center.
A biochemical panel will generally show increased serum urea nitrogen, total and direct bilirubin (BILI), and aspartate aminotransferase (AST).
Hemoglobinemia and hemoglobinuria are not seen in anaplasmosis.
IMAGING
N/A
DIAGNOSTIC PROCEDURES
Cytology on a direct, Giemsa-stained blood smear is the most common method of diagnosis in animals showing clinical signs.
Rapid card agglutination and complement fixation tests are commonly used to diagnose the carrier stage.
Recent research suggests that a nested polymerase chain reaction (PCR) test is better at accurately detecting the carrier stage than complement fixation. PATHOLOGIC FINDINGS GROSS FINDINGS
Tissues will have an anemic pallor.
Icterus may be present later in the course of disease.
Splenomegaly is common.
Hepatomegaly is found in some cases.
Petechiae are occasionally found in pericardial tissues.
HISTOPATHOLOGICAL FINDINGS
Staining of tissues may reveal organisms infecting blood cells in capillaries.
Hepatic changes may include swelling of parenchymal cells, centrilobular necrosis with bile retention and hemosiderosis
Renal changes may include degeneration of tubular cells and protein infiltrates in tubular lumens and the capsular space.
TREATMENT
Handle affected animals with caution, as anoxia can lead to aggressiveness or sudden death.
Other than antibiotic therapy, only supportive care is needed.
If PCV is below 12%, a blood transfusion may be warranted.
MEDICATIONS DRUGS OF CHOICE
If cleanup of carriers is attempted, animals should be retested 6 months after treatment.
Oxytetracycline is the treatment of choice for anaplasmosis infections and can be used according to labeled dosages.
For treatment of acute disease, administer 11 mg/kg intravenously once daily for 3-5 days.
A long-acting (or depot) form of oxytetracycline can also be used for treatment of acute disease at 20 mg/kg intramuscularly every 72 hours for one to two treatments.
In endemic areas, control can be achieved with
6.6-11mg/kg of the nondepot form or 20 mg/ml of the depot form of oxytetracycline every 21-28 days from the start of the vector season until 1-2 months after vector season ends.
Chlortetracycline in feed at 0.22-0.55 mg/kg daily year-round
Chlortetracycline in feed at 1.1 mg/kg daily during the vector season
Clearance of the carrier state can be achieved with
Four treatments utilizing a depot form of oxytetracycline at 20 mg/kg intramuscularly or subcutaneously every 72 hours
Chlortetracycline in feed at 1.1 mg/kg daily for 120 days or 11 mg/kg daily for 60 days
Observe appropriate meat and milk withdrawal times.
CONTRAINDICATIONS
If the carrier state is cleared using antibiotic therapy, cattle will become susceptible to reinfection. In endemic areas, it may not be advisable to clear the carrier state.
Drug withdrawal periods for meat and milk must be followed.
FOLLOW-UP
If cleanup of carriers is attempted, animals should be retested 6 months after treatment.
MISCELLANEOUS
There have been vaccines available at various times for use in controlling losses associated with anaplasmosis, however, their efficacy has generally been poor. A search of the Internet using the words “anaplasmosis vaccine” will enable you to find current products. Vaccines are not approved for use in all areas.
Vaccination does not prevent disease but does decrease the severity of clinical signs when animals are infected.
Some vaccines have been associated with the development of neonatal isoerythrolysis in calves so caution should be exercised when vaccinating late gestation females.
ASSOCIATED CONDITIONS
N/A
AGE-RELATED FACTORS
See Mean Age and Range above.
ZOONOTIC POTENTIAL
This disease does not have any zoonotic potential.
PREGNANCY
N/A
BIOSECURITY
N/A
PRODUCTION MANAGEMENT
N/A
SYNONYMS
N/A
SEE ALSO
Babesiosis
Bacillary hemoglobinuria Clostridium novyi infection Copper toxicity Hepatotoxic plants Leptospirosis ABBREVIATIONS
AST = aspartate aminotransferase BILI = direct bilirubin
PCR = polymerase chain reaction PCV = packed cell volume Suggested Reading
Kocan, K. M., Blouin, E. F., Barbet, A. F. 2000. Anaplasmosis control: past, present and future. Annof NY Acad Sci. 916:501-09.
Kuttler, K. L. 1984. Anaplasma infections in wild and domestic ruminants: a review. J Wildlf Dis. 20:12-20.
Palmer, G. H., Lincoln, S. 2002. Anaplasmosis. In:Large animal internal medicine, ed. B. P. Smith. Philadelphia: Mosby.
Richey, E. J. 1999. Bovine Anaplasmosis. In: Current veterinary therapy 4: food animal practice, eds. J. L. Howard, R.
A. Smith. Philadelphia: W. B. Saunders.
Author: Dawn J. Capucille

ANEMIA, NONREGENERATIVE: BOVINE
BASICS DEFINITION

Anemia in adult cattle is indicated by a PCV (or Hct) of less than 23%.
Beef cattle have higher hemoglobin, RBC, and PCV than dairy breeds.
Anemias may be nonregenerative or regenerative. The lack of reticulocytes and polychromasia with normal red cell distribution width (RDW) is indicative of a nonregenerative response or erythropoietic depression.
Lactating dairy cattle tend to have lower values than nonlactating cows.
Bulls tend to have greater RBC counts than cows.
Environmental, seasonal, and physiological differences may affect the hemogram.
Diminished oxygen tension at elevated altitudes stimulates erythropoiesis resulting in increased RBC counts.
PATHOPHYS IOLOGY
Anemia results from decreased production, or increased destruction (hemolysis) or loss (hemorrhage) of erythrocytes. Nonregenerative anemias are caused by decreased erythropoiesis.
The onset of anemia and its related signs is insidious unless there is concurrent hemolysis or hemorrhage.
Anemia of Chronic Inflammation
Established inflammation results in bone marrow depression due to alterations in iron metabolism, which results in sequestration of iron into the cells of the mononuclear phagocytic system. It is hypothesized that the iron sequestration is a nonspecific bacteriostatic process.
This functional iron deficiency causes decreased erythropoiesis. However, the depression rarely results in the classic microcytic, hypochromic anemia of dietary iron deficiency or iron deficiency resulting from chronic hemorrhage.
Iron Deficiency
Iron deficiency may be due to dietary iron deficiency or to chronic blood loss. Dietary iron deficiency is seldom recognized in cattle because soil contains a sufficient amount of iron to maintain hematopoiesis. It is possible that calves raised on concrete with a diet consisting exclusively of milk could have dietary iron deficiency.
Chronic blood loss such as with certain intestinal helminth infections may result in enough loss of iron to cause iron deficiency. Other chronic bleeding conditions, such as intestinal tract ulcers or hemorrhaging tumors (e.g., lymphoma), can also cause iron deficiency.
Classically, iron deficiency results in nonregenerative anemia (no reticulocytes or polychromasia) that has a microcytic, hypochromic erythrocyte profile.
Space Occupying Lesions Of The Bone Marrow
Myelophthisis is rare in cattle, perhaps because few cattle live to older age when an animal is more likely to develop tumors. Tumors that metastasize to the bone marrow would produce a depression anemia, which is most likely to have a normocytic, normochromic erythrocyte profile.
Cancerous lymphocytes of lymphoma do not frequently multiply in the bone marrow, but occasionally this may occur. If sufficient amount of the marrow is involved, depression anemia can be an unusual secondary feature of bovine lymphoma.
Copper Deficiency
Copper deficiency causes nonregenerative anemia due to impaired absorption and utilization of iron. The majority of copper in the blood is bound to ceruloplasmin, an enzyme that is required for the binding of iron to the transport protein, transferrin. Copper deficiency may be either primary due to deficient intake or secondary due to high molybdenum content of soils and forage. Copper deficiency results in microcytic, hypochromic anemia for the reasons outlined above for iron deficiency.
Cobalt Deficiency
Cobalt is an essential component of Vitamin B12 (cyanocobalamins). Ruminant stomach microflora synthesizes vitamin B12. Cobalt deficiency results in the depression of the vitamin B12-containing enzyme 5-methyltetrahydrofolate homocysteine methyltransferase, which causes a reduction in folate metabolism and impeded DNA synthesis in developing erythrocytes. Anemia occurs late in the course of cobalt deficiency and may be normocytic or macrocytic.
Organ Dysfunction or Failure
Nonregenerative anemia often occurs with chronic kidney diseases. This is due to decreased erythropoiesis as a result of decreased erythropoietin production. In addition, erythrocyte lifespan is decreased probably because uremic substances directly affect erythrocyte integrity (structural substances and/or metabolism).
Nonregenerative anemia may occur with liver diseases. The processes that cause the anemia are unknown, but they may be the result of decreased absorption, distribution or use of elements necessary for erythropoiesis.
Peracute and Acute Hemorrhage or Hemolysis
Apparent nonregenerative anemia may be suggested by hemogram findings for several days after rapid onset hemorrhage or hemolysis.
Hypoxia stimulation of erythropoietin production occurs rapidly, but several days of increased erythropoiesis are required before evidence of increased erythropoiesis is evident in the hemogram.
Bracken Fern Toxicosis
Chronic ingestion of bracken fern (Pteridium aquilinum) causes bladder hemorrhage and hematopoietic depression in cattle and sheep. The hemorrhage may be of sufficient magnitude and duration to cause severe anemia. Hemogram features often reveal a nonregenerative response, which is due to marrow hematopoietic suppression.
Because of the bone marrow depression, thrombocytopenia and neutropenia may be evident. Moderate to severe thrombocytopenia likely contributes to the magnitude of the bladder hemorrhage and exacerbates the anemia due to bone marrow suppression.
SYSTEMS AFFECTED
Hematopoietic: erythropoiesis is depressed. Bone marrow evaluation will reveal increased M:E (myeloid to erythroid ratio) because the myeloid activity is normal or increased, while the erythroid activity is depressed.
Cardiovascular: hypoxia causes tachycardia. Decreased blood viscosity and turbulent blood flow may occasionally result in an auscultable heart murmur.
Respiratory: hypoxia causes tachypnea.
Central nervous system, liver, and kidney are particularly sensitive to hypoxia. Clinical and laboratory features suggestive of effects on these systems may be recognized.
GENETICS
N/A
INCIDENCE/PREVALENCE
N/A
GEOGRAPHIC DISTRIBUTION
Potentially worldwide
Chronic blood loss due to intestinal parasitism may have an increased prevalence in areas endemic to associated parasites.
Copper and cobalt deficiencies are often associated with soil deficiency of these minerals. Functional copper deficiency may occur when there are excess amounts of molybdenum, zinc, and some compounds.
SIGNALMENT
Species
All cattle are susceptible to anemia.
Breed Predilections
N/A
Mean Age and Range
Anemia due to chronic gastrointestinal blood loss secondary to abomasal ulcers or intestinal parasites may occur in cattle of all ages.
Anemia due to other causes may affect any age animal.
Predominant Sex
There is no sex predilection.
SIGNS
N/A
HISTORICALFINDINGS
Nonspecific signs of anemia include weakness, lethargy, anorexia, dyspnea, tachypnea, dark feces (melena), pica (especially with mineral deficiencies). Decreased growth and productivity may occur in iron-, copper-, or cobalt-deficient animals; diarrhea may be found in copper- and cobalt-deficient animals; and faded hair coat occurs in copper-deficient animals.
PHYSICALEXAMINATION FINDINGS
Pale mucous membranes, tachycardia, tachypnea, melena occasionally observed in animals with gastric ulcers, unthrifty appearance. Faded hair coat may be seen with copper deficiency.
CAUSES AND RISK FACTORS
Anemia of Chronic Inflammation
Inflammation of any cause may result in anemia provided that the inflammatory condition is present for sufficient time. The degree of anemia will depend upon the duration of inflammation. Generally, mild anemia can be recognized by laboratory evaluation within 1 to 2 weeks after onset of inflammation.
Iron Deficiency Anemia
Any form of chronic external blood loss; blood loss in cattle most commonly results from loss through the gastrointestinal tract. Gastric ulcers and trichostrongylosis are frequent causes of GI blood loss. Neonates on all-milk diets without access to soil may develop anemia relatively rapidly because their erythrocyte mass is expanding as they grow.
Copper Deficiency Anemia
Primary copper deficiency may occur in milk-fed animals or in animals pastured on copper-deficient soils.
Secondary copper deficiency can occur with excess dietary molybdenum, sulfates, or zinc.
Cobalt Deficiency
Primary cobalt deficiency occurs in areas of cobalt-deficient soils or on pastures heavily fertilized with limestone, which reduces cobalt availability.
Secondary cobalt deficiency may occur with excess manganese, zinc, or iodine, which apparently antagonizes use of cobalt.
Anemia Secondary to Organ Dysfunction
Chronic renal failure and hepatic dysfunction may result in depression anemia.
Peracute and acute hemorrhage or hemolysis
Early (approximately the first 3 to 5 days) in any hemolytic crisis of hemorrhagic condition, hemogram often suggests erythropoietic depression because several days are required before hypoxic stimulation of erythropoiesis is manifested as recognizable features of polychromasia, reticulocytosis, etc., in the blood.
DIAGNOSIS DIFFERENTIALDIAGNOSIS
On the hemogram, nonregenerative anemia is distinguished from regenerative anemia in the lack of reticulocytosis and polychromasia. Hemogram features in the early stages of hemolysis or hemorrhage may be similar to those of depression anemia (see above, Peracute and Acute Hemorrhage or Hemolysis).
In iron deficiency, microcytosis and hypochromasia are usually evident.
In cobalt deficiency, macrocytosis may be evident.
CBC/BIOCHEMISTRY/URINALYS IS
Anemia Due to Chronic Inflammation
CBC
Generally there are mild decreases in RBC, Hgb, and PCV (anemia is rarely severe).
The hemogram reveals normocytic, normochromic, nonregenerative anemia (no reticulocytes or polychromasia with normal RDW).
Often an inflammatory leukogram consisting of neutrophilia, ± left shift, ± toxic change (often indicates bacterial etiology), ± monocytosis (presence indicates inflammation of some duration or tissue damage/necrosis is present).
Lymphopenia may indicate stress (endogenous corticosteroid release).
Thrombocytosis may be found.
Hyperfibrinogenemia is often found with active inflammation.
Serum Biochemistry
Hyperglobulinemia is often found in chronic inflammation, particularly when infectious agents such as bacteria cause the inflammation.
Hypoalbuminemia may be present with active inflammation especially if there is marked hyperglobulinemia.
Anemia Due to Iron or Copper Deficiency
CBC
There are mild to marked decreases in RBC, Hgb and PCV.
Microcytosis (low MCV) is often found
Hypochromasia (low MCHC) also occurs.
There may be either regenerative or nonregenerative response to the anemia; the latter is more common.
Characteristic changes in erythrocytes observed on blood films include increased central pallor (hypochromasia), anisocytosis and moderate to marked poikilocytosis such as dacrocytes (tear-drop shape).
Thrombocytosis is common; this may be extreme.
Serum Biochemistry
Hypoproteinemia with both hypoalbuminemia and hypoglobulinemia is a consistent finding if iron deficiency is due to sustained gastrointestinal blood loss.
Anemia Due to Cobalt Deficiency
CBC
There are mild decreases in RBC, Hgb, and PCV.
Usually the RBCs are normocytic (MCV in reference range) to occasionally macrocytic (increased MCV), normochromic (reference range MCHC), and nonregenerative anemia.
There may be a stress (corticosteroid) leukogram.
Serum Biochemistry
If ketosis develops secondary to anorexia, ketone bodies may be detected in the serum.
There may be increased liver enzyme activity-AST, SDH, GGT.
Urinalysis
If ketosis develops secondary to anorexia, ketone bodies are detectable by urine dipstick.
Anemia Due to Secondary Organ Failure/Dysfunction-Chronic Renal Failure
CBC
There are mild to moderate decreases in RBC, Hgb, and PCV.
The anemia is normocytic, normochromic, nonregenerative.
Serum Biochemistry
With kidney failure there will be increased BUN (not as striking as in monogastric animals), creatinine, and possibly phosphorus with variably low bicarbonate, sodium, and chloride.
Urinalysis
Isosthenuria (Sp. Gr. 1.008-1.012) with variable proteinuria is found. Anemia Due to Secondary Organ Failure/Dysfunction-Liver Disease CBC
There are mild to moderate decreases in RBC, Hgb, and PCV.
The anemia is normocytic, normochromic, nonregenerative.
Serum Biochemistry Increased SDH, LDH, AST, GGT; variably high bilirubin; occasionally low BUN; decreased total protein with decreased albumin are some features of liver damage.
OTHER LABORATORY TESTS
Chronic Blood Loss/Iron Deficiency
Hypoferremia (serum iron < 30 µ g/dL) is consistently found.
Transferrin saturation is decreased.
Total iron binding capacity is increased.
Fecal flotation may suggest intestinal parasites (Trichostrongylus spp.) as the cause of blood loss.
Fecal occult blood test may reveal location of blood loss (caution: some plant peroxidases can result in a false positive).
Space occupying lesions of the bone marrow
Examination of the bone marrow may reveal neoplastic lymphocytes.
Copper Deficiency
Plasma copper levels are decreased.
Cobalt Deficiency
Low serum cobalamin (vitamin B12) concentration. (Cobalt concentration is not reliable.)
OTHER DIAGNOSTIC PROCEDURES
Chronic Blood Loss/Iron Deficiency
Cytological evaluation of bone marrow specimen stained with Prussian blue for iron particles should reveal the absence of hemosiderin. Marrow evaluation for iron is only recommended when documentation of iron deficiency by other means is difficult.
PATHOLOGIC FINDINGS
Chronic Blood Loss/Iron Deficiency
Intestinal parasitism with mucosal petechiation; abomasal ulcers.
TREATMENT
Successful treatment of nonregenerative anemia usually revolves around correction of the underlying cause(s).
Treat with appropriate antimicrobials, anthelmintics, or correct dietary insufficiencies.
ACTIVITY
Restrict activity until the animal(s) can exert themselves without developing significant dyspnea.
DIET
Treat with appropriate antimicrobials, anthelmintics, or correct dietary insufficiencies. (Refer to specific chapters for types, dosages, and amounts.)
Chronic Inflammation
Determine source of inflammation and treat with appropriate antimicrobials if bacterial or fungal etiology. Hot pack external abscesses.
Chronic Blood Loss/Iron Deficiency
Identify and correct the cause of external blood loss.
Treat with appropriate anthelmintic based on specific parasite(s) detected by fecal evaluation.
Iron may be provided as an oral supplement or as a feed additive. Iron dextran injections should be avoided in cattle because it can cause anaphylaxis, especially if used repeatedly. Injected iron may cause acute iron overload resulting in massive hepatic necrosis leading to death in cattle. Injectable iron should be used with caution in cattle.
Copper and Cobalt Deficiencies
Addition of copper or cobalt to diet by feeding free-choice trace mineral/salt mix is effective, but the animals consume the mix frequently.
Renal Failure
If possible, stabilize the animal and rehydrate with fluids.
Early Peracute and Acute Hemorrhage or Hemolysis
Treat the specific condition.
In valuable animals, transfusions may be used to maintain oxygen carrying capacity until effective erythropoiesis contributes to increased oxygen-carrying capacity of the blood.
MISCELLANEOUS
See specific chapters on infectious diseases, parasitism for appropriate drugs and dosages.
See specific chapters on mineral deficiencies for supplementation and dosages.
DRUGS OF CHOICE
Appropriate antibiotics for inflammatory conditions with infectious etiologies
Appropriate anthelmintics for parasitism
CONTRAINDICATIONS
Appropriate milk and meat withdrawal times must be followed for all compounds administered to food-producing animals.
FOLLOW-UP PATIENT MONITORING
Respiration and heart rates and mucous membrane color are useful for recognizing the success of therapy.
In patients with severe anemia, CBC or PCV with a blood smear examination should be performed every 1-2 days until a significant erythropoietic response is recognized.
PREVENTION/AVOIDANCE
See specific chapters for nutritional deficiencies, intestinal parasites, etc.
POSSIBLE COMPLICATIONS
Appropriate milk and meat withdrawal times must be followed for all compounds administered to food-producing animals.
Injected iron can cause anaphylaxis (iron dextran) or liver necrosis.
EXPECTED COURSE AND PROGNOSIS
Clinical course and prognosis vary and are associated with the underlying disease condition causing the nonregenerative anemia.
MISCELLANEOUS ASSOCIATED CONDITIONS
N/A
AGE-RELATED FACTORS
Young animals on milk diets are susceptible to iron deficiency.
ZOONOTIC POTENTIAL
N/A
PREGNANCY
A mild anemia may be observed in some pregnant animals due to dilution of RBC mass by a high blood volume.
RUMINANT SPECIES AFFECTED
Potentially, all ruminant species are affected.
BIOSECURITY
N/A
PRODUCTION MANAGEMENT
In areas of mineral-deficient soils, feed should be appropriately supplemented or it should contain commodities (grain, hay, etc.) grown on properly supplemented land.
Preventative anthelmintic therapy should be practiced in areas of endemic parasitism.
SYNONYMS
Depression anemia Nonresponsive anemia SEE ALSO
Chronic renal failure Cobalt deficiency Copper deficiency Iron deficiency Liver diseases Parasitism Regenerative anemia ABBREVIATIONS
AST = aspartate aminotransferase GGT = gamma glutamyltransferase Hgb = hemoglobin
LDH = lactate dehydrogenase
MCHC = mean cell hemoglobin concentration MCV = mean cell volume
RDW = red cell distribution width SDH = sorbitol dehydrogenase Suggested Reading
Feldman, B. F., Zinkl, J. G., Jain, N. C., eds. 2000. Schalm’s veterinary hematology. 5th ed. Baltimore: Lippincott Williams and Wilkins.
Jain, N. C. 1986. Schalm’s veterinary hematology. 4th ed. Philadelphia: Lea and Febiger.
Smith, B. P., ed. 2001. Large animal internal medicine. 3d ed. Philadelphia: Mosby.
Authors: Joseph G. Zinkl and Bernard F. Feldman

ANEMIA, NONREGENERATIVE: CAMELIDS
BASICS DEFINITION

Anemia in adult llamas and alpacas is indicated by a PCV of less than 25%. A PCV of =28% in camels is indicative of anemia.
High concentrations of erythrocytes are observed in healthy camelids, but because the cells have a small mean cell volume, the PCV, or Hct, is relatively low.
Anemias may be nonregenerative or regenerative. The lack of polychromasia, reticulocytes, and nucleated erythrocytes is indicative of depression or a nonregenerative response.
PATHOPHYS IOLOGY
Anemia may result from either decreased production or increased destruction of erythrocytes. Nonregenerative anemias are most often associated with decreased erythropoiesis. The onset of anemia and its related signs is insidious unless there is concurrent RBC destruction or loss. Anemia of Chronic Inflammation
Decreased production of erythrocytes is often associated with established or chronic inflammation in camelids, but iron or copper deficiency may also cause nonregenerative anemia. A mature neutrophilia (>25,000 neutrophils/µL) ± hyperfibrinogenemia (>400 mg/dL) is consistent with inflammatory disease. The presence of immature neutrophils (e.g., left shift) is supportive of active inflammation. Inflammatory disease results in cytokine-mediated disturbances in iron metabolism and decreased availability for erythropoiesis. Lack of polychromasia and reticulocytes indicates nonregenerative anemia.
Mild, normocytic, normochromic, nonregenerative anemia has been reported in juvenile llamas affected with juvenile llama immunodeficiency syndrome (JLIDS). Anemia is probably a result of chronic and repeated infections resulting in decreased iron availability.
Iron Deficiency Anemia
Iron deficiency may be primary or secondary. In either case, iron deficiency results in moderate nonregenerative anemia due to insufficient iron for hemoglobin synthesis. Erythrocytes are microcytic (decreased MCV) due to an additional cell division during development. Hypochromasia (decreased MCHC) results from decreased hemoglobin concentration in the erythrocytes. Chronic blood loss can result in iron deficiency and nonregenerative anemia. Trichostrongylus infection causes a mildly regenerative, normocytic, normochromic blood loss anemia. Bleeding gastric ulcers can result in chronic blood loss.
Copper Deficiency Anemia
Copper deficiency causes nonregenerative anemia due to impaired absorption and utilization of iron. The majority of copper in the blood is bound to ceruloplasmin, an enzyme that is required for the binding of iron to the transport protein, transferrin. Copper deficiency may be either primary due to deficient intake or secondary due to high molybdenum content of soils and forage. Copper deficiency results in microcytic, hypochromic anemia for the reasons outlined above for iron deficiency.
Cobalt Deficiency
Cobalt is an essential component of vitamin B12 (cyanocobalamins). Camelid stomach microflora are presumed to synthesize vitamin B12. Cobalt deficiency results in the depression of the vitamin B12-containing enzyme 5-methyltetrahydrofolate homocysteine methyltransferase, which causes a reduction in folate metabolism and impedes DNA synthesis in developing erythrocytes. Anemia occurs late in the course of cobalt deficiency and may be normocytic or macrocytic.
Secondary Organ Failure
Renal failure results in decreased production of erythropoietin necessary for erythropoiesis. RBC lifespan is decreased. Uremic acids inhibit hemostasis.
Hepatic failure may result in decreased absorption, distribution, or utilization of elements necessary for erythropoiesis.
Hypothyroidism leads to decreased erythropoiesis probably through decreased tissue O2 requirements as well as a direct effect on erythrocyte production.
SYSTEMS AFFECTED
Hemic/Lymphatic/Immune
Hepatobiliary-chronic hypoxia due to marked anemia results in centrilobular necrosis. Mild hyperbilirubinemia may occur due to decreased hepatic function and mass.
Cardiovascular-hypoxia causes tachycardia; decreased blood viscosity and turbulent blood flow may occasionally result in an auscultable heart murmur.
Respiratory-hypoxia results in tachypnea.
Renal/urologic-chronic hypoxia may lead to renal tubular necrosis.
Gastrointestinal-colic may occur secondary to gastric ulcers.
GENETICS
Young llamas affected with JLIDS are often anemic. Although there are apparent familial links in affected llamas, reliable genealogical information is not available and a definitive genetic basis has not been established.
INCIDENCE/PREVALENCE
Unknown
GEOGRAPHIC DISTRIBUTION
Chronic blood loss due to intestinal parasitism may have an increased prevalence in areas endemic to associated parasites.
SIGNALMENT
Species
All camelids are susceptible to anemia. Llamas and alpacas may be more susceptible to iron and copper deficiency anemias than camels, but the condition is uncommon in all species.
Breed Predilections
N/A
Mean Age and Range
Anemia due to chronic gastrointestinal blood loss secondary to gastric ulcers may occur in llamas and alpacas of all ages including nursing animals.
Median age of llamas affected with JLIDS and that are anemic, 13.8 months; range 6 months-4 years.
Anemia due to other causes may affect any age animal.
Predominant Sex No sex predilection SIGNS
HISTORICALFINDINGS
Nonspecific signs of anemia include weakness, lethargy, anorexia, dyspnea, tachypnea; reddish-brown urine (hemoglobinuria) if anemia is severe; dark feces (melena); pica, decreased growth and productivity may occur in iron-, copper-, or cobalt- deficient animals; diarrhea in cobalt-deficient animals.
PHYSICALEXAM FINDINGS
Pale mucous membranes, tachycardia, tachypnea, icterus if anemia is severe; melena occasionally observed in llamas with gastric ulcers; unthrifty appearance and poor hair coat reported with cobalt deficiency.
CAUSES AND RISK FACTORS
Anemia of Chronic Inflammation
Any cause of inflammatory disease including internal or cutaneous infections, infectious diseases, traumatic tissue damage, or fractures
Active malignant neoplasia-lymphosarcoma, squamous cell carcinoma, mammary and uterine adenocarcinoma
Juvenile llama immunodeficiency syndrome (JLIDS)
Iron Deficiency Anemia
Any form of chronic external blood loss
Blood loss in adult camelids most commonly results from loss through the gastrointestinal tract
Gastric ulcers and trichostrongylosis are frequent causes of GI blood loss
Copper deficiency can lead to secondary iron deficiency
Neonates on all-milk diets without access to soil
Hemostatic defects
Copper Deficiency Anemia
Primary copper deficiency-milk-fed animals, pastured animals on copper-deficient soils, pregnancy may exacerbate deficiency.
Secondary copper deficiency-dietary molybdenum, sulfates or zinc excess (inhibits copper absorption).
Cobalt Deficiency
Primary cobalt deficiency-cobalt-deficient soils or pastures heavily fertilized with limestone reduces cobalt available to plants and animals.
Secondary cobalt deficiency-manganese, zinc, and iodine may antagonize utilization of cobalt.
Anemia Secondary to Organ Dysfunction
Chronic renal failure; hepatic dysfunction-hepatic lipidosis, ketosis, infectious hepatitis; endocrine disorders- hypothyroidism
DIAGNOSIS DIFFERENTIALDIAGNOSIS
Specific features in the erythrogram are used to identify not only nonregenerative (depression) anemias from regenerative anemias, but also some specific causes of the anemia such as iron deficiency.
CBC/BIOCHEMISTRY/URINALYS IS
Anemia Due to Chronic Inflammation
CBC
Normocytic, normochromic, nonregenerative anemia
Mild decreases in RBC, Hgb, and PCV (anemia is rarely severe)
Inflammatory leukogram-neutrophilia, ± left shift, ± toxic change (indicates bacterial etiology), ± monocytosis (presence indicates inflammation of some duration or tissue damage/necrosis)
Lymphopenia may indicate effects of stress (endogenous corticosteroid release)
± Thrombocytosis (reactive)
Hyperfibrinogenemia often observed with more acute or active inflammatory conditions
Serum Biochemistry
Hypoalbuminemia if active inflammation
Hyperglobulinemia if chronic inflammation
Hypoglobulinemia often observed in llamas with JLIDS, especially in the face of chronic and repeated infections
Anemia Due to Iron or Copper Deficiency
CBC
Microcytosis indicated by a low mean cell volume.
Hypochromia indicated by low mean corpuscular hemoglobin concentration.
Mild to moderate decreases in RBC, Hgb, and PCV
Anemia, either regenerative or nonregenerative; the latter is more common.
Characteristic changes in erythrocytes observed on blood films include increased central pallor (hypochromia), anisocytosis, and moderate to marked poikilocytosis such as dacrocytes (teardrop shape).
± Thrombocytosis
Serum Biochemistry
Hypoproteinemia is a consistent finding if iron deficiency is due to sustained gastrointestinal blood loss. Hypoalbuminemia and hypoglobulinemia.
Anemia Due to Cobalt Deficiency
CBC
Normocytic to occasionally macrocytic, normochromic, nonregenerative anemia
Mild decreases in RBC, Hgb, and PCV
Stress (corticosteroid) leukogram
Serum Biochemistry
If ketosis develops secondary to anorexia, ketone bodies may be detected in the serum.
Increased liver enzyme activity-AST, SDH, GGT.
Urinalysis
If ketosis develops secondary to anorexia, ketone bodies (primarily acetoacetate) are detectable by urine dipstick.
Anemia Due to Secondary Organ Failure/Dysfunction-Chronic Renal Failure
CBC
Normocytic, normochromic, nonregenerative anemia
Mild decreases in RBC, Hgb, and PCV
Inflammatory leukogram if suppurative nephritis present
Serum Biochemistry
High BUN, creatinine, ± phosphorus; variably low bicarbonate, sodium, and chloride
Urinalysis
Isosthenuria (Sp. Gr. 1.008-1.012); variable proteinuria and active sediment Anemia Due to Secondary Organ Failure/Dysfunction, e.g., Hepatic Lipidosis CBC
Normocytic, normochromic nonregenerative anemia
Mild to moderate decreases in RBC, Hgb, and PCV
Inflammatory leukogram if suppurative hepatitis present
Serum Biochemistry
High glucose, ketone bodies, SDH, LDH, AST, GGT, triglycerides, creatinine; variably high bilirubin; variable high or low BUN; low potassium, total protein, albumin, ± phosphorus; variably low bicarbonate, sodium, and chloride.
Urinalysis
Ketone bodies (note: acetoacetate and acetone are normally present in urine from pregnant alpacas, trace amount present in llama urine)
Variable specific gravity variable proteinuria and active sediment
OTHER LABORATORY TESTS
Chronic Blood Loss/Iron Deficiency
Hypoferremia (serum iron =60 µ g/dL)
Decreased transferrin saturation
Fecal flotation to rule out intestinal parasites (Trichostrongylus) as cause of blood loss
Fecal occult blood test (caution: some plant peroxidases can result in a false positive.)
Copper Deficiency Plasma copper levels Cobalt Deficiency
Low serum cobalamin (vitamin B12)concentration (cobalt concentration is not reliable).
Hepatic Lipidosis
High serum bile acids, nonesterified fatty acids (NEFA), beta-hydroxybutyrate
IMAGING
Chronic Blood Loss/Iron Deficiency
Radiographic or ultrasonographic imaging may reveal evidence of gastrointestinal disease accounting for blood loss.
OTHER DIAGNOSTIC PROCEDURES
Chronic Blood Loss/Iron Deficiency
Gastric endoscopy may reveal evidence for gastric ulceration.
Cytologic evaluation of bone marrow specimen stained with Prussian blue for iron particles should reveal the absence of hemosiderin. Marrow evaluation for iron is only recommended when documentation of iron deficiency by other means is difficult.
PATHOLOGIC FINDINGS
Chronic Blood Loss/Iron Deficiency
Intestinal parasitism with mucosal petechiation; gastric ulcers
TREATMENT
The successful treatment of nonregenerative anemia usually revolves around correction of the underlying cause. General treatment and supportive care recommendations follow. See specific disease chapters for detailed treatment information.
ACTIVITY
Restrict
DIET
Correct dietary insufficiencies as described below and within specific nutritional deficiency chapters.
Chronic Inflammation
Determine source of inflammation and treat with appropriate antimicrobials if bacterial or fungal etiology. Hot pack external abscesses.
Chronic Blood Loss/Iron Deficiency
Identify and correct the cause of external blood loss.
Oral supplementation of iron is less effective than parenteral administration if anemia is severe, but a safe and effective dose for injectable iron dextran has not been established in camelids.
Incorporation of ferrous sulfate into a mineral mix advised for prevention.
Copper and Cobalt Deficiencies
Addition of copper or cobalt to diet by feeding free-choice trace mineral/salt mix-effective only if animals consume the mix daily.
Renal Failure
Increase RBC mass (blood transfusion) if patient is symptomatic for anemia (PCV =15%).
Stabilize azotemia and carefully rehydrate with appropriate fluids.
Correct electrolyte and acid-base imbalances with appropriate fluid therapy and supplementation when necessary.
CLIENT EDUCATION
Conditions associated with severe nonregenerative anemia or pancytopenia generally carry a guarded to poor prognosis and may require long-term therapy without complete resolution.
MEDICATIONS DRUGS OF CHOICE
Specific therapy for increasing RBC mass:
If anemia is unusually severe (PCV =15%), transfusion may be required to treat life-threatening anemia. Whole blood, 0.1 ml/kg at a rate of 5-20 ml/kg/hr.
Numerous blood types are present in the llama and alpaca. However, incompatibility reactions are very rare with the first transfusion. Subsequent transfusions increase the risk for an adverse reaction. Blood cross matching is advised for repeated transfusions.
CONTRAINDICATIONS
Appropriate milk and meat withdrawal times must be followed for all compounds administered to food-producing animals.
PRECAUTIONS
N/A
POSSIBLE INTERACTIONS
N/A
ALTERNATIVE DRUGS
Oxyglobin has been used successfully in dogs, cats, and horses. If packed RBCs or whole blood is not available, Oxyglobin may be a suitable alternative in cases of severe anemia or until whole blood products are available.
FOLLOW-UP PATIENT MONITORING
Respiration and heart rate, mucous membrane color
In patients with severe anemia, CBC or PCV with blood smear examination every 1-2 days
In stabilized animals with a chronic disease or slowly improving disease course, reevaluation every 7-10 days
PREVENTION/AVOIDANCE
See specific chapters for nutritional deficiencies, intestinal parasites, etc.
POSSIBLE COMPLICATIONS
N/A
EXPECTED COURSE AND PROGNOSIS
Clinical course and prognosis vary and are associated with the underlying disease condition causing the nonregenerative anemia. Other cytopenias in addition to the anemia typically warrant a guarded to poor prognosis.
MISCELLANEOUS ASSOCIATED CONDITIONS
N/A
AGE-RELATED FACTORS
The mean age of llamas affected with JLIDS is 13.8 months.
ZOONOTIC POTENTIAL
N/A
PREGNANCY
A mild anemia may be observed in some pregnant animals due to dilution of RBC mass by a high blood volume.
RUMINANT SPECIES AFFECTED
Alpaca, camel, guanaco, llama, vicuña
BIOSECURITY
N/A
PRODUCTION MANAGEMENT
N/A
SYNONYMS
Depression anemia Nonresponsive anemia
SEE ALSO
Chronic renal failure Cobalt deficiency Copper deficiency Hepatic lipidosis Iron deficiency ABBREVIATIONS
AST = aspartate aminotransferase GGT = gamma glutamyltransferase
Hgb = hemoglobin
JLIDS = juvenile llama immunodeficiency syndrome LDH = lactate dehydrogenase
MCHC = mean cell hemoglobin concentration MCV = mean cell volume
SDH = sorbitol dehydrogenase
Suggested Reading
Fowler, M. E. 1998. Medicine and surgery of South American camelids. 2d ed. Ames: Iowa State University Press. Garry, F., Weiser, M. G., Belknap, E. 1994. Clinical pathology of llamas. Vet Clin North Am Food Anim Pract. 10:201-9.
Wernery, U., Fowler, M. E., Wernery, R. 1999. Color atlas of camelid hematology. Berlin: Blackwell Wissenschafts- Verlag,
Author: Frederic S. Almy

ANEMIA, REGENERATIVE: BOVINE
BASICS DEFINITION

Anemia in adult cattle is indicated by a PCV (or Hct) of less than 23%.
Beef cattle have higher hemoglobin, RBC, and PCV than diary breeds.
Anemias may be nonregenerative or regenerative. The presence of reticulocytes, polychromasia, and increased red cell distribution width (RDW) is indicative of a regenerative response.
Lactating dairy cattle tend to have lower values than nonlactating cows.
Bulls tend to have greater RBC counts than cows.
Environmental, seasonal, and physiological differences may affect the hemogram.
• Diminished oxygen tension at elevated altitudes stimulates erythropoiesis resulting in increased RBC counts. PATHOPHYSIOLOGY
Anemia results from decreased production or increased destruction (hemolysis) or loss (hemorrhage) of erythrocytes. Regenerative anemias are caused by hemolysis or hemorrhage.
Anemia caused by hemolysis or hemorrhage and the related signs may be insidious or acute.
Recognition of the indicators of erythropoietic response (reticulocytosis, polychromasia, and increased RDW) to hemorrhage- or hemolysis-induced hypoxia will not be evident for 3 to 6 days after the onset of anemia because the proliferation and differentiation of precursor cells of the erythropoietic series must occur. These events require several mitotic events and considerable protein, especially hemoglobin, synthesis. A single precursor cell may give rise to 16 to 32 mature RBCs.
Hemorrhagic Anemia
Hemorrhage is caused by vessel injury or disease. It may be internal (within the body) or external. With external hemorrhage, blood cells and their iron are lost from the system. Thus, the regenerative response is typically mild to moderate. Chronic external blood loss (e.g., GI bleeding) often leads to a nonregenerative anemia due to iron depletion. In peracute and acute hemorrhage, response to anemia-induced hypoxia will not be recognized by CBC parameters for 3 to 6 days after the initial hemorrhage.
Hemolytic Anemia
Hemolysis results from intravascular, extravascular (primarily in the spleen and/or liver), or a combination of both intravascular and extravascular destruction of RBCs. In contrast to hemorrhagic anemia, the regenerative response to hemolytic anemia is quite vigorous since iron is retained and is readily utilized for erythropoiesis. Extravascular hemolysis occurs as a result of erythrocyte sequestration in the spleen or liver where they are phagocytosed or lysed by the mononuclear phagocytic system. Hemolysis may be antibody and/or complement mediated, associated with infectious agents, drugs, or alterations in the immune system. Infectious agents may alter membrane antigens, form immune complexes that adsorb to the RBCs and fix complement, or cross-reacting antibody may be formed in response to the infectious agent. Less frequently, alterations in immune function may be secondary to some lymphoid malignancies. Intravascular hemolysis may be secondary to complement-mediated lysis such as with IgM-involved immune mediated anemia, neonatal isoerythrolysis or incompatible transfusions. Traumatic injury to the RBCs from intravascular fibrin deposition due to DIC or vasculitis can cause intravascular hemolysis. Oxidative injury to hemoglobin results in Heinz body formation that may cause RBC membrane damage sufficient to cause hemoglobin leakage and hemoglobinemia
SYSTEMS AFFECTED
Hemic/lymphatic/immune-moderate to marked erythrocyte hyperplasia in the bone marrow. Splenomegaly can be a feature of extravascular hemolysis.
Hepatobiliary-hypoxia due to marked anemia results in centrilobular necrosis. Hyperbilirubinemia may occur due to hypoxic hepatic injury and decreased hepatic functional mass, but icterus in patients with hemolytic anemia is primarily prehepatic.
Cardiovascular-hypoxia causes tachycardia; decreased blood viscosity and turbulent blood flow may occasionally result in an auscultable heart murmur.
Respiratory-hypoxia results in dyspnea and tachypnea.
Renal/urologic-chronic hypoxia may lead to renal tubular necrosis. Additionally, free hemoglobin may precipitate in tubules and lead to renal failure.
Central nervous system, liver, and kidney are particularly susceptible to hypoxia.
GENETICS
Congenital erythropoietic porphyria is inherited in an autosomal recessive manner in Holstein cattle. It has also been recognized in shorthorn and Jamaican cattle.
Coagulation factor VIII deficiency is inherited in a sex-linked recessive manner in Hereford cattle.
Coagulation factor XI deficiency is inherited in an autosomal recessive manner in Holstein cattle.
Bos indicus breeds exhibit resistance to babesiosis.
INCIDENCE/PREVALENCE
Anaplasmosis and babesiosis are endemic to locales with the proper tick vectors.
GEOGRAPHIC DISTRIBUTION
Hemorrhagic and hemolytic conditions occur worldwide.
Certain toxicosis and deficiencies are confined to specific regions depending upon geological origin, ecological features, or agricultural practices.
Hemolytic anemia due to infectious organisms such as Babesia and Anaplasma species occur in areas endemic for the vectors associated with these organisms.
SIGNALMENT
Breed Predilections
Hemorrhage and hemolysis may occur with cattle of all types.
Cattle on range in endemic areas for some infectious agents that cause anemia are more likely to be affected than confined cattle in the same geographic area.
Coagulation factor VIII deficiency is inherited in a sex-linked recessive manner in Hereford cattle.
Coagulation factor XI deficiency and erythropoietic porphyria are inherited as autosomal recessives in Holstein cattle.
Mean Age and Range
Anaplasmosis and babesiosis occur most frequently in adult cattle.
Neonatal isoerythrolysis occurs within 24 to 48 hours after birth.
Erythropoietic porphyria is usually recognized during the first 10 days after birth.
Inherited coagulopathies are recognized in very young cattle. They may first be manifested after castration or minor trauma.
Anemia due to other causes may affect any age animal.
Predominant Sex
Factor VIII deficiency is sex-linked. Therefore, it is a disease of newborn males.
SIGNS HISTORICALFINDINGS
Signs of anemia include weakness, lethargy, depression, inability and reluctance to exercise, decreased milk production, and anorexia.
With anaplasmosis, there may be a history of recent movement of cattle from a nonendemic area.
PHYSICALEXAMINATION FINDINGS
Pale or icteric mucous membranes, tachycardia, tachypnea, melena in animals with intestinal bleeding, frank external bleeding, petechia, ecchymosis, icterus, hemoglobinuria
Frank, extreme, external bleeding is obvious, but intestinal or internal bleeding may be difficult to recognize.
Icterus is often seen with intravascular and extravascular hemolytic anemia, but hemoglobinuria occurs only with intravascular hemolysis. Icterus may not be recognized with some cases of hemolytic anemia.
CAUSES AND RISK FACTORS
Anaplasmosis
Anaplasmosis is a hemolytic disease caused by the rickettsial organisms Anaplasma marginale and Anaplasma centrale. Transmission between animals is generally by ticks (Dermacentor andersoni in western North America), but mechanical transmission by biting flies, mosquitoes, hypodermic needles, dehorning, castrating, and ear tagging can occur.
A. marginale are small (0.5-1 µ m diameter) inclusions along the margin of mature erythrocytes. A. centrale are of similar size but are found near the center of the erythrocytes. Generally, a single organism is found, but two or more organisms can be found occasionally especially in severe cases.
A. marginale causes extravascular hemolytic anemia in adult cattle 3 years old or older. Animals less than 1 year old are resistant. Anemia develops through an immune reaction wherein antibody binds to infected erythrocytes, which are subsequently removed by mononuclear phagocytes of the spleen, liver, etc.
Major clinical features are those of hemolytic anemia including pale mucous membranes, icterus, dyspnea, tachypnea, tachycardia, fever, lethargy, and reluctance to move.
Diagnosis is based on finding organisms associated with erythrocytes or by card agglutination test.
Laboratory features include moderate to severe anemia with evidence of response including reticulocytosis, polychromasia, microcytosis (increased MCV), hypochromasia (decreased MCHC), and increased RDW along with hyperbilirubinemia.
Two vaccines are currently used to produce immunity in cattle. One consists of modified-live organisms and the other contains killed organisms. The live vaccine is only available in California. It should only be given to calves under 11 months of age. The killed vaccine can be given to cattle of any age. Two doses must be given in order to obtain full immunity. A killed vaccine that is no longer on the market has been implicated in producing neonatal isoerythrolysis (NI) in calves born to cows that were vaccinated in the last trimester. Apparently neither of the current vaccines has been evaluated for the potential for producing NI. (It is unlikely that the live vaccine would do so since it should not be used in animals of reproductive age.)
Affected cattle are typically treated with tetracycline antibiotics.
Also, tetracyclines can clear carrier cattle of A. marginale. From two to five treatments with LA-200 (long-acting tetracycline injectable product) given at 7-day intervals will clear the anaplasmosis organism from infected carrier cattle. However, cattle that are cleared will be susceptible and can be re-infected.
Babesiosis
Babesiosis is a hemolytic disease caused by the protozoan organisms Bebesia bovis and Babesia bigemina.
B. bovis and B. bigemina are piroplasm (piriform, teardrop shaped) bodies found in erythrocytes that are approximately 2 µ m (B. bovis)or4 µ m(B. bigemina) in diameter. Usually there are pairs of organisms, but greater numbers (usually multiples of 2) can be found occasionally.
Babesia species cause intravascular hemolysis, which may cause visually detectable hemoglobinuria and hemoglobinemia.
Major clinical features are those of hemolytic anemia including pale mucous membranes, icterus, hemoglobinuria, hemoglobinemia dyspnea, tachypnea, tachycardia, fever, lethargy, and reluctance to move.
Diagnosis is based on finding piriform organisms in erythrocytes. Capillary blood has higher numbers of organisms than does large vessel blood. Additionally, the infected erythrocytes are in greater numbers at the edge of blood smears than they are in the central, monolayer area. Thick blood smears improve the likeliness of finding organisms.
Laboratory features include moderate to severe anemia with evidence of response including reticulocytosis, polychromasia, microcytosis (increased MCV), hypochromasia (decreased MCHC), increased RDW, hyperbilirubinemia, hemoglobinuria, and hemoglobinemia.
Imidocarb has been used for therapy.
An attenuated vaccine has been produced and successfully used in Australia for the prevention of B. bovis.
Bos indicus breeds exhibit resistance.
Eperythrozoonosis
Mycoplasma wenyonii (basonym Eperythrozoon wenyonii) occurs worldwide as a latent infection in healthy cattle. It causes hemolytic anemia only in critically ill cattle.
Significant parasitemia without anemia but with hind limb edema and lymphadenopathy has been reported in cattle.
On blood smears, E. wenyonii are small (0.5 µ m diameter) basophilic, pleomorphic organisms. They vary from ring forms to cocci to rods.
General signs of anemia may accompany those of other diseases that allowed the organisms to cause hemolysis.
Theileriosis
Theileria parva and Theileria annulata are pathogenic for cattle. T. parva causes East Coast fever in Africa, and T. annulata causes tropical theileriosis in the Mediterranean area, the Middle East, and Asia.
T. annulata causes hemolytic anemia with hemoglobinuria.
Pleomorphic merozoites of approximately 1 µ m diameter and varying from ring- to comma-shaped are found within erythrocytes.
Trypanosomiasis
Several trypanosomes cause hemolytic and/or nonregenerative anemia in cattle. Bacillary Hemoglobinuria
BACILLARY HEMOGLOBINURIA
Bacillary hemoglobinuria is a highly fatal disease caused by Clostridium haemolyticum in damaged liver tissue.
Often there is an association with massive liver fluke (Fasciola hepatica) migration, but liver damage from toxins, inflammation, and biopsy can cause the development of hypoxic areas that allow the anaerobic organisms to grow and produce toxins (including ß toxin) that cause hemolysis.
Generally, the disease is rapidly fatal and diagnosis is made from history of sudden death and postmortem lesions. Postmortem lesions include pale and icteric mucous membranes, large volumes of red-tinged fluid in abdominal and thoracic cavities, hemoglobinuria, hemoglobin casts, and liver lesions that may include the presence of liver flukes, necrotic biopsy site, or other indicators of liver damage.
Other Bacterial Diseases That Cause Anemia
Many bacterial infections may cause anemia. Generally, the anemia is due to the erythropoietic depression that occurs with inflammation (see Anemia, Nonregenerative).
Infection with Leptospira species may cause hemolytic anemia in calves.
Postparturient Hemoglobinuria
Sporadic cases of anemia accompanied by hemoglobinuria occur throughout the world in dairy cows during the first month after calving. The anemia is often severe and may be regenerative if the cow has been anemic for several days.
Although it is not completely understood, hypophosphatemia due to loss in milk is thought to disrupt erythrocyte energy metabolism, which results in erythrocyte lysis.
Treatment is with sodium phosphate solution or transfusions (if economically reasonable).
Copper Toxicosis
Copper toxicosis most commonly causes hemolytic anemia in sheep. However, calves may develop massive hemolytic anemia when copper accumulated through long-term ingestion is released from liver storage. Copper interacts with membrane proteins leading to lysis of the cells.
Massive hemolysis leads to sudden death. Hematological features suggesting response to anemia are not found because the extreme peracute hemolysis does not allow sufficient time for the hypoxic stimulus to produce new erythrocytes.
Heinz Body Anemia Toxicosis
Heinz bodies form through oxidation of sulfur containing amino acids of hemoglobin and other proteins of erythrocytes, which denatures the proteins and results in inclusion bodies in erythrocytes. These inclusion bodies are called Heinz bodies, and they are most readily detected by microscopic examination of smears of blood that have been incubated with new methylene blue.
Erythrocytes containing Heinz bodies are removed from the blood by the mononuclear phagocyte system. This extravascular hemolysis can result in severe, rapidly developing anemia.
Numerous oxidative substances have been implicated in the production of Heinz bodies. Some oxidants include wild or domestic onions and members of the Brassica family (turnips, kale, and rape). The cause of anemia of copper toxicosis is oxidation of erythrocytes.
Animals from selenium-deficient areas are of increased risk to develop Heinz body anemia because selenium is a vital component of the erythrocyte enzyme glutathione peroxidase, which participates in the antioxidant activity of erythrocytes. Blood glutathione peroxidase activity has been used as an indicator of selenium deficiency in cattle, but this method has been replaced by trace mineral analysis.
Heinz body formation may cause massive hemolysis leading to sudden death. Hematological features suggesting response to anemia are not found because the extreme, peracute hemolysis does not allow sufficient time for the hypoxic stimulus to produce new erythrocytes.
Animals with Heinz-body-mediated anemia may be icteric and have hyperbilirubinemia provided they live long enough for hemoglobin to be catabolized to bilirubin.
Water Intoxication Toxicosis
Intake of large amounts of water can result in intravascular erythrocyte lysis due to extreme, rapidly developing blood hypotonicity.
Milk-fed calves may develop severe anemia when first given access to unlimited amounts of water.
Cattle given sudden access to water after being deprived of water such as with extreme cold when all supplies are frozen may suddenly develop severe anemia.
Features of severe water toxicosis include severe anemia, hypoproteinemia, hemoglobinuria, hypotonicity with decreased electrolyte concentrations.
Congenital Erythropoietic Porphyria
Congenital erythropoietic porphyria (CEP) is an inherited disease of cattle, particularly Holsteins.
CEP is caused by a defect in production of the heme portion of hemoglobin. In addition to decreased erythrocyte production, toxic porphyrin products are present in high concentrations in erythrocytes.
The abnormal porphyrins in high concentrations are toxic to the erythrocytes resulting in hemolysis. In addition, hemoglobin production is decreased, which results in decreased erythrocyte production.
Affected calves develop severe photosensitivity in the light parts of their hair coat. Teeth are dark and fluoresce under ultraviolet light. Urine is often dark and also fluorescent.
Traumatic or Ulceration Induced Hemorrhage
Bleeding is generally obvious with external hemorrhage, but internal hemorrhage into cavities or the intestines may be difficult to recognize.
Dark-colored feces may indicate bleeding in the upper gastrointestinal tract; red-stained feces suggest bleeding in the lower GI tract.
Red urine may be due to hemoglobin, which is suggestive of intravascular hemolysis, or hematuria (erythrocytes in urine), which is suggestive of hemorrhage into either the urinary tract or the genital system.
Chronic ingestion of bracken fern (Pteridium aquilinum) causes urinary bladder hemorrhage in cattle and sheep. (See Anemia, Nonregenerative: Bovine.)
Inherited Coagulopathies
Factor VIII deficiency (hemophilia A) has been described in Hereford cattle in Australia. Hemophilia A is inherited in a sex-linked recessive manner; therefore, it is essentially a condition of males. Clinical features include profuse bleeding and death after surgery such as castration. Diagnosis depends upon determination of prothrombin time (normal), partial thromboplastin time (markedly prolonged), and factor VIII levels (markedly decreased).
Factor XI deficiency has been described in Holstein cattle. It is inherited as a simple autosomal recessive. Spontaneous bleeding is rare, and delayed (12-14 hours), often severe hemorrhage occurs following surgery or trauma. Diagnosis depends upon determination of prothrombin time (normal), partial thromboplastin time (markedly prolonged). Specific diagnosis requires determination of factor XI levels.
Vitamin K Antagonist Rodenticide Toxicity Coagulopathies
Damaged or moldy sweet clover hay and coumarin and indandione anticoagulant rodenticides and pharmaceuticals cause bleeding by inhibiting the production of functional coagulation factors II (prothrombin), VII, IX, and X. Hemorrhages may occur in the cerebral vasculature, abdominal cavity, pericardial sac, mediastinum, thorax, subcutaneously, or into joints. Outward signs of hemorrhage may not exist.
Diagnosis depends upon determination of prothrombin time (prolonged) and partial thromboplastin time (prolonged) along with history, laboratory analysis for detection of specific anticoagulants in biological fluids, or analysis of suspect hay or silage for dicumarol content.
Therapy consists of injectable vitamin K1(1-3 mg/kg BW). Because there is great variation in the duration of activity of the various rodenticides, it may be necessary to maintain therapy for several weeks. In small animals and humans, the coagulation test PIVKA (proteins induced by vitamin K absence or antagonism) has been successfully used to determine when vitamin K therapy can be stopped. DIAGNOSIS DIFFERENTIALDIAGNOSIS
On the hemogram, regenerative anemia is distinguished from nonregenerative anemia by the presence of reticulocytosis, polychromasia, increased RDW, microcytosis, and hypochromasia.
Anemia due to either hemolysis or hemorrhage may be distinguished by evaluation of bilirubin and protein concentration. Frequently, hyperbilirubinemia occurs in hemolytic anemia. Hypoproteinemia is a common finding in external hemorrhage. However, internal hemorrhage may not cause significant decrease in plasma protein concentration.
Specific etiologic diagnosis requires evaluation of blood smears for organisms, culture of tissues, immunology-based testing, and possibly PCR for specific gene sequences.
CBC/BIOCHEMISTRY/URINALYSIS
Anaplasmosis
CBC
Moderate to marked decreases in RBC, Hgb, and PCV
Regenerative anemia with numerous typical inclusion bodies on RBCs
Inflammatory leukogram-neutrophilia, ± left shift
Lymphopenia may indicate effects of stress (endogenous corticosteroid release).
Serum Biochemistry
Hyperbilirubinemia
Normal plasma protein
Increased liver enzyme activity-AST, SDH, GGT
Babesiosis
CBC
Moderate to marked decreases in RBC, Hgb and PCV
Regenerative anemia with occasional, typical inclusion bodies in RBCs
Inflammatory leukogram-neutrophilia, ± left shift
Lymphopenia may indicate effects of stress (endogenous corticosteroid release)
Serum Biochemistry
Hyperbilirubinemia
Normal plasma protein
Increased liver enzyme activity-AST, SDH, GGT
Urinalysis Hemoglobinuria Heinz Body Anemia CBC
Moderate to marked decreases in RBC, Hgb, and PCV
Either nonregenerative or regenerative anemia depending upon the duration of the condition.
• Many typical inclusion bodies in RBCs that are best revealed with new methylene blue staining. Serum Biochemistry
Hyperbilirubinemia depending on the duration of the condition
• Normal plasma protein Postparturient Hemoglobinuria Serum Biochemistry
Hypophosphatemia in affected cows and in other cows of the dairy
Water Toxicosis
CBC
Nonregenerative anemia
Serum Biochemistry
Decreased plasma protein concentrations
Hyponatremia, hypochloremia, decreased osmolarity
Hemorrhage
CBC
Regenerative anemia but generally not as robust as in hemolytic anemia
Variable decreases in RBC, Hgb, and PCV
Serum Biochemistry
Hypoproteinemia especially with external bleeding
Increased liver enzyme activity-AST, SDH, GGT
Urinalysis
Hematuria (intact erythrocytes in urine) if bleeding is urogenital
OTHER LABORATORY TESTS
Anaplasmosis
In addition to recognizing organisms on erythrocytes, diagnosis is through the CF (complement fixation) or RCA (rapid card agglutination) tests.
Babesiosis
Complement fixation and indirect fluorescent antibody tests are available from National Veterinary Services Laboratories (USDA: APHIS).
A PCR method has been developed for detecting B. bovis carrier cattle. Its sensitivity is significantly improved over that of current methods.
Heinz Body Anemia
Possible low blood selenium concentrations
Bacillary Hemoglobinuria
Culture of liver; however, caution must be used when interpreting the results because Clostridium species often proliferate in tissues after death.
Copper Toxicosis and Selenium Deficiency
Trace metal analysis
Congenital Erythropoietic Porphyria
Blood or urine porphyrin analysis in animals of proper breed and with skin and teeth lesions
OTHER DIAGNOSTIC PROCEDURES
Bone Marrow Evaluation
Cytological evaluation of bone marrow specimen is not indicated when response to anemia-driven hypoxia is recognized by hematological features (reticulocytosis, polychromasia, macrocytosis, hypochromasia, and increased RDW).
PATHOLOGIC FINDINGS
Hemolytic Anemias
Enlarged spleen and liver may be found with many hemolytic anemias especially those of extravascular pathogenesis.
Tissues may be pale or have a red appearance. In massive hemolytic anemias (e.g., copper toxicosis), the kidneys may be dark and have a “gun metal” appearance.
Hemoglobinuria indicates extravascular hemolysis.
Liver lesions including liver flukes, biopsy site necrosis may be suggestive of bacillary hemoglobinuria.
Discolored bone and teeth in congenital erythropoietic porphyria
Hemorrhage
Large amounts of blood in intestines, thorax, abdomen, joints, etc.; petechia and ecchymosis of skin, sclera, urinary tract, mucous membrane; and ulcers of the intestinal tract may be found with various causes of hemorrhage.
TREATMENT
Successful treatment depends upon specific therapy for the underlying cause of the anemia. Appropriate milk and meat withdrawal times must be followed for all compounds administered to food-producing animals.
Transfusion may be used with animals that are of sufficient value to make the procedure economically feasible. Generally, it is unlikely that a recipient that has never received a transfusion will experience a transfusion reaction. Therefore, almost any adult bovine can be used as a donor. Occasionally, transfusion reactions may occur because of J antigen incompatibilities.
ACTIVITY
Restrict activity until the animal(s) can exert themselves without developing significant dyspnea.
DIET
Correct dietary insufficiencies such as selenium deficiency or excess copper in the diet.
CLIENT EDUCATION
Advise clients in anaplasmosis-endemic areas to purchase replacement cows from anaplasmosis-endemic areas or purchase heifers that were vaccinated for anaplasmosis as calves.
Advise clients to use proper anthelmintic therapy for liver flukes.
MEDICATIONS DRUGS OF CHOICE
Cattle with anaplasmosis are typically treated with tetracycline antibiotics.
Also, tetracyclines can clear carrier cattle of A. marginale. From two to five treatments with LA-200 (long-acting tetracycline injectable product) given at 7-day intervals will clear the anaplasmosis organism from infected carrier cattle. However, cattle that are cleared will become susceptible and can be reinfected.
Imidocarb has been used for therapy for babesiosis.
If economically feasible, anticoagulant rodenticide toxicity can be treated with injectable vitamin K1 (1-3 mg/kg BW). PIVKA can be used to determine when therapy can be discontinued.
CONTRAINDICATIONS
Appropriate milk and meat withdrawal times must be followed for all compounds administered to food-producing animals.
PRECAUTIONS
Cattle treated with tetracycline antibiotics at dosages that clear Anaplasma organisms are susceptible to reinfection.
FOLLOW-UP PATIENT MONITORING
Respiration and heart rates and mucous membrane color are useful for recognizing the success of therapy.
In patients with severe anemia, CBC or PCV with a blood smear examination should be performed every 1-2 days until a significant erythropoietic response is recognized.
PREVENTION/AVOIDANCE
If animals are to be pastured on range endemic for anaplasmosis, they should be vaccinated or purchased from an endemic area. Modified-live vaccine should be used only in calves less than 11 months old.
An attenuated vaccine has been produced and successfully used in Australia for the prevention of B. bovis. Bos indicus
breeds exhibit resistance to Babesia species.
Appropriate anthelmintic therapy should be used in order to prevent liver fluke parasitism.
Possibly initiate phosphorus supplementation if soil or feed is deficient especially in high producing dairy cows.
Possibly provide selenium supplementation if soil or feed is deficient.
POSSIBLE COMPLICATIONS
N/A
EXPECTED COURSE AND PROGNOSIS
Clinical course and prognosis vary and are associated with the underlying disease condition causing the anemia.
MISCELLANEOUS ASSOCIATED CONDITIONS
N/A
AGE-RELATED FACTORS
Adult cattle that have neither been vaccinated nor raised in endemic areas are highly susceptible to anaplasmosis, but calves develop resistance.
Adult cattle are more susceptible to babesiosis than calves.
ZOONOTIC POTENTIAL
N/A
PREGNANCY
N/A
RUMINANT SPECIES AFFECTED
Potentially, all ruminant species are affected by many of these conditions.
BIOSECURITY
N/A
SYNONYMS
Responsive anemia
SEE ALSO
Specific diseases and conditions
ABBREVIATIONS
AST = aspartate aminotransferase
CEP = Congenital erythropoietic porphyria GGT = gamma glutamyltransferase
Hgb = hemoglobin
LDH = lactate dehydrogenase
MCHC = mean cell hemoglobin concentration MCV = mean cell volume
RDW = red cell distribution width SDH = sorbitol dehydrogenase Suggested Reading
Feldman, B. F., Zinkl, J. G., Jain, N. C. 2000. Schalm’s veterinary hematology. 5th ed. Baltimore: Lippincott Williams and Wilkins.
Smith, B. P. 2001. Large animal internal medicine. 3rd ed. Philadelphia: Mosby.
Authors: Joseph G. Zinkl and Bernard F. Feldman

ANEMIA, REGENERATIVE: CAMELIDS
BASICS DEFINITION

A syndrome characterized by decreased circulating RBC mass (anemia in adult llamas and alpacas indicated by a PCV
=25%; in camels a PCV =28% indicates anemia), together with an appropriate compensatory increase in RBC production by the bone marrow.
The presence of polychromasia, reticulocytes ± nucleated erythrocytes are indicative of an appropriate regenerative response.
Because it takes the bone marrow 3-5 days for a maximum response, evidence for regeneration may not be apparent until several days after the onset of anemia.
High concentrations of erythrocytes are observed in healthy camelids, but because the cells have a small mean cell volume, the PCV, or Hct, is relatively low.
PATHOPHYS IOLOGY
Anemia may result from either decreased production or increased destruction of erythrocytes. Regenerative anemias are most often associated with two general mechanisms: blood loss (hemorrhage) or hemolysis. Chronic blood loss can result in iron deficiency and nonregenerative anemia. Trichostrongyle infection causes a mildly regenerative, normocytic, normochromic blood loss anemia.
Hemolysis in camelids most commonly occurs secondary to anti-RBC antibodies formed against altered erythrocyte membrane antigens. Infectious organisms (e.g., Leptospira interrogans, Trypanosoma, hemotrophic Mycoplasma), exposure of previously unexposed antigens, or adsorption of antigen-antibody complexes to the erythrocyte membrane can alter RBC membrane antigens and render RBCs susceptible to accelerated destruction or removal by the mononuclear- phagocytic system of the spleen and/or liver (extravascular hemolysis). Certain bacterial infections (i.e., Clostridium perfringens type A) cause direct erythrocyte damage due to hydrolysis of membrane phospholipids. The result is marked intravascular hemolysis.
RBC parasites such as Candidatus Mycoplasma haemolamae (formerly Eperythrozoon spp.) adhere to the surface of RBC membranes. Affected erythrocytes are removed by the mononuclear-phagocytic system of the spleen and/or liver. Young llamas and alpacas are more susceptible to acute infection and severe parasitemia with clinically significant extravascular hemolysis. Anemia may be nonregenerative or regenerative depending on the presence or lack of other clinical problems.
Hemorrhagic Anemia
RBCs are lost from the vasculature due to vascular injury or disease. Hemorrhage may be internal (within the body) or external. RBC lifespan is unaltered in this condition. Both blood cells and iron are lost from the body with external hemorrhagic anemia. Thus, the regenerative response is typically mild to moderate. Chronic external blood loss (e.g., GI bleeding) often leads to a nonregenerative anemia due to iron depletion.
Hemolytic Anemia
In patients with hemolytic anemia, the vasculature is typically intact. Hemolysis results from intravascular, extravascular (primarily in the spleen and/or liver) or a combination of both intravascular and extravascular destruction of RBCs. In contrast to hemorrhagic anemia, the regenerative response to hemolytic anemia is quite vigorous since iron is retained and is readily utilized for erythropoiesis. Extravascular hemolysis occurs as a result of erythrocyte sequestration in the spleen or liver where they are phagocytosed or lysed by the mononuclear phagocytic system. Hemolysis may be antibody and/or complement mediated, associated with infectious agents, drugs, or alterations in the immune system. Infectious agents may alter membrane antigens, form immune complexes that adsorb to the RBC and fix complement, or cross-reacting antibody may be formed in response to the infectious agent. Less frequently, alterations in immune function occur secondary to some lymphoid malignancies. Intravascular hemolysis may occur secondary to complement-mediated lysis such as with IgM-involved immune-mediated anemia, neonatal isoerythrolysis, or incompatible transfusions. Traumatic injury to the RBCs from intravascular fibrin deposition due to DIC or vasculitis can cause intravascular hemolysis. Oxidative injury to hemoglobin results in Heinz body formation that may cause RBC membrane damage sufficient to cause hemoglobin leakage and hemoglobinemia. The unique shape and low osmotic fragility of camelid RBCs probably render a protective effect against hemolysis from oxidative injury, unless severe.
SYSTEMS AFFECTED
Hemic/Lymphatic/Immune-moderate to marked erythrocyte hyperplasia in the bone marrow. Splenomegaly can be a feature of extravascular hemolysis.
Hepatobiliary-hypoxia due to marked anemia results in centrilobular necrosis. Hyperbilirubinemia may occur due to hypoxic hepatic injury and decreased hepatic functional mass, but icterus in patients with hemolytic anemia is primarily prehepatic.
Cardiovascular-hypoxia causes tachycardia; decreased blood viscosity and turbulent blood flow may occasionally result in an auscultable heart murmur.
Respiratory-hypoxia results in tachypnea.
Renal/urologic-chronic hypoxia may lead to renal tubular necrosis. Free hemoglobin is also nephrotoxic and can lead to renal failure.
GENETICS
Young llamas affected with juvenile llama immunodeficiency syndrome (JLIDS) are often anemic. Although there are apparent familial links in affected llamas, reliable genealogical information is not available and a definitive genetic basis has not been established.
INCIDENCE/PREVALENCE
Unknown
GEOGRAPHIC DISTRIBUTION
Chronic blood loss due to intestinal parasitism may have an increased prevalence in areas endemic to associated parasites.
SIGNALMENT
Species
All camelids are susceptible to anemia. Llamas and alpacas may be more susceptible to RBC parasitism than camels are.
Mean Age and Range
Anemia due to infection with Candidatus Mycoplasma haemolamae generally affects llamas and alpacas =1 year; range neonate to adult.
Median age of llamas affected with JLIDS and that are anemic 13.8 months; range 6 months-4 years.
Anemia due to other causes may affect any age animal.
Predominant Sex No sex predilection SIGNS
HISTORICALFINDINGS
Nonspecific signs of anemia include weakness, lethargy, anorexia, dyspnea, tachypnea; reddish-brown urine (hemoglobinuria) if hemolysis is severe; dark feces (melena).
PHYSICALEXAMINATION FINDINGS
Clinical signs of hemorrhage with blood loss; pale or icteric mucous membranes; tachycardia; tachypnea; melena occasionally observed in llamas with gastric ulcers
CAUSES AND RISK FACTORS
Blood Loss/Hemorrhagic Anemia
Blood loss may be subdivided into acute and chronic causes of hemorrhage.
Acute Hemorrhage
Trauma, lacerations, GI ulcers, and hemostatic defects such as DIC, spoiled sweet clover hay poisoning, anticoagulant rodenticides, and bracken fern poisoning.
Chronic Hemorrhage
Intestinal parasites, GI ulcers or tumors, hematuria, vascular neoplasm, vitamin K deficiency, and thrombocytopenia
Hemolytic Anemia
Many of the causes listed below have both intravascular and extravascular components, but are listed where the majority of the hemolysis occurs.
Intravascular Hemolysis
Leptospirosis, bacillary hemoglobinemia/hemoglobinuria, copper toxicity, molybdenum deficiency, propylene glycol, vitamin K3, incompatible transfusions, hypophosphatemia.
Extravascular Hemolysis
Mycoplasma haemolamae (formerly Eperythrozoon), Trypanosoma spp., occasionally drugs such as penicillin, hemangiosarcoma, autoimmune mediated hemolytic anemia (uncommon in camelids).
DIAGNOSIS DIFFERENTIALDIAGNOSIS
Regenerative anemia is differentiated from nonregenerative anemia by increased reticulocyte count, polychromasia and ± nucleated RBCs. Specific features of the erythrogram, biochemical profile, and urinalysis are used to differentiate among blood loss anemia and intravascular and extravascular hemolysis.
CBC/BIOCHEMISTRY/URINALYS IS
Anemia in adult llamas and alpacas is indicated by a PCV of less than 25%. A PCV of =28% in camels is indicative of anemia.
High concentrations of erythrocytes are observed in healthy camelids, but because the cells have a small mean cell volume, the PCV, or hematocrit, is relatively low.
Anemia Due to Blood Loss/Hemorrhage
CBC
If blood loss is chronic, one may observe normocytic to microcytic, normochromic to hypochromic anemia with mild reticulocytosis. Higher reticulocyte counts may be observed with internal hemorrhage compared to external blood loss.
Acute blood loss may result in normocytic, normochromic, nonregenerative anemia if the bone marrow has not had adequate time to respond (usually 3-5 days).
Mild to marked decreases in RBC, Hgb, and PCV (degree of anemia based upon severity and duration of blood loss). Internal hemorrhage is usually associated with less-severe anemia.
Anisocytosis, polychromasia, poikilocytosis.
Inflammatory leukogram-neutrophilia, ± monocytosis (tissue damage/necrosis due to trauma).
Lymphopenia may indicate effects of stress (endogenous corticosteroid release).
Thrombocytosis (reactive) Serum Biochemistry Hypoproteinemia is associated with chronic blood loss (e.g., GI bleeding).
Urinalysis Hematuria due to urinary tract hemorrhage. (Rarely is urinary tract hemorrhage alone severe enough to cause clinical signs of anemia.)
Intravascular Hemolytic Anemia
CBC
MCV is normal to increased. MCHC is typically low, but a falsely increased MCHC may occur due to hemoglobinemia.
Moderate reticulocytosis (counts are higher in hemolytic anemia than external hemorrhagic anemia).
Moderate to marked decreases in RBC, Hgb, and PCV.
Anisocytosis, polychromasia, abnormal erythrocyte morphology (e.g., Heinz bodies, RBC parasites, schistocytes, keratocytes)
Inflammatory leukogram (neutrophilia with left shift, ± monocytosis)
± Thrombocytosis
• Normal to increased plasma protein concentration Serum Biochemistry
Hyperbilirubinemia
Hyperproteinemia due to hyperglobulinemia
Urinalysis
Hemoglobinuria
Extravascular Hemolytic Anemia
CBC
MCV is normal to increased. MCHC is typically low.
Moderate reticulocytosis (counts are higher in hemolytic anemia than external hemorrhagic anemia).
Moderate to marked decreases in RBC, Hgb, and PCV
Inflammatory leukogram (neutrophilia with left shift, ± monocytosis)
± Thrombocytosis
Serum Biochemistry
Hyperbilirubinemia if magnitude of hemolysis exceeds liver capacity to process
Urinalysis
Hemoglobinuria is absent.
OTHER LABORATORY TESTS
Blood Loss/Hemorrhage
Fecal flotation to rule out intestinal parasites (Trichostrongylus) as cause of blood loss
Fecal occult blood test (Caution: Some plant peroxidases as part of the normal diet can result in a false positive.)
Coagulation profile to rule out hemostatic defects
Hemolytic Anemia
PCR analysis to confirm Mycoplasma haemolamae RBC parasitism
Copper levels to confirm copper toxicosis
New methylene blue stained blood smear to confirm presence of Heinz bodies
IMAGING
Blood Loss/Hemorrhage
Radiographic or ultrasonographic imaging may reveal evidence of gastrointestinal disease accounting for blood loss.
OTHER DIAGNOSTIC PROCEDURES
Blood Loss/Hemorrhage
Gastric endoscopy may reveal evidence for gastric ulceration.
Bone marrow evaluation reveals erythroid hyperplasia. Cytologic evaluation of bone marrow is only needed when there is not evidence of RBC responsiveness in the peripheral blood, but regenerative anemia is still suspected.
TREATMENT
An emergency situation exists if anemia is severe or develops rapidly. Massive hemorrhage results in hypovolemic shock and hypoxia/anoxia.
The successful treatment of regenerative anemia usually revolves around correction of the underlying cause.
General treatment and supportive care recommendations follow. See specific disease chapters for detailed treatment information.
ACTIVITY
Restrict
DIET
Correct any dietary insufficiencies as described within specific nutritional deficiency chapters.
CLIENT EDUCATION
N/A
MEDICATIONS DRUGS OF CHOICE
Specific therapy for increasing RBC mass:
If anemia is unusually severe (PCV =15%), transfusion may be required to treat life-threatening anemia: whole blood, 0.1 ml/kg at a rate of 5-20 ml/kg/hr.
Numerous blood types are present in the llama and alpaca. However, incompatibility reactions are very rare with the first transfusion. Subsequent transfusions increase the risk for an adverse reaction. Blood cross matching is advised for repeated transfusions.
Fluid therapy to correct hypovolemia may be indicated early in the course of traumatic hemorrhagic anemia.
Oral or parenteral iron supplementation may be of benefit in patients with external blood loss anemia.
CONTRAINDICATIONS
Appropriate milk and meat withdrawal times must be followed for all compounds administered to food-producing animals.
PRECAUTIONS
N/A
POSSIBLE INTERACTIONS
N/A
ALTERNATIVE DRUGS
Oxyglobin has been used successfully in dogs, cats, and horses. If packed RBCs or whole blood is not available for transfusion, Oxyglobin may be a suitable alternative in cases of severe anemia or until whole blood products are available.
FOLLOW-UP PATIENT MONITORING
Respiration and heart rate, mucous membrane color
Initially, in patients with severe anemia, CBC or PCV with blood smear examination every 24 hours. As regeneration increases RBC mass and polychromasia is apparent on blood smear evaluation, rechecks recommended at 3-5 day intervals.
PREVENTION/AVOIDANCE
See specific chapters for toxicants, nutritional deficiencies, RBC and intestinal parasites, etc.
POSSIBLE COMPLICATIONS
N/A
EXPECTED COURSE AND PROGNOSIS
Clinical course and prognosis vary and are associated with the underlying disease condition causing the anemia.
Return to normal values is expected within 10 to 14 days following the initial insult if the underlying cause has been corrected.
MISCELLANEOUS ASSOCIATED CONDITIONS
None
AGE-RELATED FACTORS
None
ZOONOTIC POTENTIAL
None
PREGNANCY
N/A
RUMINANT SPECIES AFFECTED
Alpaca, camel, guanaco, llama, vicuña
BIOSECURITY
N/A
PRODUCTION MANAGEMENT
N/A
SYNONYMS
Responsive anemia
SEE ALSO
Bacillary hemoglobinuria Bracken fern
Copper toxicity DIC
Leptospirosis Mycoplasma Rodenticide toxicity Trypanosomiasis ABBREVIATIONS
Hct = hematocrit Hgb = hemoglobin
MCHC = mean cell hemoglobin concentration MCV = mean cell volume
PCV = packed cell volume RBC = red blood cells Suggested Reading
Fowler, M. E. 1998. Medicine and surgery of South American camelids. 2d ed. Ames: Iowa State University Press. Garry, F., Weiser, M. G., Belknap, E. 1994. Clinical pathology of llamas. Vet Clin North Am Food Anim Pract. 10:201-9.
Wernery, U., Fowler, M. E., Wernery, R. 1999. Color atlas of camelid hematology. Berlin: Blackwell Wissenschafts- Verlag.
Authors: Frederic S. Almy and Tripp Almy

ANESTHESIA AND ANALGESIA
BASICS OVERVIEW

Anesthesia: local, regional (epidural, intrathecal), or general; local and regional methods most commonly employed in ruminants
Analgesia: local, regional, systemic, multimodal, short-term, long-term
Pain: an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage
Types: acute, chronic, visceral, and somatic
Suffering: a reaction to the physical or emotional components of pain with a feeling of uncontrollability, helplessness, hopelessness, intolerability, and interminableness. Suffering implies a threat to the wholeness of patient comfort within the environment.
Virtually all anesthetics and analgesics are off-label use in any ruminant species. Please see Suggested Reading below for guidelines on off-label use of analgesic and anesthetic drugs in ruminants. The relief of pain and suffering in ruminants can and should be accomplished within these guidelines.
SYSTEMS AFFECTED
CNS, musculoskeletal, respiratory
GENETICS
N/A
INCIDENCE/PREVALENCE
N/A
GEOGRAPHIC DISTRIBUTION
Worldwide
SIGNALMENT
Species
Potentially, all ruminant species
Breed Predilections
N/A
Mean Age and Range
N/A Predominant Sex N/A
SIGNS
Pain Behaviors in Ruminants: vacant stare, loss of mobility, guarding or splinting of affected limb, altered avoidance patterns, vocalization, tachypnea, repetitive motor activities, loss of socialization, repeated attempts at lateral recumbency, inappetence, reduced grooming behavior, bruxism. Behaviors and degree of distress depend on species, breed, temperament, rearing, and housing.
CAUSES AND RISK FACTORS
Acute pain: trauma, surgery, GI accident, urogenital injury/obstruction, pneumonia/pleuritis, husbandry practices
Chronic pain: osteoarthritis including CAE-related arthritis in goats, neoplasia, chronic osteomyelitis, chronic hoof rot, husbandry practices
DIAGNOSIS DIFFERENTIALDIAGNOSIS
Some pain behaviors are not pain-specific. However, for a given species, a behavior indicates pain if it is seen during and/or after a specific tissue-damaging injury, disease, or procedure, but is not seen in healthy or nondamaged animals, and not seen when local anesthesia or effective analgesics are delivered.
CBC/BIOCHEMISTRY/URINALYS IS
May be indicated as routine preoperative workup
OTHER LABORATORY TESTS
N/A
IMAGING
N/A
DIAGNOSTIC PROCEDURES
N/A
TREATMENT MEDICATIONS DRUGS OF CHOICE
Anesthetics Used in Ruminants: General Anesthesia
Often not necessary for some procedures with adequate local or regional anesthesia and sedation due to ruminant temperament
Protecting the airway is essential whether inhalant or injectable anesthetics are used; an endotracheal tube with cuff is always recommended. Proper positioning of the head during recumbency allows regurgitation to flow from the mouth. Techniques for inhalant anesthesia and monitoring are covered in depth elsewhere.
Injectable anesthesia may be administered as a single or repeated bolus, or by continuous infusion.
An IV catheter (jugular v., cephalic v., ear v.) is advised for continuous infusion; 5% guaifenesin and thiopental must be administered via jugular catheter only. Although not necessary for many ruminants, use of a preanesthetic sedative and analgesic will smooth induction and recovery.
Doses for commonly used agents are listed in Table 1.
Acepromazine is not an analgesic or a potent sedative, and has several adverse side effects in ruminants.
Analgesics Used in Ruminants
Choice of analgesic is defined by type of pain, location of pain, duration of pain, species, breed, husbandry, meat and milk withdrawal times, and other federal and state drug use restrictions. Combinations of analgesics allows lower dosing of individual drugs and better pain control. See Table 2 for individual drugs.
Opioids
Inhibit pain transmission peripherally and in the spinal cord by binding mu or kappa receptors. All opioids are controlled substances in the United States. Cardiopulmonary, GI, sedative, and excitatory side effects are possible and dose- and drug- dependent. Indications: acute pain, moderate to severe, visceral or somatic. May be given parenterally or regionally; fentanyl may be given topically in patch form. Opioids and alpha-2 agonists are synergistic; combining these drugs gives greater analgesia at lower doses for both drugs.
Alpha-2 Agonists
Produce central analgesia, sedation, and muscle relaxation by binding alpha-2 receptors in the brain and spinal cord.
Cardiopulmonary, GI, and other side effects are dose dependent and can be severe. May cause abortion in late-term gestation. Use in sheep can cause severe arterial hypoxemia. Indications: acute pain, moderate to severe, visceral, may be given parenterally or regionally, commonly used premedication for anesthesia. Opioids and alpha-2 agonists are synergistic; combining these drugs gives greater analgesia at lower doses for both drugs.
Steroids
Not analgesics but potent anti-inflammatory agents. Pain due to inflammation may be treated in part with steroids. Concurrent use of both steroids and NSAIDs should be avoided due to additive adverse renal and gastric side effects. Steroids should not be used in pregnant ruminants.
Indications: Short-term adjunct therapy in nonseptic inflammatory conditions.
NSAIDs Weak organic acids, which inhibit cyclooxygenase (COX) and reduce release of prostaglandins and thromboxanes. Anti-inflammatory, central and peripheral analgesic, and antipyretic effects, as well as adverse GI and renal effects are possible, and may relate to the COX1 and COX2 selectivity of the drug.
Indications: acute and chronic pain, mild to moderate, visceral and somatic, and for pain and concurrent sepsis or fever, may be given parenterally or orally.
Local Anesthetics
Block sodium channels and inhibit nerve transmission. Motor as well as sensory transmission is blocked. Produce anesthesia at and distal to the site of application, may be analgesic when given parenterally by infusion. Cardiovascular and CNS side effects are possible with high doses.
Table 1 Anesthetic Induction Protocols
Note: IV = intravenous; IM = intramuscular; IV/IM = via both routes, LOW ER dose IV; B = bovine; L = llama/alpaca; O = ovine; C = caprine.
1Caution: xylazine and other alpha-2 agonists can cause severe hypoxemia and pulmonary edema in sheep.
Indications: acute pain, mild to severe, visceral and somatic, and for regional anesthesia, administered subcutaneously, over peripheral nerves, and epidurally or intrathecally.
Other Agents
DMSO
Free-radical scavenger with anti-inflammatory, diuretic, vasodilatory, and anticholinesterase properties. Acts as a carrier agent for other drugs when applied topically as it readily crosses skin. DMSO is only labeled for topical use and not labeled for use in food animals.
Hyaluronic Acid and Polysulfated Glycosaminoglycans
Reported effects include inhibition of inflammatory mediators in joints and analgesia and improved range of motion for osteoarthritis pain; not licensed in food animals; oral and parenteral formulations. Author ‘s note: parenteral hyaluronic acid and polysulfated glycosaminoglycans at one-fourth the equine dose improve the comfort and mobility of small ruminants (which are not intended for food) suffering from osteoarthritis.
Ketamine
NMDA receptor antagonist that can prevent or reverse wind-up pain at subanesthetic doses. Subanesthetic use of ketamine is still largely experimental in food animals; ketamine is not labeled for use in food animals. Author ‘s note: ketamine administered IM at 0.25-0.5 mg/kg q 6-8 hours, along with opioids and NSAIDs may be helpful for severe pain such as burn injury, or for severe polyarthritis or osteomyelitis in small ruminants.
LOCALAND REGIONALANESTHETIC TECHNIQUES
Note: IV = intravenous; IM = intramuscular; IV/IM = via both routes, LOWER dose IV; PO = oral; SQ = subcutaneous; B = bovine; L = llama/alpaca; O = ovine; C = caprine.
Local
Infiltration: wound edges, incision line, inverted L block, ring block
Drugs: lidocaine, mepivacaine, bupivacaine. Epinephrine, 0.1 mL of the 1 mg/mL (1:1000) solution to 20 mL of local anesthetic prolongs the duration of lidocaine and mepivacaine. Do not use epinephrine in limb blocks or wound edges as ischemia and tissue necrosis can occur.
Dosing
B: 5 mg/kg lidocaine (125 mL of 2% solution for adult cattle), similar for mepivacaine, 2 mg/kg bupivacaine. Toxic doses: > 10 mg/kg lidocaine or mepivacaine, >4 mg/kg bupivacaine.
O, C: 2-5 mg/kg lidocaine or mepivacaine, diluting to 1% with saline extends volume without increasing dose, 1 mg/kg bupivacaine. Toxic doses: > 5 mg/kg lidocaine, mepivacaine, > 1 mg/mg bupivacaine. Combining lidocaine and bupivacaine 1:1 or 2:1 allows a long-term block with less bupivacaine volume. Toxic signs include excitation, sedation, recumbency, tonic-clonic convulsions, cardiopulmonary depression, and death.
Specific Nerve Blocks
Ocular, periocular: ocular exam, topical treatment, enucleation, periorbital surgery.
Topical: proparacaine 0.5%, 2-10 drops.
Auriculopalpebral block: B, O, C-20-24 G 2.5 cm needle placed subcutaneously over the nerve (palpable in a notch of the zygomatic arch), 2-10 mL lidocaine for aknesia of eyelids (no analgesia).
Retrobulbar
B: 15 cm 18G slightly curved needle passed through the dorsal or ventral lateral or medial eyelid behind the globe, 10- 15 mL 2% lidocaine (with epinephrine) or 5-6 mL lidocaine and 5-6 mL bupivacaine injected following aspiration as the needle is advanced.
O, C: 3.75 cm 22G slightly curved needle, 3-5 mL 2% lidocaine (with epinephrine) (or equal volumes of lidocaine and bupivacane as for B) injected following aspiration. Risks: bleeding, subarachnoid deposition of local anesthetic with possible severe neurologic side effects.
Table 2 Common Analgesics Used in Ruminants
Note: IV = intravenous; IM = intramuscular; IV/IM = via both routes, LOW ER dose IV; PO = oral; SQ = subcutaneous; B = bovine; L = llama/alpaca; O
= ovine; C = caprine.
1Caution xylazine and other alpha-2 agonists can cause severe hypoxemia and pulmonary edema in sheep, and may cause abortion in ruminants.
Peterson Eye Block: B-20-25 mL lidocaine subcutaneously and at the orbitorotundum foramen for immobilization of the globe and anesthesia of the globe and orbit.
Dehorning
B: 2.5 cm 22G or 25G needle, 5-10 mL lidocaine injected subcutaneously over the palpable cornual branch of the zygomaticotemporal (lacrimal) nerve between the temporalis and frontalis muscles midway between the lateral canthus of the eye and the lateral base of the horn.
C: 2.5 cm 22G or 25 G needle, 1-3 mL lidocaine injected subcutaneously over BOTH the zygomaticotemporal nerve midway between the lateral canthus and the base of the horn, and the infratrochlear nerve between the medial canthus and medial base of the horn at the dorsomedian margin of the orbit. For kids: 0.5 mL 2% lidocaine diluted for a ring block at the base of the horn to reduce possible toxicity.
Proximal and Distal Paravertebral Block
Anesthesia of skin, musculature, and peritoneum of the flank on the side treated, spinal nerves T13, L1, L2 for standing abdominal procedures.
Proximal
B: 2.5-5 cm from midline immediately in front of the transverse process of L1, L2, and L3. After desensitizing the skin, an 18G 4.25-15 cm spinal needle is walked off the cranial edge of the transverse process while aspirating then infusing 1-2 mL lidocaine. Following aspiration, 15 mL lidocaine are injected ventral to the intertransverse ligament, 5 mL are injected proximally with minimal resistance.
O, C: 1.5-3 cm off midline, 20G 4.25 cm spinal needle, 2-3 mL lidocaine per site. Risks: penetration of aorta, vena cava, or other vessels, caudal migration of lidocaine to L3 causing ataxia or recumbency.
Distal
B: 18G 3-7.5 cm needle inserted ventral and dorsal to the tip of the transverse process of L1, L2, and L4. Up to 20 mL lidocaine is infused in a fanned-out pattern ventrally at each site, 5 mL injected dorsally.
O, C: 20G 3 cm needle, 1-3 mL lidocaine at each site
Regional
Caudal Epidural Anesthesia:
Obstetric and surgical procedures of the tail, perineum, anus, rectum, vulva, vagina, prepuce, and skin of the scrotum
B: 18G 3 cm needle or 5 cm spinal needle midline at the S5-Co1 or Co1-Co2 junction following sterile prep and skin desensitization. After contact with the floor of the neural canal, withdraw needle slightly. Place lidocaine in the hub of the needle and slowly withdraw the needle until the lidocaine is aspirated from the hub by the negative pressure of the epidural space. Alternatively, 1 mL of air may be slowly injected as the needle is withdrawn until no resistance is felt. Inject 5-6 mL lidocaine slowly for a 450 kg animal.
O, C: 20G 1.5-3 cm needle midline at the S4-Co1 or Co1-Co2 space. Administer 0.5-1 mL lidocaine/50 kg of body weight.
L: 20 G 1.5-3 cm needle midline at the S5-Co1 space. Administer 0.22 mg/kg lidocaine.
Risks: ataxia due to cranial spread of lidocaine, infection due to nonsterile technique
Other epidural drugs
B: bupivacaine mixed with lidocaine 1:2 to extend the block duration, xylazine 0.03-0.07 mg/kg diluted to 5-7 mL with saline, xylazine 0.03 mg/kg plus lidocaine to a total volume of 5 mL. Morphine alone, 0.1 mg/kg diluted to 5-8 mL or combined with xylazine 0.01 mg/kg or detomidine, 0.01 mg/kg, may be useful for longer term analgesia.
O, C: bupivacaine as for cattle, xylazine as for cattle, but diluted to 1-2 mL, xylazine plus lidocaine as for cattle, but diluted to 1-2 mL
L: bupivacaine as for cattle, xylazine 0.17 mg/kg diluted with 2 mL/150 kg sterile water, xylazine 0.17 mg/kg plus lidocaine 0.22 mg/kg
Lumbosacral Epidural Anesthesia
Procedures performed caudal to the diaphragm in calves, sheep, and goats. The technique may be performed in cattle, but anatomic considerations and loss of sensory and motor function of the hind limbs preclude its routine utility. Cardiovascular depression can occur from sympathetic blockade.
O, C: 20 G 5-7 cm spinal needle with the bevel pointing craniad inserted midline between L6 and S1, midway between the wings of the ileum and just caudal to the dorsal spinous process of L6, following sterile prep and skin desensitization. Advance slowly until the needle pops through the interarcuate ligament to lie in the epidural space. The absence of blood or CSF in the needle hub, aspiration of saline from the needle hub, and no resistance to injection of 1 mL air all indicate correct placement. If CSF is observed (intrathecal position), reduce the dose of drug(s) to one-fourth that for epidural administration.
Drugs: lidocaine 1 mL/5-7 kg body weight, bupivacaine 0.75% 1 mL/10 kg, morphine 0.1 mg/kg diluted with saline or local anesthetic to 0.1-0.2 mL/kg. All drugs must be administered slowly.
Risks: prolonged caudal paralysis, cardiovascular effects from segmental sympathetic blockade, caudal pruritis (morphine), and infection
Adjunct Therapy
Bandages, splints, physical therapy, heat therapy, cold therapy, hydrotherapy, massage, acupuncture, topical therapy (local anesthetics, DMSO, capsaicin, diclofenac, etc.), confinement, housing (deep bedding, padding for recumbent animals, slinging, temperature-controlled environments), social and environmental enrichment
CONTRAINDICATIONS POSSIBLE INTERACTIONS
Regulatory restrictions: See Web sites below for links to FDACVM and the AMDUCA flowchart for recommendations on the use of analgesics and anesthetics in food animals.
Meat and milk withholding: See Web sites below for the link to FARAD for recommendations on meat and milk withholding times for analgesics and anesthetics in food-producing animals.
FOLLOW-UP PATIENT MONITORING
See Alpha-2 agonists and Local Anesthetics above
PREVENTION/AVOIDANCE
See Alpha-2 agonists and Local Anesthetics above
POSSIBLE COMPLICATIONS
See Alpha-2 agonists and Local Anesthetics above
EXPECTED COURSE AND PROGNOSIS
N/A
MISCELLANEOUS
Web Sites
American Association of Bovine Practitioners-http://www.aabp.org/American Association of Small Ruminant Practitioners
-http://www.aasrp.org/ American Veterinary Medical Association AMDUCA Guide and Flowsheet
-http://www.avma.org/scienact/amduca/amduca1.asp (This document is in the member center and may be accessed only by American Veterinary Medical Association members.) FDA Center for Veterinary Medicine (FDACVM)
-http://www.fda.gov/cvm/default.xhtml FDA-approved Animal Drug Products Online Database System
-http://dil.vetmed.vt.edu/Food Animal Residue Avoidance Databank (FARAD)-http://www.farad.org International Veterinary Academy of Pain Management-http://www.animalanalgesia.com Minor Use Animal Drug Program
-http://www.nrsp-7.org
ASSOCIATED CONDITIONS
N/A
AGE-RELATED FACTORS
See Local Anesthetics: Dehorning above
ZOONOTIC POTENTIAL
N/A
PREGNANCY
Alpha-2 agonist drugs may cause abortion in late-term gestation.
RUMINANT SPECIES AFFECTED
Potentially, all ruminant species are affected.
BIOSECURITY
N/A
PRODUCTION MANAGEMENT
N/A
SYNONYMS
N/A
SEE ALSO FARAD NSAIDs
ABBREVIATIONS
AMDUCA = Animal Medicinal Drug Use Classification Act CAE = caprine arthritis encephalitis
CNS = central nervous system Co1-Co2 = first and second coccygeal space COX = cyclooxygenase
DMSO = dimethyl sulfoxide
FARAD = Food Animal Residue Avoidance Databank
FDACVM = Food and Drug Administration Center for Veterinary Medicine GI = gastrointestinal
IM = intramuscular IV = intravenous
NMDA = N-methyl-D-asparate S5-Co1 = sacrococcygeal space
Suggested Reading

Ewing, K. K. 1990, Nov. Anesthesia techniques in sheep and goats. Vet Clin North Am Food Anim Pract. 6(3): 759-78. Fajt, V. R. 2001. Label and extralabel drug use in small ruminants. Vet Clin North Am Food Anim Pract. 17(2): 403-20. Greene, S. A. 2003. Protocols for anesthesia in cattle. Vet Clin North Am Food Anim Pract. 19:680-93.
Jorgensen, J. S., Cannedy, A. L. 1996, Nov. Physiologic and pathophysiologic considerations for ruminant and swine anesthesia. Vet Clin North Am Food Anim Pract. 12(3): 481-500.
Papich, M. G. 2003. Drug residue considerations for anesthetics and adjunctive drugs in food-producing animals. Vet Clin North Am Food Anim Pract. 12(3): 693-706. Skarda, R. T. 1996, Nov. Local and regional anesthesia in ruminants and swine. Vet Clin North Am Food Anim Pract. 12(3): 579-626. Tobin, E., Hunt, E. 1996, Nov. Supplies and technical considerations for ruminant and swine anesthesia. Vet Clin North Am Food Anim Pract. 12(3): 531-62.
Tranquilli, W. J., Grimm, K. A. 2003. Pharmacology of drugs used for anesthesia and sedation. Vet Clin North Am Food Anim Pract. 12(3): 501-29.
Author: Kirsten Wegner

ANESTRUS
BASICS OVERVIEW
Anestrus is the absence of behavioral signs of estrus activity or behavior, although follicular waves are generally still present.
PATHOPHYS IOLOGY
Cattle are polyestrus, but cyclicity may be influenced by factors such as:

Nutrition
Environment
Physiological conditions
Breed
Management Anestrus in cattle can be a response to aberrant release patterns at the level of the hypothalamus (GnRH) or the pituitary (LH and FSH).
SYSTEMS AFFECTED
Endocrine/metabolic, reproductive
SIGNALMENT
Breed differences are related to
Lactational status
Nutritional intake
• Estrus intensity and duration SIGNS
History of female estrous cyclicity and hormonal patterns may increase estrus detection efficiencies.
CAUSES AND RISK FACTORS
Other causes may include
Anestrus females may actually be pregnant.
Systemic disease
Lameness
Utero-ovarian disorders
Postpartum anestrus period (1-3 months) is common.
DIAGNOSIS
Estrus behavior (and lack thereof) and observations can be supported by
Estrus cyclicity records
Lack of palpable CL
No vaginal mucus discharge
No mounting activity when placed with other estrous females or males
Unresponsive to estrus synchronization treatments
DIFFERENTIALDIAGNOSIS
General health/reproductive history
CBC/BIOCHEMISTRY/URINALYS IS
N/A
OTHER LABORATORY TESTS
Serum progesterone concentration > 2 ng/ml may confirm ovulation activity and presence of functional CL, < 2 ng/ml may confirm anestrus.
IMAGING
Ultrasonic imaging in an anestrous female should reveal:
Small inactive ovaries
Small dominant follicle (10-15 mm) or evidence of follicular activity may be present.
DIAGNOSTIC PROCEDURES
Serum progesterone analysis
Transrectal ultrasonography
Rectal palpation
Visual observation
TREATMENT
Correct nutritional intake.
House anestrus females with actively cycling females.
MEDICATIONS DRUGS OF CHOICE
GnRH (200 µg) followed by PGF2alpha (according to label) treatment (7 days apart) may initiate cyclicity.
CIDR treatment (7 days) followed by estrus detection (1-7 days)
MGA (0.5-1.0 mg/head/day) for 10-14 days followed by estrus detection (1-7 days)
CONTRAINDICATIONS
N/A
PRECAUTIONS
PGF2alpha is a vasoconstrictor known to cause abortions and respiratory complications (cattle and humans).
POSSIBLE INTERACTIONS
N/A
FOLLOW-UP PATIENT MONITORING
Behavioral activity
Transrectal ultrasonography
Palpation
Serum progesterone levels
POSSIBLE COMPLICATIONS
Pyometra
Endometritis
Systemic disease
Freemartin
EXPECTED COURSE AND PROGNOSIS
Anestrus females usually regain estrus cyclicity once nutritional, reproductive, and management issues are addressed.
MISCELLANEOUS ASSOCIATED CONDITIONS
N/A
AGE-RELATED FACTORS
Older females may exhibit reduced fertility and estrus cyclicity patterns.
ZOONOTIC POTENTIAL
N/A
PREGNANCY
Many females considered to be anestrus may be pregnant (with a viable on nonviable fetus) and may abort with PGF2alpha treatment.
RUMINANT SPECIES
Cattle; other ruminants may be seasonally polyestrus.
BIOSECURITY
N/A
PRODUCTION MANAGEMENT
Consistently anestrus females in well-monitored operations with strong management and husbandry protocols should be considered for culling.
SEE ALSO
Economics of beef cattle reproductive decisions
Endometritis Estrus behavior Estrus detection
Estrus synchronization Freemartinism Pyometra ABBREVIATIONS
AI = artificial insemination
CIDR = vaginal progesterone inserts CL = corpus luteum
FSH = follicle stimulating hormone GnRH = gonadotropic releasing hormone LH = luteinizing hormone
MGA = melengestrol acetate PGF2 alpha = prostaglandin F-2alpha Suggested Reading
Beardon, H. J., Fuquay, J. W., Wilard, S. T. 2004. Applied animal reproduction. 6th ed. Upper Saddle River, NJ: Pearson-Prentice Hall.
Day, M. L. 2004. Hormonal induction of estrous cycles in anestrous Bos taurus beef cattle. Animal Reproduction Science 82-83: 487-94.
Ginther, O. J., Wiltbank, M. C., Fricke, P. M., Gibbons, J. R., Kot, K. 1996. Selection of the dominant follicle in cattle.
Biology of Reproduction 55:1187-94.
Author: John Gibbons

ANGULAR LIMB DEFORMITY
BASICS DEFINITION

Angular limb deformity (ALD) is a deviation from the normal axis of a limb (in the frontal plane) and is defined by the joint involved and the direction that the distal aspect of the limb is deviated.
Valgus deformity: the limb distal to the lesion deviates laterally.
Varus deformity: the limb distal to the lesion deviates medially.
ALDs are further described by the location of the pivot point (axis of deviation) and by the location of the site of defective growth.
Related conditions include flexural deformities, tendon injuries, joint luxations, and rotational deformities.
Spider lamb syndrome (SLS) or hereditary chondrodysplasia (HC) is a hereditary condition in young lambs characterized by a number of skeletal deformities, including angular limb deformities.
PATHOPHYS IOLOGY
ALDs are considered multifactorial in origin and have congenital/perinatal and developmental predisposing factors.
Cattle and llamas have a complete osseous ulna. In llamas, the distal ulnar epiphysis fuses with the distal radial epiphysis. This unique development of the distal portion of the ulna is associated with forelimb valgus deformities in crias. The ulnar epiphysis extends distally, crosses the radial physis, and fuses with the radial epiphysis. This early fusion demands synchronous growth to ensure normal limb development.
Most calves have a mild carpal valgus deformity of approximately 7 degrees, which does not require treatment. Varus deformities in cattle are abnormal and often need treatment.
SYSTEMS AFFECTED
Musculoskeletal, involving the tibia, radius, ulna, carpus/tarsus, and metacarpus/metatarsus
GENETICS
The questions of heritability in angular limb deformities have not been definitively answered.
ALDs in Jersey calves are genetically transmitted as a simple autosomal recessive trait.
Hereditary chondrodysplasia, or “spider-lamb syndrome” (SLS), of Suffolk and Suffolk-cross sheep is inherited as a single, autosomal recessive gene that has been localized to the distal end of chromosome 6. A defect in the gene encoding fibroblast growth factor receptor 3 (FGFR3) is suspected. DNA tests (blood or semen) are available to identify homozygous and heterozygous animals.
INCIDENCE/PREVALENCE
Valgus and varus angular limb deformities (ALD) are common and well documented in horses but rare in ruminants.
GEOGRAPHIC DISTRIBUTION
ALDs are thought to occur worldwide.
SIGNALMENT
Species
Bovine (cattle), ovine (sheep), goats (caprine), South American camelids (especially llama crias), cervids-including fallow deer (Dama dama), red deer (Cervus elaphus), white-tailed deer (Odocoileus virginianus)-and a single case report of ALD in a giraffe calf (Giraffa camelopardalis).
Breed Predilections
ALDs have been described in many different beef and dairy cattle breeds. SLS primarily affects black-faced breeds of sheep (Suffolk, Hampshire, Southdown, Shropshire, and Oxford).
Mean Age and Range
ALDs primarily affect young growing animals up to 7 months of age, but can be seen in older animals (e.g., trauma-induced ALD). SLS has two distinct clinical entities: lambs are either grossly abnormal at birth or develop the abnormal conformation at 4-6 weeks of age. Radiographic changes at birth are similar for both.
Predominant Sex
No apparent gender predisposition
SIGNS
A complete history including current age, birthing details, age at which the deformity was noticed, course and progression of deformity, and diets of affected animal and dam should be obtained.
PHYSICALEXAMINATION FINDINGS
The animal’s conformation should be assessed first by having the animal stand in a symmetrical manner on a firm, flat surface and observing it from multiple angles. Affected animals may appear to be knock-kneed or bowlegged. All limbs should be palpated and affected limbs should be manually manipulated. Clinical signs such as abnormal bending of the affected limb, increased laxity, muscle atrophy, swelling, heat, pain on manual pressure, abrasions on lateral or medial side of hoof wall, presence of orthopedic injury, and abnormal gait and locomotion are indicative of ALD.
Compensatory deviation (opposite that of the affected limb) is relatively common in the contralateral limb.
If varus deformity is found unilaterally, the contralateral limb should be examined for a significant orthopedic injury as a cause of excessive weight bearing in the deformed limb/joint.
Since cattle are considered to have a “normal” degree of medial deviation at the level of the carpus and hock, as well as normal external rotation of the lower limb, ALDs tend to be missed in the early stages of development.
SLS
In sheep affected with SLS, various degrees of angular limb deformities of fore- and/or hind limbs will be noted. Other physical exam findings include severe scoliosis/kyphosis of the thoracic spine, pectus excavatum, retarded growth rates, facial deformities such as angular deviation and/or shortening of maxilla, rounding of the dorsal silhouette, and Roman-shaped noses.
CAUSES AND RISK FACTORS
ALDs are often related to asymmetrical growth of the physis, ligament rupture, or orthopedic injuries.
Congenital Predisposing Factors
Incomplete cuboidal bone ossification (carpal and/or tarsal)
Physiological immaturity at birth
Uterine malpositioning
In utero bending stress and bone remodeling early in gestation
Twin (or triplet) pregnancy
Laxity of periarticular supporting structures
Disproportionate osseous growth of medial and lateral aspects of long bones (e.g., distal radius, tibia, metatarsus)
Nutritional imbalance during gestation
Genetic causes
Developmental Predisposing Factors
Conformational defects (causing abnormal weight distribution across a joint)
Nutritional disorders (e.g., improper dietary calcium and phosphorus ratios; copper, zinc, manganese, iron, and molybdenum concentrations)
External trauma (e.g., compression of or trauma to growth plate, malunion of fractures)
Iatrogenic (e.g., assisted delivery)
Excessive exercise
Hematogenous osteomyelitis involving the physeal region
Rapid weight gain in heavy breeds
Often, no specific cause is identified.
Camelids
May see ALDs (usually carpal valgus) in growing camelids with hypophosphatemic rickets syndrome.
Ill-thrift syndrome in llamas may be associated with ALDs as well as anemia, low serum iron concentrations, and metabolic disorders (hypothyroidism). Underlying cause not established.
DIAGNOSIS DIFFERENTIALDIAGNOSIS SLS
May be confused with arthrogryposishydranencephaly syndrome (AHS) in lambs, in which there is characteristic hyperflexion of forelimbs, cranial overextension of hind limbs, with a corkscrew deviation of the spine.
In lambs with AHS, severe deformities result from primary abnormalities of the CNS (including hydranencephaly, micromyelia, hydrocephalus, and cerebellar hypoplasia) and not of the skeleton.
Camelids
True ALDs in llamas must be differentiated from valgus deformities of the forelimbs in newborn crias that self correct without surgical treatment.
CBC/BIOCHEMISTRY/URINALYS IS
There are usually no associated laboratory abnormalities with ALD.
SLS
May see slightly elevated serum alkaline phosphatase activity; insufficient for diagnostic purposes.
Camelids
Ill-thrift syndrome: serum vitamin D (25-hydroxycholecalciferol) concentrations are often diagnostic.
May also see hypothyroidism, anemia, erythrocyte dyscrasias, hypophosphatemia, and low serum iron concentrations.
OTHER LABORATORY TESTS
N/A
IMAGING
Radiographs are critical in diagnosing ALDs-at least two views, 90 degrees apart, should be taken of the affected joint, including joints immediately proximal and distal to the affected joint.
The dorsopalmar/dorsoplantar (DP) view is needed for examination of the anatomical location of the deformity and for measurements. The pivot point is defined as the intersection between lines drawn through the long axis at the center of the proximal and distal long bone using the dorsopalmar view. Location of the pivot point identifies the type of deformity. Measure the angle of deviation with a protractor.
SLS: most consistent lesions include multiple islands of ossification of the anconeal process and malformed, displaced sternebrae. The anconeal lesions of HC are progressive, whereas similar lesions in other skeletal conditions of lambs regress.
DIAGNOSTIC PROCEDURES
Bacterial cultures may be indicated in cases of septicemia, arthritis, or osteomyelitis.
Toxicology (heavy metal and mineral analysis) and feed analysis may assist in diagnosis.
PATHOLOGIC FINDINGS
SLS
Histology (vertebrae and long bones): increase in width of the zone of proliferation and hypertrophy and unevenness of growth cartilage; failure to form or maintain orderly columns of chondrocytes.
TREATMENT APPROPRIATE HEALTH CARE
Treatment of neonatal animals with incomplete ossification involves the application of tube casts or splints to the affected limb(s) until ossification is complete (based on repeated radiographs).
NURSING CARE
Severely affected animals may be unable to rise to nurse and require additional supportive care. Protect limbs with thick,
soft bandages that fit well.
Care should be taken to maintain a soft (padding), clean, and dry environment and to minimize decubital/pressure sores, open arthritis, muscle atrophy, umbilical infections, and septicemia.
ACTIVITY
Physical confinement (stall) is recommended for the management of ALDs to limit stresses placed on affected limbs.
DIET
Nutritional imbalances have been implicated, such as ill-thrift in llamas. Treatment for this condition includes appropriate vitamin D supplementation.
Other dietary imbalances should be corrected while treating cases of ALD.
CLIENT EDUCATION
Examination and intervention of young animals with congenital angular limb deformities should be done as early as possible.
Due to the possible hereditary link with ALDs, breeding of affected animals is not recommended.
NONSURGICALCONSIDERATIONS /CONSERVATIVE TREATMENT
Many cases of ALD will resolve without surgery if the underlying cause(s) can be identified and addressed and if the animal does not damage the affected physis or joints with vigorous exercise.
Specific treatment methods are selected on the basis of age, degree of angulation, remaining growth potential of the involved physis, and experience of the veterinarian.
Minor limb deviations may be conservatively treated by manual alignment and external support of the limb (e.g., rigid splinting, bandaging, or casting/tube casts) and/or hoof (claw) trimming.
Hoof manipulations create growth-plate response to stress applied opposite the deformity, and self correction occurs. The hoof tends to turn in the direction of the longer claw or toward the side of the wider wall, resulting in straightening and derotation of the limb.
Medial (varus) deformities can be treated by trimming the medial claw shorter than the lateral claw and by placing an acrylic (methyl methacrylate) wing on the weight-bearing surface of the lateral claw (to increase lateral contact with the ground).
Treatment should be directed at the orthopedic injury when varus deformity is present secondary to a contralateral limb injury.
SURGICALCONSIDERATIONS
Surgery is recommended for older animals (near the end of active physeal growth), for those that do not respond to conservative treatments, and for animals with bone malformations that require realignment (via osteotomy).
The choice of surgical technique should take into consideration the economic value and age of the animal, severity of the deformity, and the joint involved.
Treatment Strategies Include the Following:
Growth Acceleration (Periosteal Stripping/Elevation)
In young calves and lambs with early cases of ALD, surgical growth stimulation via periosteal stripping on the concave aspect (shorter side) of the deformity has been used successfully. Based on the remaining growth potential in the physis, allow the animal to correct the deviation by physeal growth.
Growth Retardation (Transphyseal Bridging)
Transphyseal bridging is indicated for severe cases of ALD or in animals past the rapid growth phase of the radius and ulna (often recommended for animals older than 5 months of age).
By creating a temporary transphyseal bridge on the convex side of the deformity using staples or screws and wires, limb growth is slowed by restricting growth and allows the other side to continue growing, resulting in limb straightening.
The surgical implants must be removed when the limb achieves normal conformation to prevent overcorrection. This can be used in combination with periosteal stripping to increase the likelihood of full correction in animals with severe deviations.
Corrective Wedge Osteotomy
This procedure is indicated in mature animals with ALD and in neonates with congenital fracture malunion. If the growth plates are closed or if the growth plate is not involved in an ALD, a corrective osteotomy is recommended. This requires more experience and equipment and often is reserved for valuable animals when response to other therapies has failed.
The site and orientation of the wedge should be determined by clinical and radiographic examination.
• The limb needs to be stabilized by internal fixation with a plate and screws for an extended postoperative period. Camelids An ulnar osteotomy must be done in conjunction with the periosteal transection because the ulna spans the radial physis.
MEDICATIONS DRUGS OF CHOICE
Nonsteroidal anti-inflammatory agents (NSAIDs) are recommended to reduce inflammation in some cases of ALD, especially those associated with physitis.
CONTRAINDICATIONS
Prolonged NSAID administration has been associated with gastrointestinal (abomasal) ulcers.
Appropriate milk and meat withdrawal times must be followed for all compounds administered to food-producing animals.
PRECAUTIONS
Many of these affected animals are young; precautions regarding drug choices must take age into consideration.
POSSIBLE INTERACTIONS
N/A
ALTERNATIVE DRUGS
N/A
FOLLOW-UP PATIENT MONITORING
Frequent physical monitoring and repeated radiographs should be done to assess the efficacy of corrective measures and to monitor progress.
In cases of transphyseal bridging surgery, owner cooperation is required to determine when the limb has regained its normal conformation, at which time the implants must be removed to prevent overcorrection.
PREVENTION/AVOIDANCE
Avoid breeding affected animals.
POSSIBLE COMPLICATIONS
In cases of valgus deformity, efforts should be taken to prevent compensatory varus in the contralateral limb. Persistence of hoof distortion is possible if the angular deformity is not corrected.
Surgical: transphyseal bridging-overcorrection of the physis is possible. Owner cooperation is required to determine when limb has regained its normal conformation.
Possible ALD surgical complications include muscle, tendon, and ligament atrophy/laxity, hyperextension of limbs, fibrous scar tissue development, and postoperative infection.
EXPECTED COURSE AND PROGNOSIS
Prognosis is guarded, yet reasonable for ALDs associated with growth plate imbalances, such as most valgus deformities.
The prognosis for ALDs secondary to contralateral orthopedic injury (such as most varus deformities) is generally poor because it is usually centered over a joint and is dependent on the prognosis of the primary orthopedic injury.
SLS-affected individuals rarely survive the neonatal period.
Camelids: the prognosis for ill-thrift syndrome in llamas is poor; etiologic agent often not identified.
MISCELLANEOUS
ASSOCIATED CONDITIONS
Conditions associated with ALDs include osteochondrosis of the physis, epiphysitis, and incomplete ossification of the cuboidal carpal bones.
Hyena disease (premature physeal closure) has been reported in calves due to overdose of vitamins A, D3, and E.
Congenital lethal chondrodysplasia in Australian Dexter cattle = “Dexter bulldog calves.”
Congenital chondrodysplastic dwarfism in Holstein calves
Complex vertebral malformation is a familial syndrome of Holstein calves.
Syndrome known as “bentleg” or “bowie” associated with ingestion of Trachymene glaucifolia (wild parsnip) by pregnant ewes in Australia and New Zealand
AGE-RELATED FACTORS
The majority of ALDs occurs during the active growth phase of the affected bone/joint.
ZOONOTIC POTENTIAL
N/A
PREGNANCY
Many of the causes of ALDs are congenital diseases in which the in utero environment is somehow disturbed (hormones, vascular supply, teratogens, mechanical factors, or prenatal virus infections).
Cases of ALDs in goats pregnant with triplets have been reported.
Contributing factors likely include stress and in utero malpositioning.
RUMINANT SPECIES AFFECTED
Bovine, ovine, caprine, cervid, camelid
BIOSECURITY
N/A
PRODUCTION MANAGEMENT
N/A
SYNONYMS
Hereditary chondrodysplasia (spider lamb syndrome)
SEE ALSO
Arthrogryposis Cleft palate CNS anomalies
CNS: brain lesions CNS: nerve
Crooked calf syndrome
Lameness: muscle/tendon-contracted tendons
Spider lamb disease
ABBREVIATIONS
AHS = arthrogryposis-hydranencephaly syndrome ALD = angular limb deformity
CNS = central nervous system
HC = ovine hereditary chondrodysplasia NSAIDs = nonsteroidal anti-inflammatory drugs SLS = spider lamb syndrome
Suggested Reading
Duchame, N. G. 2004. Angular deformities. In:Farm animal surgery, ed. S. L. Fubini, N. G. Ducharme. Philadelphia: W.
B. Saunders.
Ferguson, J. G. 1997. Angular deformity of radiocarpal and tibiotarsal joints. In: Lameness in cattle, ed. P. R. Greenough. 3rd ed. Philadelphia: W. B. Saunders.

Kaneps, A. J. 1996. Orthopedic conditions of small ruminants, llama, sheep, goat, and deer. Advances in ruminant orthopedics. Veterinary Clinics of North America: Food Animal Practice 12(1):211-31.
Paul-Murphy, J. R., Morgan, J. P., Snyder, J. R., Fowler, M. E. 1991. Radiographic findings in young llamas with forelimb valgus deformities: 28 cases (1980-1988). JAVMA 12(15):21107-11.
Authors: Erik J. Olson and Cathy S. Carlson

ANTHRAX
BASICS DEFINITION
Anthrax is an almost invariably fatal septicemic disease caused by a large, gram-positive spore-forming bacterial rod Bacillus anthracis, which is part of the normal soil flora in most geographic areas, particularly those with alkaline soils.
PATHOPHYS IOLOGY

Spores of the causal agent gain entry to the host by ingestion, by inhalation, or through skin lesions.
Once the bacillus enters the body, it is ingested by macrophages and enters into lymphatic vessels and lymph nodes to cause lymphangitis and lymphadenitis.
The spores germinate to a vegetative form, multiply extracellularly, and are disseminated throughout the host.
The organisms produce toxins (lethal factor, edema factor, and protective antigen) that cause widespread damage of the vasculature and reticuloendothelial system to result in edema, tissue damage, shock, renal failure, anoxia, and ultimately death.
INCIDENCE/PREVALENCE
In the United States, the disease is usually seen in one or only a few animals at a time and is sporadic.
Both sporadic cases and outbreaks are often associated with disruption of the soil. This disruption brings bacterial spores to the soil surface where they are ingested. Similarly, animals grazing short grasses during drought periods may ingest spores.
Outbreaks can occur over large areas if animals are fed contaminated feeds, such as meat and bone meal.
Pastures can be contaminated by effluent from textile mills that were using animal products, such as wool, in the manufacturing process.
Morbidity varies widely but case mortality is 90%-95%.
Control efforts are successful in domestic species but wildlife can suffer large outbreaks.
GEOGRAPHIC DISTRIBUTION
The anthrax bacillus has a worldwide distribution but some areas have a higher rate of disease.
SIGNALMENT
Anthrax can affect all livestock species but the major ruminant species-cattle, goats, and sheep-are more susceptible than horses and pigs.
There are some reports of males being more susceptible than females and older animals being more susceptible than young animals but these probably reflect differences in stress and grazing habits rather than inherent differences in susceptibility.
SIGNS
Many animals die suddenly and there are no clinical signs noted.
Animals develop fever, depression, muscle tremors, dyspnea, diarrhea, and other signs related to septicemia. A smaller number of more chronic cases may develop subcutaneous edema, hematuria, rumen stasis, and decreased milk production with blood-tinged milk.
GENERALCOMMENTS
N/A
HISTORICALFINDINGS
N/A
PHYSICALEXAMINATION FINDINGS
N/A
CAUSES
Anthrax is caused by Bacillus anthracis, a large, gram-positive, spore-forming bacterial rod.
Infection can occur by ingestion, which is the most common route, by inhalation, or by contamination of skin wounds.
Primary cases are usually due to ingestion but secondary cases on the same premises may be due to contact with infectious discharges from the primary cases or by ingestion of tissues from the primary case.
RISK FACTORS
Anthrax cases are more common in years when there have been major climate changes (e.g., wet spring followed by a drought or a drought followed by heavy rains).
Disruption of the soil can bring infectious spores to the surface where they are more easily ingested or inhaled.
Close grazing of poor-quality, coarse feed can lead to oral trauma and predispose animals to infection.
DIAGNOSIS DIFFERENTIALDIAGNOSIS
Because the signs of anthrax are not specific, almost any disease can be considered in the differential diagnosis. Some that merit specific mention include acute toxicity, anaplasmosis, vena cava syndrome with exsanguination from the respiratory tract, blackleg, malignant edema, and bacillary hemoglobinuria.
CBC/CHEMISTRY/URINALYS IS
N/A
OTHER LABORATORY TESTS
N/A
IMAGING
N/A
DIAGNOSTIC PROCEDURES
Because of the zoonotic risk of anthrax and the poor response to treatment, a full clinical workup is generally not warranted.
Diagnosis is based on the demonstration of the causal organism in body fluids, and laboratory professionals best perform this testing function.
Blood from an ear tip or jugular vein in the live animal (or one dead less than 12 hours) or aqueous humor or an entire eyeball from a dead animal are all acceptable samples for finding the organism.
Bacteremia may not occur until just before death, and demonstration of the agent may be difficult in the live animal particularly if antibiotic therapy has begun.
The organism on Giemsa or Wright stain is typically seen as a square-ended bacterial rod that occurs singly or in short chains and resembles “railroad boxcars.”
PATHOLOGIC FINDINGS
Because of the danger of environmental contamination, if anthrax is suspected, a full necropsy is contraindicated.
Animals that die from anthrax undergo rapid decomposition and generally do not develop full rigor.
The carcass will be gas distended and have a “saw-horse” appearance.
Natural body orifices may have an exudate consisting of dark, unclotted, tarry blood.
On necropsy, there will be marked splenic enlargement (two to three times normal size), serosal and mucosal edema and hemorrhage, edema and hemorrhage in lymph nodes, unclotted blood, intramuscular edema, and possibly enteritis.
In sheep and goats, the disease progresses very rapidly and there may not be localized lesions in the carcass.
TREATMENT
The prognosis for animals with anthrax is poor but there are reports of animals that have survived.
The anthrax bacillus is susceptible to a wide range of antibiotics but treatment will make demonstration of the organism
in body fluids more difficult.
Streptomycin (8-10 g/day in 2 doses) or oxytetracycline (5 mg/kg/day) are recommended by some texts.
Antibiotic treatment should be for a minimum of 5 days and preferably 10 days, and the first dose should be given IV if this is a possible route with the antibiotic chosen.
An antiserum is available in some areas but is often quite expensive.
Appropriate milk and meat withdrawal times must be followed for all compounds administered to food-producing animals.
CLIENT EDUCATION
The client must be made aware of the potential of the organism to infect a variety of species, including humans, via skin wounds, ingestion, or inhalation.
Carcass disposal can be problematic.
The anthrax bacillus is generally destroyed during putrefaction of the carcass and if the carcass is not opened and if discharge of fluids into the environment does not occur, there will not be significant contamination of the site.
Since treatment is typically not successful, prevention and control should be emphasized.
MEDICATIONS
N/A
FOLLOW-UP PATIENT MONITORING
N/A
PREVENTION/AVOIDANCE
Hygiene and carcass disposal are of paramount importance.
Autolysis of the carcass destroys the vegetative forms of B. anthracis and, therefore, if carcasses are not opened up, the potential for contamination of the environment is minimized.
Carcasses should be disposed of by burning or deep (>6 feet) burial that occurs well away from water sources.
Burning may release spores into the rising heat column and disperse them, and therefore hot fires that take hold quickly are best. The risk from burning carcasses is probably less than not burning the carcass, however.
Livestock can be vaccinated with Stern-strain spore vaccine. Booster vaccination is given 4-5 weeks following the initial vaccination, and then annually thereafter.
The vaccine is a live nonencapsulated organism and therefore antibiotics should not be given within 7 to 10 days of vaccine administration.
Following vaccination, there is a 60-day withdrawal time for the carcass, and milk should be discarded for at least 72 hours.
There may be a localized reaction at the vaccination site and this can be quite severe in some animals.
Spores are very resistant and can survive in contaminated soils for 15-30 years. Therefore, anthrax is still a potential danger in areas with historic cases.
MISCELLANEOUS ASSOCIATED CONDITIONS
Animals develop fever, depression, muscle tremors, dyspnea, diarrhea, and other signs related to septicemia. A smaller number of more chronic cases may develop subcutaneous edema, hematuria, rumen stasis, and decreased milk production with blood-tinged milk.
AGE-RELATED FACTORS
There are some reports of males being more susceptible than females and older animals being more susceptible than young animals, but these probably reflect differences in stress and grazing habits rather than inherent differences in susceptibility. ZOONOTIC POTENTIAL
Anthrax is primarily a disease of herbivores, but all mammals, including humans, are susceptible and therefore care must be exercised when working in areas where spores are potentially present.
PREGNANCY
N/A
RUMINANT SPECIES AFFECTED
All ruminant species are affected.
BIOSECURITY
Anthrax is a reportable disease.
Once anthrax is diagnosed, the farm will be quarantined, all carcasses and fluids will be destroyed, survivors will be vaccinated, and the farm will be isolated for at least 2 weeks.
Because of the association between anthrax and disturbed soils and/or localized areas, animals surviving an outbreak may be moved to different pastures or holding pens in order to reduce the possibility of additional cases.
Scavenger control is important to prevent the spread of the disease.
Because of recent concerns about bioterrorism, the Federal Bureau of Investigation will likely become involved in any cases of anthrax in the United States.
PRODUCTION MANAGEMENT
Hygiene and carcass disposal are of paramount importance.
Autolysis of the carcass destroys the vegetative forms of B. anthracis and, therefore, if carcasses are not opened up, the potential for contamination of the environment is minimized.
Carcasses should be disposed of by burning or deep (>6 feet) burial that occurs well away from water sources.
Livestock can be vaccinated with Stern-strain spore vaccine. Booster vaccination is given 4-5 weeks following the initial vaccination, and then annually thereafter.
Close grazing of poor-quality, coarse feed can lead to oral trauma and predispose animals to infection.
SYNONYMS
N/A
SEE ALSO
Acute toxicity Anaplasmosis
Bacillary hemoglobinuria Blackleg
Malignant edema
Vena cava syndrome with exsanguination from the respiratory tract
ABBREVIATIONS
N/A
Suggested Reading
Anthrax. 2000. In:Veterinary medicine, ed. O. M. Radostits, C. C. Gay, D. C. Blood, K. W. Hinchcliff. 9th ed. Philadelphia: W. B. Saunders.
Mosier, D. A., Chengappa, M. M. 1999. Anthrax. In:Current veterinary therapy 4: food animal practice, ed. J. L. Howard, R. A. Smith. Philadelphia: W. B. Saunders.
Pipkin, A. B. 2002. Anthrax. In:Large animal internal medicine, ed. B. P. Smith. 3rd ed. St. Louis: Mosby.
Author: John M. Adaska

ARSENIC TOXICOSIS
BASICS OVERVIEW

Arsenic has been reported to be the second most common heavy metal intoxication of cattle after lead.
Arsenic is still used in herbicides, defoliants, and wood preservatives.
The use of arsenic-containing products has decreased in the recent past as other insecticides and herbicides become available.
SYSTEMS AFFECTED
Gastrointestinal
Renal
Nervous (phenylarsonic compounds)
Sources
Inorganic arsenic
Arsenate-natural, pentavalent form of arsenic
Trivalvent forms are manufactured inorganic arsenic: arsenic trioxide (insecticide and herbicide); trivalent arsenic (arsenite)
Pressure-treated woods (green in color): chromated copper arsenate (CCA). Cattle have been poisoned by consumption of ashes from burnt pressure-treated wood.
Inorganic arsenic is more commonly associated with intoxication in cattle.
Organic arsenic
3-nitro, 4-hydroxyphenylarsonic acid (3 nitro)-a feed additive
Thiacertarsaminde-heartworm therapy
Monosodium methanearsonate (MSMA)-herbicide
Disodium methanearsonate (DSMA)-herbicide
Toxic Dose
Toxicity depends upon the formulation, route of exposure, and duration of exposure.
Trivalent forms are 5-10 times more toxic than pentavalent forms.
For most species, the toxic oral dose of sodium arsenite is 1 to 25 mg/kg of body weight.
GENETICS
N/A
INCIDENCE/PREVALENCE
Unknown
GEOGRAPHIC DISTRIBUTION
Worldwide
SIGNALMENT
Species
N/A
Breed Predilections
N/A
Mean Age and Range
N/A
Predominant Sex
N/A
SIGNS
Sudden death (peracute toxicosis)
Acute to subacute toxicosis
Diarrhea +/- hemorrhagic
Anorexia
Dehydration
Weakness
Ruminal atony
Colic
CAUSES AND RISK FACTORS
N/A
DIAGNOSIS
Clinical signs
Possible history of exposure
Chemical determination of arsenic in tissues
Liver or kidney arsenic concentrations greater than 3 ppm
Stomach content or urinary arsenic greater than 2 ppm
Chemical determination of arsenic in water or feedstuffs
DIFFERENTIALDIAGNOSIS
Bovine viral enteritis (BVD)
Bacterial enteritis (Salmonella spp.)
Organophosphorus insecticides
Other heavy metals (lead)
Urea toxicosis
CBC/BIOCHEMISTRY/URINALYS IS
None specific to arsenic toxicosis
OTHER LABORATORY TESTS
N/A
PATHOLOGIC FINDINGS GROSS FINDINGS
Gastrointestinal: generalized or localized reddening of the gastrointestinal mucosa; hemorrhage; erosions; submucosal edema
Kidneys: pale, swollen
HISTOPATHOLOGICAL FINDINGS
Multifocal hepatic and renal necrosis
Dilation of intestinal capillaries
Submucosal congestion and edema
Intestinal epithelial necrosis
Renal tubular necrosis
TREATMENT
Symptomatic and Supportive Therapy
Very important, as animals may present late in the clinical course
Fluid therapy
Blood transfusion +/-
Antidotal Therapy-Chelation
Thioctic acid (lipoic acid or alpha lipoic acid)
More effective in cattle than dimercaprol
No commercially available source
50 mg/kg divided into two to three injection sites
Administer q 8 hours
2, 3-dimercaptosuccinic acid (DMSA)
Also known as CHEMET or Succimer
Water-soluble analog of British Anti Lewisite (BAL)
Given orally
Commercially available product (humans)
10 mg/kg per os q 8 hours (human and small animal dose)
MEDICATIONS CONTRAINDICATIONS
Appropriate milk and meat withdrawal times must be followed for all compounds administered to food-producing animals.
FOLLOW-UP MISCELLANEOUS ASSOCIATED CONDITIONS
Gastrointestinal: intestinal epithelial necrosis
Kidneys: renal tubular necrosis
AGE-RELATED FACTORS
N/A
ZOONOTIC POTENTIAL
N/A
PREGNANCY
N/A
RUMINANT SPECIES AFFECTED
Potentially all ruminant species
BIOSECURITY
N/A
PRODUCTION MANAGEMENT
Keep agricultural chemicals away from livestock at all times.
SYNONYMS
N/A
SEE ALSO
Toxicology: herd outbreaks
ABBREVIATIONS
BAL = British Anti Lewisite
BVD = bovine viral diarrhea
CCA = chromated copper arsenate
DMSA = 2, 3-dimercaptosuccinic acid
DSMA = disodium methanearsonate
MSMA = monosodium methanearsonate
Suggested Reading
Faires, M. C. 2004. Inorganic arsenic toxicosis in a beef herd. Can Vet J. 45(4): 329-31.
Hullinger, G., Sangster, L., Colvin, B., Frazier, K. 1998. Bovine arsenic toxicosis from ingestion of ashed copper- chrome-arsenate treated timber. Vet Hum Toxicol. 40(3): 147-48.
Stair, E. L., Kirkpatrick, J. G., Whitenack, D. L. 1995. Lead arsenate poisoning in a herd of beef cattle. J Am Vet Med Assoc. 207(3): 341-43.
Thatcher, C. D., Meldrum, J. B., Wikse, S. E., Whittier, W. D. 1985. Arsenic toxicosis and suspected chromium toxicosis in a herd of cattle. J Am Vet Med Assoc. 187(2): 179-82.
U.S. EPA. Chromated copper arsenate (CCA) and its use as a wood preservative. Web site visited October 8, 2004.http://www.epa.gov/pesticides/factsheets/chemicals/1file.htm.
Author: Joe Roder

ARTHROGRYPOSIS
BASICS DEFINITION

Congenital arthrogryposis is defined as a syndrome of persistent joint contracture (bilateral rigidity) present at birth and may involve one or multiple limbs (forelimbs and/or hind limbs).
Arthrogryposis is often associated with cleft palate and primary CNS lesions such as hydranencephaly and syringomyelia.
The arthrogryposis-hydranencephaly syndrome (AHS) is usually associated with flexural contracture of the limbs rather than angular limb deformities (ALDs).
Crooked calf syndrome (CCD) is a congenital deformity condition widely recognized in western North America, characterized by arthrogryposis, scoliosis, torticollis, and cleft palate. CCD is observed in calves after maternal ingestion of lupines containing the quinolizidine alkaloid anagyrine during gestation days 40-100.
Congenital arthrogryposis may be associated with denervation muscle atrophy.
PATHOPHYS IOLOGY
Congenital arthrogryposis is considered multifactorial in origin and has multiple predisposing factors and etiologies.
It can be caused by a number of etiologic agents including: plant teratogens (e.g., lupines), spinal dysraphism, prenatal viral infections (e.g., Akabane virus), and in utero hormonal and vascular defects.
It may also be attributed to a decrease or lack of motion of the fetus during critical stages of development, such as malpositioning and overcrowding caused by the size of the fetus relative to the dam.
Ingestion of teratogenic plants (e.g., Astragalus or Oxytropis spp. = locoweed; Verratrum californicum = skunk cabbage; piperidine alkaloid-containing plants such as Lupinus, Conium, and Nicotiana species).
Repeated dosing or continuous low-level ingestion over time may result in cumulative intoxication and/or teratogenesis.
Teratogenic plant alkaloids may be transferred to the placenta and induce a sedative or anesthetic effect in the fetus.
In CCD, there is often a lesion in the CNS that may result in reduced or complete absence of movement of the affected body parts in the developing fetus, especially during the period of rapid growth. Studies have demonstrated a significant reduction in number of a-motorneurons in the cervical spinal cord. May cause disruption in normal innervation of muscles leading to paresis and instability of the limb, or may result in hypotonic condition of extensor muscle and dysfunction of the radial nerve.
SYSTEMS AFFECTED
Musculoskeletal-involving forelimbs, hind limbs, or both. The carpal and phalangeal joints are most commonly affected, followed by metacarpophalangeal and metatarsophalangeal joints.
GENETICS
The questions of heritability in arthrogryposis have not been definitively answered.
Lambs
A congenital arthrogryposis exists in pedigree Suffolk and Australian Merino lambs as an inherited limb deformity.
INCIDENCE/PREVALENCE
For CCD, there are reports of up to 40% of calves from a single herd being affected. The incidence of disease varies with year, area, and herd.
Cattle records reveal that the disease usually affects < 10% of a herd.
GEOGRAPHIC DISTRIBUTION
Arthrogryposis is thought to occur worldwide. Depending on the etiologic cause, the geographic distribution may vary (e.g., crooked calf syndrome is most common in western North America).
Calf arthrogryposis has been reported from most parts of the world and in many breeds of cattle.
SIGNALMENT
Species
Bovine, ovine, caprine, camelids
Breed Predilections
Arthrogryposis has been described in many different beef and dairy cattle breeds. Certain syndromes are predominantly reported to occur in certain breeds (e.g., congenital arthrogryposis in Charolais cattle). CCD has been observed in most dairy breeds and in all breeds of beef cattle common to western North America.
No breed predilection or genetic susceptibility in cattle to the lupine-induced condition has been determined.
Mean Age and Range
Arthrogryposis tends to affect young, growing animals. The incidence of CCD is highest in heifers at first calving, but the disease has been observed in calves from cows of all ages.
For each species (cattle, sheep, and goats), there are specific periods of gestation when the fetus is susceptible to plant teratogens. The critical gestational period for exposure of cattle to lupines is 40-70 days with susceptible periods extending to 100 days.
Predominant Sex
No apparent gender predisposition SIGNS HISTORICALFINDINGS
A complete history including age, birthing details, age at which the deformity was noticed, course and progression of deformity, diets of affected animal and dam should be obtained. The animal may be normal at birth and develop the flexural deformity within hours or days.
PHYSICALEXAMINATION FINDINGS
The animal’s conformation should be assessed first by having the animal stand in a symmetrical manner on a firm, flat surface and observing it from multiple angles.
Arthrogryposis in CCD is characterized by deformities of the limbs (rigid flexion of elbows and carpal joints), and spinal column (scoliosis, lordosis, kyphosis), and rib cage abnormalities. Affected calves occasionally have torticollis and cleft palate.
The joints are often flexed and cannot be extended even after the flexor tendons are cut-distinguishing the disease from contracted tendons.
CAUSES
A number of etiological agents such as intrauterine infection with border disease virus (a pestivirus), Akabane virus, Cache Valley virus, and bluetongue virus, as well as teratogenic plant ingestion have been implicated in the pathogenesis of arthrogryposis (crooked limbs) in small ruminants.
Congenital Predisposing Factors
Uterine malpositioning
Genetic causes
Ingestion of teratogenic plants by pregnant dam (e.g., Astragalus or Oxytropis spp. = locoweed;Verratrum californicum = skunk cabbage; piperidine alkaloid-containing plants such as Lupinus, Conium, and Nicotiana species).
Conditions associated with arthrogryposis include crooked calf syndrome/congenital arthrogryposis, spider lamb syndrome (hereditary chondrodysplasia), ill-thrift syndrome in llamas, metabolic, and neurovascular disorders.
Leg deformities in young calves are most commonly associated with congenital contraction of the tendons. Flexural deformities involving contracted tendons and ligaments may be seen in many breeds of cattle and small ruminants.
RISK FACTORS
Predisposing factors for congenital arthrogryposis include male gender, posterior intrauterine presentation, and double muscling.
DIAGNOSIS
DIFFERENTIALDIAGNOSIS
Arthrogryposis and CCD differ from contracted tendons; in animals with contracted tendons, the joints are usually properly aligned and the legs are not rotated. In calves with arthrogryposis, the articular and osseous changes are usually permanent and worsen as the calf grows.
Congenital arthrogryposis rule-outs: BVD, IBR, bluetongue virus, Akabane virus, and Cache Valley virus
Arthrogryposis-hydranencephaly syndrome (AHS) in lambs may be confused with spider lamb syndrome (SLS), in which there is characteristic hyperflexion of forelimbs, cranial overextension of hind limbs, with a corkscrew deviation of the spine. In lambs with AHS, severe deformities result from primary abnormalities of the CNS and not of the skeleton. Hydranencephaly, micromyelia, hydrocephalus, and cerebellar hypoplasia are also seen with AHS.
CBC/BIOCHEMISTRY/URINALYS IS
N/A
OTHER LABORATORY TESTS
N/A
IMAGING
Radiographs can be used to diagnose angular limb deformities; at least two views, 90 degrees apart, should be taken of the affected joint.
The dorsopalmar/dorsoplantar (DP) view is needed for examination of the anatomical location of the deformity and for measurements. Shoot with radiographic beam in line with the claws.
DIAGNOSTIC PROCEDURES
Serology and virological diagnostic assays may aid in ruling out in utero viral infections (e.g., Cache Valley virus).
Feed analysis and assessment of the availability of potentially toxic plants in the environment (pasture) may assist in diagnosis.
PATHOLOGIC FINDINGS CCD
No consistent primary lesion, rather a number of varied tissue responses are observed. It is likely that these findings are at least in part due to the animal’s inability to stand.
Histology: few lesions, restricted to muscles of the forelimb, external intercostalis muscle, or radial and femoral nerves- myositis, myodegeneration, muscle necrosis and atrophy, cellulitis, and perineuritis.
TREATMENT APPROPRIATE HEALTH CARE
N/A
NURSING CARE
Severely affected animals may be unable to rise to nurse and require additional supportive care.
Protect limbs with thick, soft bandages that fit well.
Provide good footing and allow for stretching of flexor tendons.
Care should be taken to maintain a soft (padding), clean, and dry environment and to minimize decubital/pressure sores, open arthritis, muscle atrophy, umbilical infections, and septicemia.
ACTIVITY
Activity should be restricted until it is certain that the deformity is improving; however, some degree of exercise allows for stretching and lengthening of affected limb structures.
DIET
Correction of any dietary imbalances should be addressed while treating cases of arthrogryposis.
CLIENT EDUCATION
Examination of young animals with congenital arthrogryposis should be done as early as possible to assess the degree of manual correction possible.
Because of a possible hereditary component associated with some forms of arthrogryposis, breeding of affected animals is not recommended.
NONSURGICALCONSIDERATIONS /CONSERVATIVE TREATMENT
Mildly affected animals may recover spontaneously.
Weight bearing provides the necessary physical exercise to strengthen and lengthen affected tendons and musculature.
Minor deformities may be corrected by manual alignment and external support of the limb (e.g., rigid splinting, bandaging, or casting/tube casts).
SURGICALCONSIDERATIONS
Surgery may be required for animals with severe deformities and for animals that do not improve with age or conservative management.
Treatment of arthrogryposis includes surgery to improve the animal’s posture sufficient for it to obtain slaughter weight (a salvage procedure).
Surgical procedures include: transection of flexor tendon and suspensory ligament, joint capsule release, flexor tendon lengthening procedures, and joint arthrodesis.
May require postoperative splinting or casting for support
MEDICATIONS DRUGS OF CHOICE
N/A
CONTRAINDICATIONS
N/A
PRECAUTIONS
N/A
POSSIBLE INTERACTIONS
N/A
ALTERNATIVE DRUGS
N/A
FOLLOW-UP PATIENT MONITORING
Frequent physical examinations and assessing the efficacy of corrective measures should be done to monitor progress.
PREVENTION/AVOIDANCE
CCD: Avoid breeding affected animals.
Coordinate grazing times and alter breeding dates to minimize exposure. Avoid grazing the potentially teratogenic plants when pregnant cows are at the susceptible stage of pregnancy.
Control teratogenic plant populations with herbicide treatment.
POSSIBLE COMPLICATIONS
Some severe cases of arthrogryposis cannot be corrected and full extension may not be possible postoperatively.
EXPECTED COURSE AND PROGNOSIS
The prognosis is guarded for arthrogryposis, depending on the severity of the flexural deformity. Severe deformities requiring surgery often have a poor prognosis.
For arthrogryposis in cattle, approximately 80% of surgically treated animals can be kept until they reach normal slaughter weight.
If untreated, arthrogryposis is usually lethal in cattle, resulting in skin necrosis over the carpus, arthritis, and septicemia.
MISCELLANEOUS ASSOCIATED CONDITIONS
A syndrome known as “bentleg” or “bowie” has been associated with ingestion of Trachymene glaucifolia (wild parsnip) by pregnant ewes in Australia and New Zealand.
AGE-RELATED FACTORS
The majority of arthrogryposis cases occurs during the active growth phase of the affected bone/joint.
ZOONOTIC POTENTIAL
N/A
PREGNANCY
In cases of congenital arthrogryposis, the teratogenic plants are ingested by the pregnant dam and the compounds are passed to the fetus through the placenta.
RUMINANT SPECIES AFFECTED
Bovine, ovine, caprine, camelid
BIOSECURITY
N/A
PRODUCTION MANAGEMENT
Producers should be aware of the association between certain toxic plants (e.g., lupines) and angular limb deformities such as CCD.
To reduce the incidence of crooked calf syndrome, graze lupines during their least hazardous growth period and reduce exposure of pregnant cows. Lupines are most hazardous when they are young or in the mature seed stage.
Fence off heavily infested pasture areas and use intermittent, short-term grazing of lupine pastures.
SYNONYMS
N/A
SEE ALSO
Akabane virus
Cache Valley virus/disease Cleft palate
CNS anomalies CNS: brain lesions
Lameness: muscle/tendon-contracted tendons
Lupine toxicity
ABBREVIATIONS
AHS = arthrogryposis-hydranencephaly syndrome ALD = angular limb deformity
BVD = bovine viral diarrhea virus CCD = crooked calf disease/syndrome CNS = central nervous system
IBR = infectious bovine rhinotracheitis virus SLS = spider-lamb syndrome
Suggested Reading
Anderson, D. E., St. Jean, G. 1996. Diagnosis and management of tendon disorders in cattle. Advances in ruminant orthopedics. Veterinary Clinics of North America: Food Animal Practice 12(1): 89-93.
Kaneps, A. J. 1996. Orthopedic conditions of small ruminants, llama, sheep, goat, and deer. Advances in ruminant orthopedics. Veterinary Clinics of North America: Food Animal Practice 12(1): 225-26.
Panter, K. E., James, L. F., Gardner, D. R. 1999. Lupines, poison-hemlock and Nicotiana spp: toxicity and teratogenicity in livestock. Journal of Natural Toxins 8(1): 117-34.
Panter, K. E., Keeler, R. F., Bunch, T. D., Callan, R. J. 1990. Congenital skeletal malformations and cleft palate induced in goats by ingestion of Lupinus, Conium, and Nicotiana species. Toxicon 28(12): 1377-85.
Van Huffel, X., De Moor, A. 1987. Congenital multiple arthrogryposis of the forelimbs in calves. Compendium-Food Animal 9(10): F333-F339.
Authors: Erik J. Olson and Cathy S. Carlson

ASPERGILLOSIS
BASICS OVERVIEW

Aspergillus spp. are ubiquitous environmental organisms that can cause disease in many mammalian species. This saprophytic fungus is present in the soil and other decaying matter.
Aspergillus is an opportunistic pathogen and usually occurs secondary to chronic disease, immunosuppression, stress, or metabolic disturbances. It can also occur with chronic antibiotic or steroid use.
In ruminants, A. fumigatus is the most common isolate involved in clinical disease.
The disease can manifest in ruminants as one of several forms including pulmonary, intestinal, systemic, and/or as a cause of abortion or mastitis.
SIGNALMENT
In cattle, aspergillosis is a major cause of mycotic abortion. Primary pulmonary infections are rare but can be caused by inhalation of spores from contaminated feedstuffs. It can occur secondary to concurrent disease in a pulmonary or intestinal form. Mastitis caused by Aspergillus has also occasionally been seen in cattle.
Once infected, cattle may then develop a systemic aspergillosis due to invasion of blood vessels and dissemination of the organism throughout the body.
Housed calves may be more susceptible to pulmonary infection.
In sheep and goats, Aspergillus spp. may cause a primary mastitis. Disseminated aspergillosis may occur in conjunction with mastitis. Primary pulmonary infections are rare in sheep and goats.
Pulmonary and disseminated aspergillosis have also been reported in llamas and alpacas, camels, American bison, and cervidae.
SIGNS
Pulmonary
May cause few clinical signs. Mild respiratory disease and/or weight loss may be the only symptoms.
Other respiratory signs may include fever, anorexia, cough, nasal discharge, tachypnea, dyspnea, and recumbency.
Development of pneumonia may be acute.
Mastitis
Sheep and goats may have purulent mammary secretions, slight fever, and weight loss. The affected quarter becomes swollen and firm. Clinical signs from disseminated infection include depression, fever, and weight loss.
Abortion
Bovine abortions due to Aspergillus spp. usually occur in the third trimester.
Retained placenta and placentitis are seen.
Fetal lesions may consist of bronchopneumonia and dermatitis.
CAUSES AND RISK FACTORS
Chronic disease, immunosuppression, concurrent disease
Viral erosive diseases, intestinal disease, metabolic disturbances
Chronic stress, postpartum stress
Antimicrobial therapy, chronic steroid or antibiotic use
Unsanitary administration of intramammary antibiotics (dry cow treatment)
Moldy feedstuffs
DIAGNOSIS DIFFERENTIALDIAGNOSIS
Calves: enzootic pneumonia, tuberculosis, lungworms
Cattle
Pulmonary form: shipping fever, mycoplasma bovis, tuberculosis, lungworms
Intestinal form: displaced abomasums, traumatic reticuloperitonitis, abomasal ulcers
Sheep/Goats
Pulmonary form: caseous lymphadenitis, lungworms, pasteurellosis, tuberculosis, caprine arthritis/encephalitis virus (CAEV), ovine progressive pneumonia (OPP)
Mastitis form: bacterial mastitis
Llamas/alpacas: third compartmental ulcers, bacterial pneumonia, intestinal impaction
CBC/BIOCHEMISTRY/URINALYS IS
No specific findings for aspergillosis
May aid in diagnosis of underlying disease
OTHER LABORATORY TESTS
Fungal culture-identify organism; because of presence in environment, may be a contaminant.
Transtracheal wash-identify organism; also potential to be a contaminant.
Histopathology of lesions-demonstration of invasion into tissue
Immunohistochemistry-along with clinical signs and other diagnostics
IMAGING
Thoracic radiographs may show evidence of multiple densities throughout all lung fields.
PATHOLOGIC FINDINGS
Pulmonary
Severe fibrinous pneumonia (in calves) and multiple, small, white, discrete granulomas surrounded by necrotic tissue or with necrotic centers on gross pathology (ruminants)
Alpacas infected with the pulmonary form of Aspergillus niger may demonstrate severe pyogranulomatous bronchopneumonia with bronchiectasis and the presence of calcium oxalate crystals.
Mastitis
Nonspecific signs of mastitis
Demonstration of septate branched fungal hyphae on histopathology
Intestinal
Focal hemorrhagic and necrotic lesions in the omasum, rumen, reticulum, or small intestine
Demonstration of fungal elements in the tissues
TREATMENT MEDICATIONS
Surgical resection of lesions
Antifungal drugs, including intramammary application
Antifungal drugs have not been approved for use in food-producing animals.
Dosages for these agents have not been established in camelids.
Prevention would involve avoiding moldy feed, and proper administration of intramammary antibiotics.
MISCELLANEOUS ASSOCIATED CONDITIONS
N/A
AGE-RELATED FACTORS
N/A
ZOONOTIC POTENTIAL
Can affect humans due to similar environmental exposure; is not passed from animals to humans or between individual animals or humans.
ABBREVIATIONS
CAEV = caprine arthritis/encephalitis virus OPP = ovine progressive pneumonia Suggested Reading
Jensen, H. E., Olsen, S. N., Albaek, B. A. 1994. Gastrointestinal aspergillosis and zygomycosis in cattle. Vet Pathol. 31:28-36.
Wiske, S. E. 2002. Mycotic pneumonias. In: Large animal internal medicine, ed. B. P. Smith. 3rd ed. St. Louis: Mosby.
Authors: Susan L. McClanahan and Ann M. Fitzpatrick

ASPIRATION PNEUMONIA
BASICS DEFINITION
Inhalation or accidental administration of large volumes of foreign liquids, aspiration of solids (foreign bodies, plant debris, dirt) resulting in gangrenous pneumonia, or, in the case of oils, lipid pneumonia.
PATHOPHYS IOLOGY
Gangrenous pneumonia develops due to either infectious or chemical irritants damaging the airways and lung parenchyma.
SYSTEMS AFFECTED
Primarily the respiratory system; secondarily, multiple organ system dysfunction/failure
GENETICS
N/A
INCIDENCE/PREVALENCE
Uncommon, usually accidental or due to inadvertent exposure to risk factors
GEOGRAPHIC DISTRIBUTION
Potentially worldwide, depending on species and environment
SIGNALMENT

Calves, lambs, and kids receive accidental orotracheal intubation when feeding colostrum, or inhalation of meconium containing fetal fluids during difficult parturition.
Necrotic laryngitis in calves resulting in altered (turbulent) airflow through larynx and subsequent aspiration of pharyngeal secretions
Adult cattle, sheep, goats: esophageal obstruction, oropharyngeal trauma, abscesses, consumption of raw turnips, beets, oranges, or other by-product type feeds
Parturient paresis associated with recumbency in recently fresh dairy cows
Lead-poisoning-induced dysphagia
Crude oil, fuel oil, or natural gas condensate ingestion by livestock
Listeriosis or botulism resulting in cranial nerve dysfunction, regurgitation or dysphagia and aspiration of gut/pharyngeal contents
Species
Potentially all ruminant species
Breed Predilections
N/A
Mean Age and Range
N/A Predominant Sex N/A
SIGNS
Acute onset of depression, tachypnea, dyspnea, coughing, fever, foul breath odor.
Adventitious lung sounds, pleural friction rubs auscultable. In severe cases or when associated with specific conditions, recumbency, shock, and sudden death may be observed.
HISTORICALFINDINGS RISK FACTORS
Improper administration of oral medications, dystocia, exposure to viral (IBR), bacterial agents or their products (listeria,
Clostridium botulinum), using by-product feed supplements, toxin exposures, use of dips on livestock (submerged dips)
DIAGNOSIS DIFFERENTIALDIAGNOSIS
Acute bronchopneumonia, septicemia, toxic ingestion
CBC/BIOCHEMISTRY/URINALYS IS
Complete blood count may demonstrate leukocytosis, leukopenia with left shift, elevated total plasma protein, hyperglobulinemia, hyperfibrinogenemia, dehydration, and azotemia.
OTHER LABORATORY TESTS
N/A
IMAGING
N/A
OTHER DIAGNOSTIC PROCEDURES
N/A
PATHOLOGIC FINDINGS
TREATMENT
Treatment is aimed at both gram-positive and gram-negative bacterial agents, removal (if possible) of primary problem (foreign body esophagitis/choke). Protection of airway from further injury.
Prognosis often grave in cases where significant contamination of lungs with liquids has occurred.
Nonsteroidal and steroidal anti-inflammatory agents should be administered to prevent mediator-induced inflammation and shocklike sequelae.
MEDICATIONS CONTRAINDICATIONS
Appropriate milk and meat withdrawal times must be followed for all compounds administered to food-producing animals.
FOLLOW-UP
EXPECTED COURSE AND PROGNOSIS
Prognosis is often grave in cases where significant contamination of lungs with liquids has occurred.
MISCELLANEOUS ASSOCIATED CONDITIONS
N/A
AGE-RELATED FACTORS
N/A
ZOONOTIC POTENTIAL
N/A
PREGNANCY
N/A
RUMINANT SPECIES AFFECTED
Potentially, all ruminant species are affected.
BIOSECURITY
N/A
PRODUCTION MANAGEMENT
N/A
SYNONYMS
N/A
SEE ALSO
Crude oil, fuel oil, or natural gas condensate ingestion by livestock
Esophageal obstruction, oropharyngeal trauma, abscesses, consumption of raw turnips, beets, oranges or other by- product type feeds.
Lead-poisoning-induced dysphagia
Listeriosis or botulism resulting in cranial nerve dysfunction, regurgitation or dysphagia, and aspiration of gut/pharyngeal contents
Necrotic laryngitis
Parturient paresis associated with recumbency in recently fresh dairy cows
ABBREVIATIONS
IBR = infectious bovine rhinotracheitis
Suggested Reading
Adler, R., Boermans, H. J., Moulton, J. E., Moore, D. A. 1992. Toxicosis in sheep following ingestion of natural gas condensate. Vet Pathol. 29:11-20.
Davidson, H. P., Rebhun, W. C., Habel, R. E. 1981. Pharyngeal trauma in cattle. Cornell Vet. 71:15-25.
Lopez, A., Bildfell, R. 1992. Pulmonary inflammation associated with aspirated meconium and epithelial cells in calves.
Vet Pathol. 29:104-11.
Lopez, A., Lofstedt, J., Bildfell, R., Horney, B., Burton, S. 1994. Pulmonary histopathologic findings, acid-base status, and absorption of colostral immunoglobulins in newborn calves. Am J Vet Res. 55:1303-7.
Toofanian, F., Aliakbari, S., Ivoghli, B. 1979. Acute diesel fuel poisoning in goats. Trop Anim Health Prod. 2:98-101.
Author: Jeff Lakritz

ATYPICAL INTERSTITIAL PNEUMONIA
BASICS DEFINITION
Atypical interstitial pneumonia is defined as disease(s) presenting with sudden onset of dyspnea (severe respiratory distress or difficulty breathing) due to congestion or edema, hyaline membranes, alveolar epithelial hyperplasia, and interstitial emphysema. This definition is limited for the purposes of this discussion to intoxication of cattle with L-tryptophan, 4- Ipomeanol, perilla ketones.
PATHOPHYS IOLOGY
3- Methylindole
Ruminal conversion of L-tryptophan to 3-methylindole, which is absorbed from the rumen and is metabolized in the lung resulting in bronchiolar, alveolar epithelial, and endothelial damage; pulmonary edema; hyaline membranes; lung cell hyperplasia; and interstitial emphysema (see Table 1).
4- Ipomeanol

Formation of pneumotoxic 3-substituted furans (ipomeanine, 4-ipomeanol, 1-ipomeanol, and 1,4-ipomeadiol by
Fusarium solani-infected sweet potatoes.
These compounds are absorbed from rumen, and further metabolism of 4-ipomeanol and its analogs in the lung produces bronchiolar, alveolar epithelial, and endothelial injury by irreversible (covalent) binding to proteins within the cells.
The loss of cellular function results in cell death, edema, and clinical signs associated with toxicity.
Perilla Ketones (Perilla frutescens)
Cattle grazing dry grasses on sparse pastures in late summer in the southeastern United States and New Zealand (Perilla maculatta). The tall, green plant is found along the edge of wooded areas in pastures and grows well in later summer when other plants are dry. Intoxication commonly occurs in drought years.
Consumption of the plant results in absorption of perilla ketone and two related compounds causing lung injury associated with dyspnea and acute death.
SYSTEMS AFFECTED
Production management, nutrition, respiration
GENETICS
No breed predilection
INCIDENCE/PREVALENCE
Descriptions from the United Kingdom, Canada, and the western United States (3-methylindole toxicity)
Moldy sweet potato toxicity observed in southeastern United States.
Perilla ketone toxicity observed in southeastern United States.
GEOGRAPHIC DISTRIBUTION
Worldwide, depending on plant species and environment
SIGNALMENT
Species
Potentially all ruminant species
Breed Predilections
N/A
Mean Age and Range
Adult ruminants. Generally, adult brood cows or bulls (> 2 years of age). Suckling calves generally not affected and yearlings less susceptible.
Predominant Sex
N/A
SIGNS
Adult cattle moved from dry summer forage to irrigated or fertilized pastures in fall.
Herd outbreak of severe expiratory dyspnea, open-mouth breathing, excessive salivation, head and neck extension, distress and anxiousness, with quiet lung sounds
Affected animals do not generally cough. Animals forced to walk or move through alleys may collapse and die (see Table 1).
RISK FACTORS
Typical management conditions predispose to toxicity.
DIAGNOSIS DIFFERENTIALDIAGNOSIS
Parasitic bronchitis
Aspiration syndrome
Atelectasis
Pneumonia
Pulmonary hemorrhage
Congestive heart failure
Endotoxemia/sepsis
Metabolic (acidosis, hypoglycemia)
Persistent pulmonary hypertension
Severe anemia
Tracheal collapse
Anaphylaxis/allergy
Postparturient hemoglobinuria
Anaplasmosis
CBC/BIOCHEMISTRY/URINALYS IS
Stress leukogram, not generally helpful
IMAGING
N/A
OTHER DIAGNOSTIC PROCEDURES
Necropsy, demonstration of appropriate feedstuffs in rumen (perilla mint, moldy sweet potatoes), primarily lung lesions with lack of other organs affected.
PATHOLOGIC FINDINGS
Typical lesions are confined to respiratory system. Lungs are heavy and wet and have rubbery consistency (do not float). Lungs may fail to collapse and maintain rib impressions after thorax is opened.
Petechial hemorrhages in upper respiratory tract, foamy fluid in large airways, congestion, edema and hyaline membranes, hepatization of lung, interstitial emphysema, large bullae with marked accumulation of edema in interlobular septae, proliferation of alveolar epithelial cells.
TREATMENT
Management practices that prevent abrupt exposure of animals to lush green forage. Provision of feed and minerals during latter parts of summer to limit consumption of toxic plants.
Do not feed moldy sweet potatoes to livestock.
In animals that are exposed to such management conditions routinely, prior treatment with monensin or lasalocid (200 mg/head/day) for 1 day (monensin) or 6 days (lasalocid) prior to placing them on suspect pasture. Maintain access to ionophore for at least 10 days after introduction to feed.
MEDICATIONS CONTRAINDICATIONS
Appropriate milk and meat withdrawal times must be followed for all compounds administered to food-producing animals.
Steroids should not be used in pregnant animals.
FOLLOW-UP MISCELLANEOUS ASSOCIATED CONDITIONS
Endothelial damage, pulmonary edema, hyaline membranes, lung cell hyperplasia, and interstitial emphysema
Bronchiolar, alveolar epithelial and endothelial injury
The loss of cellular function results in cell death, edema, and clinical signs associated with toxicity.
Lung injury associated with dyspnea and acute death
AGE-RELATED FACTORS
Adult ruminants-generally adult brood cows or bulls (> 2 years of age); suckling calves generally not affected and yearlings less susceptible.
ZOONOTIC POTENTIAL
N/A
PREGNANCY
N/A
RUMINANT SPECIES AFFECTED
Potentially all ruminant species can be affected.
BIOSECURITY
N/A
PRODUCTION MANAGEMENT
Management practices that prevent abrupt exposure of animals to lush green forage. Provision of feed and minerals during latter parts of summer to limit consumption of toxic plants.
Do not feed moldy sweet potatoes to livestock.
SYNONYMS
Fog fever
SEE ALSO
3-Methylindole toxicity
Moldy sweet potato toxicity
Perilla toxicity
Plants associated with respiratory disease
Toxicology herd outbreak
Toxic plant chapters
ABBREVIATIONS
Suggested Reading
Breeze, R. 1985. Respiratory disease in adult cattle. Vet Clin North Amer: Food Animal Practice 1:311-46.
Kerr, L. A., Johnson, B. J., Burrows, G. E. 1986, Oct. Intoxication of cattle by Perilla frutescens (purple mint). Vet Hum Toxicol. 28(5):412-16.
Kerr, L. A., Linnabary, R. D. 1989, Jun. A review of interstitial pneumonia in cattle. Vet Hum Toxicol. 31(3):247-54.
Loneragan, G. H., Gould, D. H., Mason, G. L., Garry, F. B., Yost, G. S., Lanza, D. L., Miles, D. G., Hoffman, B. W., Mills, L. J. 2001, Oct. Association of 3-methyleneindolenine, a toxic metabolite of 3-methylindole, with acute interstitial pneumonia in feedlot cattle. Am J Vet Res. 62(10):1525-30.
Medeiros, R. M., Simoes, S. V., Tabosa, I. M., Nobrega, W. D., Riet-Correa, F. 2001, Aug. Bovine atypical interstitial pneumonia associated with the ingestion of damaged sweet potatoes (Ipomoea batatas)in northeastern Brazil. Vet Hum

Toxicol. 43(4):205-7.
Author: Jeff Lakritz

AVOCADO TOXICOSIS
BASICS OVERVIEW
Lactating animals that consume avocado leaves may develop noninfectious mastitis and agalactia.
Source

Avocado plant (Persea americana)
Leaves, fruit, bark, and seeds reported to cause toxicosis
Drying the leaves does not reduce toxic potential.
Toxin
Thought to be due to a “persin,” which has been identified as (Z,Z)-1-(acetyloxy)-2-hydroxy-12,15-heneicosadien-4- one that can be isolated from the leaves of the avocado plant.
The exact mechanism of action of this toxin on target is not known.
Toxic Dose
Symptoms of noninfectious mastitis and agalactia have been noted with 60-100 mg/kg of the toxin in an experimental setting.
SYSTEMS AFFECTED
Mammary glands, cardiovascular (mouse model) at doses higher than those that cause agalactia
INCIDENCE/PREVALENCE
N/A
GEOGRAPHIC DISTRIBUTION
N/A
SIGNALMENT
Species
Cattle, goats, sheep Predominant Sex Female
SIGNS
Noninfectious mastitis
Agalactia
CAUSES AND RISK FACTORS
N/A
DIAGNOSIS
Mastitis that is not explained by an infectious agent
History of exposure to the plant
CBC/BIOCHEMISTRY/URINALYS IS
N/A
PATHOLOGIC FINDINGS
Histopathology
Agalactia/mastitis
Extensive coagulative necrosis of the secretory acinar epithelium
Interstitial edema
Congestion
Edema
Cardiotoxicity (described in a mouse model)
Necrosis of myocardial fibers
Myocardial fibrosis if animals survive
TREATMENT
No specific antidote or treatment
Symptomatic and supportive therapy is indicated.
MEDICATIONS
None
FOLLOW-UP PREVENTION/AVOIDANCE
Prevent exposure of lactating animals to these plants.
Ideally, animals should not be exposed to this plant.
EXPECTED COURSE AND PROGNOSIS
Mastitis should resolve within 1 week to 10 days.
Agalactia requires a longer period of time for resolution.
Milk production may not reach original levels.
MISCELLANEOUS ASSOCIATED CONDITIONS
Mastitis
AGE-RELATED FACTORS
N/A
ZOONOTIC POTENTIAL
N/A
PREGNANCY
N/A
RUMINANT SPECIES AFFECTED
Potentially all ruminant species are affected
BIOSECURITY
N/A
PRODUCTION MANAGEMENT
Restrict grazing of livestock from avocado groves.
SYNONYMS
N/A
SEE ALSO
Mastitis: noninfectious Toxicology: herd outbreaks ABBREVIATIONS
N/A
Suggested Reading
Craigmill, A. L., Eide, R. N., Shultz, T. A., Hedrick, K. 1984. Toxicity of avocado (Persea americana (Guatamalan var)) leaves: review and preliminary report. Vet Hum Toxicol. 26(5): 381-83.
Craigmill, A. L., Seawright, A. A., Mattila, T., Frost, A. J. 1989. Pathological changes in the mammary gland and biochemical changes in milk of the goat following oral dosing with leaf of the avocado (Persea americana). Aust Vet J. 66(7): 206-11.
Oelrichs, P. B., Ng, J. C., Seawright, A. A., Ward, A., Schaffeler, L., MacLeod, J. K. 1995. Isolation and identification of a compound from avocado (Persea americana) leaves which causes necrosis of the acinar epithelium of the lactating mammary gland and the myocardium. Nat Toxins. 3(5): 344-49.
Author: Joe Roder

B VITAMINS
BASICS OVERVIEW

The B vitamins are a family of water-soluble micronutrients, which act primarily as coenzymes, and are essential to normal metabolism.
The B vitamins are thiamine (B1), riboflavin (B2), niacin (B3), pyridoxine (B6), the cobalamins (B12), biotin, folic acid, pantothenic acid, and inositol.
Common feedstuffs usually contain substantial amounts of several of the B vitamins.
Ruminal microorganisms synthesize B vitamins in quantities that, under most conditions, meet metabolic needs; therefore, there are no specific dietary requirements for B vitamins in animals possessing a functioning rumen.
Preruminants are susceptible to deficiencies, but these are rare when the principle feed is milk.
Under certain nutritional, management, or disease conditions, deficiencies may result in disease, the most clinically significant being polioencephalomalacia (PEM) associated with vitamin B1 deficiency.
The trace element cobalt (Co) is required for the synthesis of vitamin B12 and a lack of this vitamin is responsible for the ill thrift associated with Co deficiency.
SIGNALMENT
B-vitamin deficiencies are noted in all ruminants, with growing animals most at risk. Sheep are most susceptible to vitamin B12 deficiency.
SIGNS
Vitamin B1 deficiency-a history of acute neurologic disease in growing ruminants fed highly fermentable carbohydrate is suggestive. Clinical signs include excitability, circling behavior, abnormal vision, head pressing, followed by depression, convulsions and coma.
Vitamin B12 deficiency-often accompanied by a history of ill thrift in animals offered what would appear to be an adequate ration. Animals may have been fed a ration grown in a region known to possess Co-deficient soils. Clinical signs include retarded growth, muscular weakness, anemia, ketosis and general poor condition. In sheep, a syndrome termed
ovine white liver disease has been identified that is characterized by ill thrift together with serous ocular discharge, fatty degeneration of the liver and sometimes photosensitization.
Other B vitamin deficiencies-are extremely rare or unknown in ruminants under typical management conditions, but are most likely to result in nonspecific signs of ill thrift, poor growth, skin lesions, poor coat condition, and central nervous system abnormalities.
CAUSES AND RISK FACTORS
Deficiencies of vitamin B1 can occur when there is production or ingestion of inactive B vitamin analogs, or excessive destruction of B vitamins in the rumen. This occurs most commonly under conditions of ruminal lactic acidosis, induced by diets containing a high proportion of concentrate or other source of highly fermentable carbohydrate such as very lush
pasture. A diet of highly fermentable carbohydrate can induce changes in ruminal flora so that rumen bacteria produce excessive amounts of thiaminase, reducing the amount of thiamine available for intestinal absorption. Some plants, such as bracken fern (Pteridium aquilinum) contain thiaminase.
In vitamin B12 deficiency, ruminal microorganisms are incapable of producing sufficient cobalamins due to a lack of Co. The concentration of Co in crops and forages depends on a variety of factors including Co concentration of the soil, plant species, rate of plant growth, and soil pH, drainage, and fertilization. Soils are generally considered Co deficient if they contain less than 2 ppm Co. Such soils are widely distributed throughout the world.
DIAGNOSIS DIFFERENTIALDIAGNOSIS
Vitamin B1 deficiency-clinical signs are nonspecific and may be confused with PEM associated with water deprivation and toxicosis due to sulfur, salt, lead, amprolium, lasalocid, and some anthelmintics. Differential diagnoses should include the following causes of encephalitis or meningoencephalitis: focal symmetric encephalomalacia (Clostridium perfringens
type D); thrombotic meningoencephalitis (Hemophilus somnus); nervous coccidiosis; listeriosis; rabies, and herpes virus. Toxicoses due to ethylene glycol, lead and selenium, and deficiencies of vitamin A and magnesium should also be considered.
Vitamin B12 deficiency-differential diagnoses that should be considered are gross malnutrition; intestinal parasitism; paratuberculosis; and deficiencies of vitamin D, selenium, and copper. Diagnosis may be complicated by the fact that cattle are more susceptible to intestinal parasitism under conditions of vitamin B12 deficiency.
CBC/BIOCHEMISTRY/URINALYS IS
No consistent abnormalities are observed.
OTHER LABORATORY TESTS
Vitamin B1 deficiency-antemortem diagnostic aids for thiamine deficiency include the following: blood concentrations of thiamine, lactate, and pyruvate; erythrocyte transketolase activity, and fecal thiaminase activity. Many laboratories do not offer these tests routinely and, due to the acute nature of the condition, postmortem diagnosis is more commonly performed (see below).
Vitamin B12 deficiency-diagnosis may be made by measuring serum or liver vitamin B12 concentrations or serum methylmalonic acid concentration.
PATHOLOGIC FINDINGS
Gross pathologic signs of vitamin B1 deficiency are symmetric and include cortical swelling and flattened gyri with thinning and yellowing of the cortex. Necrotic areas of the brain may autofluoresce under ultraviolet light. A diagnosis of PEM can be confirmed by histopathology.
TREATMENT
If clinical signs are noted in one or more animals, it is likely that a large proportion of the herd or flock is subclinically affected.
Vitamin B1 deficiency-provide good quality roughage and/or remove thiaminase-containing forage. Cease treatment with any medications that might be associated with PEM.
Vitamin B12 deficiency-supplementation is usually applied on a flock or herd basis.
MEDICATIONS
Vitamin B1 deficiency-thiamine hydrochloride solution 10-20 mg/kg IM or SC three times daily. The same dose can be given IV if diluted in isotonic intravenous fluids and administered slowly. Corticosteroids and diuretics to reduce cortical swelling may be useful.
Vitamin B12 deficiency-injection of vitamin B12 solution SC at a dose of 100-300 µg weekly or 2000-3000 µg weekly for small and large ruminants, respectively, is effective.
Weekly oral treatment with a dilute cobalt sulfate solution at 7 mg Co per animal (small ruminants), or 35-70 mg Co per head (large ruminants) is also effective.
CONTRAINDICATIONS
Appropriate milk and meat withdrawal times must be followed for all compounds administered to food-producing animals.
FOLLOW-UP PREVENTION/AVOIDANCE
Vitamin B1 deficiency-provide adequate roughage in the diet to avoid lactic acidosis. Avoid feeding plants containing thiaminase. Add thiamine mononitrate to the ration at 125 g per tonne. Ruminants should be introduced to high-grain diets gradually and large variations in intake should be avoided.
Vitamin B12 deficiency-ensure Co is supplied at a rate of at least 0.1 mg/kg DM in the total ration. Rations supplemented at this level, or salt licks containing 0.1% Co (as cobalt carbonate), should prevent the disease. Oral administration of intraruminal boluses made of metal oxides or soluble glass, where available, provides supplementary Co
for periods in excess of 1 year. Cobalt sulfate applied to pasture (1.5 kg/ha every 3-4 years) can be effective also. An injectable product containing microencapsulated vitamin B12 has been developed in New Zealand for supplementation of sheep and is effective for up to 8 months after treatment.
EXPECTED COURSE AND PROGNOSIS
Vitamin B1 deficiency-response to treatment should be noted within minutes. Individuals that are recumbent and showing severe neurologic signs at the time of treatment have a poorer prognosis. Recovered individuals may be left with residual neurologic deficits.
Vitamin B12 deficiency-response to Co or vitamin B12 supplementation is usually good and improvement is noted within days of treatment, however affected growing animals may never attain full mature weight.
MISCELLANEOUS ASSOCIATED CONDITIONS
Ruminal lactic acidosis in vitamin B1 deficiency
Intestinal parasitism in vitamin B12 deficiency
RUMINANT SPECIES AFFECTED
All ruminant species are affected.
PRODUCTION MANAGEMENT
There is some evidence that the health and production of high-producing dairy cattle may be enhanced by supplementation of some B vitamins (niacin, biotin, and folic acid) and Co even though these cattle are not at risk of overt deficiency. Most researched is the effect of biotin on the incidence of lameness in dairy cattle.
SEE ALSO
Chapters on nutrition, vitamins, PEM, lameness
ABBREVIATIONS
Co = cobalt
DM = dry matter
PEM = polioencephalomalacia
Suggested Reading
Lee, J., Knowles, S. O., Judson, G. J., Freer, M., Dove, H. 2002. Trace element and vitamin nutrition of grazing sheep. In: Sheep nutrition. Wallingford, UK: CABI Publishing.
Loneragan, G. H., Gould, D. H. 2002. Polioencephalomalacia. In: Large animal internal medicine, ed. B. P. Smith. 3rd ed. St. Louis, MO: Mosby.
Maas, J. 2002. Cobalt deficiency in ruminants. In: Large animal internal medicine, ed. B. P. Smith. 3rd ed. St. Louis, MO: Mosby.
National Research Council. 2001. Nutrient requirements of dairy cattle. 7th rev ed. Washington, DC: National Academy of Sciences.

Author: Jeff Wichtel

BABESIOSIS
BASICS DEFINITION

Although it has been eradicated in the United States for 60 years, babesiosis remains an important disease in cattle throughout the world where the tick vector is prevalent.
The causative agent is an intraerythrocytic protozoan that produces intravascular hemolysis in the ruminant host.
PATHOPHYS IOLOGY
Babesiosis is contractible via inoculation of infected blood.
Ticks are considered to be the principal vectors (see Table 1), although transmission may also occur via blood- contaminated needles or instruments.
The organism is transmitted by several one-host ticks; the genus Boophilus is particularly important.
Female ticks become infected during blood engorgement on infected cattle, with subsequent replication of the Babesia in the tick’s embryos. As the tick embryos develop into larvae, nymphs, and adults, the Babesia persist and can be transmitted to new mammalian hosts during tick feeding. For B. bigemina, only nymph or adult ticks are capable of transmitting the disease. The infection does not persist beyond the larval stage in B. bovis.
Although considered rare, vertical transmission within the mammalian host has been reported.
Once inoculated, the incubation period is 2 to 3 weeks.
In endemic areas, wherein passive humoral immunity is transferred from dam to offspring, clinical signs of disease are uncommon in cattle less than 6 months of age.
Immunosuppressed or immunologically naïve individuals are susceptible to parasitemia, and clinical signs of disease develop. If an animal survives the initial episode of infection, active immunity rapidly ensues, thereby controlling parasitemia.
Immunity to the disease after natural exposure may be as long as 1 to 2 years, however, the development of immunity may be insufficient to completely eliminate the organism, allowing for the persistence of the organism without clinical signs of disease (premunition).
These subclinical “carriers” of Babesia serve as a silent reservoir for persistent infection within a herd.
Carriers also may experience episodic clinical signs of recrudescence as protective immunity and the extent of parasitemia wax and wane.
Although some individuals may eventually eliminate the infection, other chronic carriers eventually succumb to the disease.
Upon inoculation, infective sporozoites enter red blood cells wherein binary fission occurs within 14 days of inoculation. When replication is complete, the organisms are released by erythrolysis to propagate infection in new red blood cells.
Thus the predominant clinical signs of disease are fever and intravascular hemolysis. Other factors that may contribute to hemolysis include increased red blood cell fragility, removal of infected cells by the mononuclear phagocytic system, and the development of secondary autoimmune hemolytic anemia.
Anemia develops, and in severe cases (typically immunosuppressed or immunologically naïve adults), death from hypoxemia may ensue.
With B. bovis infection, the release of inflammatory mediators in response to infection may also lead to intense hypotension, cardiovascular shock, and disseminated intravascular coagulation.
B. bigemina may also replicate within the endothelium of the cerebrum, causing local hypoxemia and the development of “cerebral babesiosis,” characterized by acute onset of signs of cerebral disease.
SYSTEMS AFFECTED
Hemic: regenerative anemia, intravascular hemolysis, disseminated intravascular coagulation, hemoglobinemia, hemoglobinuria, icterus
Cardiovascular: hypoxemia, hypotension
Cerebral: ataxia, blindness, maniacal behavior
GENETICS
Zebu, Afrikaner, and Santa Gertrudis cattle are less susceptible to babesiosis than are other breeds of cattle.
INCIDENCE/PREVALENCE
The disease is widespread in endemic areas.
The existence of asystematic carriers obscures accurate estimate of the true prevalence of infection.
Wide application of sensitive PCR testing will be necessary to establish the actual rate and distribution of infection.
GEOGRAPHIC DISTRIBUTION
Cases have been reported throughout the world. The disease is endemic in tropical climates where the tick vectors flourish (see Table 1).
Rigid measures to control the Boophilus tick population were primarily responsible for eradication of babesiosis from the United States.
SIGNALMENT
Species
Cattle and small ruminants are the principal hosts, but cases have been reported in other ruminants, such as water buffalo, reindeer, and the American bison.
Breed Predilections
N/A
Mean Age and Range
Any age may be affected, but younger calves in endemic areas, wherein infected dams have provided passive immunity to their offspring, rarely develop infection prior to 6 months of age.
Immunosuppressed, debilitated, stressed, or immunologically naïve adult ruminants are more susceptible to infection and often are more severely affected by the disease.
Predominant Sex
N/A
SIGNS GENERALCOMMENTS
Severely debilitated, immunosuppressed, or immunologically naïve individuals in endemic areas are most susceptible to disease.
Seasonality of the disease is mostly dependent on the peak occurrence of the tick vector population.
HISTORICALFINDINGS
Concurrent illness; progressive depression, weakness, and lethargy; poor growth; poor coat quality; separation from the herd; anorexia; tick infestation; hemoglobinuria; fever; and icterus
PHYSICALEXAMINATION FINDINGS
The onset of clinical signs depends on the size of the inoculum.
Signs of disease can develop within 1 week of inoculation of infected blood, but may not be apparent for 2 to 3 weeks.
High fever, depression, anorexia, and progressive weakness occur first.
The predominant clinical signs develop with the onset of intravascular hemolysis that occurs as reproducing merozoites destroy erythrocytes in the circulation.
Tachycardia and tachypnea may be profound and depend on the degree and rate at which the anemia develops. A low- grade systolic murmur may be present over the heart base as the viscosity of the blood decreases.
Hemoglobinemia and pallor of the mucous membranes precede hemoglobinuria and the development of icterus. Pregnant cows often abort their fetuses.
In severe cases, death occurs as a result of anoxic shock. If the infected animal survives the initial episode of hemolysis, convalescence is prolonged until anemia has regenerated (weeks to months).
Emaciation, poor condition, and failure to thrive, and the existence of the carrier stage are common developments during convalescence.
Infection of the endothelium of the central nervous system in cattle with B. bigemina may result in clinical signs of cerebral disease, including maniacal behavior, hyperexcitability, seizures, bruxism, opisthotonus, blindness, ataxia, and coma.
The prognosis for this form of the disease typically is grave.
A unique phenomenon of anal sphincter spasm in cattle infected with B. divergens may produce the additional clinical sign of pipe stream feces.
CAUSES
Babesiosis is caused by infection with protozoa from the phylum Apicomplexa, order Piroplasmida, genus Babesia.
There are at least six species of Babesia that affect cattle and two species that affect small ruminants (see Table 1). B. bovis is frequently considered to be the most pathogenic of the Babesia species; B. major and B. ovate are less pathogenic to nonpathogenic.
RISK FACTORS
Immunologically naïve (typically mature cattle) or immunosuppressed or otherwise debilitated individuals in endemic areas wherein the tick vectors reside are most at risk for contracting the infection.
DIAGNOSIS DIFFERENTIALDIAGNOSIS
Any cause of intravascular hemolysis in cattle would result in similar signs including leptospirosis, bacillary hemoglobinuria, Heinz body anemias (onion, rape, kale toxicity), theileriosis, postparturient hemoglobinuria, and autoimmune hemolytic anemia.
Differentials for extravascular hemolysis should also be considered.
Copper toxicity should be considered as differential diagnoses in sheep.
CBC/BIOCHEMISTRY/URINALYS IS
Anemia
Regenerative anemia 5 to 7 days after onset (signs of regeneration include an increased MCV, anisocytosis, polychromasia, basophilic stippling, reticulocytes, Howell Jolly bodies, nucleated red blood cells)
Hemoglobinemia (pink plasma, MCH, and MCHC increased)
Hemoglobinuria (red-brown urine, urine dipstick positive for blood; positive for hemoglobin with saturated ammonium sulfate test)
Hyperbilirubinemia (unconjugated)
Hypokalemia
Thrombocytopenia
Metabolic acidosis
OTHER LABORATORY TESTS
Babesia species may be seen within erythrocytes in a peripheral Wright- or Giemsa-stained blood smear. B. bovis is often difficult to find in the peripheral blood.
The protozoa appear as nonpigmented, pyriform to irregular, round or amoeba-shaped organisms.
Often, the protozoa appear in groups of two, with the “tops” of the pear-shaped organisms joined at an angle to form a “v.”
Parasitemia is often low, or affected cells are removed from the circulation, therefore absence of visible protozoa does not preclude the diagnosis.
The humoral response to Babesia can usually be detected within a week of infection.
Numerous serologic assays have been developed to detect Babesia, but the complement fixation, ELISA, and the indirect fluorescent antibody tests are most commonly used.
Because humoral immunity postinfection is long lived, it may be difficult to distinguish active infection from previous exposure.
Highly sensitive and specific PCR assays recently have been developed as extremely useful tools in the diagnosis and
surveillance of active infection in both ticks and cattle.
IMAGING
N/A
DIAGNOSTIC PROCEDURES
N/A
PATHOLOGIC FINDINGS
Sudden death is not uncommon. Depending on the stage of the disease, diffuse pallor of the tissues or icterus is present.
Splenomegaly, hepatomegaly, edema, body cavity effusion, petechial and ecchymotic hemorrhages on the heart and gastrointestinal tract, thin blood, thrombi, gallbladder distension, and the presence of red-brown urine in the urinary bladder are common findings.
In chronically infected cattle, emaciation is an additional expected feature. B. bigemina tends to proliferate in peripheral vessels, whereas B. bovis multiplies in visceral blood vessels.
Direct fluorescent antibody staining and PCR assay of blood or tissues are the most specific tests used to confirm the diagnosis postmortem.
TREATMENT APPROPRIATE HEALTH CARE
Inpatient or outpatient care
NURSING CARE
If anemia is severe and clinical or laboratory evidence of hypoxemia is evident (intense lethargy or weakness, profound tachycardia or tachypnea, severe anemia, acidosis, increased anion gap), a whole blood transfusion is indicated.
The normal total blood volume is approximately 8% of the body weight (i.e., 0.08 x body weight in kilograms equals the total blood volume in liters). Typically, transfusing one-fourth to one-third of the total blood volume is adequate.
ACTIVITY
Confined
DIET
N/A
CLIENT EDUCATION
See Prevention/Avoidance below.
Immunologically naïve cattle moving into endemic areas should be vaccinated prior to movement.
SURGICALCONSIDERATIONS
N/A
MEDICATIONS DRUGS OF CHOICE
Numerous drugs have been used for the treatment of babesiosis.
The most commonly used drugs include diminazene diaceturate (Berenil; 3-5 mg/kg IM), phenamidine diisethionate (Lomadine; 8-13 mg/kg, SQ or IM), imidocarb dipropionate (Imizol; 1-3 mg/kg, SQ or IM), and amicarbalide diisethionate (Diampron; 5-10 mg/kg IM). Imidocarb therapy may prevent reinfection for up to 2 months.
Overzealous use of babesiocidal drugs may abruptly reduce parasitemia to a level that is inadequate for establishment of protective immunity.
CONTRAINDICATIONS
Meat and milk withdrawal periods must be maintained.
PRECAUTIONS
N/A
POSSIBLE INTERACTIONS
N/A
ALTERNATIVE DRUGS
N/A
FOLLOW-UP PATIENT MONITORING
Heart rate, respiratory rate, attitude, appetite, PCV, body weight
PREVENTION/AVOIDANCE
Most control programs are tailored to the particular circumstances of infection in the herd.
Complete eradication in a herd within an endemic area leaves that herd susceptible to future reinfection from surrounding herds.
Thus most control programs are aimed at balancing the degree of infection with an appropriate level of immunity. This is most effectively achieved by reducing the tick population with acaricides and vaccination with live or live-attenuated organisms to establish a state of premunition.
As older animals are more sensitive to the effects of infection, vaccination with live organisms is often followed with babesiostatic drugs.
Newer vaccines using cell culture or recombinant proteins are promising, but are not currently widely available. There is little cross protection between species of Babesia.
Table 1
POSSIBLE COMPLICATIONS
Death from hypoxemic anemia or cerebral babesiosis is not uncommon. Treatment frequently does not eliminate the carrier state.
EXPECTED COURSE AND PROGNOSIS
Carriers and recrudesce are common in endemic areas. Infection with B. bovis is generally more severe than infection with other species.
The presence of cerebral babesiosis warrants a grave prognosis.
The mortality rate is high in adult immunologically naïve or immunosuppressed individuals.
MISCELLANEOUS ASSOCIATED CONDITIONS
N/A
AGE-RELATED FACTORS
Younger cattle in endemic areas are rarely infected.
ZOONOTIC POTENTIAL
Although rare, immunosuppressed humans may be susceptible to infection.
PREGNANCY
Immunization of pregnant cows with live or live-attenuated vaccines may induce neonatal isoerythrolysis.
RUMINANT SPECIES AFFECTED
Cases of babesiosis have been reported in cattle, small ruminants, white-tailed deer, American bison, water buffalo, reindeer, Asian elk, Tartarean roe deer, and African buffalo.
Recent application of PCR techniques revealed that 16% of the cottontail rabbit population on Nantucket Island, Massachusetts, were carriers for B. divergens.
The significance of this finding has not been fully determined, but widespread use of PCR assays may unveil a wider range of distribution of the organism.
BIOSECURITY
N/A
PRODUCTION MANAGEMENT
N/A
SYNONYMS
Bovine malaria Piroplasmosis Redwater Texas fever Tick fever Tristeza
SEE ALSO
Autoimmune hemolytic anemia Bacillary hemoglobinuria Copper toxicity
Heinz body anemias (onion, rape, kale toxicity) Intravascular hemolysis
Leptospirosis
Postparturient hemoglobinuria Theileriosis ABBREVIATIONS
ELISA = enzyme-linked immunosorbent assay IM = intramuscular
MCH = mean corpuscular hemoglobin
MCHC = mean corpuscular hemoglobin concentration MCV = mean corpuscular volume
PCR = polymerase chain reaction SQ = subcutaneous
Suggested Reading
Goethert, H. K., Telford, S. R. 2003. Enzootic transmission of Babesia divergens among cottontail rabbits on Nantucket Island, Massachusetts. Am J Trop Med Hyg. 69(5):455-60.
Goff, W. L., McElwain, T. F., Suarez, C. E., Johnson, W. C., Brown, W. C., Norimine, J., Knowles, D. P. 2003. Competitive enzyme linked immunosorbent assay based on a rhoptry associated protein 1 epitope specifically identifies Babesia bovis infected cattle. Clin Diagn La Immunol. 10(1):38-43.
Regassa, A., Penzhorn, B. L., Bryson, N. R. 2003. Attainment of endemic stability to Babesia bigemina in cattle on a South African ranch where nonintensive tick control was applied. Vet Parasitol. 116(4):267-74.
Vos, A. J., Bock, R. E. 2000. Vaccination against Babesia. Annals of the New York Academy of Sciences. 916:540-45.
Yeruham, I., Avidar, Y., Aroch, I., Hadani, A. 2003. Intrauterine infection with Babesia bovis in a 2-day-old calf. J Vet Med B Infect Dis Vet Public Health 50(2):60-62.
Author: Michelle Henry Barton

BACILLARY HEMOGLOBINURIA
BASICS DEFINITION
Peracute, highly fatal, anaerobic infection of cattle and other ruminants caused by rapid proliferation of Clostridium haemolyticum (Clostridium novyi type D) after hepatic insult and resulting in sudden death or fulminant disease with characteristic necrotic hepatic infarct, hemolysis, hemoglobinuria, and toxemia.
OVERVIEW

Disease primarily of cattle and sheep caused by proliferation of and toxin(s) released by C lostridium haemolyticum
(Clostridium novyi type D)
Spores of Cl. haemolyticum are normally found in the soil and GIT (liver, feces) and urine of healthy cattle and sheep grazing on contaminated pastures.
Disease results when a hepatic insult or damage creates an area of anaerobiosis in the liver appropriate for spore germination and resulting vegetative cell multiplication and toxin production.
Hepatic insult often results from migration of liver flukes (Fasciola hepatica, Dicrocoelium dendriticum, or Cysticercus cellulosae) or trauma (iatrogenic or spontaneous).
Disease causes sudden death or fulminant toxemia.
Clinical signs and pathologic lesions primarily due to toxin(s) produced by organism
Organism produces at least three exotoxins.
Principle toxin, ß-toxin, is a phospholipase C with lethal necrotizing (hydrolyzes lecithin and sphingomyelin) and hemolytic (hemolyzes erythrocytes) activity.
Tropomyosinase
?-toxin: a lipase
Toxins induce localized hepatic necrosis, toxemia, and intravascular hemolysis.
Seasonal disease occurring mostly in summer and fall
Outbreaks in feedlot cattle fed hay from infected fields
Disease is spread from contaminated pasture to uninfected area by carrier animals, flooding or natural water drainage, or feeding of contaminated hay or bones of infected animals.
PATHOPHYS IOLOGY
Clostridium haemolyticum is endemic in moist or swampy areas with a high soil pH (~8).
Organism spores survive in soil and bones from affected animal carcasses for years.
Once ingested by animal during grazing, spores are transported via lymphatic and blood to liver and tissue where they remain dormant.
Asymptomatic but infected cattle harbor the organism in their GIT, liver, and tissues and may shed it in feces and urine.
Any liver insult or damage that results in suitable anaerobic conditions fosters conversion of spores to vegetative organisms and bacterial proliferation.
Vegetative growth associated with production and release of potent exotoxins, which induce hepatic necrosis, hemolysis, and severe toxemia
A single ischemic pale hepatic infarct is highly suggestive of the disease.
SIGNALMENT
Occurs in western United States, along the Gulf of Mexico, Wisconsin, Florida, New Zealand, Australia, Mexico, Venezuela, Chile, Great Britain, Ireland, Middle East
High incidence in animals grazing irrigated or poorly draining alkaline pastures
Usually affects mature cattle
Highly conditioned cattle seem most susceptible.
Mature sheep affected sporadically
No sex or breed predilection
SIGNS
Sudden death with no premonitory signs
Duration of symptoms usually ranges from 12 hours to 4 days
Peracute toxemia
High fever (103°F -106°F; 39.5°C-41°C)
Severe depression
Tachycardia
Abdominal pain
Ileus
Hypolactia/agalactia
Anorexia
Dark feces
Dysentery with blood and mucus
Arched-back stance
Grunting
±Brisket edema
Abortion in pregnant cows
Recumbency
Shock
Death within 12 to 48 hours
Intravascular hemolysis
Dyspnea
Progressive tachycardia
Hemoglobinuria
Red stain to perineal wool
Progressive anemia
Icterus
± Tachypnea
Immune carriers: animals exposed to subclinical infections
Pathologic Lesions
Rapid onset of rigor mortis
Anemic (pale) infarct of liver is virtually pathognomonic.
Usually a single infarct but occasionally multiple of varying size
Dark-red zone of hyperemia around infarcts
Red urine in kidney and bladder
Dehydration
Icterus
Anemia
Subcutaneous gelatinous edema
Petechial or diffuse subcutaneous hemorrhage
Bloody fluid in abdominal, pericardial, and thoracic cavities
Trachea has bloody exudate and mucosal hemorrhages
Intestinal tract is hemorrhagic and may contain free or clotted blood.
±Subcutaneous edema
±Hemorrhages in renal parenchyma
CAUSES AND RISK FACTORS
Pasturing of cattle in areas where liver flukes reside
Geographic areas with wet or swampy conditions and high soil pH
Irrigated pastures
Hepatic insult(s) in cattle, which creates an appropriate anaerobic environment for germination of spores include migration of liver flukes, liver abscesses, septicemia, metabolic anoxia of liver, hepatotoxins, trauma, biopsy, and high nitrate diets.
In sheep, telangiectasis, necrobacillosis, and Cysticercus tenuicollis are also precipitating factors.
Unvaccinated cattle, sheep
DIAGNOSIS
History of grazing cattle in pasture containing liver flukes or of a known insult to the liver
Gross necropsy lesions
Identification of large, gram-positive rods on impression smear from liver lesion
Culturing of Cl. haemolyticum from tissue from the edge of liver infarct fresh carcass
Demonstrate organism in liver by clostridial fluorescent antibody test (FAT) or immunohistochemistry
Toxin identification
Demonstration of only ß lecithinase in peritoneal effusion
Saline extract of liver infarct
Definitive diagnosis by culture and GLC confirmation that isolate is Cl. haemolyticum
Complete blood count
Evidence of hemolysis in plasma or serum
Anemia
Primarily leukocytosis ± left shift
May have leukopenia with left shift
±Anaerobic blood cultures (acute stage)
Serum chemistry panel often reflects severe insult to liver and accompanying changes in other organ systems, hydration status, or hypophagia
Elevated liver enzymes (SDH, GGT, AST)
Hyperbilirubinemia
Azotemia
Elevated creatine kinase, if recumbent
Electrolyte abnormalities
Metabolic acidosis
DIFFERENTIALDIAGNOSIS
Leptospirosis
Postparturient hemoglobinuria
Hemolytic anemia from cruciferous plants
Enzootic hematuria (bracken fern toxicosis)
Anaplasmosis
Chronic copper poisoning
Black disease
Acute pyelonephritis
Hemorrhagic cystitis
CBC/BIOCHEMICAL/URINALYS IS
Progressive anemia
Leukocytosis with neutrophilia
Hemoglobinuria
OTHER LABORATORY TESTING IMAGING
Hepatic Ultrasound
Infarct
Disruption of normal parenchyma
Vascular changes
DIAGNOSTIC PROCEDURES
Caution interpreting Gram stains, culture, or FAT of liver
Cl. haemolyticum is a normal inhabitant of the liver
Cross reacts with Cl. novyi type B on FAT
Ultrasound of liver
Blood culture
TREATMENT
Seldom successful
High doses of aqueous potassium or sodium penicillin, intravenously (44,000 IU/kg QID) preferred
High doses of procaine penicillin IM
Tetracycline has also been recommended.
Blood transfusion(s) as indicated; minimum of 4-6 liters for adult cattle
Antitoxic serum, if available
Intravenous fluids to maintain normovolemia, and electrolyte and acid-base balance
Appropriate treatment of secondary organ disease or dysfunction
If recovery, treat for liver flukes
MEDICATIONS DRUGS OF CHOICE
High doses of penicillin or tetracycline
Blood transfusion
Antitoxic serum
Polyionic fluids
CONTRAINDICATIONS
Monitor for blood transfusion reaction
Appropriate milk and meat withdrawal times must be followed for all compounds administered to food-producing animals.
FOLLOW-UP
EXPECTED COURSE AND PROGROSIS
Mortality in untreated animals is 95%.
Mortality in treated animals is high.
On endemic farms, death losses may be as high as 25%.
Heavy mortalities when naïve, unvaccinated cattle brought onto infected pastures
Recovered animals may become poor doers: chronic weight loss, poor production
Cattle surviving subclinical attacks of disease may act as immune carriers.
MISCELLANEOUS ASSOCIATED CONDITIONS
Toxemia, hypovolemia, and severe anemia may result in damage to other organs.
Renal or pulmonary emboli
Renal infarcts
Cardiac arrhythmias
Pigment nephropathy
ZOONOTIC POTENTIAL
N/A
RUMINANT SPECIES AFFECTED
Cattle
Adult sheep primarily
Uncommonly elk, other ruminants
BIOSECURITY
N/A
PRODUCTION MANAGEMENT
Cattle should not be grazed on liver fluke infested pastures.
Treat cattle with anthelmintics effective against liver flukes.
Aquatic snails are intermediate hosts and needed for the flukes to complete their life cycle; use muskicide to remove snails, or fence cattle away from areas with standing water.
Avoid feeding practices that induce ruminal acidosis or rumenitis to decrease liver abscess formation.
In United States, vaccination recommended in spring; do not vaccinate within 21 days before slaughter.
Calf vaccination
Commercial bacterin-toxoids Cl. haemolyticum
Vaccinate calves twice 3-4 weeks apart at 3-4 months of age
Booster annually or every 6 months in endemic areas
Deworm sheepdogs to reduce C. tenuicollis infection.
Avoid pasture contamination by removing contaminated feces or properly disposing (burn, deep burial, remove from premises) of decomposing carcasses of affected animals.
SYNONYMS
Icterohemoglobinuria Infectious icterohemoglobinuria Red water
SEE ALSO
Acute pyelonephritis Anaplasmosis
Black disease
Chronic copper poisoning
Enzootic hematuria (bracken fern toxicosis) Hemolytic anemia from cruciferous plants Hemorrhagic cystitis
Leptospirosis Liver flukes
Postparturient hemoglobinuria
ABBREVIATIONS
AST = aspartate transaminase FAT = fluorescent antibody test
GGT = gamma-glutamyltransferase GIT = gastrointestinal tract
GLC = gas-liquid chromatography IM = intramuscular
QID = four times daily
SDH = sorbitol dehydrogenase
Suggested Reading
Dennis, S. 1998. Clostridial diseases. In: Merck veterinary manual, ed. S. E. Aiello. 8th ed. Whitehouse Station, NJ: Merck & Co.
Hoyt, J., Snyder, J., Snyder, S. 2002. Bacillary hemoglobinuria. In: Large animal internal medicine, ed. B. Smith. St. Louis: Mosby.
Lewis, C. J. 2000. Clostridial diseases. In: Diseases of sheep, ed. W. B. Martin, I. D. Aitken. 3rd ed. Oxford: Blackwell Science.
Pugh, D. G. 2002. Diseases of the integumentary system. In: Sheep and goat medicine. Philadelphia: W. B. Saunders.
Rebhum, W. C. 1995. Miscellaneous infectious diseases. In: Diseases of dairy cattle. Media, PA: Williams and Wilkins.
Authors: Susan Semrad and Sheila McGuirk

BACKGROUNDING BEEF CALVES
BASICS OVERVIEW

The term “backgrounding” is used to describe many different systems in which cattle are grown after weaning but before being placed into a feedlot.
Some people may use backgrounding and preconditioning interchangeably but backgrounding can include much more than just a preconditioning period.
Backgrounding programs are often called stocker programs in the southern and southwestern United States.
The ultimate goal of a backgrounding program is to enable calves to gain frame and muscle mass without gaining excessive condition.
Most backgrounding programs rely on forage-based diets and may take advantage of inexpensive regional feeds such as grain by-products or crop residues.
Backgrounding programs may provide more flexibility and market opportunity for producers and may give producers a good way to use available forages and/or feeds.
Numerous backgrounding systems exist, and one system is not appropriate for all producers or all types of cattle.
Backgrounding programs may be used for home-raised calves, or calves may be purchased from other producers and placed into a backgrounding program. Some producers provide custom backgrounding services for other producers.
Types of Backgrounding Systems: Preconditioning, Wintering, Growing, Grazing Wheat Pasture, Fast-Track Systems, Calf-Fed Finishing Systems
Preconditioning
Preconditioning is a 30-45-day period occurring immediately after weaning in which calves are weaned, taught to eat dry feed from a bunk, and taught to drink from a water tank.
Numerous health management practices such as vaccination, dehorning, implants, and castration can occur during this time.
Efforts should be made to reduce stress as much as possible during this period so it is beneficial to perform the health management factors described above at least a few weeks prior to weaning.
Preconditioning may be part of a larger backgrounding program or it may occur alone with calves being placed directly in the feedlot after the preconditioning period.
Gains during this period are usually minimal.
Wintering
This system focuses on using large quantities of forage (e.g., crop residues, hay, and dormant pastures) to carry calves through the winter.
Targeted gains range between 0.5 and 1.5 lbs/hd/day.
The overall goal is to minimize winter-feed cost and keep cattle healthy.
Calves may be sold in the spring when prices are favorable or grazed through the summer to take advantage of additional cheap gains.
Smaller framed British or British-cross cattle tend to fit this system well.
These cattle tend to have excess finish and light carcass weights if placed directly on feed after weaning.
Overwintering coupled with summer grazing allows these cattle to gain adequate frame and muscle prior to finishing so that their finished carcass weights better meet the industry standards.
Large-framed exotic or exotic-cross cattle do not fit this system well because they become too large and finish with carcass weights that exceed the industry standards.
Growing
This system targets higher rates of gain (1.5-2.5 lbs/hd/day) over a shorter period of time.
This system utilizes a mixture of forage and grains and is a good way to utilize forages or grains grown on the farm.
The cattle best suited to this system include moderate framed exotic and British breed cattle that may become too large in an overwintering system but become too fleshy if grown at a faster rate.
Grazing Wheat Pasture
This system is the most common backgrounding system in the U. S. southern plains states.
Calves are placed on wheat pasture around the middle of November and removed around the middle of March if wheat is to be harvested. If the producer elects not to harvest wheat grain, the pasture can be “grazed out” usually until the middle of May.
The rates of gain and type of cattle are similar to those for other growing systems.
Fast-Track Systems
These systems involve feeding rations that are quite similar to those fed in a finishing program.
The goal is to get cattle to gain as fast as possible and gains should be 3 lbs/hd/day or more.
The fast-track systems are best suited to large-framed exotic or exotic-cross cattle with genetic potential for rapid gains.
They require a much higher level of management and have an increased risk of digestive problems.
Calf-Fed Finishing Systems
These systems involve placing calves directly on feed after weaning or after a preconditioning program.
Calf-fed finishing systems are better suited to commercial feedlots and are best suited for large-framed exotic cattle.
This production system may get cattle finished earlier and allow the producer to take advantage of seasonal variations in price.
Backgrounding Facilities
Pens
Pens should be designed to provide adequate space, protection from cold winds, adequate bunk space, adequate water supply, ease of handling, and safety.
Calves in backgrounding systems generally require 150-300 square feet of space per calf.
Pens should slope away from the feed bunk and have adequate drainage to reduce mud.
Concrete aprons should be provided around feed bunks and waterers to reduce mud.
Properly designed mounds should be included to provide calves a dry place to rest.
Pen size should be no greater than 150 head per pen.
Feed and Water
Calves fed once daily should have 18-26 inches of bunk space per calf.
Calves fed twice daily should have 8-11 inches of bunk space per calf.
If self-feeders are used, 3-4 inches of trough space per calf is required.
Bunks should be easy to clean.
Feeding on the ground should be avoided due to increased wastage and disease transmission.
Placing waterers along fence lines will help new calves find the water.
Handling Facilities
Handling facilities should be designed to promote smooth flow of calves through the system.
Numerous publications are available describing facilities design.
Advantages of Backgrounding
Calves can be grown to optimum size to increase feeding efficiency and maximize returns.
Homegrown feed resources can be marketed through backgrounded calves.
Backgrounding gives producers more flexibility and allows marketing of calves at times when demand and prices may be higher.
Calves may be healthier and enter the feedlot with less stress when they have been backgrounded.
PATHOPHYS IOLOGY
Stress is a major contributor to disease in weaning-age calves. Reducing the stress of weaning by performing health management practices prior to weaning should help reduce disease in these calves.
Stress is also a major contributor to disease in cattle entering a feedlot.
Backgrounding programs may reduce the stress of feedlot placement by giving the calves the opportunity to learn to eat from a bunk and drink from a water tank. Getting calves used to eating dry feeds is also a benefit.
Properly backgrounded calves should have greater resistance to disease because of proper vaccination during the backgrounding period.
Increasing the age and maturity of calves through backgrounding prior to feedlot placement also should increase disease resistance.
SYSTEMS AFFECTED
The respiratory and gastrointestinal systems are most commonly affected by disease in weaned calves and cattle placed in the feedlot; production management
GENETICS
Calf genetics play a very important role in deciding if and how to background calves.
Numerous backgrounding systems exist and the system should be carefully matched to the type of cattle in order to take maximum advantage of the system.
INCIDENCE/PREVALENCE
N/A
GEOGRAPHIC DISTRIBUTION
Most cattle are shipped to the Great Plains states for finishing and slaughter.
Backgrounding programs may be performed on the farm or ranch of origin or calves may be purchased from several producers and shipped to a backgrounding program.
Preconditioning calves on the farm or ranch of origin provides the best health benefits because stress and commingling are reduced at the time of weaning.
SIGNALMENT
The type of cattle best suited for a particular backgrounding program depends on the genetics of the calf.
See Types of Backgrounding Systems above for a description of the types of cattle best suited to each program.
SIGNS
Calves should be watched very closely for signs of disease throughout a backgrounding period, especially during the preconditioning and early backgrounding phase.
The most common diseases affecting calves at this time are respiratory and gastrointestinal diseases.
CAUSES
The causes of disease during the backgrounding period are numerous and most commonly include diseases of the respiratory and gastrointestinal tract.
RISK FACTORS
Stress and commingling with calves from other farms are two of most important risk factors for disease in calves during a backgrounding program.
DIAGNOSIS DIFFERENTIALDIAGNOSIS
N/A
CBC/BIOCHEMISTRY/URINALYS IS
N/A
OTHER LABORATORY TESTS
N/A
IMAGING
N/A
DIAGNOSTIC PROCEDURES
N/A
PATHOLOGIC FINDINGS
Postmortem examinations should be performed on all cattle that die during a backgrounding program in order to make appropriate management decisions about disease prevention and treatment.
TREATMENT APPROPRIATE HEALTH CARE
If possible, management practices such as castration, dehorning, implants, and vaccination should occur prior to weaning.
If necessary, these practices can be performed during the backgrounding, or preconditioning, period.
These practices should not be performed at the time of weaning because of the increased stress to the calves. If performed during the preconditioning period, they should be performed after the calves have had some time to recover from the stress of weaning.
NURSING CARE
N/A
ACTIVITY
N/A
DIET
Much of the advantage of a backgrounding program is gained from feeding forage-based diets to achieve moderate rates of gain.
Depending on the type of backgrounding system and the type of cattle being fed, the diet will vary from mostly forage to diets that may be similar to those used in a feedlot.
Adequate nutrition is very important to the success of a backgrounding system.
Calves must be provided adequate protein and energy to provide for maintenance needs as well as to provide the desired amount of gain.
A balanced mineral supplement should be available at all times because proper trace mineral nutrition is essential for optimum immune system function.
Calves should have constant access to a clean water source and should be watched closely to make sure they are drinking adequately during the initial phase of the backgrounding period.
Feeding management
Calves should be fed long-stemmed grass hay from the bunks for 4-7 days to help get them accustomed to the bunks. Once calves are eating from the bunks, a starter ration can be top dressed over the hay to get calves started on the ration.
Allowing waterers to run over for a few days will help calves find the waterers. The sound of running water will attract the calves.
Bunks should be kept clean and any old or moldy feed should be removed.
See the Suggested Reading list below for more information on feeding management.
CLIENT EDUCATION
N/A
SURGICALCONSIDERATIONS
N/A
MEDICATIONS DRUGS OF CHOICE
Calves should receive respiratory virus and clostridial vaccines prior to weaning or as part of the preconditioning program.
Several antibiotics are labeled for metaphylactic (mass medication) use and may be beneficial in high-risk calves.
Treatment protocols should be established to provide adequate and consistent treatment.
CONTRAINDICATIONS
Appropriate milk and meat withdrawal times must be followed for all compounds administered to food producing animals.
MISCELLANEOUS ASSOCIATED CONDITIONS
N/A
AGE-RELATED FACTORS
Young calves may be at increased risk of developing disease during the backgrounding period.
Younger calves may also be less likely to respond to vaccines due to the interference of colostral antibodies.
ZOONOTIC POTENTIAL
N/A
PREGNANCY
Calves should not be exposed to bulls during the backgrounding period due to the risks associated with pregnancy in feeder heifers.
Many heifers will reach puberty during the backgrounding period and should not be pastured with intact bulls.
RUMINANT SPECIES AFFECTED
Cattle
BIOSECURITY
Biosecurity should be considered in order to protect calves from as much disease exposure as possible.
If calves from other sources are being backgrounded, they should be maintained separately, if possible, to prevent the introduction of disease in the home-raised calves.
PRODUCTION MANAGEMENT
Backgrounding systems should have a production management plan in order to provide and monitor production, nutrition, and disease occurrence.
SYNONYMS
Growing programs Preconditioning programs Stocker programs
SEE ALSO
Beef nutrition
Bovine respiratory disease complex Coccidiosis
Feed bunk management
Vaccination and deworming programs for beef cattle
ABBREVIATIONS
Lbs/hd/day = pounds of gain per head per day
Suggested Reading
Avent, R. K., Ward, C. E., Lalman, D. L. Economic value of preconditioning feeder calves. Oklahoma State University Extension Publication F-583. 2003.
Lalman, D., Smith, R. Effects of preconditioning on health, performance and prices of weaned calves. Oklahoma State University Extension Publication F3529. 2003.
Lardy, G. 1999, Jan. Feeding management for backgrounders. North Dakota State University Extension Publication AS-1158. Available at: http://.ext.nodak.edu/extpubs/ansci/beef/as1158w.htm
Peel, D. S. 2003, July. Beef cattle growing and backgrounding programs. Veterinary Clinics of North America Food Animal Practice, pp. 365-85.

Stoltenow, C., Lardy, G. 1999, Jan. Preconditioning programs: vaccination, nutrition, and management. North Dakota State University Extension Publication AS-1160. Available at: http://.ext.nodak.edu/extpubs/ansci/beef/as1160w.htm
Authors: John Gilliam and Alfredo DiCostanzo

BACTERIAL ENDOCARDITIS
BASICS DEFINITION
An acute, subacute, or chronic infection involving one or more of the heart valves or parietal endocardium resulting in variably sized masslike lesions on or near the valves, valvular insufficiency or stenosis, and progression to heart failure.
OVERVIEW

Most common valvular or endocardial disease in adult cattle but often unrecognized or misdiagnosed
Vegetative lesions result from hematogenous infection of valvular or mural (parietal) endocardium
Gram-positive organisms, Arcanobacterium pyogenes, a-streptococci, most commonly cultured from blood of affected cattle
Tricuspid valve most frequently and severely affected in cattle
Often more than one valve involved
Initial clinical signs are vague and variable; later signs relate to cardiac insufficiency or septic thromboembolism
Long-term antimicrobial and supportive therapy required
General prognosis is guarded to poor for productivity and long-term survival
PATHOPHYS IOLOGY
Unclear whether bacteria in bloodstream directly adhere to endocardium or valvular surfaces or enter hematogenously through capillaries at base of valve.
Circulating bacteria enter endocardial surface(s) and initiate infection.
Local proliferation of bacteria (bacterial colonies grow in laminar fashion).
Endothelial damage exposes collagen and enhances platelets and fibrin; fibrin is a major component of the vegetative lesion.
Certain bacteria synthesize polysaccharides (dextrans) and fibronectin, which enhance their ability to adhere to and colonize endothelial surfaces (vascular walls, heart valves) and thrombi.
Bacteria adhering to valve surface activates coagulation cascade via release of tissue thromboplastin and extrinsic pathway.
Reseeding of endothelial surface with continued bacteremia.
Preexisting structural damage to endothelium (valvular or mural) and nonbacterial thrombi may or may not be required to initiate disease.
Heart failure, right-sided more commonly than left-sided, may subsequently develop.
In cattle, tricuspid valve is most frequently affected followed by mitral, pulmonary, and aortic valve, and endocardium adjacent to valves.
Multiple valve involvement reported.
Bacterial embolism to secondary organs is common.
Lesions may be small to large enough to occupy most of adjacent heart chamber.
Three histologic zones in lesions: (1) inner zone composed of fibrous tissue, (2) intermediate zone contains fibrin and bacterial colonies, and (3) superficial zone of fibrin and blood cells.
Gross necropsy findings: (1) valvular lesions, often vegetative or fibrotic, thickening and distortion of valve leaflet, (2) embolic lesions to other organs, (3) signs of right-sided or congestive heart failure (e.g., hydrothorax, hydroperitoneum, passive congestion of liver, subcutaneous edema).
SIGNALMENT
Seen worldwide
Primarily in mature cattle
More common in adult, small ruminants than in young
No sex or breed predilection
SIGNS
Frequently animal has history of temporary remission of clinical signs during antibiotic therapy.
Clinical signs are often variable and vague.
Tachycardia is the most consistent finding.
Decreased appetite
Weight loss
Intermittent or constant fever
Lameness, septic arthritis
Hypolactia
Heart murmur noted in ~50% of cattle cases
Primarily holosystolic or pansystolic on right side because of propensity for tricuspid valve to be affected
Diastolic and continuous also reported
Location, timing, and point of maximum intensity of murmur depends on valve(s) affected
±Thrill
Cardiac arrhythmias in ~10% of affected cattle
±Variable intensity of heart sounds
±Painful on palpation over heart region
Less common signs: weakness, diarrhea, abdominal pain, pale mucous membranes
As disease progresses, signs of heart failure, primarily right-sided, develop
Right-sided heart failure: ventral, mandibular, or brisket edema, jugular or mammary vein distention ± vein pulsation, tachycardia, hepatomegaly
Left-sided heart failure: tachycardia, tachypnea, dyspnea, coughing, abnormal lung sounds on auscultation
Occasionally, affected cattle die suddenly without observed clinical signs
Signs of secondary organ (lung, kidney) involvement (infection, infarction) or embolic disease
CAUSES AND RISK FACTORS
At least eight bacterial species have been isolated from cattle with bacterial endocarditis.
Arcanobacterium (Actinomyces) pyogenes, a-hemolytic streptococci are most commonly isolated.
Other common isolates: Escherichia coli, Micrococcus spp., Staphylococcus aureus, Pseudomonas spp., Klebsiella pneumoniae, Proteus mirabilis, Clostridium spp. Bacterioides spp., Fusobacterium necrophorum.
Uncommon isolates: Mycoplasma mycoides, Erysipelothrix rhusipathia, Helcococcus ovis.
Predisposing factors include chronic infection, chronic bacteremia, and underlying damage to valvular or endocardial surface.
Risk factors include ruminal acidosis (acute, subacute, chronic), thrombophlebitis, infection site (mastitis, metritis, septic arthritis, tail infection, pneumonia, omphalophlebitis, abscesses, etc.), traumatic reticulopericarditis, decubital ulcers, traumatic myocarditis, indwelling intravenous catheter, iatrogenic lesions.
DIAGNOSIS
Based on compatible history and clinical findings (murmur, persistent tachycardia), positive blood cultures, and confirmed by echocardiographic identification of consistent lesions
History and physical examination
Tachycardia
±Cardiac murmur
±Fever
±Obvious sites of infection
Hyperfibrinogenemia
Hypergammaglobulinemia due to infectious or inflammatory process
Aerobic and anaerobic blood cultures and sensitivity
Blood sample(s) obtained before antimicrobial therapy is initiated
Minimum of 10 ml of blood collected aseptically
Two to three cultures drawn 1-2 hours apart from separate venipuncture sites preferred but not often obtained
Culture in broth medium
Antimicrobial removal device (ARD) used if animal previously received antimicrobial drugs
Alternatively, if animal’s condition permits, withdraw antimicrobial therapy for 24 to 48 hours before obtaining blood samples for culture
Failure to obtain a positive blood culture does not rule out the presence of bacterial endocarditis
Examination of buffy-coat smears or leukocyte monolayer preparation stained with gram or Giemsa stain
Echocardiography
Visualize and measure size of vegetative lesion on or around heart valve leaflets.
Lesions appear as echogenic shaggy, smooth, or cystic masses.
Valve thickening with ventricular hyperkinesis.
±Enlargement of chambers on affected side.
±Acoustic reverberation and production of microbubbles.
CBC/BLOOD SERUM CHEMISTRY/URINALYS IS
Complete blood count
±Nonregenerative anemia
Most commonly leukocytosis ± left shift; monocytosis
May have normal leukogram or leukopenia with left shift
Cattle have less consistent leukocyte response compared to other species
Serum chemistry panel often reflects accompanying changes in other organ systems, hydration status, or hypophagia
Azotemia
Elevated GGT
Elevated creatine kinase if recumbent
Electrolyte abnormalities from anorexia
Urinalysis if renal infection or infarct suspected
OTHER LABORATORY TESTING
Electrocardiogram if arrhythmia present
Transtracheal wash for cytology and microbiologic cultures if signs of pulmonic disease
Thoracic radiographs of limited value in evaluating cardiac disease in cattle
Arterial blood gas to evaluate oxygenation status
Venous blood gas to evaluate metabolic status
IMAGING
Echocardiogram: vegetative lesion on or near one or more heart valves, most commonly tricuspid valve, ± secondary chamber enlargement (right atrial).
Negative study does not rule out diagnosis of bacterial endocarditis.
DIAGNOSTIC PROCEDURES
Thorough history and physical examination
Blood cultures
Echocardiogram
Adult cattle: sector scanners, 3.5 mHz (or smaller) transducer
Young calf or small ruminant: 5.0 mHz
May need to scan adult cattle from both sides
DIFFERENTIALDIAGNOSIS
Bacterial, viral, or protozoal myocarditis Brisket disease
Cardiac lymphosarcoma or other neoplasm Congenital cardiac abnormalities Congestive heart failure
Cor pulmonale
Dilative cardiomyopathy Endocardiosis
Nutritional myodegeneration Parasitic endocarditis
Septic pericarditis
Toxic myocardial necrosis (ionophore toxicity, gossypol toxicity, plant toxicosis)
TREATMENT
Long term and often costly
Often palliative rather than curative
Aimed at (1) sterilizing lesion and stopping spread of infection and (2) controlling signs of heart failure
Ideally, antimicrobial therapy based on sensitivity of bacteria isolated from blood culture or other site of infection
Parenteral administration of bactericidal antimicrobials required for a minimum of 4 to 6 weeks and often as long as 8 to 12 weeks
Ideally, initial therapy includes broad spectrum antimicrobials given intravenously (IV) to provide maximum blood levels
In cattle, penicillin and beta-lactam drugs are frequently first-choice therapy due to high percentage of gram-positive organisms isolated from affected animals
Early withdrawal of therapy may result in relapse
Often, extralabel use of antimicrobial is required because few are labeled for long-term therapy
Anti-inflammatory/antipyretic agents: aspirin, flunixin meglumine
Anticoagulants to limit enlargement of vegetative lesions and thromboembolic disease; bovine platelets respond poorly to antithrombotic effects of aspirin
If signs of heart failure are present, diuretics and dietary sodium restriction are added to therapy
Maintenance of normal blood electrolyte concentrations, acid-base status, and hydration
Appropriate treatment of secondary organ disease or dysfunction
Correct hypokalemia (± hypocalcemia) associated with anorexia and diuretic therapy
Oxygen supplementation if hypoxemic
MEDICATIONS DRUGS
Penicillin: 22,000 IU/kg: Aqueous potassium penicillin IV QID or procaine penicillin IM BID
Amoxicillin: 10 mg/kg IM BID
Ampicillin: 20 mg/kg IV TID; 10 to 20 mg/kg IM BID
Rifampin: 5 mg/kg PO BID, as adjunct therapy to enhance antibiotic penetration into lesion
Anti-inflammatories: flunixin meglumine, aspirin
Anticoagulants: aspirin, 30 to 100 mg/kg PO every 12 to 24 hours; heparin, 30 U/kg SC every 12 hours (of questionable value)
Furosemide: 0.5 to 1 mg/kg IV every 12 to 24 hours
Potassium supplement (50 to 200 g/day PO) if on potassium-wasting diuretics
CONTRAINDICATIONS /POSSIBLE INTERACTIONS
Appropriate milk and meat withdrawal times must be followed for all compounds administered to food producing animals.
FOLLOW-UP
EXPECTED COURSE AND PROGNOSIS
Most cases die or are culled due to poor prognosis and expense of therapy.
One study reported 29% of affected cattle survived until discharge.
Long-term survival rate and productivity level is not known.
Prognosis is generally guarded to poor for recovery and productivity.
Animals diagnosed early and treated aggressively with small or single lesions have a fair to good prognosis.
Monitoring resolution of disease or lesion.
Regression of clinical signs
Return of fibrinogen and serum protein concentrations to normal
Echocardiogram to measure size of lesion(s)
Repeat blood culture 3-4 days after discontinuing antimicrobial therapy
Reasons for therapeutic failure.
Advanced stage of disease at initiation of therapy
Premature withdrawal of therapy
Ongoing valvular thrombosis due to endothelial damage
Bacterial recolonization of valve
Change in sensitivity or type of infecting bacteria
MISCELLANEOUS ASSOCIATED CONDITIONS
Cardiac arrhythmias including sinus tachycardia, premature ventricular contractions, and atrial fibrillation
Septic arthritis
Passive hepatic congestion
Congestive heart failure
Myocardial disease
Most common sequelae include embolic pneumonia, renal infarction, suppurative arthritis, hepatic emboli
Less common sequelae: cerebral and adrenal emboli, epididymitis, pleural effusion
ZOONOTIC POTENTIAL
N/A
RUMINANT SPECIES AFFECTED
Mostly mature cattle
Goats, sheep
BIOSECURITY
N/A
PRODUCTION MANAGEMENT
Observe appropriate milk and meat withdrawal times for drugs administered.
Treatment of unregistered animals with bacterial endocarditis is often not undertaken due to costs.
Genetically valuable animals often treated to enhance options for genetic salvage procedures (e.g., semen collection, embryo collection, cloning).
Infection results in decreased milk and meat production.
SEE ALSO
Bacterial, viral, or protozoal myocarditis Brisket disease
Cardiac lymphosarcoma or other neoplasm Congenital cardiac abnormalities Congestive heart failure
Cor pulmonale
Dilative cardiomyopathy Endocardiosis
Nutritional myodegeneration Parasitic endocarditis
Septic pericarditis
Toxic myocardial necrosis (ionophore toxicity, gossypol toxicity, plant toxicosis)
ABBREVIATIONS
ARD = antimicrobial removal device BID = twice daily
IM = intramuscular IV = intravenous
PO = per os, by mouth QID = four times daily SC = subcutaneous TID = three times daily Suggested Reading
Diseases of the heart. 1999. In: Radostits, Gay, Blood, Hinchcliff, ed., Veterinary medicine: a textbook of diseases of cattle, sheep, pigs, goats, and horses, 9th ed., pp. 387-89. New York: WS Saunders.
Dowling, M. P., Tyler, J. W. 1994. Diagnosis and treatment of bacterial endocarditis in cattle. JAMA 204(7):1013-16.
Kasari, T. R., Roussel, A. J. 1989. Bacterial endocarditis: Part I. Pathophysiologic, diagnostic, and therapeutic considerations. Compendium Continuing Education 11 (5):259-64.
Reef, V. B., McGuirk, S. 2002. Diseases of the cardiovascular system. In: Smith, B., ed., Large animal internal medicine, 3d ed, pp. 454-58. St. Louis: Mosby.
Roussel, A. J., Kasari, T. R. 1989. Bacterial endocarditis in large animals: Part II. Incidence, causes, clinical signs and pathologic findings. Compendium Continuing Education 11:769-73.
Tyler, J. W., George, L., Bartram, P. A. 1991. Endocarditis in a cow. JAMA 198(8): 1410-12.
Authors: Susan Semrad and Sheila McGuirk

BACTERIAL MENINGITIS
BASICS DEFINITION

Meningitis is defined as a bacteria-associated inflammatory process that involves the meninges of the brain and/or spinal cord.
Disease is most commonly seen in neonates but may also occur in older animals as a result of osteonecrosis induced by thermal cauterization during dehorning, extension of localized infection from skull fractures or coccygeal vertebrae (poor docking hygiene), or secondary to left-sided bacterial endocarditis.
PATHOPHYS IOLOGY
Bacterial meningitis occurs by direct extension of an infectious agent into the calvarium or by hematogenous spread to the CNS from a distant site.
The relative lack of bactericidal and opsonic activities in the CNS predisposes animals to meningeal infection.
The inflammatory response resulting from bacterial invasion of the subarachnoid space is due in large part to the activity of host-derived mediators (cytokines), and it is this inflammatory response that is responsible for the long-term neurological sequelae and death associated with bacterial meningitis.
Defects of cerebrospinal fluid (CSF) drainage occurring secondary to meningeal inflammation lead to hypertensive hydrocephalus.
SYSTEMS AFFECTED
Nervous system
GENETICS
None reported
INCIDENCE/PREVALENCE
The disease is common in neonatal farm animals. One survey reported a 43% prevalence of septic meningitis in necropsied calves (Green and Smith, 1992).
GEOGRAPHIC DISTRIBUTION
Worldwide occurrence
SIGNALMENT
Neonates of all species, especially calves
SIGNS HISTORICALFINDINGS
There may be a history of prematurity, dystocia, or lack of colostral intake.
There may be a history of hyperesthesia, stiff neck, depression, seizures, or blindness, with or without a history of another illness, such as enteritis or polyarthritis.
There may be a history of trauma, recent dehorning, or tail docking, or there may be information relating to the presence of a wound near the calvarium or vertebrae (usually older ruminants), or an infection of the sinuses, middle ear, or inner ear.
PHYSICALEXAMINATION FINDINGS
Acute meningitis may or may not be accompanied by fever in the neonate.
Depression, anorexia, omphalophlebitis, polyarthritis, and ophthalmitis are frequent concurrent findings.
Neurological Examination Findings
Ataxia, with or without spasticity and mild tetraparesis, hyperesthesia, neck pain, depression, wandering, star-gazing, and abnormal vocalization, may be seen.
Lethargy, recumbency, anorexia, loss of suckle reflex, coma, opisthotonus, convulsions, tremors, and hyperesthesia are the most common clinical signs in calves.
CAUSES
Meningitis most commonly results from hematogenous extension of a preexisting bacterial infection, or results from traumatic penetration of the CNS.
Failure of passive transfer of maternal antibodies predisposes to hematogenous meningitis.
The bacteria involved most commonly are those associated with neonatal sepsis.
Gram-negative bacteria are the predominant cause of infection in large animal neonates although polymicrobial infections also occur.
Escherichia coli is the most common bacterium isolated. Other isolates include Klebsiella pneumonia, Salmonella spp. (S. dublin and S. typhimurium), Staphylococcus spp., Streptococcus spp., and Bacillus spp. in calves; Klebsiella pneumonia, Salmonella spp., Streptococcus spp., Arcanobacterium pyogenes, Erysipelothrix rhusiopathiae, and occasionally Leptospira interrogans, Listeria monocytogenes, Mycoplasma spp., and Fusobacterium necrophorum in sheep and goats in North America.
RISK FACTORS
Both maternal and neonatal factors contribute to the development of sepsis in the neonate. They include bacterial placentitis, perinatal stress, prematurity, dystocia, birth asphyxia, unsanitary or adverse environmental conditions, overcrowding, failure of passive transfer of maternal antibodies, contamination of the environment with pathogenic bacteria, and the presence of enteritis, omphalitis, or respiratory infections in the neonate.
DIAGNOSIS DIFFERENTIALDIAGNOSIS
Metabolic disease (e.g., hypoglycemia, hypomagnesemia)
Cerebral edema
Hydrocephalus
Encephalitis (e.g., viral)
Toxicity
CBC/BIOCHEMISTRY/URINALYS IS
Leukocytosis with a left shift is common in calves.
Respiratory acidosis, hypernatremia, hyponatremia, hyperkalemia, hypomagnesemia, and hypoglycemia may be observed also.
OTHER LABORATORY TESTS
Low serum immunoglobulin concentrations may be observed.
In the presence of neurological signs, a positive blood culture supports a diagnosis of bacterial meningitis secondary to neonatal infection. Other samples, such as synovial fluid, also may culture positive.
IMAGING
Radiographs and/or ultrasound may be indicated when trauma or extension of a localized infection is suspected.
DIAGNOSTIC PROCEDURES
Definitive diagnosis is based on the presence of a neutrophilic pleocytosis, xanthochromia, turbidity, high total protein concentration in the CSF, and, ideally, positive culture from the CSF. Although often unrewarding, Gram stain and culture should be attempted.
TREATMENT APPROPRIATE HEALTH CARE
Early diagnosis and aggressive treatment are imperative for a successful outcome. By the time clinical signs are present, treatment is often unrewarding.
Within the herd, minimize perinatal stress, ensure passive transfer of maternal antibodies, and employ proper dehorning technique and hygiene during tail docking.
NURSING CARE
Provision of adequate nutritional support and a clean, comfortable environment; protection from self-inflicted trauma; and maintenance of body temperature, fluid, and acid-base balance are critical for a successful outcome.
ACTIVITY
N/A
DIET
N/A
CLIENT EDUCATION
Treatment may be expensive and mortality rate high despite appropriate therapy.
SURGICALCONSIDERATIONS
N/A
MEDICATIONS DRUGS OF CHOICE
Antimicrobials
NOTE: * = Not approved for use in food animals in the United States; ** = Approved for use in cattle, except lactating cows, in the United States; extralabel dose
Antimicrobial therapy is the hallmark of treatment.
Drugs that penetrate the blood-CSF barrier are lipid soluble, nonionized at physiologic pH, not extensively protein bound, and of low molecular weight. Drugs that satisfy these criteria and that are approved for use in food animals are limited, but include trimethoprim sulfa and sulfonamides (except lactating dairy animals). Inflammation markedly enhances CSF concentrations of penicillins, particularly cephalosporins, which normally penetrate poorly. Other drugs, such as aminoglycosides, do not penetrate CSF even in the presence of inflammation.
Selection of an antimicrobial drug in ruminants should also be based on the pharmacokinetics and pharmacodynamics of the drug in neonates, the likelihood of antimicrobial resistance, and the potential for violative antimicrobial tissue residues.
Bacteriocidal drugs are superior to bacteriostatic drugs.
Where possible, the selection of antimicrobial drugs should be based on either smears stained by Gram stain or culture from infected areas. Treatment should not be delayed, however, until results of sensitivity testing are known. Empiric antimicrobial therapy should include gram-negative and gram-positive spectrum.
Antibiotics should be administered by intravenous routes in order to attain maximum peak blood and CSF concentrations.
The efficacy of specific antimicrobial therapy for treatment of meningitis in food animals is unknown because of the lack of CSF pharmacokinetic data in ruminants. Specific antimicrobial therapy could include, but is not limited to trimethoprim sulfa (30 mg/kg, IV, q 12 h); cefazolin (20 mg/kg, IV, q 6 h); florfenicol (20 mg/kg, IV, q 12 h)**.
Relapses may occur as meningeal inflammation subsides and CNS concentrations of (nonlipophilic) antimicrobial drug(s) fall.
Antimicrobial drug therapy should continue for at least 7 days after resolution of all clinical signs.
Anticonvulsants
The following drug doses have been extrapolated from recommended doses for equine neonates.
Diazepam (5-10 mg/45 kg, slowly IV, repeated if necessary) is used for short-term control.
If two to three doses of diazepam fail to control convulsions, a loading dose of phenobarbital (10-20 mg/kg diluted in 30 ml saline, IV over 15 minutes) should be given. Oral therapy (5-10 mg/kg, q8htoq12h)is then used for maintenance for long-term control.
Pentobarbital (2-4 mg/kg, IV, slowly) has been advocated, but depth of anesthesia must be monitored to prevent respiratory arrest.
Other Treatments
Consider DMSO (1 gm/kg, IV as a 10% solution in 5% dextrose or saline), corticosteroids (dexamethasone at 0.15 mg/kg 15-20 minutes before the first dose of antibiotic, then every 6 hours for 4 days), or a combination of both if progression is rapid.
Following rehydration, nonsteroidal anti-inflammatory drugs may be beneficial (flunixin meglumine, 0.5-1.0 mg/kg, IV, q 12 h to q 24 h; ketoprofen, 2.2 mg/kg, IV, q 24 h; or aspirin, 100 mg/kg, PO, q 24 h in neonates)
A plasma transfusion may be required.
Additional therapy may be required to resolve secondary complications (i.e., antiulcer medications, ophthalmic drugs, etc.).
CONTRAINDICATIONS
Acepromazine should not be used as a sedative due to its ability to lower the seizure threshold.
Drug withdrawal times must be determined for all drugs used to treat food-producing animals.
PRECAUTIONS
Care should be exercised when dosing anticonvulsant drugs in neonates because of the increased permeability of their blood brain barrier.
POSSIBLE INTERACTIONS
N/A
ALTERNATIVE DRUGS
N/A
FOLLOW-UP PATIENT MONITORING
Close monitoring of vital parameters and metabolic indices is warranted during antimicrobial therapy, especially in animals showing seizure activity.
PREVENTION/AVOIDANCE
The key to prevention of meningitis in neonates is paying attention to the events leading up to and including parturition, and ensuring adequate colostral intake.
Proper dehorning technique and hygiene during tail docking will decrease the incidence of meningitis in older animals.
POSSIBLE COMPLICATIONS
N/A
EXPECTED COURSE AND PROGNOSIS
Prognosis in neonatal ruminants with septic meningitis is poor, despite treatment. The key to a successful outcome relies on early recognition of CNS involvement and institution of aggressive, appropriate therapy.
MISCELLANEOUS ASSOCIATED CONDITIONS
Generalized sepsis typically accompanies septic meningitis in neonates.
AGE-RELATED FACTORS
Neonates are most commonly affected.
ZOONOTIC POTENTIAL
N/A
PREGNANCY
Diseases affecting the dam during gestation may predispose the neonate to partial or complete failure of passive transfer after birth.
RUMINANT SPECIES AFFECTED
All species are susceptible.
BIOSECURITY
N/A
PRODUCTION MANAGEMENT
Measures taken that reduce perinatal stress will reduce the incidence of septic meningitis in the neonate.
Proper dehorning technique and hygiene during tail docking will reduce the incidence of septic meningitis in older animals.
SYNONYMS
Meningoencephalitis
Meningomyeloencephalitis
Suppurative meningitis
SEE ALSO
Neonatal sepsis
ABBREVIATIONS
CNS = central nervous system CSF = cerebrospinal fluid DMSO = dimethyl sulfoxide IV = intravenous
PO = per os, by mouth q = for
Suggested Reading
Aldridge, B. M., Garry, F. B., Adams, R. 1993. Neonatal septicemia in calves: 25 cases (1985-1990). J Amer Vet Med Assoc. 203:1324-29.
Cebra, C., Cebra, M. 2002. Diseases of the hematologic, immunologic, and lymphatic systems (multisystem diseases). In: Sheep and goat medicine, ed. D. G. Pugh. Philadelphia: W. B. Saunders.
Fecteau, G and George, L. 2004. Bacterial meningitis and encephalitis in ruminants. Veterinary Clinics of North America: Food Animal Practice. 20(2):363-77.
Fecteau, G., Van Metre, D. C., Paré, J., Smith, B. P., Higgins, R., Holmberg, C. A., Jang, S., Guterbock, W. 1997. Bacteriological culture of blood from critically ill neonatal calves. Can Vet J. 38:95-100.
Green, S. L., Smith, L. L. 1992. Meningitis in neonatal calves: 32 cases (1983-1990). J Am Vet Med Assoc. 201:125-28.
Prescott, J. F. 2000. Infections of the nervous system: meningitis and encephalitis. In: Antimicrobial therapy in veterinary medicine, ed. J. G. Prescott, J. D. Baggot, R. D. Walker. 3rd ed. Ames: Iowa State University Press.
Author: Maureen E. G. Wichtel

BEEF BULL MANAGEMENT
BASICS OVERVIEW

It is well known that the reproductive program in each herd has a major influence on productivity and is directly linked to profitability.
Good reproductive performance requires diligent management of many important and interrelated factors.
The performance of herd bulls during natural service is dependent upon not only their health and proper management but also the health of the females they will be breeding.
To be successful, programs should start with good planning and genetic selection considerations for the important traits necessary for each herd and continue through the implementation stages of the breeding season.
At the end of the production cycle, success is measured by overall reproductive efficiency and the performance of the offspring.
SYSTEMS AFFECTED
Male reproductive, production management, nutrition
GENETICS
N/A
INCIDENCE/PREVALENCE
N/A
GEOGRAPHIC DISTRIBUTION
Worldwide distribution
SIGNALMENT
Species
Beef cattle
Breed Predilections
All breeds
BULLMANAGEMENT PROGRAMS
Bull management programs begin with the purchase of new herd sire prospects.
The genetic direction of the herd is of obvious importance.
In addition to inherent genetic traits, bulls must be healthy, fertile, and capable of expressing the desirable traits.
Bulls should be purchased from seed-stock breeders that have documented herd health programs that minimize the likelihood of infectious diseases.
The bulls should be immunized against common diseases and, if necessary, treated for parasites or tested for diseases indicated from a biosecurity standpoint.
All bulls should undergo a complete breeding soundness evaluation (BSE) performed by a competent veterinarian to assess their general physical and reproductive soundness. This includes newly purchased bulls and a yearly reexamination of herd bulls.
In addition to the general physical examination, it is important to collect semen and evaluate the sample for spermatozoal motility and morphology.
Bulls should meet the minimum standards established by the Society for Theriogenology (BIF).
Each component of the BSE such as scrotal circumference (SC) should be accurately measured and utilized within the context of age, weight, nutritional status, and contemporary group.
SC is a good indicator trait for age at puberty in offspring; it is highly correlated with daily sperm production and is mildly correlated with the percentage of normal spermatozoa.
Body condition, structural correctness of feet and legs, and general soundness are also important factors for new sire prospects.
BULLTO FEMALE RATIO
The number of bulls required to adequately cover a given number of breeding females is related to a variety of factors. An arbitrary classification of some considerations follows:
Factors Influencing Bull to Female Ratio (BFR)
Pasture or range conditions and cattle distribution

Terrain
Water availability and location(s)
Carrying capacity
Pasture adaptation
Pasture size

Individual bull variation

Age
Condition
Fertility
Mating ability
Social behavior
Injury

Operation and management

Length of breeding season
Animal breeding and selection
Reproductive disease
Nutrition and body condition
Management observation

Defining the optimum BFR is difficult because certain factors influencing each set of circumstances are unpredictable.
The expected number of estral females available to the bull(s) on any given day is an important point that must be considered.
Anecdotal reports indicate that smaller breeding pastures with fewer animals are more efficient and provide more uniform distribution of bulls and females. This obviously limits the total number of females exposed to dominant bulls when compared to large multisire pastures where females congregate in a sexually active group. This is a group of estral females that band together from preestrus through standing estrus.
The bull(s) join this group and are constantly moving throughout the pasture. This is of most concern in very large groups of females because the bulls tend to run together.
It is possible for single bulls to cover 60 breeding females in limited breeding seasons and produce comparable reproductive rates to a much lower BFR.
Generally, BFRs of 1:25 or 1:30 for mature bulls and BFRs of 1:15 or 1:20 for yearling bulls have been utilized for range areas with minimal observation and little breeding season management.
This may be an important area of management consideration if optimizing efficiency and reducing expenditures is desirable.
Other Considerations
The time each cow settles in relation to the start of the breeding season influences the weaning weight of her offspring and the ability to select replacement heifers with adequate age in a yearly production cycle.
In limited breeding seasons, efficient management requires early conception and higher overall pregnancy rates.
It is important to identify and optimize the use of bulls with preferred genetic traits, especially as producers move toward value-based marketing through vertically coordinated programs.
The use of frequent observation of breeding pastures and immediate detection and correction of problems is important.
Molecular Evaluation
More recent technology utilizing a commercially available set of DNA microsatellite markers to identify each sire’s progeny from multisire breeding pastures has been developed.
Proteomics shows promise in terms of accurately identifying progeny. As new technology advances, it may reach an economic level that could permit its use in commercial herds.
The identification of progeny in multisire breeding pastures will permit an accurate genetic evaluation system for a greater number of young sires.
This potential could rapidly revolutionize bull selection programs and permit the ability to select and optimize the use of bulls with superior reproductive and genetic traits.
SELECTION GUIDELINES
Select superior bulls from a genetic standpoint.
Carefully screen the health of all new bulls.
Conduct a breeding soundness evaluation on all bulls and select bulls that are above average in scrotal circumference, motility, and percent normal sperm morphology.
Conduct breeding soundness evaluations on bulls yearly, preferably just before breeding season begins.
Develop a method to identify some progeny of each sire.
Observe mating ability of bulls during breeding at the start and several times during the breeding season.
Utilize knowledge of social behavior, terrain, calving pattern, bull performance, and other factors to determine the number of bulls, bull to female ratio, and grouping of bulls.
MISCELLANEOUS ASSOCIATED CONDITIONS
Lameness, infertility, nutritional deficiencies
AGE-RELATED FACTORS
N/A
ZOONOTIC POTENTIAL
N/A
PREGNANCY
It is possible for single bulls to cover 60 breeding females in limited breeding seasons and produce comparable reproductive rates to a much lower BFR.
Generally, BFRs of 1:25 or 1:30 for mature bulls and BFRs of 1:15 or 1:20 for yearling bulls have been utilized for range areas with minimal observation and little breeding season management. This may be an important area of management consideration if optimizing efficiency and reducing expenditures are desirable.
The time each cow settles in relation to the start of the breeding season influences the weaning weight of her offspring and the ability to select replacement heifers with adequate age in a yearly production cycle.
Therefore, in limited breeding seasons, efficient management requires early conception and higher overall pregnancy rates.
RUMINANT SPECIES AFFECTED
Beef bulls
BIOSECURITY
N/A
PRODUCTION MANAGEMENT
The performance of herd bulls during natural service is dependent not only upon their health and proper management but also upon the health of the females they will be breeding.
To be successful, programs should start with good planning and genetic selection considerations for the important traits necessary for each herd and continue through the implementation stages of the breeding season.
SYNONYMS
N/A
SEE ALSO
Animal identification Beef bull behavior Beef cattle nutrition
Body condition scoring Record keeping
Reproductive disease chapters Semen evaluation ABBREVIATIONS
BFR = bull to female ratio
BSE = breeding soundness evaluation DNA = deoxyribonucleic acid
SC = scrotal circumference
Suggested Reading
Blockey, M. A. deB. 1989. Relationship between serving capacity of beef bulls as predicted by the yeard test and their fertility during paddock mating. Australian Vet J. 66(11): 348-51.
Chenoweth, P. J. 2000. Rationale for using bull breeding soundness evaluations. Comp Cont Ed, Food Anim Suppl. 22(2): s48-s55.
Lunstra, D. D., Laster, D. B. 1982. Influence of single-sire and multiple-sire natural mating on pregnancy rate of beef heifers. Theriogenology 18(4): 373-80.
McGrann, J. M., Leachman, L. 1995, Jul. Seedstock beef cattle: SPA. Vet Clin North Am Food Anim Pract. 11(2): 375- 88.
Rupp, G. P., Ball, L., Shoop, M. C., Chenoweth, P. J. 1977. Reproductive efficiency of bulls in natural service: Effects of male to female ratio and single- vs multiple-sire breeding groups. JAVMA 171(7): 639-42.
Sanderson, M. W., Gay, J. M. 1996, Feb 15. Veterinary involvement in management practices of beef cow-calf producers. J Am Vet Med Assoc. 208(4): 488-91.
Wiltbank, J. N., Parish, N. R. 1986. Pregnancy rate in cows and heifers bred to bulls selected for semen quality.
Theriogenology 30:779-83.
Author: Gary P. Rupp

BERSERK MALE SYNDROME/ABERRANT BEHAVIOR SYNDROME
BASICS OVERVIEW

Berserk syndrome or berserk male syndrome (BMS), aberrant behavior syndrome (ABS)
As with any behavioral difficulty, there is a wide range in the severity of syndrome expression.
A berserk male is a male camelid who has been improperly imprinted on humans, is extremely aggressive, and is very territorial. The extreme case is possibly incurable. However, most ABS camelids are not this severe and a more favorable prognosis is accorded.
Territorial males typically direct their aggression toward other male llamas and their aggressiveness is misdirected at humans. In a domestic camelid, this syndrome is unacceptable for caretaker safety.
Symptoms that indicate a camelid is at significant risk for developing ABS generally begin between 12 and 18 months of age; severe ABS begins between 2 and 3 years of age.
Behavioral signs include: screaming, excessive spitting, attacking humans and other animals, charging, biting, butting, and lying on people.
BMS/ABS is the result of a male llama being abnormally socialized to people at an early age. Common causes include bottle feeding, excessive handling, limited discipline of poor behaviors, removal from mother/peers, and isolation from the rest of the herd.
Male crias are imprinted upon people and essentially see them as another llama in the herd.
ABS crias communicate with people through behaviors like spitting, chest butting, and wrestling.
Territoriality of males increases over time.
SYSTEMS AFFECTED
Behavioral
GENETICS
N/A
INCIDENCE/PREVALENCE
N/A
GEOGRAPHIC DISTRIBUTION
Worldwide in camelids
SIGNALMENT
Species
Camelids
Breed Predilections
N/A
Mean Age and Range
Symptoms that indicate a camelid is at significant risk for developing ABS generally begin between 12 and 18 months of age; severe ABS begins between 2 and 3 years of age.
Predominant Sex
Males
SIGNS
Clinical Signs
ABS camelids may have the following history:
Bottle or tube fed/supplemented
Separated from mother, generally early in life
Separated from other camelid peers
Early veterinary treatment, sometimes extensive
Handled by numerous inexperienced people with the exclusion of camelid peers
Behavioral Signs
Does not respond to training
ABS camelids are usually under 4 years old.
Regularly follow people within a 2-foot distance.
Orgle at humans
Quite human aggressive
Drop to a U-neck position near humans
Flip tail over back into an aggressive positioning
Aggressively pursue people and run up to people on sight
TREATMENT
Castration is mandatory. Early castration is preferred. Castration generally helps and may in fact alleviate the syndrome in some cases. Once the syndrome is diagnosed, castration should be accomplished.
Postcastration, remove the camelid completely from his territory. He should be moved into an established pasture of an aggressive older male. This should be done as soon as possible postsurgery. The new pasture should be out of the visual territory of the previous pasture. The animal should be maintained in this mixed pasture for several months prior to a training program.
Training program with a qualified camelid trainer/behaviorist is necessary if a poor postsurgical/mature peer response occurs.
In severe cases, euthanasia is indicated.
FOLLOW-UP PREVENTION/AVOIDANCE
Raise young males with one or more assertive adult males/geldings. These animals will teach the young crias needed socialization and “manners.”
Young intact males should be raised within the territory of an established male.
Pushiness or aggressiveness should be firmly/positively corrected early on.
Begin behavior training at an early age.
Regular brushing/grooming while haltered allows socialization to humans.
Do not allow crias to invade personal human space (2-foot distance rule).
Halter training can begin around 2 months of age and is done slowly allowing camelid acceptance. All training should be directed toward eliminating cria aggression.
Early camelid training must establish you as the alpha leader and the cria should learn to follow instructions.
Do not allow attention at people’s feet by crias.
Genetic Selection
Don’t breed from aggressive camelid stock; select less-aggressive dams and sires.
Select against territorial instincts.
Select away from guarding instincts, if possible.
Keeping geldings away from females early on. Mixing can encourage possessive behavior and territoriality in ABS crias.
Do not breed males before 4-5 years of age.
Castrate all young males that show excessive fear, aggression, or territoriality or challenge adult animals/humans.
MISCELLANEOUS ASSOCIATED CONDITIONS
N/A
AGE-RELATED FACTORS
Camelids are at significant risk for developing ABS symptoms generally between 12 and 18 months of age; severe ABS begins between 2 and 3 years of age.
ZOONOTIC POTENTIAL
N/A
PREGNANCY
N/A
RUMINANT SPECIES AFFECTED
Camelids
BIOSECURITY
N/A
PRODUCTION MANAGEMENT
See above
SYNONYMS
Berserk male syndrome or aberrant behavior syndrome
SEE ALSO
Body condition scoring Camelid nutrition Euthanasia and disposal Tooth root abscess ABBREVIATIONS
ABS = aberrant behavior syndrome BMS = berserk male syndrome Suggested Reading
Ebel, S. 1989, Mar. The llama industry in the United States. Vet Clin North Am Food Anim Pract. 5(1):1-20.
Fowler, M. 1989, Mar. Llama medicine. Physical examination, restraint and handling. Vet Clin North Am Food Anim Pract. 5(1):27-35.
Fowler, M. E. 1996, Mar. Husbandry and diseases of camelids. Rev Sci Tech. 15(1):155-69.
McGee, M. 1994, Jul. Llama handling and training. Vet Clin North Am Food Anim Pract. 10(2):421-34.
Author: Scott R. R. Haskell

BESNOITIOSIS
BASICS DEFINITION

Infection with a coccidian protozoa of genus Besnoitia, family Sarcocystidae, which primarily affects the skin, subcutis, blood vessels, mucous membranes, and tissues of cattle, horses, goats, and other herbivores
Organism is closely related to genus Toxoplasma.
OVERVIEW
Chronic debilitating disease primarily of cattle, goats, and rarely horses
Affects antelope, blue duiker, and blue wildebeest in Africa, caribou in Canada, and wildlife in Australia
Endemic disease in some tropical and subtropical areas, sporadic elsewhere
High morbidity, significant economic loss, and low mortality in endemic areas
Reported in cattle in southwest Europe (France, Portugal), Africa, South America (Venezuela), Israel, Kazakhstan, South Korea, Asia, and Soviet Union
Reported in goats in Iran, New Zealand, Africa
Reported sporadically in horses in Africa, southern Europe, Mexico, and in two imported burros in the United States
Not reported in cattle in North America
Reported in North America in wildlife including opossum, caribou, reindeer, and mule deer; other wildlife that prey upon definitive host (i.e., cats) may also be affected.
Three of the seven classified species occur in domestic livestock and four in wildlife.
Life cycle involves a definitive host and an intermediate host.
Besnoitia are host specific for intermediate hosts.
Besnoitia besnoiti in cattle
B. bennetti infects horses, donkeys, mules
B. caprae in goats (not sheep)
B. tarandi in reindeer, mule deer, and caribou
B. jellisoni and B. wallacei infect rodents
B. darlingi from lizards, opossums, and snakes
B. sauriana in lizards
Cats are the definitive host for some Besnoitia spp. infecting wildlife; sexual reproduction occurs in the intestines of the definitive host.
Transmission to wildlife may be fecal-oral route by ingestion of oocysts (contaminated feeds or water) shed in cat (final host) feces.
Definitive host and mechanism of transmission for species affecting domestic livestock is unknown.
Mechanical transmission via biting insects/flies (tabanids, tsetse, ticks) possible in cattle and goat; ingestion of feedstuffs or water contaminated with cat feces
Transmission via semen suspected.
Experimentally, can transmit some Besnoitia spp. by needle inoculation of cyst-containing tissues into suitable host.
Organism localizes in thick-walled cyst(s) in the skin, blood vessels, mucous membranes of upper respiratory tract and subcutaneous and other tissues.
Anasarca gives way to sclerodermatitis with loss of hair and epidermis and development of severe dermatitis.
Condition may become generalized and disseminated
PATHOPHYS IOLOGY
Upon entrance into a susceptible intermediate host, sporulated oocysts release sporozoites that produce tachyzoites via endodyogeny.
Parasitemia is associated with tachyzoites (endozoites) replicating in the host’s macrophages, fibroblasts, and endothelial cells.
Tachyzoites are released from endothelial cells and reinvade other endothelial cells causing vasculitis, increased permeability, anasarca, and thrombosis in capillaries and small veins of the dermis, subcutis, and testes (known as anasarca stage).
Tachyzoites migrate into connective tissues and initiate cyst formation within endothelium and fibroblasts. They mature here to form bradyzoite cysts (cystozoites).
Cellular destruction and release of inflammatory mediators during replication of organisms in endothelial, histiocytic, and other cells result in clinical signs and formation of large thick-walled cysts filled with bradyzoites.
Connective tissue reaction around the cysts produces a thickening of the skin and resulting circulation disturbances, alopecia, and necrosis (scleroderma stage).
Cysts are most commonly within the dermis, subcutaneous connective tissues, conjunctiva, sclera, scrotum, and mesentery.
Location of cyst formation and size help determine which clinical signs predominate in any given case.
SIGNALMENT
No age, sex, or breed predilection
SIGNS
Many affected animals are asymptomatic except for cysts in scleral conjunctiva.
Cattle commonly have two stages of the disease: an acute stage associated with endozoite proliferation and a chronic stage with scleroderma and cyst formation.
Incubation period in cattle is 6 to 10 days.
Cattle: Signs Seen During Acute Phase
Fever
Warm, painful ventral swellings and reluctance to move
Anasarca (generalized edema of skin)
Tachypnea
Tachycardia
Hypophagia
Swollen lymph nodes
Nasal discharge (rhinitis)
Lacrimation
±Diarrhea
Loss of condition
Hypolactia
Photophobia
±Orchitis
±Abortion
Small whitish to clear pinpoint nodules on scleral conjunctiva and nasal, pharyngeal, and laryngeal mucosa
Cattle: Signs Seen During Chronic Phase
Skin lesions progress to severe dermatitis over most of body
Sclerodermatitis
Infected cysts in the skin and subcutaneous tissue
Subcutaneous lumps
Variable alopecia
Hyperpigmentation
Skin thickens, wrinkles, and cracks
Thickened folds of skin around neck, shoulders, rump
Inspiratory dyspnea
Secondary bacterial infection or myiasis of skin
Bulls frequently become sterile: scrotal skin affected, and orchitis, epididymitis, periorchitis, vascular lesions in testes
Teat lesions
Mouth lesions in suckling calves
Loss of hair, especially on face and lower legs in wildlife
Other Lesions That May Be Seen with Generalization of Disease
±Focal or disseminated myositis, keratitis, periostitis, endostitis, lymphadenitis, pneumonia, arteritis, perineuritis
Severe weight loss
In Goats
Rarely see acute stage
Animals present in chronic stage with dermatitis and respiratory dyspnea
Thickening, lichenification, alopecia, fissures, and oozing serum of legs (carpus/tarsus) and ventral abdomen
Lesions severe on scrotum and fetlocks
±Subcutaneous papules over hindquarters
Postmortem Lesions
Parasitic cysts in dermis, subcutaneous and other fascia
Pharyngitis, laryngitis, tracheitis
Cysts present in scrotum and testes of males
Sandlike granules and cysts in nostrils and turbinates
Sandlike granules in vascular endothelium
Widespread vascular lesions
Dermatitis
Secondary lesions in skeletal and heart muscle, and lungs
Histology: parasite evident in cystic lesions
CAUSES AND RISK FACTORS
Endemic area
Disease outbreaks in cattle and goats occur during fly/insect season
Contamination of feedstuffs with cat feces
High feral cat population
DIAGNOSIS
Diagnosis is based upon history and geographical area.
Appearance of cyst in scleral conjunctivas or nasal mucosa
Identification of crescent-shaped bradyzoites surrounded by a collagen capsule in skin or scleral conjunctival scrapings or skin biopsy
Ear-tip biopsy commonly used in goats
Affected animals are often asymptomatic.
DIFFERENTIALDIAGNOSIS
Lumpy skin disease
Sweating sickness
Ectoparasites: ticks, fungi, mites
CBC/BIOCHEMISTRY/URINALYS IS
No characteristic changes
±Hyperproteinemia, hypergammaglobulinemia
OTHER LABORATORY TESTS
Serum antibodies by indirect immunofluorescence or ELISA
Tests have only moderate sensitivity
IMAGING
N/A
DIAGNOSTIC PROCEDURES
Scleral conjunctival or skin scrapings
Skin biopsy
TREATMENT
Isolate affected animals.
No specific treatment; treat symptomatically.
Supportive therapy; dermatitis, enteritis, fever.
Reported clinical cure in donkey after prolonged administration of trimethoprim-sulfamethoxazole.
Reportedly in rabbits, antimony and sulfanilamide complex prevented cyst formation.
Oxytetracycline may have some value if given early in the course of the disease.
MEDICATIONS
N/A
DRUGS OF CHOICE
N/A
CONTRAINDICATIONS
Appropriate milk and meat withdrawal times must be followed for all compounds administered to food-producing animals.
FOLLOW-UP
Case fatality about 10%
Long convalescence period (many months)
Sterility and infertility may be transient or permanent
MISCELLANEOUS PREVENTION
Reduce exposure to biting insects and ticks.
Avoid exposure of wildlife to feces of infected cats.
Avoid feed contamination with cat feces.
Control feral cat population.
Vaccine produced using B. besnoiti isolated from wildebeest and grown on tissue culture is effective.
Durable immunity in all vaccinates
Subclinical infection occurred at low level.
ASSOCIATED CONDITIONS
Secondary bacterial or myiasis
±Focal or disseminated myositis, keratitis, periostitis, endostitis, lymphadenitis, pneumonia, arteritis, perineuritis
ZOONOTIC POTENTIAL
N/A
RUMINANT SPECIES AFFECTED
Cattle
Goat
Wild ruminants: antelope, wildebeest
BIOSECURITY
N/A
PRODUCTION MANAGEMENT
Affected animals remain carriers for life.
Chronic cystic stage results in severe production loss.
Economic losses in endemic areas due to mortality (<10%), sterility (temporary or permanent), loss of condition, and lower market value, and damage to hide.
Carcasses approved if localized lesions only, no systemic involvement
Carcass condemned if disseminated lesions with emaciation
SYNONYMS
“Dimple” in goats Globidiosis
SEE ALSO
Ectoparasites: ticks, fungi, mites Lumpy skin disease
Sweating sickness
ABBREVIATIONS
ELISA = enzyme-linked immunosorbent assay
Suggested Reading
Besnoitiosis. 1998. In: The Merck veterinary manual, eds. S. E. Aiello, A. May, 8th ed. Whitehouse Station, NJ: Merck & Co., Inc.
Diseases caused by protozoa. 1999. In: Veterinary medicine: a textbook of diseases of cattle, sheep, pigs, goats, and horses, ed. O. M. Radostits et al., 9th ed. London: W. B. Saunders.
Lloyd, J. E. 1999. Dermatologic diseases. In: Current veterinary therapy 4, food animal practice, eds. J. L. Howard, R.
A. Smith. Philadelphia: W. B. Saunders.
Parasitic diseases. Manual on meat inspection for developing countries. http://www.fao.org/docrep/003/t0756e/T0756E04.htm; accessed August 25, 2007.
Smith, M. C., Sherman, D. M. 1994. Skin. In: Goat medicine. Philadelphia: Lea & Febiger.
Authors: Susan Semrad and Karen A. Moriello

BLACK LOCUST TOXICITY
BASICS OVERVIEW

There are two lectins present in the bark of the Robinia pseudoacacia (black locust) tree. They are the major lectin RPbAI and the minor lectin RPbAII. The seeds and leaves are also toxic.
Plants from this family are in the same family as the Abrus precatorius (rosary pea) and the Ricinus communis (castor bean), as well as the Phoradendron (mistletoe) and Phytolacca americana (pokeweed).
The lectins act as hemagglutinins and bind to mucous membranes, where they impair nutrient absorption and inactivate rRNA-particularly within the crypt epithelium. Also, due to the inhibition of protein synthesis, they impair the immune system and put the animal at risk for secondary bacterial infection.
GEOGRAPHIC DISTRIBUTION
These trees are typically found in the woods of the eastern United States but are also used as landscape trees throughout the United States.
SIGNALMENT
Toxicity from the black locust is more prevalent in the summer and fall, when there is less forage available to grazing animals.
Any ruminant on pasture can be potentially exposed to this toxin.
SIGNS
Clinical signs can be acute or chronic and can consist of inappetance, bloody diarrhea, and salivation. Weakness and incoordination can be present due to posterior paralysis. There can be dyspnea, dehydration, laminitis, and recumbency. A weak pulse may be present due to systemic shock.
Death is infrequent.
CAUSES AND RISK FACTORS
The major risk factor is animals grazing on sparse pasture in the late summer and fall.
DIAGNOSIS DIFFERENTIALDIAGNOSIS
Vomitoxin from moldy concentrates or arsenic toxicity as well as other causes of gastroenteritis
CBC/BIOCHEMISTRY/URINALYS IS
There will be increased hepatic enzymes-AST, ALT, LDH, GOT, and GGT. There can be increased BUN and creatinine. Decreased serum total protein, specifically albumin, can be present. There can be hemoconcentration (increased PCV and TP) due to the dehydration.
OTHER LABORATORY TESTS
RBC agglutination, precipitin test
IMAGING
N/A
DIAGNOSTIC PROCEDURES
Presence of black locust seeds or plant materials in the forage or rumen contents upon necropsy is most diagnostic.
PATHOLOGIC FINDINGS GROSS FINDINGS
Postmortem lesions are generally restricted to the GI tract.
There can be fatty hepatic change and erosions of abomasal and intestinal epithelium.
There can be pulmonary hemorrhage, edema, and emphysema.
HISTOPATHOLOGICAL FINDINGS
You may find central lobular hepatic necrosis, lymphoid necrosis, and crypt cell epithelial necrosis.
Histopathological evidence of pulmonary hemorrhage, edema, and emphysema may be evident.
There may be necrosis of the renal convoluted tubules.
TREATMENT
Treatment consists of antiserum for ricinus toxicity, sedatives for convulsions, arecoline hydrobromide and saline cathartics.
MEDICATIONS
N/A
CONTRAINDICATIONS
Appropriate milk and meat withdrawal times must be followed for all compounds administered to food-producing animals.
FOLLOW-UP PATIENT MONITORING
The recovery period can be extensive.
PREVENTION/AVOIDANCE
Control black locust plants in pastures.
POSSIBLE COMPLICATIONS
Secondary bacterial infections due to impairment of the immune system.
EXPECTED COURSE AND PROGNOSIS
Prognosis is usually good once the forage is removed from the diet, but recovery can be prolonged.
MISCELLANEOUS ASSOCIATED CONDITIONS
Inappetance, bloody diarrhea, and salivation
Weakness and incoordination due to posterior paralysis
There can be dyspnea, dehydration, laminitis, and recumbency.
Death is infrequent.
AGE-RELATED FACTORS
N/A
ZOONOTIC POTENTIAL
N/A
PREGNANCY
N/A
RUMINANT SPECIES AFFECTED
Potentially, all ruminant species can be affected.
BIOSECURITY
N/A
PRODUCTION MANAGEMENT
Control black locust plants in pastures.
SYNONYMS SEE ALSO
Arsenic toxicity
Other causes of gastroenteritis Toxicology: herd outbreaks Vomitoxin ABBREVIATIONS
ALT = alanine transferase AST = aspartate transferase BUN = blood urea nitrogen
GGT = gamma-glutamyl transferase GOT = glutamyl oxaloacetic transaminase LDH = lactate dehydrogenase
PCV= packed cell volume RBC = red blood cell
TP = total protein
Suggested Reading
Aiello, S. E., ed. 1998. Merck veterinary manual. 8th ed. Whitehouse Station, NJ: Merck and Co.
Barri, M. E., El Dirdiri, N. I., Abu Danir, H., Idris, O. F. 1990, Dec. Toxicity of Abrus precatorius in Nubian Goats.
Veterinary and Human Toxicology 32(6): 541-45.
Van Damme, E. J., et al. 1995, Mar. The bark of Robinia pseudoacacia contains a complex mixture of lectins. Characterization of the proteins and the cDNA clones. American Society of Plant Physiologists, Plant Physiology. 107(3): 833-43.
Author: Heidi Coker

BLINDNESS
BASICS DEFINITION
Loss of vision in one or both eyes
PATHOPHYS IOLOGY
Can be due to the blocking of light from entering the eye correctly (cataracts), retinal disease, optic nerve lesions, or brain lesions
SYSTEMS AFFECTED
Ophthalmic, CNS
GENETICS

Congenital cataracts reported in cattle, sheep, rare in goats. Autosomal recessive in several breeds of cattle: Jersey, Hereford, Holstein-Friesian
Albinism/subalbinism primarily in cattle and sheep, optic disc with dominant form of incomplete albinism in Hereford cattle
Retinal degeneration of Toggenburg goats
INCIDENCE/PREVALENCE
N/A
GEOGRAPHIC DISTRIBUTION
Worldwide
SIGNALMENT
Species
Cattle, sheep, goats, camelids; potentially all ruminant species
Breed Predilections
Congenital cataracts have been reported in cattle, sheep, rare in goats.
Autosomal recessive in several breeds of cattle: Jersey, Hereford, Holstein-Friesian cattle
Albinism/subalbinism in cattle and sheep; dominant form of incomplete albinism in Hereford cattle
Retinal degeneration of Toggenburg goats
Mean Age and Range
N/A Predominant Sex N/A
SIGNS HISTORICALFINDINGS
Inability to see, bumping into objects, unwilling or hesitant to move, eyes wide open, startles easily or overreacts when touched or when bumps an object
Eyes may show an abnormal sheen due to degeneration of the retina. Determine if the disease is in a specific individual or multiple members of the herd/flock.
Young animals may lack a menace response yet not be blind; need to watch them navigate an obstacle course.
PHYSICALEXAMINATION FINDINGS CAUSES AND RISK FACTORS
Congenital cataracts can be associated with microphthalmia and retinal lesions from in utero exposure to BVD during days 76-150 of gestation, secondary to inflammation, toxins, and metabolic disease. In cattle can be secondary to IBK,

malignant catarrhal fever, IBR, or retinal dysplasia of cattle. In sheep, bluetongue is often associated with retinal detachment.

Chorioretinitis: in cattle, it can be associated with neonatal septicemia, TEME, rabies, toxoplasmosis, tuberculosis, and listeriosis. In sheep, this can be associated with mycoplasmosis, listeriosis, elaeophorosis, toxoplasmosis, bluetongue, and scrapie.
Retinal degenerations are more commonly acquired vitamin A deficiency in cattle.
Bracken fern (Pteris aquiline) toxicity and PEM are common in sheep.
DIAGNOSIS DIFFERENTIALDIAGNOSIS
Causes:
Toxins
There are many plant and fungal toxins, the most common are listed here.
Stypandra glauca (blind grass)-causes retinal degeneration and optic nerve neuropathy
Astragalus mollisimus (locoweed)-causes dry eye and retinal degeneration
Bracken fern (Pteris aquiline)-causes polioencephalomalacia and degeneration of outer retinal layers
Sweet clover-coumarin causing intraocular hemorrhaging
Lead toxicity
Sulfur-see edema and decreased pupillary light response.
Trauma to the brain
Neoplasia-in the occipital cortices, lateral geniculate bodies, or optic radiations
Systemic Disease
Meningitis/encephalitis-see pale swollen optic disc with hazy margins.
Bluetongue in sheep-causes retinal dysplasia
Listeriosis
Neonatal septicemia
Equine herpes type 1 virus in llamas-optic nerve and retinal degeneration
Mycoplasmas-in goats can cause corneal opacification
Diabetes mellitus in ram lambs can cause cataracts.
Parasitic
Elaeophorosis, toxoplasmosis, trypanosomiasis-cause inflammation of fundus; elaeophorosis can cause cataracts.
Echinococcus granulosis-hydatid cysts in the brain
Paraelaphostrongylus tenuis (meningeal worm) in llamas
Deficiencies
Thiamine
Vitamin A
Water deprivation
CNS hypoxia-postanesthesia or other prolonged hypoxia
Congenital/Degenerative
Retinal degeneration of Toggenburg goats
Hydrocephalus
Congenital malformations
Glaucoma
Cataracts
Wool blindness of sheep
CBC/BIOCHEMISTRY/URINALYS IS
Consistent with an underlying cause
Ram lambs with diabetes mellitus-induced cataracts will have elevated glucose.
OTHER LABORATORY TESTS
Practitioners use direct ophthalmoscopy more frequently than indirect ophthalmoscopy. It is important to view the tapetal fundus several inches from the patient and then move to 1-2 inches from the patient’s eye when the optimum focus is achieved and the animal has adapted to the restraint. The diopter setting is usually started at “0” and adjusted to between +3 to -3 diopters to provide the sharpest image possible.
Indirect ophthalmoscopy complements direct ophthalmoscopy.
IMAGING
Ultrasound evaluation of the corneal surfaces, the anterior and posterior lens surfaces, the retina, and any abnormal intraocular material will aid intraocular diagnosis. This is especially useful when dense corneal opacity or mature cataract obscures the view of the fundus.
OTHER DIAGNOSTIC PROCEDURES
Examination of the cornea is incomplete without utilization of topical ophthalmic stains.
Fluorescein is used to demonstrate the presence or absence of corneal ulcers. For topical use, fluorescein-impregnated paper strips are preferred to fluorescein solution to insure sterility.
PATHOLOGIC FINDINGS
TREATMENT
Ensure nutrition and management are adequate, remove from toxin sources.
Remove objects that can cause ocular trauma.
Affected animals will need to be hand-fed and watered separately due to inability to compete with the rest of the herd.
CLIENT EDUCATION
MEDICATIONS DRUGS OF CHOICE
Pharmaceutical choice depends on the specific etiology.
Trauma-corticosteroids and IV DMSO may help decrease swelling.
Polioencephalomalacia-thiamine HCl 6-10 mg/kg IM or IV, antibiotics
CONTRAINDICATIONS
Appropriate milk and meat withdrawal times must be followed for all compounds administered to food-producing animals.
Topical corticosteroids and anesthetics are contraindicated when the cornea retains fluorescein stain.
PRECAUTIONS
N/A
POSSIBLE INTERACTIONS
N/A
ALTERNATIVE DRUGS
FOLLOW-UP PATIENT MONITORING
With optic nerve lesions, on initial exam the fundus may appear normal. It can take 4 weeks for the optic disc to become pale
and the retinal vessels to start regression. PREVENTION/AVOIDANCE POSSIBLE COMPLICATIONS
Permanent vision loss
EXPECTED COURSE AND PROGNOSIS
Prognosis for the return of sight is very guarded, but depends on the degree of damage and the etiology.
MISCELLANEOUS ASSOCIATED CONDITIONS
Note: animals with a disease causing mental dullness or vestibular signs may appear blind.
AGE-RELATED FACTORS
Young animals may lack a menace response yet not be blind; need to evaluate them while navigating an obstacle course.
Diabetes mellitus will induce cataracts in ram lambs
ZOONOTIC POTENTIAL
N/A
PREGNANCY
Many diseases that cause blindness may also induce abortion.
RUMINANT SPECIES AFFECTED
Potentially, all ruminant species are affected.
BIOSECURITY
Quarantine new animals, isolate affected animals.
PRODUCTION MANAGEMENT
Ensure nutrition and management are adequate; remove from toxin sources.
Remove objects that can cause ocular trauma.
Fence off toxic plants to prevent grazing.
Minimize the incidence of nutritional PEM.
SYNONYMS
Bright blind Glass eyed Moon blind SEE ALSO
Corneal ulceration Ectropion Entropion Enucleation FARAD
Keratoconjunctivitis Microphthalmia Ocular surgery ABBREVIATIONS
BVD = bovine viral diarrhea CNS = central nervous system DMSO = dimethyl sulfoxide
FARAD = Food Animal Residue Avoidance Databank IBK = infectious bovine keratoconjunctivitis
IBR = infectious bovine rhinotracheitis
IM = intramuscular IV = intravenous
PEM = polioencephalomalacia
TEME = thromboembolic meningoencephalitis
Suggested Reading
Gelatt, K. N. 2000. Essentials of veterinary ophthalmology. Baltimore: Lipincott, Williams and Wilkins.
Hirono, I., Ito, M., Yagyu, S., Haga, M., Wakamatsu, K., Kishikawa, T., Nishikawa, O., Yamada, K., Ojika, M., Kigoshi, H. 1993, Dec. Reproduction of progressive retinal degeneration (bright blindness) in sheep by administration of ptaquiloside contained in bracken. J Vet Med Sci. 55(6):979-83.
Moore, C. P. 1996. Signs of ocular disease. In: Large animal internal medicine, ed. B. P. Smith. 2nd ed. St. Louis: Mosby.
Niles, G. A., Morgan, S. E., Edwards, W. C. 2000, Oct. Sulfur-induced polioencephalomalacia in stocker calves. Vet Hum Toxicol. 42(5):290-91.
O’Toole, D., Raisbeck, M., Case, J. C., Whitson, T. D. 1996, Jan. Selenium-induced “blind staggers” and related myths. A commentary on the extent of historical livestock losses attributed to selenosis on western US rangelands. Vet Pathol. 33(1):109-16.
Whitley, R. D., Moore, C. P. 1984, Nov. Ocular diagnostic and therapeutic techniques in food animals. Vet Clin North Am Large Anim Pract. 6(3):553-75.
Author: Melissa N. Carr

BLOAT
BASICS DEFINITION
Gas distension of the rumen and reticulum. Primary, or frothy, bloat occurs when rumen gas is trapped in bubbles/froth, and cannot be eructated. Secondary, or free gas, bloat occurs because of physical blockage of the esophagus or from decreased vagal nerve function.
PATHOPHYS IOLOGY

Normal rumen bacterial fermentation produces gases that are eructated from the rumen.
Primary, or frothy, bloat occurs when the gas is trapped in bubbles/froth, and cannot be eructated. Immature legumes and clovers are rapidly fermented by rumen microflora, resulting in release of chloroplast particles that trap gas bubbles and prevent their coalescence.
Additionally, liquid is trapped in the foam, reducing the passage of liquid from the rumen. This serves to enhance bacterial growth and increase gas and foam production. Feeding finely ground grains can also cause frothy bloat.
Secondary, or free gas, bloat occurs because of physical blockage of the esophagus or from decreased vagal nerve function. Expansion of the rumen within the abdominal cavity eventually compresses the diaphragm decreasing lung volume and oxygenation and the venous return to the post cava causing hypovolemia.
Young calves can bloat from fermentation of milk or milk replacer in the rumen.
SYSTEMS AFFECTED
Gastrointestinal, cardiovascular
GENETICS
N/A
INCIDENCE/PREVALENCE
Normally very low incidence, generally less than 1%
Incidence of primary bloat may be over 25% if animals are grazed on immature legumes/clover or fed excessive amounts of highly fermentable carbohydrates, such as finely ground grains.
GEOGRAPHIC DISTRIBUTION
Worldwide
Epidemiology
Primary bloat is associated with grazing or feeding immature legumes/clover. Finely ground grain diets are also associated with frothy bloat.
Secondary bloat is associated with feeds that can block the esophagus such as potatoes/beets and with masses that either block the esophagus or interfere with the vagus nerve in the mediastinum.
Examples are tumors from lymphoma, enlarged lymph nodes from tuberculosis, and chronic bacterial pneumonia.
SIGNALMENT
Species Affected Ruminants, especially cattle Breed Predilections
N/A
Mean Age and Range
N/A Predominant Sex N/A
SIGNS
Distension of the left flank from gas accumulation, tachycardia from hypoxia. Rumen contractions may decrease but often remain normal. Abdominal discomfort is evident.
Severe cases may show open mouth breathing and staggering. Animal may become recumbent from hypoxia.
GENERALCOMMENTS
Bloat should be considered a medical emergency due to potential death from hypoxia and hypovolemia.
HISTORICALFINDINGS
Sheep and cattle grazing on lush pastures, especially young legumes or clovers; high-concentrate diets with finely ground grains; history of chronic pneumonia
PHYSICALEXAMINATION FINDINGS
Distension of the dorsal left flank. Cattle with chronic vagal indigestion may have concurrent distension of ventral right flank due to rumen emptying defect (“papple-shape”).
Tachycardia often present
CAUSES
Ingestion of immature legumes and clovers or finely ground grains
Blockage of the esophagus or interference with the vagus nerve
RISK FACTORS
Grazing or feeding early legumes or clovers; feeding finely ground grains or rapidly fermented carbohydrates
Factors associated with the spread of tuberculosis or bovine leukemia virus; chronic bacterial pneumonia
DIAGNOSIS DIFFERENTIALDIAGNOSIS
Ruminants often bloat postmortem. Necropsy signs of antemortem bloat include compression of blood and lymph flow in the neck and thorax, resulting in enlarged cervical vessels and lymph nodes. There is often a visible “white line” demarcation in the esophagus near the thoracic inlet from compression of the distal esophagus and congestion in the proximal esophagus.
Lymphoma, enlarged lymph nodes from tuberculosis, and chronic bacterial pneumonia
CBC/BIOCHEMISTRY/URINALYS IS
N/A
OTHER LABORATORY TESTS
N/A
IMAGING
N/A
OTHER DIAGNOSTIC PROCEDURES
Passing a stomach tube differentiates primary (frothy) from secondary (free gas) bloat. Esophageal blockages may often be detected while passing the stomach tube.
GROSS AND HISTOPATHOLOGIC FINDINGS
Distension of the rumen and reticulum with gas; congestion of cervical lymph nodes and vessels; “white line” demarcation in esophagus at interface of compressed and congested tissue
TREATMENT
Depends on the cause and degree of hypoxia. Severely hypoxic animals should be intubated to relieve the free gas. The tube often plugs with froth or dips below the fluid level in the rumen, requiring clearing the tube by blowing into it or moving the end within the rumen.
It may be necessary to place a rumen trocar in the dorsal left flank. Mild to moderate cases of frothy bloat often respond to surfactants such as poloxalene (25-50 g per animal).
Inpatient Versus Outpatient
N/A
CLIENT EDUCATION
Advise clients about the danger of grazing or feeding immature legumes/clovers especially to hungry animals.
Discuss the importance of a functional rumen mat in cattle on high-concentrate diets.
Discuss early recognition of bloat and treatments such as poloxalene and stomach tubing.
MEDICATIONS DRUGS OF CHOICE
Poloxalene (25-50 g per animal) for primary bloat
CONTRAINDICATIONS
N/A
PRECAUTIONS
N/A
POSSIBLE INTERACTIONS
N/A
ALTERNATE DRUGS
Mineral oil or vegetable oils may act as antifoaming agents.
FOLLOW-UP PATIENT MONITORING
Watch for recurrence.
PREVENTION/AVOIDANCE
Avoid feeding or grazing risk plants such as legumes or clovers. Do not overfeed finely ground grain or other highly fermentable carbohydrates.
Prevent infections with bovine leukemia virus and tuberculosis.
POSSIBLE COMPLICATIONS
Physical damage to the vagus nerve or branches of the vagus from excessive rumen distension may result in rumen dysfunction and possibly recurrence.
Trocarization may result in localized or diffuse peritonitis.
EXPECTED COURSE AND PROGNOSIS
Spontaneous recovery in mild cases and those patients sufficiently relieved by stomach tube/trocar or treated with poloxalene
Death from hypoxia in severe cases
MISCELLANEOUS PREVENTION
N/A
ASSOCIATED CONDITIONS
Lymphoma, vagal indigestion, tuberculosis
AGE-RELATED FACTORS
Young calves may bloat from fermentation of milk or milk replacer in the rumen.
ZOONOTIC POTENTIAL
N/A
PREGNANCY
N/A
SYNONYMS
Bloat, ruminal tympany
SEE ALSO
Chronic bacterial pneumonia
Enlarged lymph nodes from tuberculosis Lymphoma Vagal indigestion ABBREVIATIONS
N/A
Suggested Reading
Majak, W., Hall, J. W., McCaughey, W. P. 1995. Pasture management strategies for reducing the risk of legume bloat in cattle. Journal of Animal Science 73:1493-98.
Radostits, O. M., Gay, C. C., Blood, D. C., Hinchcliff, K. W., eds. 2000. Veterinary medicine: a textbook of diseases of cattle, sheep, pigs, goats and horses. 9th ed. London: W. B. Saunders.
Author: James P. Reynolds

BLUE-GREEN ALGAE POISONING
BASICS OVERVIEW

Over 50 genera of freshwater blue-green algae (also referred to as cyanophytes or cyanobacteria) exist worldwide that produce two major types of toxins: neurotoxic alkaloids, such as anatoxins, and hepatotoxic peptides, such as microcystins.
Very few cases of anatoxin poisoning (often produced by Anabaena flos-aquae) have been reported in cattle with clinical signs resembling organophosphorus insecticide poisoning (depolarizing neuromuscular blocking agent), such as muscle weakness and paralysis.
Microcystin toxicosis is much more common than anatoxin poisoning and numerous cases have been reported in cattle and sheep worldwide. Therefore, microcystin toxicosis is discussed in detail.
Microcystins are primarily produced by Microcystis aeruginosa, but many other cyanobacteria produce these peptides such as other Microcystis spp., Anabaena spp., Oscillatoria spp., and Nostoc spp.
Microcystins are usually confined within the algal cells and are released only when cells are damaged (e.g., when cells encounter the acidic environment of the stomach).
Microcystins enter the hepatocytes through a carrier-mediated transport system and cause inhibition of protein phosphatase (1 and 2A) in the hepatocytes. Dissociation and necrosis of hepatocytes lead to intrahepatic hemorrhage and diffuse centrilobular hepatocellular degeneration.
Sudden death is possible as a result of hemorrhagic shock.
Death in animals usually occurs within hours to days postexposure.
Animals that survive the acute phase of poisoning can recover, but may develop clinical signs related to liver disease (e.g., hepatogenous photosensitization; drop in production).
Respiratory-pulmonary edema and congestion have been reported in acute cases.
GENETICS
N/A
INCIDENCE/PREVALENCE
Blue-green algae poisoning occurs seasonally during warm weather conditions. The blooms are most common in the summer and fall when bodies of water are stagnant and warm and contain ample nutrients.
A breeze blowing across the water may help concentrate the organisms near a shore.
GEOGRAPHIC DISTRIBUTION
Worldwide
Epidemiology
Not all animals in a herd may be affected. Several important factors are related to occurrence of poisoning. Favorable algae growth conditions are usually required to produce sufficiently high concentrations of algae in water. Nutrient pollution of lakes and ponds with phosphorus and nitrogen leads to eutrophication and accelerated algae growth.
Long periods of sustained sunshine, which produce warm water temperatures, are usually necessary. A breeze blowing across the water has also been identified as critical in some situations for concentrating algae near a shore where cattle congregate on the leeward side during hot weather.
Microcystins are the most prevalent hepatotoxins and are produced by several cyanobacteria genera including Microcystis, Planktothrix, Anabaena, and Oscillatoria. Anatoxins are produced mainly by Anabaena spp. in addition to Aphanizomenon, Microcystis, and Oscillatoria spp. Saxitoxin production is associated with a few specific freshwater cyanobacteria species found in the genera of Anabaena, Aphanizomenon, Cylindrospermopsis, Lyngbya, and Planktothrix.
SIGNALMENT
All ruminant species are susceptible to blue-green algae toxins. Microcystin poisoning has been reported in cattle and sheep.
Dead animals are often found close to water bodies that have a “painted green” or “scumlike” bloom.
SIGNS
Animals exposed to blue-green algae toxins are often found dead near water that has a thick algal bloom. Cattle may have algae on their limbs.
Abrupt onset of apprehension and distress occurs within hours of microcystin exposure.
This is quickly followed by pale mucous membranes, ruminal atony, diarrhea, weakness, nervousness, ataxia, and anorexia. In severe cases, the animals become recumbent and comatose.
Death may occur within 24 hours of exposure, but may be delayed several days.
Animals that survive the initial toxicosis may develop hepatogenous photosensitization.
CAUSES AND RISK FACTORS
Exposure to water contaminated with toxin-producing cyanobacteria
Warm, dry weather and stagnant water and a breeze that blows across water, allowing the organisms to concentrate near a shore
High concentrations of nutrients in the water, such as nitrates and phosphates from sewage, detergents, industrial pollution, and fertilizers increase the risk for a blue-green algae bloom.
DIAGNOSIS DIFFERENTIALDIAGNOSIS
Other hepatotoxicants-metals (detection in liver and kidney, histopathological lesions), aflatoxins (detection in feed, often chronic), pyrrolizidine alkaloids (evidence of plant consumption, histopathologic lesions, chronic disease)
Hepatopathy-serum clinical chemistry and liver biopsy
Nitrate toxicosis-chocolate-colored blood, exposure to nitrate-accumulating plants
Cyanide poisoning-mucous membranes are initially bright cherry red, evidence of exposure to cyanogenic plants, chemical analysis for cyanide in gastrointestinal contents, liver, or muscle
Larkspur poisoning-mainly found in the western states; bloat is a common finding, evidence of exposure to Delphinium
spp.
Grass tetany-hypomagnesemia
Electrocution or lightning strike
Organophosphorus or carbamate insecticide exposure-commonly associated with gastrointestinal irritation and neurological signs, evaluation of cholinesterase activity, detection of pesticides in gastrointestinal contents
Lead poisoning-determination of blood lead concentration
Exposure to neurotoxic plants, such as poison hemlock, water hemlock, tree tobacco, lupine-chemical analysis for plant toxins in gastrointestinal contents, history of presence of plants in the environment
Exposure to cardiotoxic plants, such as oleander, milkweed, and azalea-chemical analysis for plant toxins in gastrointestinal contents, history of presence of plants in the environment
CBC/BIOCHEMISTRY/URINALYS IS
Increased GGT, AST, SDH, and GLDH
OTHER LABORATORY TESTS
Direct microscopic examination of water and gastrointestinal contents
Mouse bioassay
Detection of microcystins in water or rumen contents by high-performance liquid chromatography/mass spectrometry
Analysis of suspect water by direct competitive ELISA
IMAGING
N/A
DIAGNOSTIC PROCEDURES
N/A
PATHOLOGIC FINDINGS
Postmortem lesions in animals that died of exposure to microcystins include hepatomegaly, congested and hemorrhagic liver.
Histopathologically, microcystin toxicosis results in centrilobular hepatocellular degeneration and necrosis; dilatation and engorgement of sinusoids; and loss of hepatic cords.
Postmortem lesions are generally nonspecific in animals that died of exposure to neurotoxic blue-green algae toxins (e.g., anatoxins).
TREATMENT
Treatment of animals exposed to blue-green algae toxins is primarily supportive and symptomatic. Supportive therapy should include administration of intravenous fluids, corticosteroids, and calcium.
Poisoned animals should be removed immediately from the source.
Adsorption of toxins with activated charcoal has been suggested.
Rumenotomy or a rumen lavage may be considered in valuable animals.
CLIENT EDUCATION
Create awareness for potential of blue-green algae toxicity, especially during sunny, warm weather and other favorable environmental conditions.
A heavy water bloom of algae producing a surface scum is usually necessary for poisonings to occur.
MEDICATIONS DRUGS OF CHOICE
No antidote is available.
Activated charcoal, mineral oil, or saline cathartics
Corticosteroids
Vitamin E and selenium supplementation
CONTRAINDICATIONS
N/A
POSSIBLE INTERACTIONS
N/A
ALTERNATIVE DRUGS
Hepatic uptake blockers, such as rifampicin and cyclosporin A, may be helpful, but their usefulness in the treatment of cardiac glycoside-poisoned ruminants has not been evaluated.
FOLLOW-UP PATIENT MONITORING
Monitoring of liver enzymes is helpful.
Monitor serum electrolytes.
PREVENTION/AVOIDANCE
Keep animals away from water bodies with visible algal blooms.
Precipitation of algal cells:
Lime (100-250 mg/l) to precipitate cells without rupturing them
Suspend ferric alum block (1 kg/10,000 L)
Suspend gypsum block (50 kg/1000 L)
Algaecide (lysis of algal cells): copper sulfate at 20-40 g/50,000 L (target concentration: 0.2-0.4 ppm). After treatment with copper sulfate, animals must be removed from the water source for approximately 7 days.
Use of straw bales (100 g/1000 L) to control algal blooms has also been reported. Barley straw seems to be more effective when compared to wheat or other straws.
POSSIBLE COMPLICATIONS
Hepatogenous photosensitization
EXPECTED COURSE AND PROGNOSIS
Animals poisoned with microcystins are often found dead.
Microcystin poisoning progresses rapidly, and treatment is often too late. If animals exhibit clinical signs of liver failure, the prognosis is poor.
Animals that survive 24 to 72 hours after exposure usually survive but may develop clinical signs associated with hepatic failure.
MISCELLANEOUS ASSOCIATED CONDITIONS
Hepatopathy
AGE-RELATED FACTORS
N/A
ZOONOTIC POTENTIAL
N/A
PREGNANCY
N/A
BIOSECURITY
N/A
PRODUCTION MANAGEMENT
N/A
SYNONYMS
N/A
SEE ALSO
Aflatoxins and pyrrolizidine alkaloids
Cardiotoxic plants (i.e., oleander, milkweed, azalea)
Cyanide poisoning
Grass tetany-hypomagnesemia
Larkspur poisoning
Lead poisoning
Neurotoxic plants (i.e., poison hemlock, water hemlock, tree tobacco, lupine)
Nitrate toxicosis
Organophosphorus or carbamate insecticide exposure
ABBREVIATIONS
AST = aspartate aminotransferase
ELISA = enzyme linked immunosorbent assay
GGT = gamma-glutamyl transferase
GLDH = glutamate dehydrogenase
SDH = sorbitol dehydrogenase

Suggested Reading
Dawson, R. M. 1998. The toxicology of microcystins. Toxicon. 36:953-62.
Puschner, B., Galey, F. D., Johnson, B., et al. 1998. Blue-green algae toxicosis in cattle. J Am Vet Med Assoc. 213:1605- 7.
Roder, J. D. 2004. Blue-green algae. In: Clinical veterinary toxicology, ed. K. H. Plumlee. St. Louis: Mosby.
Authors: Asheesh Tiwary, Birgit Puschner, Terry W. Lehenbauer

BLUETONGUE
BASICS OVERVIEW
Bluetongue (BT) is an arthropod-borne, noncontagious viral infection of ruminants caused by BT virus (BTV), of the genus O rbivirus within the Reoviridae family.

Transmission of BTV among susceptible hosts occurs through the bite of certain species of infected Culicoides or biting midges.
The main vector of BTV in North America is Culicoides sonorensis (C. sonorensis; previously known as C. varipennis); in Australia, C. brevitarsis; and in Africa, Asia, and Europe, C. imicola.
In the absence of a competent vector, transmission of BTV to cattle occurs occasionally by insemination with infected semen and transplacentally.
Due to its potential for rapid spread across borders, and its capability to produce serious economic losses, the Office International des Epizooties (OIE) includes BT in their A list of diseases.
PATHOPHYS IOLOGY
Bluetongue virus infection presents initially with dyspnea and increased respirations followed by fever, hyperemia of the ears, lips, and muzzle, and ulceration of the oral mucosa. The tongue can become cyanotic and swollen, hence the disease name, bluetongue. Lameness and widespread muscle necrosis are additional sequellae.
SYSTEMS AFFECTED
Cardiovascular-vascular injury leading to hemorrhages, congestion, heart failure.
Musculoskeletal-intramuscular edema, hemorrhages, coronitis.
Reproductive-infection during pregnancy can cause fetal loss or malformations.
Gastrointestinal-vascular damage causes ulcerations and hemorrhages in the oral cavity, fore stomachs, and intestine.
Respiratory-vascular damage leads to congestion and edema.
GENETICS
N/A
INCIDENCE/PREVALENCE
N/A
GEOGRAPHIC DISTRIBUTION
Twenty-four BTV serotypes (BTV-1 to -24) have been found worldwide. Four of them are endemic in the United States (BTV-10, BTV-11, BTV-13, BTV-17). BTV-2, although not prevalent in the United States, has been isolated sporadically in the past.
BTV infection occurs in tropical and temperate regions of Africa, Asia, Australia, and the Americas. Periodic incursions of the infection also occur in southern Europe.
The distribution of BTV is limited by the distribution of the vector. BTV is considered to be present between approximate latitudes 35°S and 40°N. In some regions the presence of BTV may extend to 50°N. BTV transmission occurs only when weather conditions are favorable and adult vectors are active.
In the United States, BTV infection is more prevalent in the southern and western parts of the country, and most infections occur in late summer and fall. Variations in weather patterns may affect the distribution of the vector and BTV transmission.
SIGNALMENT
BTV infects a wide range of domestic and wild ruminants. Severe disease occurs almost exclusively in sheep and some species of deer, most notably the white-tailed deer of North America. Cattle commonly have inapparent infections.
Mortality rates and severity of disease in sheep may vary, with fine-wool breeds and older sheep considered to be more susceptible.
SIGNS
BTV infection can cause inapparent infection or acute fulminant disease.
Clinical disease is largely restricted to sheep and white-tailed deer; in cattle and goats, infection is usually asymptomatic. Infected bulls may shed BTV in their semen.
The incubation period ranges from 2-15 days.
The acute fulminant form is characterized by fever of up to 107.6°F (42°C), leukopenia, anorexia, weight loss, depression, with edema and swelling of the face, lips, muzzle, and ears, reddening of the oral mucosa, and salivation.
Crusting and accumulation of mucopurulent discharge in the muzzle and nostrils are common. In a small percentage of cases, the tongue appears edematous and purplish-blue (hence the name of the disease) as a result of cyanosis.
Hemorrhages, erosions, and ulcers in gums, cheeks, tongue, and nostrils are often present.
Lameness, stiffness, and prostration may develop as a result of muscle degeneration and laminitis. Laminitis may manifest as swelling, hyperemia, and hemorrhage of the hoof laminae and coronary band. Lameness may progress to “knee walking” or recumbency.
Death due to bronchopneumonia or secondary bacterial infections may occur 8 to 10 days after the initial signs appear. Some severely affected sheep may recover.
BTV infection of pregnant sheep or cattle may result in abortion, stillbirths, fetal malformation, or the birth of live but weak offspring (dummy lambs/calves). These negative effects have been linked to the use of modified-live vaccines (MLV) rather than to natural infection with wild-type BTV. Ovine fetuses are more susceptible to the teratogenic effects when infection occurs during the fifth and sixth weeks of gestation.
Pregnant sheep may abort during the acute phase of BT disease in the absence of fetal infection as a result of maternal stress.
CAUSES AND RISK FACTORS
Ruminants living in areas where the vector, Culicoides, and bluetongue virus coexist
DIAGNOSIS DIFFERENTIALDIAGNOSIS
Differential diagnosis includes other ulcerative diseases of the respiratory and digestive tracts of ruminants such as foot- and-mouth disease, orf, sheep pox, peste des petits ruminants, photosensitization, and diseases that cause stiffness and lameness including polyarthritis, and foot rot.
In white-tailed deer, BT needs to be differentiated from epizootic hemorrhagic disease (EHD).
The differential diagnosis of BTV fetal infection, malformations, and abortions includes infection with Cache Valley, Akabane, border disease, Rift Valley fever, Nairobi sheep disease, Wesselsbron disease, genetic defects, and ingestion of teratogenic plants.
CBC/BIOCHEMISTRY/URINALYS IS
N/A
DIAGNOSTIC PROCEDURES
Serological assays available for the demonstration of BTV antibodies include complement fixation, virus neutralization, the agar gel immunodiffusion (AGID) test, and several ELISA formats.
Only the AGID and competitive ELISA (cELISA) are recommended by the OIE as prescribed tests for international movement of ruminants.
Virus isolation can be done by inoculation of susceptible sheep or embryonated chicken eggs with heparinized blood or homogenized lymph nodes, spleen, or lung of infected animals. Subsequent adaptation to cell culture and serotyping of the virus may be necessary. Blood and tissue samples for diagnosis need to be preserved at 4°C, and not frozen.
BTV can be isolated from blood of infected sheep and cattle for up to 11 and 49 days postinfection, respectively. BTV nucleic acids can be detected by reverse transcription-polymerase chain reaction (RT-PCR) for up to 222 days postinfection. However, blood from sheep and cattle is infectious for C. sonorensis for only 21 days after infection of the ruminant host.
Sheep and cattle whose blood contains BTV nucleic acid as detected by RT-PCR, but not infectious virus as determined by virus isolation, are unlikely to play an important role in the epidemiology of BTV infection.
BTV antibodies can be demonstrated in precolostral serum samples of lambs infected in utero. BTV virus also can be isolated in some of these lambs due to immune tolerance and persistent infection.
PATHOLOGIC FINDINGS GROSS FINDINGS
BTV infection in sheep and white-tailed deer may result in extensive vascular injury that leads to congestion, edema, hemorrhage, disseminated intravascular coagulation, and tissue necrosis.
The vascular damage results in ulcerations and hemorrhage of the tongue, oral mucosa, hard palate, dental pad, and sometimes fore stomachs and intestine.
The lips, gums, and tongue may be edematous, congested, or cyanotic.
There is subcutaneous and intramuscular edema and hemorrhages.
The superficial lymph nodes may be enlarged and edematous.
The most consistent lesion in sheep is hemorrhages in the tunica media at the base of the pulmonary artery. Hemorrhages are also present in the aorta, epicardium, endocardium, and myocardium.
Pale areas as a result of necrosis may be found in skeletal and cardiac muscles.
Pulmonary congestion and edema as a result of heart failure, and pneumonia due to secondary bacterial infections, may be present.
Fetal lesions consist of hydranencephaly, poroencephaly, and arthrogryposis.
HISTOPATHOLOGIC FINDINGS
The characteristic lesion consists of microvascular thrombosis resulting in congestion, edema, hemorrhage, and tissue necrosis.
TREATMENT
There are no specific treatments for BT.
NURSING CARE/ACTIVITY/DIET
Secondary infections may be treated with broad-spectrum antibiotics. Anti-inflammatory and pain relief medications can be used to limit the symptoms. Affected animals should be placed in shaded pens protected from the environment and provided with clean water and good-quality hay or feed.
MEDICATIONS DRUGS OF CHOICE
N/A
CONTRAINDICATIONS
N/A
POSSIBLE INTERACTIONS
N/A
ALTERNATIVE DRUGS
N/A
FOLLOW-UP PATIENT MONITORING
N/A
PREVENTION/AVOIDANCE
Modified live virus vaccines are available in some parts of the world.
In the United States, MLV containing serotype 10 is available. In addition, MLV vaccines containing serotypes 10, 11, or 17 can be obtained for use only in California. Lambs can be vaccinated close to weaning and the breeding stock at least 3 weeks before breeding or after lambing. Pregnant animals should not be vaccinated because of the potential teratogenic effects.
To induce protection, the BTV serotype of the vaccine must correspond to the serotype of the virus in the region.
Limiting vector exposure by housing sheep during peak feeding times (from dusk to dawn) may reduce the risk of exposure, but vectors may be active during daytime when overcast.
Reduction of the vector population through the use of insecticides or by making vector habitat unsuitable can aid in BT control.
Many countries impose restrictions to the movement of livestock and germ plasm from infected areas.
MISCELLANEOUS AGE-RELATED FACTORS
N/A
ZOONOTIC POTENTIAL
There is no evidence to indicate that BTV is infectious to humans.
PREGNANCY
Modified live BTV vaccines may cause pregnancy loss and teratogenesis.
RUMINANT SPECIES AFFECTED
Sheep, cattle, white-tailed deer BIOSECURITY/PRODUCTION MANAGEMENT:
N/A
SYNONYMS
Muzzle disease
Pseudo foot-and-mouth disease Sore muzzle
SEE ALSO
Epizootic hemorrhagic disease
ABBREVIATIONS
BT = bluetongue
BTV = bluetongue virus
EHD = epizootic hemorrhagic disease
ELISA = enzyme-linked immunosorbent assay MLV = modified live vaccine
OIE = Office International des Epizooties
RT-PCR = reverse transcription-polymerase chain reaction
Suggested Reading
Aradaib, I. E., Smith, W. L., Osburn, B. I., Cullor, J. S. 2003. A multiplex PCR for simultaneous detection and differentiation of North American serotypes of bluetongue and epizootic hemorrhagic disease viruses. Comp Immunol Microbiol Infect Dis. 26:77-87.
Bonneau, K. R., DeMaula, C. D., Mullens, B. A., MacLachlan, N. J. 2002. Duration of viremia infectious to Culicoides sonorensis in bluetongue virus-infected cattle and sheep. Vet Microbiol. 88: 115-25.
Breard, E., Hamblin, C., Hammoumi, S., Sailleau, C., Dauphin, G., Zientara, S. 2004, Aug. The epidemiology and

diagnosis of bluetongue with particular reference to Corsica. Res Vet Sci. 77(1):1-8.
Clavijo, A., Heckert, R. A., Dulac, G. C., Afshar, A. 2000. Isolation and identification of bluetongue virus. J Virol Methd. 87:13-23.
MacLachlan, N. J., Conley, A. J., Kennedy, P. C. 2000. Bluetongue and equine arteritis viruses as models of virus- induced fetal injury and abortion. Anim Reprod Sci. 60-61:643-51.
Mellor, P. S., Wittmann, E. J. 2002. Bluetongue virus in the Mediterranean basin, 1998-2001. Vet J. 164:20-37.
Author: Andrés de la Concha-Bermejillo

BODY CONDITION SCORE: CAMELIDS AND CAMELS
BASICS DEFINITION
Body condition score is a subjective technique of categorizing animals based on the amount of adipose tissue stores.
SYSTEMS AFFECTED

Musculoskeletal
Nutritional
Production management
GENETICS
N/A
INCIDENCE/PREVALENCE
N/A
GEOGRAPHIC DISTRIBUTION
Worldwide
SIGNALMENT
Species
Camelids and Camels Breed Predilections N/A
Mean Age and Range
N/A Predominant Sex N/A
SIGNS HISTORICALFINDINGS
PHYSICALEXAMINATION FINDINGS
Body Areas to Be Assessed
Dorsal aspect of the thorax, just caudal to the withers
Fiberless area behind the elbows
Region between the hind legs
Brisket area
NOTE: Palpation of the pelvis is less than ideal due to the inherent thin skin, light muscling, and minimal fat cover in this area.
BODY CONDITION SCORES: GENERALCONSIDERATIONS AND CAUTION
Camelids have a great variability of body type and conformation even within the same species. Therefore weight alone is not a good indicator of body condition.
Body condition scoring (BCS) does not replace actual weighing. Both should be considered if possible.
A single score is usually not helpful. It is the variation of the BCS that needs to be stressed.
Fiber coat may be misleading. Animals require direct palpation.
Accumulations of adipose tissue characteristics are essential in assessing BCS. Evaluating adipose cover over the rib cage and the axilla region is important to the overall scoring process. It should be understood that body condition scoring is a subjective measure of a herd nutrition and care program.
Pelvic area is always bony.
Neck is not a good indicator of body condition score.
Characteristic regions of fat deposition in camelids: Shoulders; briskets; cranial ribs; inner thighs; perineum; camel: hump (or humps).
Body condition scoring is a good management tool to evaluate if the nutritional demands required by specific physiologic situations (particularly lactation and late pregnancy) are being met.
In addition, body condition scores allow monitoring animals through a change in feed or feeding systems.
In range animals’ changes in body conditions, scores are important in the evaluation of the nutritive value of pastures.
BCS Technique
BCS should be assessed at least four times and ideally six times a year.
Best times for assessment of body condition scores for the herd in general are
Before winter
In the middle of winter
In spring
In summer
In fall
Best times for assessment of body conditions scores for breeding females are
Early pregnancy
Midpregnancy
At parturition
Six weeks after parturition (corresponds in general with the early pregnancy in rebred females)
At weaning (corresponds in general to midpregnancy in rebred females) Technique for evaluation
General appreciation from a distance for camels and camelids and if animals are sheared (llamoids).
Depending on the body area, palpation evaluates fat deposit or both muscle mass and fat deposit.
Palpate over the lumbar (loin) areas to feel the spinous and transverse processes and evaluate presence or absence of depression and its depth or roundness. Evaluating the angle from between the thumb on one side of the spinous process and the other fingers on the other side.
Inspect and palpate the paralumbar fossa and evaluate the depth of the shelf created by the transverse process of the lumbar vertebrae.
Palpate over the ribs to feel the fat cover in that region.
Raise the tail and inspect the perineal area and the inguinal area for shape (curvature and fat deposition).
Palpate the brisket for roundness and shape.
Palpate the shoulders for fat deposit.
In camels, inspect the size and shape of the hump.
Body Condition Scores
Scores are given from 1 (emaciated animals) to 5 or 9 (obese animals) depending on preference.
Generally, people using the 5-point system use intermediate scores in increments of 0.25 to 0.5.
The ideal BCS
Males: 3 to 3.25 before the breeding season. Males will lose 0.5 to 1.0 points during the breeding season. Camels in free mating systems may lose up to 2 points during rutting season.
Females: 2.5 to 3.25 for open or lactating females; 3.25 to 3.5 in the last trimester of pregnancy. Lactating females should not loose more than 0.5 to 0.75 points.
Score 1: Emaciated Animal Extreme loss of muscle mass Thin face
Deep depression over the lumbar area
Gaunt, visible, tucked-in paralumbar fossa No perineal fat, sharp visible ischial tuberii Inverted “V” inner thighs shape
Narrow prominent V-shaped brisket
Ribs easily identified, depressed intercostals area Camels: flat back or flopped-over hump
Score 2: Thin
Muscle mass is minimal.
Lumbar area depression slightly filled in but easily palpable Lumbar fossa prominent
Some fat deposition in the perineal area Gradual filling of the inner thighs
Gradual filling on the brisket and loss of sharp edges of the sternum Camels: moderate hump
Score 3: Moderate
Normal muscle mass and smooth appearance
Lumbar area depression palpable with slight pressure Lumbar fossa not evident
Perineum filled in Inner thighs rounded
Brisket: sternum still palpable but starting to become round
Ribs can still be palpated with some pressure. Camels: shoulder and rump muscles can still be delineated, hump normal size with angular dorsal edge
Score 4: Fat
Musculature not well defined-“buried in fat” Lumbar area rounded to nearly flat
No shelf formed by the transverse process of the lumbar vertebrae Perineum filled in, no depression under the tail
Inguinal area filled in Brisket flat
Ribs can only be palpated with firm pressure.
Camel: hump round and wide at the base, shoulders very thick
Score 5: Obese
Smooth, rounded appearance due to excessive fat deposition Lumbar area completely rounded
Bony structures difficult to palpate Bulging perineum
Thick tail-head
Convex inguinal appearance Rounded brisket
Camels: obviously fat on shoulders, hump very large and round
MISCELLANEOUS ASSOCIATED CONDITIONS
N/A
AGE-RELATED FACTORS
N/A
ZOONOTIC POTENTIAL
N/A
PREGNANCY
Pregnancy may affect body condition scoring.
RUMINANT SPECIES AFFECTED
Camelids and camels
BIOSECURITY
N/A
PRODUCTION MANAGEMENT
Body condition scoring should be performed on all animals within the herd at minimum on a quarterly basis.
SYNONYMS
N/A
SEE ALSO
Body condition scoring by species
ABBREVIATIONS
BCS = body condition score
Suggested Reading
Fowler, M. E. 1989. Medicine and surgery of South American camelids. Ames: Iowa State University Press.
Johnson, L. W. 1994. Update on llama medicine. Veterinary Clinics of North America Food Animal Practice 10:198-99.
Tibrary, A., Anouassi, A. 1997. Management of reproduction in camelidae. In: Theriogenology in camelidae, pp. 453-

Rabat, Morocco: Actes Edition.
Van Saun, R. J. 2003. Feeding alpacas. In: Hoffman, E. (ed), The complete alpaca book, pp. 179-232. Santa Cruz, CA: Bonny Doon Press.
Authors: Ahmed Tibary and Debbie Terrel

BORDER DISEASE
BASICS OVERVIEW

Neonatal condition of lambs as a result of a viral infection of the dam during pregnancy. The virus crosses the placenta and infects the lamb.
The border disease virus (BDV) is closely related to other pestiviruses such as hog cholera virus (HCV), which causes classical swine fever, and bovine viral diarrhea virus (BVDV).
Also called hairy shaker and fuzzy lamb disease
SYSTEMS AFFECTED
Reproductive, musculoskeletal, central nervous system
GENETICS
N/A
INCIDENCE/PREVALENCE
Unknown
GEOGRAPHIC DISTRIBUTION
Worldwide
SIGNALMENT
Sheep
Goats
Pregnant cattle inoculated early in gestation with border disease virus frequently abort and develop antibodies to bovine viral diarrhea. Swine may possibly be affected.
Species
Sheep and goats Breed Predilections N/A
Mean Age and Range
Clinical manifestations in the fetus depend on the stage of gestation when infection occurs.
Predominant Sex
N/A
SIGNS
Clinical signs are determined by the animal’s age when infected.
Animals infected as adults are subclinical. However, when the ewe is infected during pregnancy, the virus crosses the placenta and infects the fetus. Disease is suspected with increased numbers of barren ewes or ewes bearing mummified or malformed lambs.
Clinical manifestations in the fetus depend on the stage of gestation when infection occurs.
Placentitis occurs 10-30 days postinfection and may cause fetal expulsion, resorption, or mummification.
Early gestational infections may result in immune tolerance in the lamb. These lambs are permanent carriers and shedders of the virus, but do not develop clinical signs of disease.
Other surviving fetuses infected < 90 days gestation may not develop immune tolerance. These lambs develop the characteristic signs of border disease.
Affected lambs are of small size with possible skeletal defects such as dropped pasterns or mandibular brachygnathia
Involuntary tonic/clonic muscular tremors and ataxia
Hypertrophy of primary hair follicles results in a long, coarse, and straight birth coat. It is sometimes described as “hairy.” The coat may also be pigmented.
Kids and some rough-coated breeds of sheep do not demonstrate the characteristic hair changes.
CAUSES AND RISK FACTORS
The main sources of infection are the asymptomatic, persistently infected sheep. These animals shed the virus in saliva, respiratory secretions, urine, feces, or semen. Transmission occurs across mucous membranes.
DIAGNOSIS DIFFERENTIALDIAGNOSIS
Other causes of abortion such as Salmonella spp., Campylobacter spp., Chlamydia spp., Toxoplasma gondii, and
Rickettsia spp.
In lambs other neurological conditions such as enzootic ataxia (swayback), bacterial meningoencephalitis, focal symmetrical encephalomalacia, and “daft lamb” disease
CBC/BIOCHEMISTRY/URINALYS IS
N/A
OTHER LABORATORY FINDINGS
Possibility of decreased levels of thyroid hormones contributing to growth retardation
IMAGING
N/A
DIAGNOSTIC PROCEDURES
Fluorescent antibody tests for viral antigens performed on tissues of affected lambs. Tissues for collection include: abomasum, pancreas, kidneys, thyroid, testicles, and skin biopsies.
Serology includes serum neutralization, agar gel immunodiffusion (AGID), and complement fixation tests of ewes. Ewes infected as adults develop serum neutralization (SN) titers ranging from 1:20 to 1:320. Animals with congenital infection may have negative SN titers or titers < 1:10.
Precolostral blood cultures: colostral antibody can mask virus for up to 2 months.
• RT-PCR PATHOLOGIC FINDINGS GROSS FINDINGS
Hydranencephaly
Undersized cerebral cortex
Severe cases may have cavitations or cysts of the cerebrum and/or spinal cord.
Doming of the frontal bones of the skull
Abnormal curvature of the ribs
Brachygnathia
Abnormal “hairy” appearance of birth coat due to increased proportion of primary hair follicles
Abnormal skin pigmentation
Placentitis and placental necrosis can occur.
HISTOPATHOLOGICAL FINDINGS
White matter lesions in the CNS
Increase in intrafascicular glial cells with myelinlike lipid droplet accumulation
CNS and spinal cord hypomyelinogenesis
Endothelial swelling and thrombotic occlusion of the vessels in the placenta
TREATMENT
No effective treatment
MEDICATIONS
None
CONTRAINDICATIONS
N/A
FOLLOW-UP PATIENT MONITORING
N/A
PREVENTION/AVOIDANCE
Serology should be performed. Most dams of affected lambs should have high levels of antibody and be immune to further challenge by the same strain of the virus in subsequent pregnancies. Ewes with negative antibody titers may be persistently infected. Blood cultures and examination of skin biopsies by fluorescent antibody tests should be performed on these animals to identify carriers.
Pregnant noninfected ewes should be kept separated from the rest of the flock for the first 60 days of gestation.
Infected lambs should be culled from the flock before breeding season.
There are no approved vaccines for use against border disease virus in the United States. Bovine viral diarrhea vaccines for cattle are not recommended for use in sheep.
POSSIBLE COMPLICATIONS
N/A
EXPECTED COURSE AND PROGNOSIS
Affected lambs that survive the first few months will gradually resolve neurologic signs and fleece abnormalities.
MISCELLANEOUS ASSOCIATED CONDITIONS
Bovine viral diarrhea (BVD) and hog cholera virus (HCV) are very closely related pestiviruses.
AGE-RELATED FACTORS
Age at time of infection determines clinical signs in the individual.
ZOONOTIC POTENTIAL
N/A
PREGNANCY
Clinical disease or death in lambs is the result of infection of the dam during gestation.
SYNONYMS
Also called hairy shaker and fuzzy lamb disease.
SEE ALSO
Other causes of abortion such as Salmonella spp., Campylobacter spp., Chlamydia spp., Toxoplasma gondii, and Rickettsia spp. Other neurological conditions such as enzootic ataxia (swayback), bacterial meningoencephalitis, focal symmetrical encephalomalacia, and “daft lamb” disease
ABBREVIATIONS
BDV = bovine diarrhea virus HCV = hog cholera virus
SN = serum neutralization
RT-PCR = reverse transcription polymerase chain reaction
Suggested Reading
Jones, T. C., Hunt, R. D., King, N. W. 1997. Border disease of sheep, veterinary pathology. 6th ed. Baltimore, Maryland: Williams & Wilkins.
Loken, T. 1995, Nov. Border disease in sheep. Vet Clin North Am Food Anim Pract. 11(3): 579-95.
Nettleton, P. F., Gilray, J. A., Russo, P., Dlissi, E. 1998, May-Aug. Border disease of sheep and goats. Vet Res. 29(3-4): 327-40.
Pratelli, A., Bollo, E., Martella, V., Guarda, F., Chiocco, D., Buonavoglia, C. 1999, Oct. Pestivirus infection in small ruminants: virological and histopathological findings. New Microbiol. 22(4): 351-56.
Thur, B., Hilbe, M., Strasser, M., Ehrensperger, F. 1997, Dec. Immunohistochemical diagnosis of pestivirus infection associated with bovine and ovine abortion and perinatal death. Am J Vet Res. 58(12): 1371-75.
Vilbek, S., Paton, D. J. 2000, Jul-Aug. A RT-PCR assay for the rapid recognition of border disease virus. Vet Res. 31(4): 437-45.
Author: Lisa Nashold

BORNA DISEASE
BASICS OVERVIEW

Borna disease is a sporadic, transmissible, progressive encephalitis.
The virus does not have a direct cytopathic effect.
Virally infected cells initiate a T cell immune response, which leads to tissue destruction.
SYSTEMS AFFECTED CNS
GENETICS
N/A
INCIDENCE/PREVALENCE
Unknown
GEOGRAPHIC DISTRIBUTION
Borna disease was historically endemic to areas of Germany and Switzerland. Confirmed outbreaks of the disease have generally been in middle and eastern Europe and in horses in the Middle East.
Clinically normal animals have tested positive for the RNA virus responsible for the disease in many areas of the world including the United States.
SIGNALMENT
Natural infections occur in sheep and horses. Goats and cattle can also be affected.
BDV has been experimentally transmitted to a wide range of animals including chickens, rabbits, rats, guinea pigs, and monkeys.
Antibodies have been identified in monkeys, humans, and birds.
SIGNS
Borna disease is a progressive neurologic disease.
Initial signs are generally nonspecific and include anorexia, fever, excessive salivation, yawning, and chewing movements.
Early neurologic signs include hyperesthesia, ataxia, head pressing, head tremors, muscle contractions, and depression.
Transient signs of irritability, kicking, biting or compulsive movements may occur.
In later stages of disease, animals may lean against objects or maintain a sawhorse stance. Convulsion or coma is possible.
Nystagmus is observed in terminal cases.
CAUSES AND RISK FACTORS
Borna disease virus (BDV) is an enveloped RNA virus from the Flaviviridae family.
Actively infected, convalescent, and immune carrier animals shed the virus in nasal secretions, saliva, urine, or milk.
Infection often occurs due to contaminated food and water.
The virus moves to the CNS by intra-axonal transport via nerves in the nose and throat area.
Disease outbreaks are more commonly seen in spring and early summer.
The virus is transmitted between birds by the tick Hyalomma anatolicum. An arthropod vector is not necessary for transmission in other species.
An outbreak of disease in horses in the Middle East was associated with a dense population of infected wild birds.
Rodents have also been suspected as a source of infection.
DIAGNOSIS DIFFERENTIALDIAGNOSIS
Other encephalopathies such as St. Louis encephalitis or West Nile virus
Scrapie, bovine spongiform encephalopathy, chronic wasting disease in elk and deer
Rabies
Metabolic or digestive disorders-milk fever, nervous ketosis
CNS tumor
Oestrus ovis infestations in sheep
Pseudorabies
CBC/BIOCHEMISTRY/URINALYS IS
N/A
OTHER LABORATORY FINDINGS
In some cases, serum and CSF may contain antibodies to BDV.
IMAGING
N/A
DIAGNOSTIC PROCEDURES
Polymerase chain reaction (PCR) viral amplification and in situ hybridization have been used to demonstrate viral RNA in neurons, astrocytes, Schwann cells, and ependymal cells.
PATHOLOGIC FINDINGS GROSS FINDINGS
No characteristic gross lesions
HISTOPATHOLOGICAL FINDINGS
Inclusion bodies in neuronal nucleus known as Joest or Joest-Degen bodies are found in ganglion cells of the hippocampus and olfactory lobes of the cerebral cortex. They are considered pathognomonic for Borna disease.
Other lesions are characteristic of encephalitis including perivascular cuffing, ganglion cell degeneration, and gliosis.
Neuronophagic nodules may be found.
Lesions are typically found in gray matter of the cerebral hemispheres and brain stem. The most severe lesions are found in the olfactory bulbs, caudate nucleus, and hippocampus.
Cerebellum is spared.
TREATMENT
No specific treatment is available.
Supportive therapy with mannitol may temporarily relieve cerebral edema. Anti-inflammatory medications may reduce discomfort.
MEDICATIONS
No specific medications
CONTRAINDICATIONS
Appropriate milk and meat withdrawal times must be followed for all compounds administered to food-producing animals.
FOLLOW-UP PATIENT MONITORING
Surviving animals may have permanent neurological deficits.
PREVENTION/AVOIDANCE
Animals should not be fed and watered together in large numbers and should be kept separate from horses and cattle.
Insect and tick control may be helpful.
Incoming animals should be quarantined for 2 months due to the long incubation period of the disease, and tested twice during this period for the presence of antibodies.
BDV is resistant to drying and other adverse environmental conditions.
POSSIBLE COMPLICATIONS
N/A
EXPECTED COURSE AND PROGNOSIS
Unlike other viral encephalitides, the incubation period can vary from 3 weeks to months or possibly years. The average incubation period is usually from 2 to 3 months.
Duration of clinical illness is normally 1-3 weeks.
Mortality rates can range from 60% to 95% in animals exhibiting clinical signs.
Surviving animals may remain permanently neurologically impaired.
MISCELLANEOUS ASSOCIATED CONDITIONS
The viruses of Borna disease and near eastern encephalitis are indistinguishable.
Serologically distinct from the viruses that cause West Nile virus (WNV), eastern equine encephalitis (EEE), western equine encephalitis (WEE), Venezuelan encephalitis (VE)
AGE-RELATED FACTORS
N/A
ZOONOTIC POTENTIAL
BDV antibodies have been found in humans with various neuropsychiatric disorders such as schizophrenia. The actual significance of BDV in these disorders has yet to be determined.
PREGNANCY
N/A
SEE ALSO
Bovine spongiform encephalopathy Chronic wasting disease in elk and deer Metabolic or digestive disorders: milk fever, nervous ketosis Oestrus ovis infestations in sheep Other encephalopathies such as St. Louis encephalitis or West Nile virus Pseudorabies Rabies Scrapie
ABBREVIATIONS
APHIS = Animal and Plant Health Inspection Service BDV = Borna disease virus
CNS = central nervous system CSF = cerebral spinal fluid
EEE = eastern equine encephalitis PCR = polymerase chain reaction VEE = Venezuelan equine encephalitis WEE = western equine encephalitis
WNV = West Nile virus
Suggested Reading
Jones, T. C., Hunt, R. D., King, N.W. 1997. Borna disease, veterinary pathology. 6th ed. Baltimore, Maryland: Williams & Wilkins.
Smith, B. 2002. Borna disease (near eastern encephalitis), large animal internal medicine. 3rd ed. St. Louis: Mosby.
Timoney, J. F., Gillespie, J. H., Scott, F.W., Barlough, J. E., ed. 1992. Borna disease. In: Hagan and Bruner ‘s microbiology and infectious diseases of domestic animals. 8th ed. Cornell University, Ithaca, NY: Comstock Publishing Associates a division of Cornell University Press.
USDA. 2002. Sept. Borna disease, factsheet. Riverdale, Maryland: APHIS, Veterinary Services.
Author: Lisa Nashold

BOTULISM
BASICS OVERVIEW

Toxins produced by the bacteria Clostridium botulinum cause botulism.
There are eight botulinum toxins produced by the bacteria. These toxins are antigenically distinct toxins and identified as types A, B, C1,C2, D, E, F, and G. Each of these toxins is found in different environments and affect different species of animals.
Botulinum toxin types B, C, and D are the most common toxins to cause toxicity in cattle.
PATHOPHYS IOLOGY
Intoxication by Clostridium botulinum is primarily by ingestion of the preformed toxin in a contaminated feed source. Spoiled oat, rye, and barley silage and hay are common sources for type B botulinum intoxication.
The ingestion of poultry litter containing bird parts or the ingestion of other forages contaminated with toxin-ladened animal parts is a source for type C botulinum toxin.
Type D botulinum intoxication is common in phosphorus-deficient areas where toxin-contaminated bones are ingested. The ingestion of contaminated water (usually type C and D botulinum toxin) from nutrient-rich ponds has also been a source of intoxication.
Wound infections can also lead to botulinum intoxication but is rare in ruminants.
SYSTEMS AFFECTED
Ingestion of preformed toxin is the usual means of intoxication of ruminates.
The toxin is absorbed by the intestines and distributed to the nerves that innervate the muscles (neuromuscular junction).
The toxin attaches to the nerve and is incorporated into the cytoplasm where it acts as a metaloprotease that inactivates proteins needed to release the neurotransmitter acetylcholine.
INCIDENCE/PREVALENCE
With modern production processes, the potential for animals ingesting toxin-laden food sources can occur, resulting in catastrophic consequences to the affected herd.
Areas of the world where intoxication is a fairly common occurrence and is considered an endemic problem include Australia, South Africa, and South America.
GEOGRAPHIC DISTRIBUTION
The various botulinum toxins tend to have a unique geographical area of the world. Clostridium botulinum type B is commonly found in Europe and the eastern United States. Clostridium botulinum type C is commonly found in the western United States. Clostridium botulinum type D is commonly found in South Africa, South America, and Australia.
SIGNALMENT
Most cases involve adult or young growing animals.
Cattle are extremely sensitive to the toxins. Cattle have been determined to be 12.88 times more sensitive to botulinum toxin type C on a kilogram basis than the mouse. The median toxic dose for botulinum toxin type C in lactating dairy cows is 0.38 ng/kg.
SIGNS
The rapidity of development of clinical signs depends on the amount of toxin ingested.
Clinical signs develop usually between 48 and 72 hours after ingestion, but may appear as early as 24 hours and as late as 10-14 days after ingestion.
Animals first appear to be constipated with dry feces and may seem uneasy on their feet. Over the next 24 to 48 hours, the animals become weaker with staggering and muscle fasciculation of large muscle groups. Animals will lean against fences and walls for support. When lying down they will remain in sternal recumbency.
On clinical examination, the animals will usually lose tail tone with the tail easily handled and elevated. Animals lose tongue tone. An animal will remain alert and actively try to eat but cannot chew properly resulting in food being dropped from the mouth. The lack of tongue control causes the animal to be unable to clean its nose resulting in a dirty dry nose. Some animals will drool. When drinking water, the animal may stick its nose down deep into the water trough to get a drink.
Labored abdominal breathing is usually seen in animals late in the course of the intoxication.
CAUSES AND RISK FACTORS
Ingestion of spoiled hay or silage made from oats, barley, or rye is a common cause of intoxication for botulinum toxin type B.
Ingestion of contaminated animal parts in hay, silage, or poultry litter is a common cause in botulinum toxin type C intoxication.
In phosphorus-deficient areas of the world, ingestion of toxin-contaminated bones are a common source of intoxication particularly for type D botulinum toxin.
Ingestion of water from shallow, warm, nutrient-rich ponds has been implicated in the intoxication of some animals.
DIAGNOSIS DIFFERENTIALDIAGNOSIS
Diagnosis of botulism can be difficult and is usually one of exclusion of other causes.
Hypocalcemia, hypomagnesemia, and hypokalemia should be ruled out. However, there is a decreased chance of an acute outbreak involving multiple animals with a deficiency of calcium, magnesium, or potassium.
Monensin and other ionophore toxicities can cause cardiac and skeletal muscle lesions leading to weakness in the animals.
Gossypol toxicity can cause cardiac problems leading to weakness in the animals.
Organophosphate and carbamate toxicity due to interference with neurotransmitters
Chlorinated hydrocarbon (organochlorine insecticides) interferes with sodium and potassium channels leading to weakness, tremors, ataxia, and salivation.
CBC/BIOCHEMISTRY/URINALYS IS
CBC and blood chemistries should be normal in affected animals.
DIAGNOSTIC PROCEDURES
Confirmation of a positive case of botulinum intoxication can be difficult.
Feed samples from the previous 2 to 5 days should be immediately evaluated for botulinum toxin contamination.
Animal samples to submit for botulinum toxin testing are serum, liver, rumen content, and cecal content. The testing procedure usually performed is the mouse protection bioassay. However, agar immunodiffusion testing and ELISA testing for the toxin can also be performed.
Bacterial culturing of fresh rumen and cecal content from animals immediately euthanized or freshly dead for Clostridium botulinum organism can also aid in a diagnosis.
The finding of preformed toxin in any of the feed or tissues submitted and/or the finding of Clostridium botulinum
organisms present in the fresh rumen or cecal content suggests that the animal was intoxicated by botulinum toxin.
PATHOLOGIC FINDINGS GROSS FINDINGS
Gross lesions are few. No histopathologic lesions are noted.
The rumen may have a decreased fill of forage and forage in the rumen may be dry due to the animal’s inability to swallow and drink water.
TREATMENT APPROPRIATE HEALTH CARE
The toxin is long acting and can affect the animal for several weeks, which makes treatment difficult.
Treatment is mainly supportive with the animal receiving fluids for dehydration and hand-feeding to maintain the animal’s caloric intake. Animals must remain in sternal recumbency or bloat will occur. Animals should be made to move and rise to prevent crush injuries to large muscle groups.
The treatment of cattle with a pentavalent antitoxin has been of little success and is expensive.
Avoid antimicrobials that potentiate muscle weakness (aminoglycosides, tetracycline, procaine penicillin)
In some areas of the world, vaccination of cattle with a toxoid for types B, C, and D botulinum toxin has been successful in preventing outbreaks.
CLIENT EDUCATION
The most common source of intoxication is through feed.
Insure ensiled feed (e.g., rye, oat, and barley silage and hay) has been fermented correctly. No animal parts are present in the feed.
MEDICATIONS CONTRAINDICATIONS
Avoid aminoglycosides, tetracycline, and procaine penicillin for treatment of wounds since these can potentiate muscle weakness.
Appropriate milk and meat withdrawal times must be followed for all compounds administered to food-producing animals.
FOLLOW-UP PATIENT MONITORING
Monitor cattle for dehydration and bloating. Keep animals in sternal recumbency so that bloat will not occur.
Watch for muscle damage in recumbent animals.
PREVENTION/AVOIDANCE
Clients need to insure that silage is properly fermented and no animal parts are inadvertently incorporated into hay or feed.
EXPECTED COURSE AND PROGNOSIS
The prognosis is poor in most affected animals. Prolonged and intense supportive care is often needed lasting several weeks to months.
MISCELLANEOUS ASSOCIATED CONDITIONS
N/A
AGE-RELATED FACTORS
Most cases involve adult or young growing animals.
ZOONOTIC POTENTIAL
Since this is an intracellular toxin bound to the nerves, the chance of individuals working with affected animals becoming intoxicated is minimal. Affected animals should be disposed of by burial or rendering.
Animals should not be sent to slaughter for human consumption.
No evidence of milk contamination with the toxin from intoxicated cows has been identified.
PREGNANCY
N/A
RUMINANT SPECIES AFFECTED
Cattle, sheep, and goats are most commonly affected.
BIOSECURITY
N/A
PRODUCTION MANAGEMENT
Insure ensiled feed (e.g., rye, oat, and barley silage and hay) has been fermented correctly. No animal parts are present in the feed.
SYNONYMS
Bulbar paralysis Lamziekte
Loin disease
SEE ALSO
Chlorinated hydrocarbon (organochlorine insecticides) Gossypol toxicity
Hypocalcemia Hypokalemia Hypomagnesemia
Monensin and other ionophore organophosphate and carbamate toxicity
ABBREVIATIONS
N/A
Suggested Reading
Galey, F. D., Terra, R., Walker, R., Adaska, J., Etchebarne, M. A., Puschner, B., Fisher, E., Whitlock, R. H., Rocke, T., Willoughby, D., Tor, E. 2000. Type C botulism in dairy cattle from feed contaminated with a dead cat. J Vet Diagn Invest. 12(3):204-9.
Kelch, W. J., Kerr, L. A., Pringle, J. K., Rohrbach, B. W., Whitlock, R. H. 2000. Fatal Clostridium botulinum toxicosis in eleven Holstein cattle fed round bale barley haylage. J Vet Diagn Invest. 12(5):453-55
Martin, S. 2003. Clostridium botulinum type D intoxication in a dairy herd in Ontario. Can Vet J. 44(6):493-95.
Moeller, R. B., Jr., Puschner, B., Walker, R. L., Rocke, T., Galey, F. D., Cullor, J. S., Ardans, A. A. 2003. Determination of the median toxic dose of type C botulinum toxin in lactating dairy cows. J Vet Diagn Invest. 15(6):523-26.
Author: Robert B. Moeller, Jr.

BOVINE EPHEMERAL FEVER
BASICS OVERVIEW
Bovine ephemeral fever (BEF) is a seasonal, arthropod-transmitted, viral disease of cattle and water buffalo that occurs in the subtropics or temperate regions of Africa, Australia, and Asia.
SIGNALMENT

BEF is a seasonal disease whose severity varies from year to year and region to region. Epidemics may occur periodically and are characterized by rapid onset within days or a few weeks of many animals in a region.
Ephemeral fever is most prevalent in the wet season in the tropics and in summer to early autumn in the subtropics or temperate regions when conditions favor the presence of biting arthropods. BEF disappears abruptly in winter.
Morbidity may be as high as 80%; overall mortality is usually 1-2%, although it is higher in well-conditioned cattle (10- 20%).
SIGNS
The clinical signs occur suddenly and vary in severity. They include biphasic or polyphasic fever, shivering, inappetence, lacrimation, serous nasal discharge, drooling, dyspnea, atony of the fore stomachs, depression, stiffness and lameness, and a sudden decrease in milk yield. Cattle may also become recumbent and paralyzed for 8 hr to > 1 wk.
After recovery, milk production often fails to return to normal levels until the next lactation.
Abortion, with total loss of the season’s lactation, occurs in ~5% of cows pregnant in months 8 and 9 of the last trimester.
Bulls, market cattle, and heavily producing dairy cows are the most severely affected, but even so, spontaneous recovery usually occurs within a few days.
CAUSES AND RISK FACTORS
The disease is caused by ephemeral fever virus, a Rhabdovirus (single-stranded, negative sense RNA in the same family as rabies virus).
The virus can be mechanically transmitted by IV inoculation of blood from infected viremic cattle to susceptible cattle. The virus has been recovered from some Culicoides (biting midge) and mosquito species (Anopheles and Culicine spp.) collected in the field and has been shown to multiply in Culicoides and Culex mosquitoes in the laboratory. The role of the insect in mechanical transmission has not been established.
Transmission by contact or fomites does not occur, and the virus does not appear to persist in recovered cattle.
DIAGNOSIS DIFFERENTIALDIAGNOSIS
Parturient paresis (milk fever, hypocalcemia) is an afebrile disease of mature dairy cows that occurs most commonly within 72 hours of parturition. The clinical signs progress through three stages: Stage 1, changes in attitude (i.e., hypersensitivity and excitability); Stage 2, generalized paresis; Stage 3, circulatory collapse, coma, and death.
CBC/BIOCHEMISTRY/URINALYS IS
Clinical cases have a neutrophilia with bands.
OTHER LABORATORY TESTS
Viral serum neutralization, complement fixation, and the blocking ELISA tests are used for serology. Virus isolation can also be done but isolation usually requires mouse inoculation.
IMAGING
N/A
DIAGNOSTIC PROCEDURES
Diagnosis of BEF is usually based on history and clinical signs (rapid onset of febrile signs for 2-5 days with spontaneous recovery).
The clinical outbreak is confirmed by serology in paired serum samples collected during illness and 2-3 weeks later with a fourfold rise in antibodies.
PATHOLOGIC FINDINGS
The gross lesions of BEF include polyserositis affecting joint, pleural, and peritoneal surfaces. Some lung edema is evident, atelectasis, cellulitis, and focal necrosis of skeletal muscle. The lymph nodes are edematous.
The histological findings include neutrophilia, leukocytosis, and high fibrinogen deposition.
Hemosiderosis of the lymph nodes and spleen from loss of erythrocytes early in infection has been observed.
The venules and capillaries of the tendon sheath, synovial membranes, muscle, and fascia have perivascular neutrophilic infiltration, focal or complete necrosis of vessel walls, thrombosis, and perivascular fibrosis.
TREATMENT
Complete rest is the most effective treatment, and recovering animals should not be stressed or worked because relapse is likely.
Isotonic fluids can be administered IV to treat dehydration. Oral dosing should be avoided unless the swallowing reflex is functional.
MEDICATIONS DRUGS OF CHOICE
Anti-inflammatory drugs can be given early and in repeated doses for 2-3 days.
IV or subcutaneous administration of calcium borogluconate has been found to be beneficial in some animals.
Antibiotics can be administered to prevent secondary bacterial infections.
CONTRAINDICATIONS
During acute illness, no oral therapy should be given to avoid inhalation pneumonia due to the inability of the animal to swallow.
PRECAUTIONS/POSSIBLE INTERACTIONS
Appropriate milk and meat withdrawal times must be followed for all compounds administered.
ALTERNATIVE DRUGS
N/A
FOLLOW-UP PATIENT MONITORING
Animals should be encouraged to stand within 2-5 days. The animals should be rolled over several times a day to help avoid loss of circulation to the underside limbs, which will result in permanent muscle damage.
The heavier the animal is, the more critical it is to get it back on its feet as quickly as possible.
PREVENTION/AVOIDANCE
A modified live vaccine is available that confers good protection. An inactivated vaccine is also available but it gives only 6 months of protection.
POSSIBLE COMPLICATIONS
Pneumonia, mastitis, hind limb paralysis, abnormal gait, abortion in late pregnancy, and temporary (up to 6 months) infertility in bulls
EXPECTED COURSE AND PROGNOSIS
A complete recovery occurs in 95-97% of cases. BEF virus infection confers life-long immunity to cattle.
MISCELLANEOUS ASSOCIATED CONDITIONS
Pneumonia, mastitis, hind limb paralysis, abnormal gait, abortion in late pregnancy
AGE-RELATED FACTORS
N/A
ZOONOTIC POTENTIAL
N/A
PREGNANCY
Infection in the last trimester can result in abortion.
RUMINANT SPECIES AFFECTED
Bovine and water buffalo
BIOSECURITY
The virus cannot be spread by direct animal-to-animal contact. However, it can be spread from infected animals to susceptible animals by injection, so single-use needles should be used.
PRODUCTION MANAGEMENT
N/A
SYNONYMS
Bovine epizootic fever Dengue fever of cattle Lazy man’s disease Stiff sickness
Three day fever Three day sickness SEE ALSO
Abnormal gait and abortion in late pregnancy Hind limb paralysis
Mastitis Parturient paresis Pneumonia
ABBREVIATIONS
BEF = bovine ephemeral fever
ELISA = enzyme-linked immunosorbent assay IV = intravenous
Suggested Reading
Kirkland, P. D. 2002, Nov. Akabane and bovine ephemeral fever virus infections. Vet Clin North Am Food Anim Pract. 18(3): 501-14.
Nandi, S., Negi, B. S. 1999, Apr. Bovine ephemeral fever: a review. Comp Immunol Microbiol Infect Dis. 22(2): 81-91.
NSW Department of Primary Industries/Agriculture. Bovine ephemeral fever: three-day fever. May 18, 2001. Agfact A0.9.50 (first edition) http://www.agric.nsw.gov.au/reader/cattlehealth/a0950.htm
Author: Christopher C. L. Chase

BOVINE LAMENESS
BASICS DEFINITION
Lameness is an alteration of gait. Clinically affected cattle are reluctant to move and may spend a great proportion of the day lying down. The affected limb typically has reduced contact time. Cattle will preferentially stand in such a manner that the affected limb bears little weight.
SYSTEMS AFFECTED
Musculoskeletal
GENETICS
N/A
GEOGRAPHIC DISTRIBUTION
Potentially worldwide depending on environment
SIGNALMENT
Species
Bovine
Breed Predilections
N/A
Mean Age and Range
N/A Predominant Sex N/A
General Considerations

Lameness is one of the most costly diseases of dairy cattle. Only mastitis and reproductive failure have greater economic impact.
The vast majority of lameness can be localized to the hind limb.
The vast majority of lameness in cattle is associated with hoof lesions.
The vast majority of hoof lesions in the hind limb are located in the lateral claw.
Hoof lesions are typically bilaterally symmetrical. Similar lesions are present in the right and left hoof.
With the exception of interdigital cellulitis, parenteral antibiotics have little benefit in most lame cows.
DIAGNOSIS DIFFERENTIALDIAGNOSES
Laminitis: acute laminitis, chronic laminitis, septic white line disease, horizontal hoof cracks, thimbles
Sole ulcers
Sole abscesses
Corkscrew claw
Interdigital cellulitis (foot rot)
Digital dermatitis (heel warts)
Heel erosions
Vertical hoof cracks, sand cracks
Interdigital fibroma
LAMINITIS
Definition
An inflammatory process that disrupts the junction of sensitive and insensitive lamina of the hoof. Acute disease will often cause permanent changes in hoof structure, which predispose to other hoof lameness.
Acute laminitis-Clinical signs include hemorrhage at the white line, warm foot, softening of the coronary band, and prominent digital pulses. It is often difficult to localize the lesion to a specific hoof and most patients are lame in multiple hooves. Concrete floors accentuate gait abnormality. Hind limbs may be drawn under the body in an attempt to shift weight off the front feet
Chronic laminitis-Loss of normal white line structure permits widening of white line and altered hoof angle and a loss of parallelism with P3. The toe becomes abnormally long. Weight is shifted onto heel and off of toe, potentiating abnormal hoof growth. The hoof wall often has raised horizontal ridges or rings; in severe cases horizontal fissures or thimbles may be present
Septic white line disease-junction of sensitive and insensitive lamina is compromised and may separate permitting debris and infection to dissect along white line. Severe cases may have draining tracts erupt from coronary band.
Diagnosis based on physical examination, radiographs rarely performed to document rotation of P3 and altered hoof angle
Cause
Subclinical or clinical grain engorgement-a single episode can permanently disrupt laminar growth and integrity; grain engorgement is typically occult/subclinical in dairy and feedlot cattle; repetitive episodes will potentiate lesions and abnormalities; cattle with grossly abnormal hoof growth usually do not have clinical signs of acute laminitis; specific dietary causes include high proportions of easily fermented carbohydrates and short dietary fiber length.
Septicemia-common primary causes include metritis, mastitis, peritonitis, and pneumonia.
Trauma-heat (use of power sander on hooves), concrete floors
Treatment
Acute laminitis-treat underlying diseases (septicemia or grain engorgement), place cows on softer surface (dirt vs. concrete) for 5 to 7 days, and administer nonsteroidal anti-inflammatory agents (flunixin meglumine).
Chronic laminitis-perform corrective hoof trimming. Preferentially shorten the toe, altering the hoof angle. Remove all infected, underrun or unattached hoof.
Prevention/Management
Dairy-limit concentrates to a maximum of 60% of diet. Insure adequate long-stem fiber in the diet. Screen total mixed rations on a routine basis to assess proportionate fiber length of feed. Monitor rumen pH to screen for subclinical grain engorgement. Consider inclusion of buffers in diet. Increase frequency of feeding. Eliminate component feeding. Provide routine hoof trimming. Recognize that a degree of laminitis is “normal” in dairy cows.
Beef-attempt to limit frequency of severe disease. If possible and economical, adopt slow transition to high (>90%) concentrate diets. Consider inclusion of dietary ionophores and provide access to more comfortable footing.
SOLE ABSCESSES
Definition
Abscesses located at the junction of sensitive and insensitive lamina.
Cause
This disease occurs when sensitive (living) tissues are exposed by a penetrating wound or separation of the white line (laminitis). Lesions are most common on the lateral claw of the hind foot. Structure of hoof wall limits drainage and host’s ability to clear infections.
Clinical Signs and Diagnosis
Infection dissects along the junction of sensitive and insensitive tissues forming a circumscribed abscess covered by a “false sole.” The history often includes fluctuating degree of lameness. Enclosed abscesses produce pressure and severe lameness. Drainage to the exterior will often cause short-term dramatic improvement in gait. Untreated infection may eventually involve deeper tissue (P3, navicular bone, flexor tendons, coffin joint, etc.), and cause irreparable damage.
Treatment
Pare out abscesses and underrun areas completely. If deep, sensitive tissues need to be debrided, consider a Baer block (distal intravenous anesthesia). Affix a wooden block to the unaffected digit making the lesion non-weight bearing. Lesions are typically not bandaged. If deep tissues are infected, consider soaking the foot one to two times a day for 10-15 minutes. Soak solutions typically contain betadine and Epsom salts (MgSO4). Simple uncomplicated lesions do not require antibiotic
therapy.
Prevention
Prevention of laminitis and trauma, routine hoof trimming
SOLE ULCERS (RUSTERHOLTZ ULCER, PODODERM ATITIS CIRCUMSCRIPTA)
Clinical Signs and Diagnosis
Sole ulcers are typically located at the juncture of the sole and heel on the lateral claw of the hind foot.
Lesions typically consist of a circular defect in the sensitive layers of the sole with a mass of proliferative granulation tissue protruding through the defect. An intact sheet of insensitive sole typically covers early lesions. Later lesions may have a defect in the wall of the sole.
The cause, origin, and pathogenesis of this disease are unknown. Postulated causes include laminitis, frostbite, and conformational defects.
Treatment
Excise sole wall overlying the defect in sensitive hoof wall and expose the defect in sensitive hoof wall. Remove the proliferative granulation tissue. Apply mild cautery or administer local treatment of lesions with compounds that kill living tissue (10% formaldehyde). Affix a wooden block to the unaffected digit making the lesion non-weight bearing.
Prevention
Design of specific preventative programs is difficult given unknown etiology. Routine hoof trimming recommended in dairy cattle.
CORKSCREW CLAW (SCREWCLAW)
Definition/Clinical Description
Corkscrew claw is an excessive growth of the abaxial wall of either the lateral hoof of the hind foot (most common) or medial claw of the front foot, which curves under the ventral surface of hoof. This growth pattern causes the toe to not bear weight. Long toes and an altered hoof angle usually accompany the rolling of the hoof wall.
Additionally, infected heel cracks and sole ulcers are commonly seen in cattle with screwclaw.
Cause
The conformation of cattle seems to predispose some beef cattle to this disorder. Affected beef cattle are usually heavily muscled with a wide rump. These cattle stand with their hind limbs abnormally close together and preferentially bear weight on the abaxial aspect of the lateral claw. Laminitis and preexisting damage to the hoof wall or coronary band are probably important predisposing causes.
Treatment
Corrective hoof trimming is the most appropriate treatment. Aggressive shortening of the affected abaxial hoof wall. Hoof trimming should provide a flat solar surface, which is perpendicular to abaxial hoof wall.
Prevention
Farmers should consider selection of breeding stock (especially bulls) for proper hoof conformation. The practitioner may consider aggressive corrective hoof trimming of young actively growing animals (less than 18 months of age). This procedure will force proper placement of feet, permitting animals to grow into a structure or conformation, which permits flat placement of hoof. Although this procedure may improve the health and survival of individual animals, it may mask conformational defects, which may have a genetic component.
INTERDIGITALCELLULITIS (FOOT ROT, INTERDIGITALPHLEGMON)
Definition
Infection of the skin and subcutaneous tissues of the interdigital cleft
Cause
Primary etiologic agent is Fusobacterium necrophorum, a gram-negative anaerobe. Trauma and abrasions of the interdigital skin are important predisposing factors.
Clinical Signs and Diagnosis
Has the appearance of a wound with gray, devitalized edges. Lesion has a foul, necrotic odor characteristic of anaerobic infections. The foot dorsal to the coronary band is often swollen, warm, and erythematous.
Untreated disease or delayed treatment may result in deeper tissues being affected and cause irreparable damage.
Treatment
Optimal treatment is systemic antibiotics. Common treatments include long-acting oxytetracycline (20 mg/kg IM) and procaine penicillin G (20,000 IU/kg IM). Some dairy clients will treat with ceftiofur (1-2 mg/kg) because this does not necessitate milk withholding. The author finds this treatment less efficacious.
Topical therapy is less effective and unreliable.
Contraindications
Appropriate milk and meat withdrawal times must be followed for all compounds administered to food-producing animals.
Prevention
Avoid traumatic footing and irregular flooring surfaces like frozen mud, gravel, or grain stubble. Consider use of trace- mineralized salt containing organic iodine compounds.
DIGITALDERMATITIS (HEEL WARTS , HAIRY HEEL WARTS )
Definition
A warty to verrucous lesion located on the bulbs of the heels or the caudal interdigital cleft
Cause
Disease appears to be caused by an as yet unnamed spirochete bacterium. Organism functions as a contagious pathogen and is readily passed among cattle in a herd. This disease is very common in dairy cattle and seen occasionally in beef cattle.
Clinical Signs and Diagnosis
Lesions vary in appearance from warty and verrucous lesions to a raw, circumscribed granulation bed surrounded by a white to gray skin edge. Long hairlike fibrils often protrude from lesions.
Lesions are confined to areas of haired skin and typically spare the hoof wall. These lesions are very painful when palpated.
Treatment
Large lesions should be debrided. Application of topical tetracycline or lincocin with or without bandages is effective. Dairy herds often spray the bulbs of the heel with topical antibiotic to either treat lesions or limit their severity.
Contraindications
Appropriate milk and meat withdrawal times must be followed for all compounds administered to food-producing animals.
Prevention
Herds free of digital dermatitis should practice strict biosecurity to prevent introduction of the agent.
Providing dry environment seems to limit the spread and severity of lesions. In endemically infected herds farmers may spray the bulbs of the heel with topical antibiotics to limit lesion severity. A vaccine is available; however, its efficacy has not been documented in controlled clinical trials.
Farriers and hoof trimmers should disinfect hoof tools after treating affected cattle.
HEELEROSIONS (SLURRY HEEL, HEELCRACKS)
Clinical Signs and Diagnosis
Deep erosive cracks that originate from the junction of heel and sole on the axial surface of hoof and extend caudally through the heel at a 45-degree angle.
These lesions may extend as deep as the sensitive tissue and may become infected, dissecting cranial and caudal under the surface of the sole and heel.
Lesions typically are present on both the medial and lateral claw of both hind feet. Lesions are predisposed by wet conditions and preexisting chronic laminitis.
Treatment
Completely pare out lesions. Consider corrective hoof trimming with particular emphasis on shortening the toe, which will shift weight off the heels and onto the toes. Affix a wooden block to the normal digit if only one claw is affected.
Prevention
Implement routine hoof trimming in dairy cattle. Avoid excessively wet conditions. Management of the diet to prevent laminitis.
VERTICAL HOOF CRACKS (SAND CRACKS)
Clinical Signs and Diagnosis
Vertical cracks are typically located on the anterior to anterior-lateral surface of the hoof. They are most common on the front feet.
Lesions are more common in beef cattle than dairy cattle. The underlying hoof wall is greatly thickened.
Cracks that do not extend to the coronary band rarely cause lameness. Hoof wall adjacent to the crack may become underrun. In some instances, granulation tissue may protrude through the crack.
Dry conditions and firm, hard footing may predispose, but the exact cause is unknown.
Treatment
Pare out fissure (crack) completely. Thin (grind) hoof wall over and to either side of the fissure. This procedure will make that portion of the hoof non-weight bearing and shift weight onto the sole of the hoof. This procedure will limit flexing of hoof wall and coronary band, providing nearly immediate pain relief in many cattle.
Normal hoof wall will grow out at a rate of approximately one-fourth inch/month. Replacement of entire edge of the hoof will require a minimum of 1 year. Repetitive hoof trimming may be needed to insure the affected portion of the hoof remains non-weight bearing.
Protruding granulation tissue should be removed and its regrowth limited by topical application of 10% formaldehyde.
Prevention
Unknown
INTERDIGITALFIBROMA (CORNS)
Proliferation of fibrous connective tissue and skin in the interdigital space. Most corns do not cause lameness. Corns that are not infected and not in contact with the ground rarely cause gait abnormalities. One should be careful not to attribute lameness to corns and miss other problems, which may cause irreversible damage if not treated. Laxity of intercornual ligaments probably predisposes.
Treatment
Surgical resection of corn
MISCELLANEOUS ASSOCIATED CONDITIONS
N/A
AGE-RELATED FACTORS
N/A
ZOONOTIC POTENTIAL
N/A
PREGNANCY
N/A
RUMINANT SPECIES AFFECTED
Potentially, all ruminant species are affected.
BIOSECURITY
N/A
PRODUCTION MANAGEMENT
N/A
SYNONYMS
Corkscrew claw (screwclaw)
Digital dermatitis (heel warts, hairy heel warts) Heel erosions (slurry heel, heel cracks)
Interdigital cellulitis (foot rot, interdigital phlegmon) Interdigital fibroma (corns)
Sole ulcers (Rusterholtz ulcer, pododermatitis circumscripta)
Vertical hoof cracks (sand cracks)
SEE ALSO
Acute laminitis Chronic laminitis Corkscrew claw
Digital dermatitis (heel warts) Heel erosions
Horizontal hoof cracks Interdigital cellulitis (foot rot) Interdigital fibroma
Laminitis Sand cracks
Septic white line disease Sole abscesses
Sole ulcers Thimbles
Vertical hoof cracks
ABBREVIATIONS
IM = intramuscular
Suggested Reading
Blowey, R. 1992, Mar. Diseases of the bovine digit. Part 1: Description of common lesions. Practice. 14(2):85-90.
Leach, K. A., Logue, D. N., Randall, J. M., Kempson, S. A. 1998, Jan. Claw lesions in dairy cattle: methods for assessment of sole and white line lesions. Vet J. 155(1): 91-102.
Offer, J. E., Logue, D. N., Offer, N. W., Marsden, M. 2004, Jan. The effect of concentrate composition on lameness and hoof health in dairy cows. Vet J. 167(1): 111-13.
Raber, M., Lischer, Ch. J., Geyer, H., Ossent, P. 2004, May. The bovine digital cushion-a descriptive anatomical study. Vet J. 167(3): 258-64.
van Amstel, S. R., Shearer, J. K., Palin, F. L. 2004, Mar. Moisture content, thickness, and lesions of sole horn associated with thin soles in dairy cattle. J Dairy Sci. 87(3): 757-63.
Author: Jeffrey W. Tyler

BOVINE LEUKEMIA
BASICS DEFINITION
Bovine leukemia is a term used for two hematopoietic oncogenic diseases: sporadic bovine leukosis (SBL), which does not have an infectious cause, and enzootic bovine leukemia (EBL), a disease caused by a retrovirus, bovine leukemia virus (BLV). PATHOPHYS IOLOGY

Four clinical syndromes are recognized: calf, thymic, skin, and adult. The first three syndromes are called sporadic bovine leukosis because there is no evidence for the etiology.
The adult form, enzootic bovine leukosis (EBL), is caused by infection of B cells with the bovine leukosis virus (BLV).
BLV infections are lifelong infections. Thirty percent of the animals develop elevated lymphocyte counts (lymphocytosis). The development of solid tumors (lymphomas) from BLV occurs in a small percentage of animals.
There is no relationship between lymphocytosis and the progression to lymphomas.
Over 50% of the lymphomas contain a mutation in the p53 tumor suppression gene. These lymphomas develop most frequently in the lymph nodes, abomasum, heart, spleen, kidneys, uterus, spine, and retrobulbar lymphatic tissue.
SYSTEMS AFFECTED
Lymphoreticular system, skin
GENETICS
There is a genetic component to BLV susceptibility.
Cattle with the major histocompatibility complex allotype, BoLA-w8, have been shown at higher risk of being seropositive.
The BoLA-DA12.3 allotype is prone to increased persistent lymphocytosis (increased numbers of B cells), while the BoLA-DA7 allotype is resistant to lymphocytosis.
INCIDENCE/PREVALENCE
The three syndromes of sporadic bovine leukosis are very rare and usually occur in animals less than 2 years of age.
Seroprevalence to BLV, the causative agent of EBL, varies from 0%-100% by herd. In 1996, 89% of dairy herds and 43.5% of dairy cows in the United States were BLV seropositive. In 1997, a survey of beef herds showed that 38% of all beef operations and 10.3% of all beef cows were BLV seropositive.
The development of EBL following a BLV infection is a rare event.
The incidence of animals developing EBL (leukemia/lymphosarcoma) varies among herds with the average annual incidence in infected cattle estimated to be 0.3%-1.0%.
Most animals that develop EBL are > 2 years of age with peak incidence at 5-8 years of age.
GEOGRAPHIC DISTRIBUTION
Sporadic bovine leukosis occurs worldwide.
The geographic distribution of enzootic bovine leukosis is also worldwide but is dependent on the distribution of BLV. North and South America, Eastern Europe, Russia, and portions of Australia are BLV-endemic areas.
SIGNALMENT
SBL is a disease mainly of young cattle.
Three SBL syndromes are recognized: calf, thymic, and skin. The calf form usually appears in animals < 6 months old and results in generalized proliferation of lymph nodes, liver, spleen, and bone marrow and in lymphoblastic leukemia in about 50% of the animals. The thymic form occurs at 6-30 months of age and the primary neoplasm involves the thymus although lymph nodes and other organs can be affected also. Skin lymphosarcoma form is extremely rare. This syndrome has cutaneous tumors that spontaneously disappear and the animal appears healthy. The syndrome is usually only temporary and the skin tumors reappear along with lymphoid tumors in other tissues. All three SBL syndromes are usually fatal.
BLV infections are asymptomatic and can be recognized only by a serological test that detects BLV antibody. Animals become seropositive 4-12 weeks after exposure.
Persistent lymphocytosis develops in ~30% of infected cattle, but this lymphocytosis is not associated with any clinical signs of disease.
EBL occurs in 0.3-1.0% of BLV-infected animals. These animals will have enlarged superficial lymph nodes (retropharyngeal, mandibular, prescapular, subiliac, mammary) that are two to three times larger than normal size with no signs of inflammation. Lymphomas will infiltrate and affect the function of the abomasum, heart, spleen, kidneys, uterus, spine, and eyes [retrobulbar lymphatic tumor (exophthalmia)].
The clinical signs may include weight loss, decreased milk production, loss of appetite, rear-limb weakness, fever, protruding eyeballs, gastrointestinal obstruction, and heart failure. These animals frequently suffer from anemia.
Pregnant animals develop more rapid symptoms probably due to the immunosuppression associated with pregnancy.
The lymphoma form of EBL is always fatal.
CAUSES
There are no known etiological agents for SBL.
Bovine leukemia virus, a C-type retrovirus, causes EBL. Retroviruses are enveloped, single-stranded RNA viruses. They integrate their genes into the B lymphocytes and the cattle are infected for life. This virus is highly cell associated and does not survive well outside the host.
RISK FACTORS
Transmission of BLV occurs primarily by transfer of blood lymphocytes between animals. The use of common bleeding needles and surgical equipment (tattoo pliers, dehorners, castration knives, etc.) without proper disinfection are the most common mechanisms of transmission.
Rectal palpation with a common sleeve is another high-risk practice.
Virus is rarely present in nasal secretions, saliva, urine, or semen, except when those fluids are contaminated by blood or cellular exudate.
Insects may act as mechanical vectors of blood. BLV can be transmitted to fetuses in utero, but usually < 10% of calves from infected dams carry the virus at birth.
When embryos from cows infected with BLV are transferred to BLV-negative cows, the calves produced are routinely free of infection.
Transmission of BLV to calves through colostrum or milk can occur but is rare because of the presence of BLV colostral antibody.
DIAGNOSIS DIFFERENTIALDIAGNOSIS
Other tumors can be differentiated only by histology.
Lumpy jaw caused by Actinomyces bovis causes hard swellings on the jaw and neck. These infections usually have some areas filled with purulent material and some of the abscesses may have already drained and may not have purulent material.
CBC/BIOCHEMISTRY/URINALYS IS
Persistent lymphocytosis (PL), identified as absolute lymphocytosis in two consecutive complete blood counts obtained 3 months apart, occurs in approximately 30% of BLV-infected cattle.
Circulating lymphocytes can be morphologically normal or exhibit morphologic features of “reactive” B cells.
When bone marrow becomes lymphomatous in cattle with BLV-induced malignant lymphoma (ML), leukemia with lymphocyte counts as high as 100,000/µl can occur. In leukemic cattle, circulating lymphoid cells can appear “immature or blastic.”
Some cattle with BLV-induced ML have lymphopenia, probably because circulating lymphoid cells are “trapped” in lymphomatous tissues.
Lymphocytosis, usually in the 8000 to 20,000/ul range can also occur with other chronic infectious diseases, like tuberculosis, trypanosomiasis, or brucellosis.
OTHER LABORATORY TESTS
N/A
IMAGING
N/A
DIAGNOSTIC PROCEDURES
Two commercial serology tests for the detection of BLV antibody are available: the agar gel immunodiffusion (AGID) and the antibody capture ELISA. These two tests have similar sensitivity and specificities. However, they fail to detect between 35% and 39% of BLV serologically positive animals.
Reverse transcriptase-polymerase chain reaction (RT-PCR) assays for the detection of the virus in milk and blood are available and are more sensitive and less likely to have false negatives seen with the serological tests. RT-PCR can also detect the infection prior to the presence of antibody.
PATHOLOGIC FINDINGS
Grossly, EBL can be suspected when tumors of the visceral lymph nodes, uterus, abomasum, heart (especially right atrium), liver, spleen, and kidneys are found. These tumors are usually soft and gray-white, and can include friable areas of necrosis.
Microscopically, massive lymphoid cell infiltration is observed in the affected organs as they replace normal cells.
TREATMENT APPROPRIATE HEALTH CARE
Supportive treatment but prognosis is poor
ACTIVITY
N/A
DIET
N/A
CLIENT EDUCATION
Essential practices for controlling BLV infections are
using hypodermic needles that are designed to be discarded after one injection
using a different obstetrical sleeve to palpate each cow
washing and then disinfecting any instruments that may be contaminated with blood. The use of two sets of instruments with one soaking in disinfectant while the other is being used should be encouraged.
using electric dehorners rather than gouges or saws. The latter cause profuse hemorrhage and are difficult to sanitize.
SURGICALCONSIDERATIONS
N/A
MEDICATIONS DRUGS OF CHOICE
N/A
CONTRAINDICATIONS
N/A
PRECAUTIONS
N/A
POSSIBLE INTERACTIONS
N/A
ALTERNATIVE DRUGS
N/A
FOLLOW-UP PATIENT MONITORING
N/A
PREVENTION/AVOIDANCE
BLV-infected animals are a source of infection to all other animals.
The low occurrence of clinical disease in herds with high seroprevalence to BLV frequently makes the priority of culling BLV seropositive animals low.
Four essential practices for controlling BLV infections are listed above under Client Education.
BLV eradication programs have been developed in Europe and in New York. The New York State Bovine Leukosis Virus Eradication and Certification Program (NYSBLVECP) was designed to help producers in establishing a BLV-free herd. The NYSBLVECP guidelines include the four practices outlined above along with many other steps for separation and rearing of infected animals and young stock.
Although BLV-seropositive animals pose a risk to the herd, using only serology will lengthen the time to identify and eradicate BLV from a herd.
BLV-positive animals with lymphocytosis are a larger risk because of their higher concentrations of BLV-infected lymphocytes. Removing these animals will have a faster impact on reducing the BLV risk in the herd.
There are no commercial BLV vaccines available. Two experimental BLV vaccines, a modified-live gene deleted and a DNA vaccine, have been developed and prevented BLV infection in over 85% of the animals.
POSSIBLE COMPLICATIONS
N/A
EXPECTED COURSE AND PROGNOSIS
With SBL, the prognosis is poor and the course of the disease from the first appearance of tumors will be only weeks to months.
The vast majority of BLV infections are inapparent. Although 30% of BLV-seropositive animals will develop lymphocytosis, these animals are not at a greater risk for developing EBL.
Animals with clinical signs of EBL have a poor prognosis and the course of the disease from the first appearance of tumors is short similar to SBL.
MISCELLANEOUS ASSOCIATED CONDITIONS
N/A
AGE-RELATED FACTORS
Animals < 2 years of age develop SBL. Most animals that develop EBL are > 2 years of age with peak incidence at 5-8 years of age.
ZOONOTIC POTENTIAL
No risk
PREGNANCY
The immunosuppression of pregnancy appears to accelerate the development of BLV lymphomas.
RUMINANT SPECIES AFFECTED
Bovine and ovine
BIOSECURITY
BLV-infected animals have the potential of producing infectious BLV for life.
BLV-seropositive animals need to be considered a reservoir of the virus.
New arrivals should be tested prior to introduction for BLV antibodies.
In a BLV-positive herd, testing for lymphocytosis also may be advisable to identify animals with higher numbers of BLV-infected lymphocytes that would pose a higher risk to the herd.
The use of single-use materials (needles, gloves, etc.), as described above, along with proper disinfection of surgical instruments are essential components of a BLV biosecurity plan.
Depending on the level of control desired, BLV seropositive and seronegative animals should be housed separately.
Seronegative animals should always be processed before seronegative animals.
PRODUCTION MANAGEMENT
The economic impact of BLV on dairy cows is $59 per year per cow resulting from a ~3% decrease in milk production per cow.
The overall economic impact of BLV on milk production for the United States is $525 million per year.
SYNONYMS
Bovine leukemia Bovine leukosis
Enzootic bovine leukosis
SEE ALSO
Differential diagnosis Laboratory diagnosis
Lumpy jaw caused by Actinomyces bovis
Sampling techniques
ABBREVIATIONS
AGID = agar gel immunodiffusion BLV = bovine leukemia virus EBL = enzootic bovine leukemia
ELISA = enzyme-linked immunosorbent assay ML = malignant lymphoma
NYSBLVECP = New York State Bovine Leukosis Virus Eradication and Certification Program PL = persistent lymphocytosis
RT-PCR = reverse transcriptase-polymerase chain reaction SBL = spontaneous bovine leukemia
Suggested Reading
Choi, K. Y., Liu, R. B., Buehring, G. C. 2002. Relative sensitivity and specificity of agar gel immunodiffusion, enzyme immunosorbent assay, and immunoblotting for detection of anti-bovine leukemia virus antibodies in cattle. J Virol Meth. 104:33-39.
Evermann, J. F., Jackson, M. K. 1997. Laboratory diagnostic tests for retroviral infections in dairy and beef cattle. Vet Clin North Am Food Animal Pract. 13:87-106.
Hopkins, S. G., DiGiacomo, R. F. 1997. Natural transmission of bovine leukemia virus in dairy and beef cattle. Vet Clin North Am Food Animal Pract. 13:107-28.
Kabeya, H., Ohashi, K., Onuma, M. 2001. Host immune responses in the course of bovine leukemia virus infection. J Vet Med Sci. 63:703-708.
Author: Christopher C. L. Chase

BOVINE PAPULAR STOMATITIS
BASICS DEFINITION

A mild viral disease of calves characterized by proliferative lesions around the mouth caused by a parapoxvirus.
Infections are usually asymptomatic, but raised papules may be observed on nasal planum, hard palate, nares, and occasionally on the esophageal or ruminal mucosa.
There are no lesions at the coronary band.
SYSTEMS AFFECTED
Epithelium of nares, oral cavity, esophagus, and rumen
GENETICS
No association with breed or genetics observed; commonly observed in dairy calves and recent arrivals in feedlots
INCIDENCE/PREVALENCE
Worldwide distribution
SIGNALMENT
Young dairy calves, feedlot calves shortly after arrival. Commonly observed in calves from 1 to 12 months of age
Rare in adult cattle
SIGNS
Acute lesions consist of 2-4 mm macules on the nares and muzzle that progress rapidly to papules with raised periphery and depressed center. Lesions later develop in the oral cavity.
Lesion size may increase to 1 cm in diameter or greater (coalescence of multiple lesions) and regress within several days to weeks.
Most animals are afebrile, eat normally, and have no clinicopathlogic alterations associated with viral infection.
PATHOPHYS IOLOGY
Viral infection results in early hyperemia and inflammation in focal regions of the nares and mouth. Secondary lesions may occur for up to 4 months.
Histopathological evaluation of lesions demonstrates degeneration of epithelial cells and eosinophilic inclusions in degenerated cells.
Hyperplasia of the papillae of the lamina propria is observed.
Ulceration of lesions is accompanied by bacterial infection and sloughing of the epithelium.
A chronic form of BPS has been described associated with more severe clinical signs (salivation, diarrhea, anorexia, and fever). The ulcers in chronic cases become encrusted with exudates.
Similar to contagious ecthyma and pseudocowpox in sheep and goats, bovine papular stomatitis is zoonotic and common in veterinary personnel.
RISK FACTORS
Calves born to cows affected by BPS when young
Adult cows may serve as reservoir for future calf infection.
Recent introduction of naïve animals to feedlot
DIAGNOSIS DIFFERENTIALDIAGNOSIS
Foot-and-mouth disease, vesicular stomatitis, and bovine virus diarrhea/MD, pseudocowpox viruses. Lesions are not found at coronary band, and generally are asymptomatic.
CBC/BIOCHEMISTRY/URINALYS IS
No abnormalities consistently associated with viral lesions
IMAGING
N/A
DIAGNOSTIC PROCEDURES
Polymerase chain reaction, electron microscopy and histopathology are useful in the diagnosis of BPS.
Histopathological evaluation of lesions demonstrates degeneration of epithelial cells and eosinophilic inclusions in degenerated cells.
Confirmation of BPS in a new area requires virus isolation and identification.
Typical parapoxvirus virions can be seen using transmission electron microscopy of biopsy samples.
TREATMENT MISCELLANEOUS PREVENTION
Symptomatic treatment of severely affected animals.
Prevention can focus on biosecurity and production of vaccines using locally obtained viral strains.
ASSOCIATED CONDITIONS
N/A
Young dairy calves, feedlot calves shortly after arrival; commonly observed in calves from 1 to 12 months of age
Rare in adult cattle
ZOONOTIC POTENTIAL
Similar to contagious ecthyma and pseudocowpox in sheep and goats, bovine papular stomatitis is zoonotic and common in veterinary personnel. The mild clinical manifestations make the condition relatively minor; however, the occasional case may have more severe lesions.
PREGNANCY
N/A
BIOSECURITY
PRODUCTION MANAGEMENT
N/A
SYNONYMS
N/A
SEE ALSO
Bovine virus diarrhea/MD Foot-and-mouth disease, Pseudocowpox viruses Vesicular stomatitis ABBREVIATIONS
BPS = bovine papular stomatitis MD = mucosal disease Suggested Reading
Buttner, M., Rziha, H. J. 2002. Parapoxviruses: from the lesion to the viral genome. Journal Veterinary Medicine B49:7-16.
Delhon, G., Tulman, E. R., Afonso, C. L., Lu, Z., de la Concha-Bermejillo, A., Lehmkuhl, H. D., Piccone, M. E., Kutish, G. F., Rock, D. L. 2004. Genomes of the parapoxviruses Orf virus and bovine papular stomatitis virus. Journal of Virology 78:168-77.
Guo, J., Rasmussen, J., Wunschmann, A., de la Concha-Bermejillo, A. 2004. Genetic characterization of orf viruses isolated from various ruminant species of a zoo. Veterinary Microbiology 99: 81-92.
Inoshima, Y., Morooka, A., Sentsui, H. 2000. Detection and diagnosis of parapoxvirus by the polymerase chain reaction. Journal of Virological Methods 84: 201-8.
Stroebel, J. C., Gerdes, G. H. 1996. Bovine papular stomatitis-an incidental finding. Journal of the South African Veterinary Association 67: 104.
Yeruham, I., Abraham, A., Nyska, A. 1994. Clinical and pathological description of a chronic form of bovine papular stomatitis. Journal of Comparative Pathology 111: 279-86.
Author: Jeff Lakritz

BOVINE PETECHIAL FEVER
BASICS DEFINITION

Bovine petechial fever is an infectious disease of cattle characterized by petechial and echymotic hemorrhages on mucosal membranes. The disease is also known as Ondiri disease.
Bovine petechial fever is endemic in some parts of East Africa (Kenya and possibly Tanzania). The disease has not been reported in North America.
SIGNALMENT
There is no sex or age predisposition. Bos taurus breeds are more susceptible than Bos indicus.
The disease also has been reported in sheep, goats, and wild ruminants following experimental infection, but natural infection has been reported only in cattle.
SIGNS
Affected animals have a fluctuating fever.
The most consistent signs are petechiation and echymosis of mucous membranes. Unilateral conjuctival edema, hyphema, epistaxis, and anemia are present in some severe cases.
Dairy cattle imported into endemic areas often exhibit a profound drop in milk production.
CAUSES
The cause is Ehrlichia (Cytoecetes) ondiri. The organism is endemic in wild animals particularly the bushbuck (Tragelaphus scriptus) of highlands above 5000 feet in East Africa. Cattle acquire the disease when grazing on edges of thick, humid forests particularly when they are grazed in these areas at the end of the dry season.
Bovine petechial fever is common in cattle that have been recently introduced to these areas while indigenous cattle appear to acquire resistance.
The disease is thought to be transmitted by an arthropod vector. The vector has yet to be identified, but epidemiological findings suggest a tick vector.
RISK FACTORS
Grazing in or adjacent to thick, high elevation East African forests and the presence of the bushbuck, the reservoir of the organism, are important risk factors. Recently introduced animals are more susceptible.
DIAGNOSIS
Ehrlichia ondiri is diagnosed on demonstration of the organism in peripheral blood monocytes and granulocytes after Giemsa staining but cannot be cultured.
DIFFERENTIALDIAGNOSIS
Differential diagnosis includes bracken fern poisoning and tropical diseases including acute trypanosomiasis and theileriosis.
Bracken fern poisoning is associated with pastures containing the plant and affected animals have hematuria.
Trypanosomiasis occurs in the tropics where the vector, the tsetse (Glossina sp.) fly is found.
Theileriosis is also common in areas where the tick vector Rhipicephalus sp. is present. Trypanosomiasis causes lymphadenopathy and the organism can be demonstrated in blood smears. Theileriosis causes lymphadenopathy and can be demonstrated in blood smears and lymph node aspirates.
TREATMENT
Tetracyclines are effective as a treatment. Recovered animals are immune to reinfection for at least 2 years.
MEDICATIONS CONTRAINDICATIONS
Appropriate milk and meat withdrawal times must be followed for all compounds administered to food-producing animals.
FOLLOW-UP PROGNOSIS
Prognosis is guarded. The mortality is up to 50% in affected animals.
The disease is important in imported animals introduced into risk areas where significant losses are recorded.
MISCELLANEOUS ASSOCIATED CONDITIONS
N/A
AGE-RELATED FACTORS
N/A
ZOONOTIC POTENTIAL
N/A
PREGNANCY
N/A
RUMINANT SPECIES AFFECTED
The disease also has been reported in sheep, goats, and wild ruminants following experimental infection, but natural infection has been reported only in cattle.
BIOSECURITY
N/A
PRODUCTION MANAGEMENT
Bovine petechial fever is common in cattle that have been recently introduced to infected areas while indigenous cattle appear to acquire resistance.
Grazing in or adjacent to thick, high elevation East African forests and the presence of the bushbuck, the reservoir of the organism, are important risk factors. Recently introduced animals are more susceptible.
SYNONYMS
Ondiri disease
SEE ALSO
Bracken fern poisoning Theileriosis Trypanosomiasis ABBREVIATIONS
N/A
Suggested Reading
Davies, G. 1993. Bovine petechial fever (Ondiri disease). Vet Microbio. 34:103-21.
Radostits, O. M., Gay, C. C., Blood, D. C., Hinchcliff, K. W. 2000. Veterinary medicine, 9th ed. New York: W. B. Saunders.
Author: Munashe Chigerwe

BOVINE RESPIRATORY DISEASE COMPLEX (BRD)
BASICS OVERVIEW

Bovine respiratory disease (BRD) complex refers to the general development of respiratory disease in cattle. In most cases, it specifically refers to respiratory disease outbreaks among multiple animals. BRD most commonly occurs in cattle fed for slaughter, although it can also occur in cattle raised for milk production.
BRD is commonly called “shipping fever.”
It is estimated that over $3 billion are spent annually on prevention, treatment, and production losses related to BRD in the United States fed cattle industry.
The etiology of BRD is very often multifactorial, and may include viruses, bacteria, parasites, nutrition, environmental stressors, and host susceptibility. The severity of BRD outbreaks is often influenced by the relative combination of these factors.
SIGNALMENT
BRD can occur in any age and class of cattle.
Younger animals under stressful conditions are most at risk.
SIGNS
Clinical signs may vary depending on the agents involved and the severity of infection.
The first sign often recognized is a reduction in appetite. Cattle may not show typical enthusiasm for coming to the feed bunk when fed.
Cattle off feed may have a sunken appearance in the left para lumbar fossa as a result of decreased rumen fill.
Affected animals often separate from their herd mates.
Movement of affected animals is typically slower than nonaffected herd mates. They may show a reluctance to rise.
A general appearance of depression is often appreciated.
Affected cattle often stand with their heads down and extended.
Cattle may have a serous to mucopurulent nasal discharge.
Serous ocular discharge is often present.
Coughing is often evident, especially when cattle are forced to move.
Depending on the severity, shallow to labored and rapid breathing may be evident.
Cattle affected with BRD typically have a fever ranging from 103.5°F to 105.5°F.
A cranial ventral distribution of lung sounds consistent with bronchopneumonia and lung consolidation is found on auscultation. Moist crackles are heard with bronchopneumonia when the bronchi contain watery secretion or exudation. As the exudate thickens, the sound changes to a dry crackle. Consolidated areas of lung associated with bronchopneumonia (or large abscesses) contain no air and are completely silent.
CAUSES AND RISK FACTORS
Viruses commonly implicated in BRD include bovine herpesvirus 1 (BHV-1), bovine viral diarrhea virus (BVDV), bovine respiratory syncytial virus (BRSV), parainfluenza-3 (PI-3), bovine respiratory corona virus (BRCV), and adenoviruses.
Bacteria commonly involved in BRD include Mannheimia haemolytica (formerly Pasteurella haemolytica), Pasteurella multocida, Mycoplasma bovis, Haemophilus somnus, and Actinomyces pyogenes.
Environmental factors that increase the risk of BRD include poor sanitation, poor ventilation, overcrowding, lack of adequate feed bunk space, lack of adequate water availability.
Stressful events such as transportation, mixing of cattle from multiple sources, castration, dehorning, vaccination, starvation, and weaning increase the risk of BRD developing.
DIAGNOSIS DIFFERENTIALDIAGNOSIS
Allergic interstitial pneumonia
Pulmonary edema
Pleuritis
Pulmonary fibrosis
Lungworms
CBC/BIOCHEMISTRY/URINALYS IS
N/A
OTHER LABORATORY TESTS
Culture and antimicrobial sensitivity are often done on lung samples collected at necropsy or following transtracheal bronchial alveolar lavage.
DIAGNOSTIC PROCEDURES
Nasal swabs are of limited value, as many of the pathogens involved in BRD inhabit the nasal passages normally.
Transtracheal bronchial alveolar lavage will identify pathogens most likely involved with pneumonic process.
Necropsy provides the most useful information on the etiological agents and pathological processes involved. Necropsies on cases early in the course of the disease and prior to antibiotic therapy yield the best results.
GROSS FINDINGS
Gross lesions will depend on the pathological agents involved in the BRD outbreak and the chronicity of the disease process.
Necrotizing lesions of the upper respiratory tract and trachea may be present.
Pneumonic lesions are typically distributed in a bilateral cranial ventral pattern, often with a sharp line of demarcation between the normal and abnormal lung.
There may be varying degrees of pleural adhesion between lung lobes and to the chest wall.
The lung parenchyma typically has a lobulated pattern that imparts a marbled appearance both on the pleural and cut surface.
Affected parenchyma is firm in palpation and may range in color from pink to tan to red to red-black depending on the amount of necrosis present.
Necrotic tissue may progress to abscessation.
HISTOPATHOLOGICAL FINDINGS
N/A
TREATMENT
Antimicrobials directed against common BRD bacteria.
Moving sick cattle to separate pens may be indicated to reduce the stress of competing with healthy cattle.
MEDICATIONS
Common antimicrobial classes used for treatment of BRD include penicillins, cephalosporins, oxytetracyclines, floroquinalones, macrolides.
Ancillary treatments such as nonsteroidal anti-inflammatory drugs, corticosteroids, antihistamines, and vitamin injections may be of value on a case-by-case basis, but in general have limited application in treatment of BRD.
CONTRAINDICATIONS
Some antibiotics are not approved for certain classes of cattle, such as lactating dairy cattle.
Meat and milk withhold times must be considered before administrating any medication to food-producing cattle.
POSSIBLE INTERACTIONS
N/A
FOLLOW-UP PATIENT MONITORING
Daily observation of attitude and appetite will provide a good indication of treatment success.
Gaining of weight is associated with a good prognosis while continued weight loss is a poor sign.
Reduction of rectal temperature in 24-48 hours posttreatment is associated with a good prognosis.
PREVENTION/AVOIDANCE
Immunization against common pathogens associated with BRD
Minimizing stressful events
Maintaining well-ventilated and sanitary environments with plenty of bunk space and water availability
POSSIBLE COMPLICATIONS
Pericarditis
Endocarditis
Pleuritis
Polyarthritis is often a sequela of Mycoplasma bovis and Haemophilus somnus pneumonia.
EXPECTED COURSE AND PROGNOSIS
Prognosis is generally favorable if intervention occurs early.
If intervention is started early, most cattle respond to treatment in 24-72 hours.
Failure to respond to initial treatments generally indicates advanced disease and the prognosis should be guarded.
MISCELLANEOUS ASSOCIATED CONDITIONS
N/A
AGE-RELATED FACTORS
N/A
ZOONOTIC POTENTIAL
Agents commonly involved in BRD are not zoonotic.
PREGNANCY
N/A
SEE ALSO
Bovine respiratory syncytial virus Bovine viral diarrhea virus Haemophilosis
Infectious bovine rhinotracheitis virus Mannheimiosis
Mycoplasma bovis Parainfluenza-3 virus ABBREVIATIONS
BHV-1 = bovine heresvirus 1
BRCV = bovine respiratory corona virus BRD = bovine respiratory disease
BRSV = bovine respiratory syncytial virus BVDV = bovine viral diarrhea virus
PI-3 = parainfluenza-3
Suggested Reading
Bovine respiratory disease: sourcebook for the veterinary professional. 1996. Chatham, NJ: Veterinary Learning Systems.
Chirase, N. K., Greene, L. W., Purdy, C. W., Loan, R. W., Auvermann, B. W., Parker, D. B., Walborg, E. F., Jr., Stevenson, D. E., Xu, Y., Klaunig, J. E. 2004, Jun. Effect of transport stress on respiratory disease, serum antioxidant status, and serum concentrations of lipid peroxidation biomarkers in beef cattle. Am J Vet Res. 65(6):860-64.
Martin SW, Nagy E, Armstrong D, Rosendal S. 1999, Aug. The associations of viral and mycoplasmal antibody titers with respiratory disease and weight gain in feedlot calves. Can Vet J. 40(8):560-67, 570.
Woolums, A. R., Mason, G. L., Hawkins, L. L., Brown, C. C., Williams, S. M., Gould, J. A., Fox, J. J., Sturgeon, S. D., Anderson, J. L., Duggan, F. E., Sanchez, S., Barrett, P. B., Chitwood, S.W. 2004, Nov. Microbiologic findings in feedlot cattle with acute interstitial pneumonia. Am J Vet Res. 65(11):1525-32.
Author: Daniel L. Grooms

BOVINE RESPIRATORY SYNCYTIAL VIRUS
BASICS DEFINITION
Bovine respiratory syncytial virus (BRSV) induces a mild to severe lower respiratory disease in cattle. This infection is one of the viral factors associated with bovine respiratory disease complex.
PATHOLOGIC FINDINGS

BRSV induces damage to the respiratory epithelium with a concomitant influx of inflammatory cells (neutrophils and cytotoxic lymphocytes) and cytokines (tumor necrosis factor). This lowers arterial oxygen by 30%-40%.
The damage to epithelium coupled with inflammatory changes increases the susceptibility of the lung to secondary bacterial infection.
Severe BRSV infections can cause severe damage to bronchiolar and alveolar epithelial tissue resulting in the formation of bullae and interstitial emphysema.
SYSTEMS AFFECTED
Respiratory
GENETICS
N/A
INCIDENCE/PREVALANCE
BRSV is endemic in cattle.
BRSV is seldom seen in calves less than 2 weeks of age, and is most prevalent and severe in animals between 1 month and 8 months of age.
BRSV disease is rarely seen in cattle > 9 months of age. Adult cattle can occasionally experience severe disease.
Seroprevalence in herds is often > 90%.
GEOGRAPHIC DISTRIBUTION
Worldwide
SIGNALMENT
BRSV infection results in respiratory signs. These respiratory signs can be mild, with increased respiratory rate and increased harshness in respiratory sounds, to severe, with dyspnea, forced expiration, and open-mouth breathing.
Spontaneous cough can be easily induced and can vary from dry and nonproductive to moist.
Nasal discharge can vary from none to serous to mucopurulent.
Conjunctivitis and lacrimal discharge are seen infrequently. There is an increased rectal temperature (104-108°F [40- 42°C]), depression, and decreased feed intake.
Secondary pneumonia with bacterial pathogens (Mannheimia haemolytica, Pasteurella multocida, Haemophilus somnus) or Mycoplasma bovis is a frequent sequela.
CAUSES
BRSV is an enveloped, negative, single-stranded RNA virus in the pneumovirus group of the paramyxovirus family. The virus is easily inactivated by desiccation, heat, and disinfectants.
RISK FACTORS
Stress (weaning, shipping, etc.) will increase the risk. Excessive levels of dust have been reported to increase clinical BRSV.
Maternal antibody will inhibit vaccine response but will not prevent infection. However, it will lessen the clinical course of disease.
Concurrent infection with other viral agents, particularly bovine viral diarrhea virus (BVDV), exacerbates BRSV clinical disease.
DIAGNOSIS DIFFERENTIALDIAGNOSIS
Three other bovine viruses-BVDV, bovine parainfluenza-3 virus (PI-3), and bovine herpesvirus 1 (BHV-1)-commonly cause similar respiratory disease.
BHV-1 is associated with rhinotracheitis and upper respiratory disease. BHV-1-infected calves frequently have mucopurulent discharge and conjunctivitis.
BVDV is associated with oral ulcers, mucopurulent discharge, and upper respiratory disease.
PI-3 infection is usually a mild lower respiratory disease.
Bovine coronavirus (BCV) has also been associated with respiratory disease. In younger calves, it is seen in calves suffering from enteritis and diarrhea. BCV in 5-13-month-old cattle causes symptoms of dyspnea, nasal discharge, and increased respiratory rate.
Atypical interstitial pneumonia (AIP) is characterized by sudden onset of disease with subsequent death. AIP animals have labored breathing with loud expiration, frothing at the mouth, and open-mouth breathing. They have harsh respiratory sounds with crackles and rhonchi. These animals usually have a recent history of grazing lush pastures or having a ration change in a feedyard.
CBC/BIOCHEMISTRY/URINALYS IS
BRSV causes a slight lymphopenia 3-10 days postinfection.
OTHER LABORATORY TESTS IMAGING
N/A
DIAGNOSTIC PROCEDURES
BRSV is a very difficult virus to detect by virus isolation. Animals need to be sampled in the incubation or acute phase of infection (3-7 days).
Transtracheal washes have been used to detect BRSV using polymerase chain reaction (PCR). Antigen detection kits have been developed and can detect BRSV antigen.
Other procedures that have proved useful in detection of BRSV antigen are fluorescent antibody tests of fresh tissue and immunohistochemistry staining of cell cultures or formalin-fixed paraffin embedded tissues.
Paired serum samples can be used in the diagnosis of BRSV infection. However, the antibody titer of animals with well- developed clinical disease may be higher in acute samples than the samples taken 2-3 weeks later.
BRSV antibody response often develops rapidly, and clinical signs follow virus infection by up to 7-10 days.
Single serum samples showing high antibody titers from a number of animals in a respiratory outbreak may be useful in making a diagnosis if coupled with clinical signs.
Younger calves infected with BRSV in the presence of maternally acquired antibody may not seroconvert.
PATHOPHYS IOLOGY
Gross lesions include a diffuse interstitial pneumonia with subpleural and interstitial emphysema along with interstitial edema. These lesions are similar to and must be differentiated from AIP.
Regional suppurative bronchopneumonia of bacterial origin is usually present.
Histologic examination reveals necrotizing and proliferative bronchiolitis with alveolitis that is sometimes proliferative along with hyaline membrane formation and edema.
Syncytial cells are present in bronchiolar epithelium and lung parenchyma.
TREATMENT APPROPRIATE HEALTH CARE
The therapy for BRSV is supportive. Severely diseased animals that are dehydrated may receive oral and/or intravenous fluids.
ACTIVITY
Handling of BRSV-infected animals should be minimized to decrease the risk of secondary bacterial infections.
DIET
Concentrate and silage should not be fed to severely diseased animals.
CLIENT EDUCATION
Minimize handling of animals, decrease animal exposure to high levels of dust, and use preventative vaccines.
SURGICALCONSIDERATIONS
N/A
MEDICATIONS DRUGS OF CHOICE
Corticosteroids or nonsteroidal anti-inflammatory drugs (NSAIDs) may have some benefit to lessen the severity of BRSV disease.
Antimicrobial treatment is utilized to reduce secondary bacterial infections.
CONTRAINDICATIONS
Appropriate milk and meat withdrawal times must be followed for all compounds administered to food-producing animals.
PRECAUTIONS
N/A
POSSIBLE INTERACTIONS
N/A
ALTERNATIVE DRUGS
N/A
FOLLOW-UP PATIENT MONITORING
Respiratory characteristics along with rectal body temperatures should be frequently monitored to assess BRSV clinical progression and also the development of secondary bacterial infections that would result in bovine respiratory disease complex (BRDC).
PREVENTION/AVOIDANCE
Both modified-live-virus (MLV) and inactivated-virus BRSV vaccines are available.
Vaccination is an important part of a BRSV control program.
POSSIBLE COMPLICATIONS
Some formaldehyde-inactivated BRSV vaccines have been shown to increase the severity of BRSV disease. This method of inactivation is not currently used for commercial vaccines.
Maternal antibodies in calves interfere with development of an effective BRSV immune response with MLV vaccines.
EXPECTED COURSE AND PROGNOSIS
Uncomplicated BRSV infections will resolve in 10-14 days.
Animals that have secondary infections usually will develop bronchopneumonia with varying levels of morbidity and mortality.
MISCELLANEOUS ASSOCIATED CONDITIONS
BRDC is a frequent sequela to BRSV infections.
AGE-RELATED FACTORS
Younger animals (between 1and 8 months of age) are usually affected.
ZOONOTIC POTENTIAL
N/A
PREGNANCY
N/A
RUMINANT SPECIES AFFECTED
Bovine, ovine
BIOSECURITY
BRSV survives very poorly in the environment and is susceptible to UV light, desiccation, heat, and disinfectants. The virus will survive better in the winter.
Animals exhibiting clinical signs of BRSV should be isolated from other cattle as transmission of BRSV occurs by the oronasal route.
In pens of animals that have had a BRSV outbreak, it would be prudent to clean the water sources.
PRODUCTION MANAGEMENT
In herds with a history of BRSV in their calves, a BRSV vaccine program should be implemented.
SYNONYMS
N/A
SEE ALSO
Atypical interstitial pneumonia Bovine coronavirus
Bovine herpesvirus 1 Bovine parainfluenza-3 virus Bovine viral diarrhea virus ABBREVIATIONS
AIP = atypical interstitial pneumonia BCV = bovine coronavirus
BHV-1 = bovine herpesvirus 1
BRDC = bovine respiratory disease complex BRSV = bovine respiratory syncytial virus BVDV = bovine viral diarrhea virus
MLV = modified-live virus
NSAIDs = nonsteroidal anti-inflammatory drugs PCR = polymerase chain reaction
PI-3 = bovine parainfluenza-3 virus
Suggested Reading
Larsen, L. E. 2000. Bovine respiratory syncytial virus (BRSV) review article. Acta Vet Scand. 41:1-24.
Woolums, A. R., Anderson, M. L., Gunther, R. A., Schelegle, E. S., LaRochelle, D. R., Singer, R. S., Boyle, G. A., Frieberthauser, K. E., Gershwin, L. J. 1999. Evaluation of severe disease induced by aerosol inoculation of calves with bovine respiratory syncytial virus. AJVR 60:473-80.
Author: Christopher C. L. Chase

BOVINE SPONGIFORM ENCEPHALOPATHY
BASICS DEFINITION
Bovine spongiform encephalopathy (BSE) is a progressively fatal, neurodegenerative disease of cattle and is a type of transmissible spongiform encephalopathy.
PATHOPHYS IOLOGY

Since its first diagnosis in the United Kingdom in 1986, different theories about the origin of BSE have been proposed.
The most common theory is that BSE mutated from the scrapie agent found in sheep, and changes in the rendering processes for livestock feed allowed this prion to survive and be fed to cattle. Then further rendering of infected cattle carcasses to make meat and bone meal amplified the agent.
Another theory is that BSE has always existed in cattle but went virtually unrecognized until 1986 when the outbreaks occurred in the UK.
SYSTEMS AFFECTED
Nervous
GENETICS
Offspring of BSE-infected cattle seem to have an increased risk of developing BSE but exact etiology is unknown at this time.
Vertical or venereal transmission has not been proven.
INCIDENCE/PREVALENCE
Annual incidence data are only available for the countries in which BSE has been diagnosed and in cattle over 24 months of age because the incubation period is thought to be more than one year.
The 2003 data range from as low as 0.16 cases per million bovines over 24 months of age in Canada to 137.19 cases per million bovines over 24 months of age in Portugal.
GEOGRAPHIC DISTRIBUTION
Infected indigenous cattle have been found in Austria, Belgium, Canada, Czech Republic, Denmark, Finland, France, Germany, Greece, Ireland, Israel, Italy, Japan, Lichtenstein, Luxembourg, Netherlands, Poland, Portugal, Slovakia, Slovenia, Spain, Switzerland, United Kingdom, and the United States. Imported cattle with BSE have been reported in the Falkland Islands and Oman.
SIGNALMENT
Species
Cattle, bison
Breed Predilections
NA
Mean Age and Range
Generally affects cattle between 3 and 6 years of age and the incubation period ranges from 2 to 8 years.
Predominant Sex
NA
SIGNS HISTORICALFINDINGS
Usually an insidious onset of neurologic signs in cattle older than 3 years of age.
PHYSICALEXAMINATION FINDINGS
Slowly progressive, degenerative neurological disease. Cattle will often be ataxic, primarily on the hind limbs with hypermetria. They will also have hyper-reflexia, muscle fasciculation and tremors, fall down, and behavior changes such as nervousness and frenzy. Over time, the animal will become anorexic and lose weight and body condition; dairy animals will have decreased milk production.
CAUSES
The agent that causes BSE is smaller than most viruses and highly resistant to common disinfectants, heat, UV light, and ionizing radiation.
While it has not been observed microscopically, there are three main theories as to the causative agent. First is that it is just an unconventional virus. Second is that it is an incomplete virus or virino. Third, and the most widely accepted theory, is that small prions, or proteinaceous infectious particles, cause normal prion proteins to change to an abnormal form and cause degenerative changes in the brain of infected cattle.
RISK FACTORS
Cattle consuming scrapie-infected meat and bone meal or other ruminant by-products that may be contaminated with the BSE agent
DIAGNOSIS DIFFERENTIALDIAGNOSIS
Rabies, lead poisoning, nervous ketosis, listeriosis, polioencephalomalacia, hypomagnesemia, intracranial tumors, and spinal cord trauma
CBC/BIOCHEMISTRY/URINALYS IS
There is no antemortem test for BSE as the host does not mount an immune response to the agent.
OTHER LABORATORY TESTS IMAGING DIAGNOSTIC PROCEDURES
N/A
PATHOLOGIC FINDINGS
Gross lesions are restricted to carcass changes such as emaciation and damage to the hide from ataxia and nervousness.
Histopathologic detection of neurodegeneration lesions in the brain (bilaterally symmetrical spongiform changes in the grey matter) will help confirm the diagnosis. Immunohistochemistry, immunoblotting, and ELISA to demonstrate accumulations of the prion (PrPres) protein are needed for definitive diagnosis.
TREATMENT
APPROPRIATE HEALTH CARE, NURSING CARE, ACTIVITY
There is no treatment for this disease.
DIET, CLIENT EDUCATION
Restrictions have been put in place in many countries that preclude the feeding of ruminant products back to ruminants, but clients should be made aware of this as a risk factor and prevent contamination of any cattle feed on their farms.
SURGICALCONSIDERATIONS
N/A
MEDICATIONS DRUGS OF CHOICE
N/A
CONTRAINDICATIONS
N/A
POSSIBLE INTERACTIONS
N/A
ALTERNATIVE DRUGS
N/A
FOLLOW-UP PATIENT MONITORING
N/A
PREVENTION/AVOIDANCE
Do not feed ruminant products to ruminants.
POSSIBLE COMPLICATIONS
N/A
EXPECTED COURSE AND PROGNOSIS
This is a progressively fatal neurodegenerative disease and 100% of the cases will die.
MISCELLANEOUS ASSOCIATED CONDITIONS
N/A
AGE-RELATED FACTORS
Most often seen in cattle between 3 and 6 years of age.
ZOONOTIC POTENTIAL
There is evidence to suggest that persons consuming BSE-contaminated products may develop a disease called variant Creutzfeldt-Jakob disease.
The exact incubation period for this disease is unknown but it is thought to be decades. It too is a progressively fatal neurologic disease with 28 years of age being the mean age at death of those affected with vCJD.
Since the first discovery of vCJD in 1996 through November 2006, there have been 200 cases worldwide, with the majority of cases in the UK (164) and France (21). The United States has reported 3 cases, but the patients had resided in the UK (2) and Saudi Arabia (1) the majority of their lives.
There are recommendations regarding blood donations, surgical equipment, and organ transplants from countries where vCJD has been diagnosed to prevent further spread of this disease.
PREGNANCY
Vertical transmission of BSE has not been documented but offspring of BSE-infected cattle are at higher risk for developing the disease; offspring are usually culled.
RUMINANT SPECIES AFFECTED
Bovine, bison
BIOSECURITY, PRODUCTION MANAGEMENT
N/A
SYNONYMS
Mad cow disease
SEE ALSO
Chronic wasting disease Hypomagnesemia Intracranial tumors Lead poisoning
Listeriosis Nervous ketosis
Polioencephalomalacia Rabies
Scrapie
Spinal cord trauma.
Variant Creutzfeldt-Jakob disease
ABBREVIATIONS
BSE = bovine spongiform encephalopathy ELISA = enzyme linked immunosorbent assay PrPres = abnormal prion protein
vCJD = variant Creutzfeldt-Jakob disease
Suggested Reading
Aiello, S. E., ed. 1998. Merck veterinary manual, 8th ed. Whitehouse Station, NJ: Merck and Co.
Bovine Spongiform Encephalopathy disease card from the OIE website accessed May 9, 2004, at http://www.oie.int/eng/maladies/fiches/a B115.htm.
Bovine Spongiform Encephalopathy from the United States Department of Agriculture, Animal and Plant Inspection Service website accessed May 9, 2004, at “http://www.aphis.usda.gov/lpa/issues/bse/bse.xhtml.
Bovine Spongiform Encephalopathy in the Manual of Standards for Diagnostic Tests and Vaccines. Paris, Office International des Epizooties, 2000, Chapter 2. 3. 13.
Centers for Disease Control and Prevention. BSE and vCJD Infectious Disease information websites accessed May 9, 2004, and January 16, 2007, at http://www.cdc.gov/ncidod/diseases/submenus/sub bse.htm.
Authors: Danelle Bickett-Weddle and Neal Bataller

BOVINE VIRAL DIARRHEA VIRUS
BASICS OVERVIEW

Bovine viral diarrhea (BVD) is a multifaceted disease with complicated pathogenesis and one of the most significant viral infections of cattle.
Bovine viral diarrhea virus (BVDV) is capable of infecting and causing pathology in many different organ systems.
Cattle can become acutely infected with BVDV at any age. This is also referred to as primary infection or transient infection.
Fetal infection prior to day 125 of gestation can result in the development of immunotolerance to the BVDV and the development of a persistent infection (PI) with the virus.
Cattle persistently infected with BVDV shed large amounts of virus during their lifetime. They are the major source of virus spread within and between farms.
SIGNALMENT
All ages and classes of cattle are susceptible to infection with BVDV.
INCIDENCE/PREVALENCE
BVDV is a ubiquitous pathogen of ruminants with high seroprevalence worldwide (up to 60% of adult cattle have antibodies). Infections with BVDV are endemic in many countries and are often associated with severe economic losses for the cattle industry.
GEOGRAPHIC DISTRIBUTION
Worldwide
Species
BVDV was thought to be species-specific but is now known to cause infection in species other than cattle including llama, alpaca, pigs, sheep, goats, white-tail deer, and mule deer.
Breed Predilections
N/A
Mean Age and Range
N/A Predominant Sex N/A
SIGNS
Infections are mostly subclinical in nature. However, there has been an emergence of new virulent BVD viruses that cause thrombocytopenia and hemorrhagic disease.
BVDV infection may result in subclinical acute infections; severe acute infections characterized by fever, leukopenia, and thrombocytopenia; persistent infections; reproductive disease presenting as congenital defects, repeat breeding, abortion, or mummification; enteric disease, respiratory disease; and immunosuppression. The severity of disease depends upon host and viral factors.
Acute infection may be defined as the infection of an immunocompetent animal with BVDV.
Following infection with BVDV, a short incubation period of 5-7 days is followed by viremia, which generally lasts for 1-2 days but may persist for 15 days.
A mild, biphasic elevation in body temperature and leukopenia may be evident.
Lactating cattle may have an associated decrease in milk production.
Some strains are pneumotropic and may cause severe fibrinopurulent bronchopneumonia in the presence of Mannheimia hemolytica.
Mucosal disease is characterized by fever, anorexia, depression, profuse salivation, nasal discharge, severe diarrhea, hemorrhages and erosions in gastrointestinal tract, and a very high case fatality rate (see Mucosal Disease in this volume).
BVDV subtype 2 is usually involved in severe acute BVD characterized by severe thrombocytopenia with hemorrhages (prolonged bleeding from venipuncture sites; hemorrhages on sclera of eye and inner surface of eyelids; hemorrhages on mucosal surfaces of cheeks, lower gingiva, tongue, and soft palate), fever, pneumonia, diarrhea, and sudden death in 10- 100% of infected animals.
BVDV can result in immunosuppression following acute infection resulting in secondary infections caused by opportunistic pathogens. BVDV has been implicated most often as an immunosuppressive component of the bovine respiratory disease complex.
In calves: diphasic pyrexia, leukopenia, anorexia, diarrhea, immunosuppression
In pregnant animals: early embryonic death, abortion, congenital infection (if infected within 45 to 125 days of gestation). At 12 days of gestation, infection usually results in the birth of PI animals. Signs may include cerebral hypoplasia, retinal atrophy, cataract, growth retardation, arrested bone development, and pulmonary hypoplasia.
CAUSES AND RISK FACTORS
BVDV is an RNA virus and a member of the genus Pestivirus in the family Flaviviridae.
The BVDV is antigenically related to classical swine fever virus (CSFV) of pigs and border diseases virus (BDV) of sheep. All pestiviruses are antigenically cross reactive.
The subtypes of BVDV include BVDV 1a, BVDV 1b, BVDV 2a, and BVDV 2b. All of these viruses can be either cytopathic (cp) or noncytopathic (ncp); the cp strains have an additional nonstructural protein. Both virulent and nonvirulent strains have been reported. Virulence does not depend on biotype (cp or ncp) or genotype.
The major risk factor for BVDV being introduced into a farm is the acquisition of new cattle. Other risk factors include sharing of pastures with other cattle (direct or fence line) and lack of a BVDV vaccination program.
Transmission
The virus is shed in most secretions and excretions of infected animals including tears, milk, saliva, urine, feces, nasal secretions, and semen.
Two main methods of virus transmission include postnatal horizontal transmission and gestational vertical transmission from a viremic dam to her fetus. Transmission may occur by aerosols, nose-to-nose contact, and via semen, rectal palpation, and embryo transfer. PI animals are much more efficient transmitters of BVDV than transiently infected animals because they shed large amounts of virus for a long period of time.
Infection at 120-150 days of gestation may result in abortion, resorption, stillbirths, or PI animals.
After 120 days, infection results in abortion, stillbirth, congenital defects, and normal appearing calves.
Virus can survive for several days or even weeks in a cool, protected environment and hence fomites (nose tongs, halters, etc.) play a role in virus transmission.
Flies can also transmit the virus.
The virus can be present in milk and colostrums.
DIAGNOSIS DIFFERENTIALDIAGNOSIS
Differential diagnosis for calves with diarrhea as the result of BVDV includes any pathogen known to cause diarrhea in neonatal calves. In adult cattle, differential diagnoses would include winter dysentery and salmonella.
Differential diagnosis for abortions caused by BVDV includes BHV-1, neospora, leptospirosis, and brucellosis.
Differential diagnosis for thrombocytopenia induced by BVDV includes sweet clover poisoning, coumarol poisoning, and vitamin K deficiency.
CBC/BIOCHEMISTRY/URINALYS IS
Severe leukopenia is characteristic in the early stages of acute BVD, with total leukocyte count in the range of 1000- 5000/µl being common.
Isolates of BVDV associated with hemorrhagic BVDV can result in severe thrombocytopenia and subsequently anemia.
IMAGING
N/A
DIAGNOSTIC PROCEDURES
Virus isolation from serum, whole blood, nasal swabs, or lymphoid tissue
PCR on serum, whole blood, nasal swabs, or lymphoid tissue
Identification of a fourfold increase in virus-neutralizing antibody titers in acute and convalescent serum samples
Persistent infection with BVDV can be diagnosed by identification of virus from serial samples taken 3 weeks apart using virus isolation, antigen detection ELISA, or PCR, or identification of BVDV antigen in skin samples by immunohistochemistry.
Virus/Viral Antigen Detection
Viral antigen can be found in brain, spinal cord, kidney, spleen, lymph nodes, testicular tubules, and endothelial cells of PI animals.
High throughput methods are now available for whole-herd screening to identify and remove PI animals.
For direct detection of viral antigen, cryostat sections of fresh tissues are stained with fluorescein-conjugated anti-BVDV antibody and then examined under a fluorescent microscope. The presence of apple-green fluorescence indicates a positive test.
Immunohistological staining of formalin-fixed, paraffin-embedded skin biopsies (ear notch samples) using 15C5 monoclonal antibody has been used to detect PI animals and is often considered better than histopathology and direct immunofluorescence (DFA) of tissues.
Antigen-capture ELISA (AC-ELISA) can be used for the detection of BVDV antigen in buffy coat cells, serum, and ear notch samples. Monoclonal antibody directed against a conserved antigenic domain of a nonstructural protein (NS2/3) of pestiviruses is used as a capture antigen followed by detection of antigen-antibody complex with enzyme-conjugated antibody. Serum can be used for the detection of PI animals by ACELISA. Acute animals are rarely detected by this test because the virus is present in the blood of acutely infected animal for only a short time.
Bovine turbinate (BT) cells, primary bovine embryo kidney (pBEK) cells, and cell lines originating from bovine embryonic trachea (EBTr) and buffalo lung (IMR-31) can be used for the isolation of BVDV from nasal discharge, peripheral blood leukocytes (PBL), lungs, semen, blood, serum, fetus, and feces. The isolated virus can be confirmed/identified by DFA, immunoperoxidase monolayer assay (IPMA), monolayer enzyme-linked immunosorbent assay (M-ELISA), AC-ELISA, or RT-PCR. The presence of anti-BVDV antibody in serum and buffy coat samples may interfere with virus isolation.
Antibody Detection
An indirect measure of virus infection is the detection of virus-specific antibodies in the sera of animals. Unfortunately, it is often difficult to differentiate among antibodies produced in response to acute infection, vaccination, or transfer of maternal antibodies from dam to offspring. In cattle, calves are usually born without antibody but seroconvert after colostrum consumption. These passive antibodies wane after 3-8 months. Hence, the presence of antibody in colostrum- deprived calves can be due only to active infection (either in utero or postnatal) or vaccination.
Seroconversion of sentinel animals can be used as an evidence for possible exposure to PI animals. Many tests are available for the detection of anti-BVDV antibodies, namely, virus-neutralization (VN), indirect immunofluorescence (IIF) assay, indirect immunoperoxidase (IIP) assay, and ELISA tests.
The virus neutralization (VN), also known as serum neutralization (SN), is considered to be the gold standard test for the detection of anti-BVDV antibodies and is used worldwide. The test can be used for the detection of antibodies against BVDV 1 or BVDV 2 depending upon the virus used in the test. In most situations, cp strains of BVDV are used in the test so that the presence of neutralizing antibodies can be detected by inhibition of viral infectivity as detected by the absence of viral cytopathology. Titers due to active infection can be differentiated from vaccination titers by demonstrating a fourfold rise in antibody titers using paired (acute and convalescent) serum samples. Virus neutralizing antibodies usually appear 3-4 weeks after infection and persist for years. Titers induced by vaccination may also persist for a long time. Passive antibodies decline at 105-230 days (but may persist for more than a year).
ELISA tests have been developed for the detection of anti-BVDV antibodies in serum samples. The antigens used in ELISA tests include whole-virus antigen, nonstructural protein (p125/80), monoclonal antibodies, and peptides. The advantages of the ELISA test include its sensitivity, ease, and objectivity in reading results, nondependability on cell cultures.
Indirect immunoperoxidase and indirect immunofluorescence tests also have been used for the detection of anti-BVDV antibodies.
Nucleic Acid Detection
Detection by reverse transcription-polymerase chain reaction (RT-PCR) has been found to be more sensitive and rapid than virus isolation. In addition, contrary to virus isolation, RT-PCR is not affected by the presence of antibodies in serum samples.
Due to its high sensitivity, RT-PCR is considered as an alternative to current standard methods for detecting BVDV, especially in pooled samples such as bulk tank milk. However, RT-PCR does not differentiate between nucleic acid from live or inactivated virus and may yield false positive results.
The prolonged stability of viral nucleic acid as compared to the virus itself has led to a simple method for the collection, storage, transport, and testing of blood samples. In this procedure, 10 µ l of blood or serum is applied to a Whatman No. 1 paper, the sample is air dried and then tested.
Several single- and two-tube RT-PCR assays have been described for the detection of BVDV RNA in serum, buffy coat cells, and fresh and formalin-fixed tissues (including ear notches).
Diagnosis by Testing Bulk Milk
Screening of bulk milk for antibody or antigen has been used to detect BVDV infection in cattle herds. The milk is centrifuged to remove fat and undiluted skim milk is tested for antibodies using an ELISA test. There is an excellent correlation between the level of antibodies in the bulk-tank milk and the prevalence of BVDV-antibody-positive cows.
RT-PCR assay to screen bulk milk samples for BVDV is also a sensitive and economic method for the detection of PI animals within a group because virus titers are usually higher in milk than in serum samples.
GROSS FINDINGS
In most cases, acute BVDV presents with no gross lesions that are specific.
Cattle may have lesions similar to those found with mucosal disease including erosions in the oral cavity, esophagus, rumen, abomasums, and small intestine, especially over areas of the Peyer’s patches.
Widespread petechial and ecchymotic hemorrhages may be present in cattle suffering from hemorrhagic syndrome.
No specific lesions are seen in aborted fetuses.
Cerebellar hypoplasia can be seen grossly in congenitally affected calves.
HISTOPATHOLOGICAL FINDINGS
Lymphoid depletion of the Peyer’s patches, lymph nodes, spleen, and thymus are common with acute BVDV infections.
TREATMENT
Cattle acutely infected with BVDV typically recover over time.
In severe cases, supportive therapy is indicated.
There is no treatment for cattle persistently infected with BVDV.
CLIENT EDUCATION
Eradication
Sweden was one of the first countries to introduce a national BVDV control program in 1993, which now forms the basis for control programs in many other countries.
The eradication programs are based mostly on detection and elimination of PI animals and immunization of breeding females prior to first gestation.
Vaccination is not allowed in Denmark. Therefore, it is easy in that country to detect infected animals by testing for the presence of antibodies.
The primary aims of eradication programs are the establishment of BVDV-free herds and prevention of reinfection of these herds so that there is a gradual decrease in the number of infected herds. This model works well in countries where cattle density is low and vaccination is not allowed but may not work in countries where both virus prevalence and cattle densities are high and where vaccination is permitted.
MEDICATIONS
N/A
CONTRAINDICATIONS
N/A
FOLLOW-UP PATIENT MONITORING
N/A
PREVENTION/AVOIDANCE
Implementation of a whole-herd vaccination program against BVDV is recommended.
Vaccinations should include antigens against both type 1 and type 2 BVDV.
Newly acquired cattle should be screened for persistent infection.
Newly acquired cattle should be quarantined for a minimum of 3 weeks.
Vaccination
Vaccination to prevent fetal infections is likely the most important measure to control the occurrence of PI calves.
Effective vaccines against infectious agents must account for both antigenic and genetic diversity, and they should provide fetal protection.
It should be remembered that colostral antibodies, which may last for 6 months, may interfere with vaccination.
Both modified-live (MLV) and killed vaccines are available. Most vaccines in the United States include BVDV 1a cp strains, although some vaccines do contain BVDV 2 cp strains.
Only a single dose of MLV vaccine is needed for initial immunization as opposed to killed vaccine that may require 2 or more doses. However, MLV vaccines are susceptible to inactivation by chemicals and/or exposure to higher temperatures. The MLV may also lead to mucosal disease when an animal persistently infected with an ncp strain is exposed to a closely related cp strain included in MLV.
Because of multiple doses needed and the added cost of adjuvants, killed vaccines turn out to be more expensive. However, they are recommended for dairy herds where pregnant animals are always likely to be present. Killed vaccines are also recommended for bulls in AI centers.
POSSIBLE COMPLICATIONS
The use of modified-live vaccines against BVDV in pregnant cattle is contraindicated unless specified by the product manufacturer.
Modified-live vaccines may be immunosuppressive and therefore should be used with caution.
EXPECTED COURSE AND PROGNOSIS
Most cattle recover within 10 to 14 days.
MISCELLANEOUS ASSOCIATED CONDITIONS
Mucosal disease occurs in cattle persistently infected with BVDV following a superinfection with an antigenically related cytopathic BVDV strain.
Cytopathic BVDV may also arise by mutation of the infecting ncp virus.
AGE-RELATED FACTORS
Colostral antibodies can protect newborn calves for 2-4 months.
ZOONOTIC POTENTIAL
BVDV is not considered a zoonotic agent.
Fetal infection with BVDV can result in abortion, congenital defects, persistent infection, or seroconversion. The result of fetal infection is dependent on the virus strain and biotype and the stage of gestation when fetal infection occurs.
In utero infection of the fetus with ncp BVDV prior to 120 days of gestation leads to immune tolerance and the birth of persistently infected (PI) calves that are unthrifty and poor doers and act as a source of virus for the rest of the herd. PI families can arise by breeding PI animals.
SEE ALSO
BHV-1
Brucellosis Coumarol poisoning Leptospirosis Mucosal disease Neospora Salmonella
Sweet clover poisoning Vitamin K deficiency Winter dysentery ABBREVIATIONS
BDV = border diseases virus of sheep BHV = bovine herpes virus
BT = bovine turbinate
BVD = bovine viral diarrhea BVDV = bovine viral diarrhea virus CP = cytopathic
CSFV = classical swine fever virus DFA = direct immunofluorescence
ELISA = enzyme-linked immunosorbent assay IIF = indirect immunofluorescence assay
IIP = indirect immunoperoxidase assay IPMA = immunoperoxidase monolayer assay mAbs = monoclonal antibodies
M-ELISA = monolayer enzyme-linked immunosorbent assay NCP = noncytopathic
PBL = peripheral blood leukocytes PCR = polymerase chain reaction PI = persistent infection
RT-PCR = reverse transcription-polymerase chain reaction SN = serum neutralization
VN = virus neutralization
Suggested Reading
Baker, J. C., Houe, H., eds. 1995, Nov. Bovine viral diarrhea virus. Vet Clin North Am Food Anim Pract. 11(3):521-47.
Bitsch, V., Ronsholt, L. 1995, Nov. Control of bovine viral diarrhea virus infection without vaccines. Vet Clin North Am Food Anim Pract. 11(3):627-40.
Campbell, J. R. 2004, Mar. Effect of bovine viral diarrhea virus in the feedlot. Vet Clin North Am Food Anim Pract. 20(1):39-50.
Fray, M. D., Paton, D. J., Alenius, S. 2000, Jul 2. The effects of bovine viral diarrhoea virus on cattle reproduction in relation to disease control. Anim Reprod Sci. 60-61:615-27.
Grooms, D. L. 2004, Mar. Reproductive consequences of infection with bovine viral diarrhea virus. Vet Clin North Am Food Anim Pract. 20(1):5-19.
Kelling, C. L. 2004, Mar. Evolution of bovine viral diarrhea virus vaccines. Vet Clin North Am Food Anim Pract. 20(1):115-29.
Authors: Daniel L. Grooms and Sagar Goyal

BRACKEN FERN TOXICITY
BASICS OVERVIEW

All ruminant species are at risk of developing toxicosis. Most cases of poisonings have been reported in cattle.
Bracken fern, or brake fern (Pteridium aquilinum), is a native perennial fern, 1 to 6 feet tall, with triangular, coarse, pinnately compound fronds. It has a deep-seated, black, elongate, branched, hairy, horizontal rhizome. Spores develop late in the summer and are found rolled under the blade edges. This is the only Pteridium species that is considered toxic in the United States. Other Pteridium species have been shown to contain the toxic principle in other parts of the world.
The plant prefers moist to dry woods and open slopes, with good drainage. It tends to occur naturally in very dense stands.
The young plants and rhizomes are the most toxic part of the plant, green or dried.
Disease in ruminants is generally seen following chronic exposures of variable concentrations of the plant in the diet.
Poisonings with this plant are relatively uncommon.
Diseases reported in ruminants include bone marrow suppression, enzootic hematuria, bladder and gastrointestinal carcinomas, and progressive retinal degeneration.
Key to controlling the disease is prevention. Bracken fern is susceptible to a wide variety of herbicides.
PATHOPHYS IOLOGY
Ptaquiloside is thought to be the main toxic principle. Other agents reported to be toxic include quercetin and shikimic acid. The species of animal exposed, and the dose and duration of exposure, are thought to be the limiting factors in determining which disease the animal succumbs to.
Bone marrow suppression has been observed in clinically affected animals; there is suppression of all cell lines (radiomimetic effect).
Clinically affected animals generally present with signs associated with thrombocytopenia and neutropenia; anemia may occur as a result of blood loss or later as the red cells disappear from circulation (long life span).
Bovine enzootic hematuria (“red water”) has been reported in cattle chronically exposed to bracken fern. This syndrome is linked to the development of bladder lesions, some of which are neoplastic. Hematuria and bladder neoplasms predominate in cattle, but papillomas, sarcomas, and carcinomas of the jaw and gastrointestinal tract can occur in sheep. Exposures of months or years are required to cause these types of changes. It has been speculated that viruses (bovine papillomavirus type 2 and type 4) may play a role in the development of neoplastic lesions.
Experimentally, bracken fern exposure for 4 to 12 months has been associated with progressive retinal degeneration in sheep.
Polioencephalomalacia has been reported in sheep chronically exposed to the plant (rare).
SYSTEMS AFFECTED
Bone marrow, urinary tract, gastrointestinal tract, and eye
GENETICS
N/A
INCIDENCE/PREVALENCE
Unpredictable and uncommon
GEOGRAPHIC DISTRIBUTION
Worldwide
SIGNALMENT
Cattle are most commonly affected.
Species
All ruminants appear susceptible; most poisonings have been reported to occur in cattle.
Breed Predilections
N/A
Mean Age and Range
Enzootic hematuria and tumors are generally observed in older animals, following months or years of exposure.
Predominant Sex
N/A
SIGNS
Cattle afflicted with bone marrow suppression generally present with bloody nasal discharge, petechiation and ecchymoses, and weakness. Secondary bacterial infections are common (e.g., lung), and signs of dyspnea, decreased appetite, and hyperthermia can be observed.
Red to brown urine is a common change in those cattle suffering from enzootic hematuria.
Signs can be varied depending on the tumor site.
Sheep suffering from retinal degeneration show bilateral pupil dilatation and have a glassy-eyed appearance (“bright blindness”).
CAUSES AND RISK FACTORS
Poisonings can occur as a result of grazing the fresh plant (thought to be unpalatable) or following chronic consumption of contaminated hay.
The plant is toxic green or dry; the most toxic parts of the plant are the young developing fronds (fiddleheads or crosiers) and rhizomes.
Clinical disease is generally seen when animals consume significant amounts of plant material (up to 20% of their diet) for 30 days or more.
DIAGNOSIS DIFFERENTIALDIAGNOSIS
Thrombocytopenia has been reported with BVD virus infection.
CBC/BIOCHEMISTRY/URINALYS IS
Thrombocytopenia and neutropenia; anemia is observed later on.
Inflammatory leukogram, hyperproteinemia, elevated fibrinogen can be due to secondary infectious processes.
Hematuria
OTHER LABORATORY TESTS
Prolonged bleeding times
IMAGING
N/A
DIAGNOSTIC PROCEDURES
Examination of the bone marrow may reveal pancytopenia-risky procedure in compromised patients.
PATHOLOGIC FINDINGS
Petechiation and ecchymoses, multiple hemorrhages throughout the tissues, pale bone marrow, edematous and ulcerated GIT
Numerous neoplastic conditions of the GIT and urinary tract-papillomas, transitional cell carcinomas, squamous cell carcinomas, adenocarcinomas, hemangiomas
Retinal degeneration and atrophy of the outer layers
TREATMENT
Find and remove the suspect source or remove animals from the contaminated environment.
Most animals respond poorly to treatment.
Broad-spectrum antibiotic use, animal stress reduction, and good nursing care can be utilized.
Appropriate milk and meat withdrawal times must be followed for all compounds administered to food-producing animals.
MEDICATIONS
N/A
CONTRAINDICATIONS
Appropriate milk and meat withdrawal times must be followed for all compounds administered to food-producing animals.
FOLLOW-UP
N/A
PATIENT MONITORING
Monitor platelet, neutrophil, and red blood cell values.
Check for onset of secondary infections.
PREVENTION/AVOIDANCE
Be able to recognize bracken fern in the field or in hay, and avoid excessive grazing.
Herbicide application can be successful in eliminating the plant.
POSSIBLE COMPLICATIONS
N/A
EXPECTED COURSE AND PROGNOSIS
Animals suffering from bone marrow suppression almost never recover.
MISCELLANEOUS ASSOCIATED CONDITIONS
Monogastrics exposed to bracken fern suffer from neurologic disease that is thought to be related to a thiamine deficiency.
AGE-RELATED FACTORS ZOONOTIC POTENTIAL
Since ptaquiloside is a direct-acting carcinogen, people conceivably can be affected through direct consumption of the plant or ingesting meat or milk from exposed animals.
PREGNANCY
N/A
RUMINANT SPECIES AFFECTED
Cattle are most commonly reported to be affected; but there are reports of sheep, llamas, and other ruminants being affected.
BIOSECURITY
N/A
PRODUCTION MANAGEMENT
Avoid feeding “weedy” hay.
Avoid grazing in bracken dense areas, provide adequate forage, and instill appropriate stocking densities.
SYNONYMS
Bracken fern, brake fern Bright blindness
SEE ALSO
BVD
Toxicology: herd outbreaks
ABBREVIATIONS
BVD = bovine viral diarrhea GIT = gastrointestinal tract Suggested Reading
Plumlee, K. H., Nicholson, S. S. 2004. Ptaquiloside. In: Clinical veterinary toxicology, ed. K. H. Plumlee. St. Louis: Mosby.
Pteridium. 2001. In: Toxic plants of North America, ed. G. E. Burrows, R. J. Tyrl. Ames: Iowa State University Press.
Author: Patricia Talcott

BRASSICA SPP. TOXICITY
BASICS OVERVIEW

Ingestion of Brassica spp. can cause various diseases including goiter, enteritis, and Heinz body anemia in ruminant animals.
Forages or roots of the genus Brassica include kale, rape, turnips, mustards, cabbage, brussels sprouts, and others.
Brassica spp. contain glucosinolates, which have goitrogenic effects and induce gastrointestinal irritation.
These plants also contain S-methylcysteine sulphoxide (SMCO), which causes Heinz body anemia.
Other diseases associated with Brassica spp. ingestion include polioencephalomalacia, photosensitization, and acute bovine pulmonary emphysema and edema.
There are three groups of glucosinolates, which can be enyzmatically broken down into different metabolites: isothiocyanates, thiocyanate ion, and thiones.
Isothiocyanates are found in mustard oils contained in plant seeds. These are irritants to the gastrointestinal mucosa causing enteritis and diarrhea.
Thiocyanate ion can cause goiter when ingested in small amounts over extended periods of time, particularly if the dietary content of iodine is low. Thiocyanate ion reduces iodine uptake by the thyroid and can be treated with exogenous iodine.
Thiones are a potent goitrogen, which interferes with the formation of thryoxine. Treatment with iodine does not alleviate clinical signs.
“Rape blindness” has been observed in cattle and sheep grazing on rape. Other neurological signs such as head pressing and behavioral changes have been noted. These signs may be as a result of a mild degree of polioencephalomalacia or hepatotoxicity.
Acute bovine pulmonary emphysema and edema have been observed in cattle on Brassica spp. plants. Brassica spp. forage may precipitate 3-methylindole-associated disease.
PATHOPHYS IOLOGY
Thiocyanate ion can cause goiter when ingested in small amounts over extended periods of time, particularly if the dietary content of iodine is low.
Thiocyanate ion reduces iodine uptake by the thyroid and can be treated with exogenous iodine. Thiones are a potent goitrogen, which interferes with the formation of thryoxine.
Another toxin is S-methylcysteine sulphoxide (SMCO), which is converted to dimethyl disulphide (DMDS) by the rumen or gut organisms.
DMDS interferes with disulphide exchange reactions, which results in changes in red blood cell membranes and hemoglobin. This can lead to Heinz body formation and anemia.
Brassica spp. have also been associated with primary and secondary or hepatogenous photosensitization.
SYSTEMS AFFECTED
Hemic
Lymphoreticular
Gastrointestinal
Nervous
Respiratory
Integumentary
GENETICS
N/A
INCIDENCE/PREVALENCE
N/A
GEOGRAPHIC DISTRIBUTION
Potentially worldwide depending on species and environment
SIGNALMENT
Brassica spp. poisoning has been reported in cattle, sheep, goats, and pigs. Goiter may be seen in animals of any age. Feeding Brassica spp. to pregnant dams may result in neonates with goiter.
Hemolytic anemia occurs after 1-3 weeks of ingestion of a diet consisting mainly of Brassica spp. plants. Enteritis can occur after ingestion of large amounts of rapeseed and Brassica spp. seeds containing mustard oils.
Pulmonary emphysema has been reported only in cattle.
Species
Potentially all ruminant species
Breed Predilections
N/A
Mean Age and Range
Any age Predominant Sex N/A
SIGNS HISTORICALFINDINGS
Clinical signs for goiter include thyroid enlargement, weakness, lethargy, and recumbency. Animals with goiter may show signs of weight loss or failure to gain weight.
Animals in hemolytic anemia crisis may show signs of lethargy, anorexia, dyspnea, coffee-colored urine and mucous membranes, icterus, hypoxic abortion, and cardiovascular shock. Death results from respiratory failure secondary to anemia.
Clinical signs associated with enteritis include diarrhea, dysentery, abdominal pain, salivation, and occasionally vomiting. Anorexia, ruminal stasis, and scant, sticky feces may also be noted with gastrointestinal disturbances.
Signs of photosensitization include erythema and blistering of affected areas, particularly areas of light-pigmented skin.
PHYSICALEXAMINATION FINDINGS CAUSES AND RISK FACTORS
Brassica poisoning can be found in any commercial operation that provides Brassica plants or seeds as feed.
Glucosinolate concentration can vary between Brassica plant species and can vary with season. The highest concentration of glucosinolates can be found in seeds, but are present in all parts of the plants. Plants become more toxic as they mature.
The SMCO content of Brassica plants also increases with maturity and the flowers and seeds are particularly toxic.
DIAGNOSIS DIFFERENTIALDIAGNOSIS
A nutritional deficiency of iodine can cause goiter. Goiter may also be caused by the ingestion of couch grasses (Cynodon aethiopicus, C. nlemfuensis) and white clover (Trifolium repens).
Differential diagnoses for signs of hemolytic anemia include onion toxicity, red maple toxicity as well as leptospirosis, hypophosphatemia in postparturient cows, babesiosis, anaplasmosis, chronic copper poisoning, as well as immune- mediated and drug-induced hemolytic anemias.
Differential diagnoses for Brassica spp.-induced signs of gastritis are numerous including ingestion of oak species,
Nerium spp. (oleander),Geigeria spp., Eupatorium rugosum, and others, as well as parasitic, viral, and bacterial etiologies.
Many species of plants, grasses, and blue-green algae can cause primary and secondary photosensitization.
CBC/BIOCHEMISTRY/URINALYS IS
Assays of serum glucosinolate levels are available.
Heinz bodies and decreased serum hemoglobin levels can be observed on complete blood counts.
TREATMENT
There is no specific treatment for Brassica spp. poisoning. Removal of Brassica spp. feedstuffs and relocating animals away from pastures populated with Brassica spp. are recommended.
Administration of iodine may be beneficial in cases of iodine deficiency. Blood transfusions may be necessary in cases of severe hemolytic anemia.
MEDICATIONS
DRUGS OF CHOICE CONTRAINDICATIONS
Appropriate milk and meat withdrawal times must be followed for all compounds administered to food-producing animals.
PRECAUTIONS
N/A
POSSIBLE INTERACTIONS
N/A
FOLLOW-UP PREVENTION/AVOIDANCE
Removal of Brassica spp. feedstuffs and relocating animals away from pastures populated with Brassica spp. are recommended.
EXPECTED COURSE AND PROGNOSIS
Fair to guarded if removed from plant
MISCELLANEOUS ASSOCIATED CONDITIONS
N/A
AGE-RELATED FACTORS
N/A
ZOONOTIC POTENTIAL
N/A
PREGNANCY
Feeding Brassica spp. to pregnant dams may result in neonates with goiter.
RUMINANT SPECIES AFFECTED
Potentially all ruminant species are affected.
BIOSECURITY
N/A
PRODUCTION MANAGEMENT
Removal of Brassica spp. feedstuffs and relocating animals away from pastures populated with Brassica spp. are recommended.
SYNONYMS
N/A
SEE ALSO
Anaplasmosis Babesiosis
Blue-green algae
Chronic copper poisoning Ingestion of oak species Leptospirosis
Nutritional deficiency of iodine Oleander
Onion toxicity
Primary photosensitization Red maple toxicity ABBREVIATIONS
DMDS = dimethyl disulphide
SMCO = S-methylcysteine sulphoxide
Suggested Reading
Bell, J. M. 1984, Apr. Nutrients and toxicants in rapeseed meal: a review. J Anim Sci. 58(4): 996-1010.
Bray, T. M., Kirkland, J. B. 1990. The metabolic basis of 3-methylindole-induced pneumotoxicity. Pharmacol Ther. 46(1): 105-18.
Gonzalez, J. M., Yusta, B., Garcia, C., Carpio, M. 1986, Oct. Pulmonary and hepatic lesions in experimental 3- hydroxymethylindole intoxication. Vet Hum Toxicol. 28(5): 418-20.
Morton, J. M., Campbell, P. H. 1997, Feb. Disease signs reported in south-eastern Australian dairy cattle while grazing
Brassica species. Aust Vet J. 75(2): 109-13.
Stoewsand, G. S. 1995, Jun. Bioactive organosulfur phytochemicals in Brassica oleracea vegetables-a review. Food Chem Toxicol. 33(6): 537-43.
Taljaard, T. L. 1993, Jun. Cabbage poisoning in ruminants. J S Afr Vet Assoc. 64(2): 96-100.
Author: Natalie Coffer

BREEDING SOUNDNESS EXAMINATION AND INFERTILITY IN MALE CAMELIDS
BASICS DEFINITION

Breeding soundness examination of the male camelid is becoming an integral part of many prepurchase examinations requested by breeders. This examination is not intended to measure fertility but to help identify males with reproductive problems.
The reproductive system of the male camelid presents several anatomical and physiological peculiarities (see Camelid Reproduction). The practitioner should be familiar with these peculiarities in order to complete a thorough examination of a male.
SYSTEMS AFFECTED
Reproductive
GENETICS
N/A
INCIDENCE/PREVALENCE
N/A
GEOGRAPHIC DISTRIBUTION
Worldwide
SIGNALMENT
Species
Camelids
Breed Predilections
N/A
Mean Age and Range
N/A Predominant Sex Male
SIGNS
HISTORY AND PHYSICALEXAMINATION
History and Signalment
Age of the animal is important. Problems such as inability to mount or exteriorize the penis or even substandard fertility can be due to sexual immaturity
Origin and type of management
Breeding records
Previous health problems
Reason for examination
Physical Examination
Reproductive performance of the male can be affected by diseases of other systems.
Prolonged febrile condition or debilitating diseases can affect testicular function and spermatogenesis.
A complete health history, including previous illnesses, vaccination, and recent treatments, should be taken.
A general physical examination should be performed including general appearance and body condition of the animal.
During the sire-selection process, particular attention should be given to the presence of congenital or potentially heritable conditions.
Reason for Examination
Reasons for examination can be generally divided into two categories: prepurchase examination of a herd sire and examination for infertility or obvious genital lesions.
It is very important to define exactly the problem(s) to be addressed: existence of visible lesions, suspicion of infertility due to many unsuccessful breedings, or a change in the reproductive behavior (reduced libido).
An approximate date of the onset of the problem should be obtained as well as conditions: did the problem appear suddenly or was it a slow, progressive process?
Examination of the Prepuce and Penis
Examination should be done when there is an obvious problem at this level, such as an abnormally pendulous prepuce, presence of edema, or laceration.
Examination of the prepuce may require sedation of the animal.
Ability to exteriorize the penis is best observed during a live cover.
The penis is normally extended when the male assumes the breeding position but full erection is completed intravaginally.
Penile attachment to the prepuce is normal in young, prepuberal animals but can signal the presence of adhesions in the mature male. In llamoids, the penis should be completely free at 3 years of age.
Examination of the Testicles and Scrotal Content
The scrotal region is examined from a distance to evaluate testicular descent and integrity of the skin in the area.
Both testes should be present and visible within the scrotum in the perineal region.
In older males, the scrotum may sometimes be pendulous.
One of the testicles is usually situated slightly more ventral than the other, but both should be nearly equal in size (difference less than 15%).
Testicles are predisposed to traumatic lesions including bites by other males.
Palpation of the scrotum and its contents is necessary to appreciate the regularity of the contour of the testes as well as their consistency.
The surface of the testes should be smooth and regular.
The testes are normally resilient. They become hard and fibrotic or very soft in the case of degenerative changes.
The scrotal sac should be free from fluid.
The tail of the epididymis is palpable as a small hard nodule.
Testicular size is an important indicator of sperm production capacity. Size of the testis can be evaluated by measuring its length and width using precision calipers or ultrasonography. In the llama, the long axis should measure at least 1.1 cm in a yearling and 3.2 cm by 2 to 3 years of age. In alpacas, the testes’ long axis should be at least 3.5 cm in order to achieve good fertility in a herd. The length and width of the testicle in adult males should be 5-7 cm and 3-4 cm in llamas and 4-5 cm and 2.5-3 cm in alpacas.
Ultrasound of the testicle should be part of the routine breeding soundness examination. It is preferably done with a linear 7.5 MHz transducer (see Camelid Reproduction).
Examination of the Accessory Sex Glands
When examination of the accessory sex glands is required, transrectal ultrasonography is the best method to accomplish this.
The bulbourethral glands are found just cranial and on each side of the anal sphincter.
Following the pelvic portion of the penis cranially images the prostate.
Evaluation of Mating Behavior
Mating ability of the male is best observed in the presence of a receptive female.
During this evaluation, the succession of normal behavioral patterns is recorded as well as the times needed for each step: chasing, forcing down, mating, intromission, and duration of copulation.
Behavioral problems at mating can be due to shyness, inexperience, or lack of libido.
Semen Collection
Semen collection presents many difficulties due mainly to the nature of copulatory behavior and the slow (dribbling) process of ejaculation in camelids.
Semen collection using an artificial vagina is possible but requires training and the use of a specially designed dummy mount fitted with a collection apparatus. The average duration of collection is about 30 minutes in llamas and 22 minutes in alpacas.
Electroejaculation, using ram probes in llamoids and bovine probes in camels, has been accomplished under various degrees of sedation or anesthesia.
Response to the electrical stimulus varies greatly from one individual to the other.
Erection is possible during electroejaculation but failure to obtain an ejaculate or only a few sperm cells is common.
The ejaculate obtained by electroejaculation is often of poor quality and contaminated with urine and cellular debris.
In practice, the techniques most commonly used are vaginal aspiration and electroejaculation.
Vaginal aspiration is accomplished by allowing a male to complete breeding with a receptive female. Upon completion of the mating an infusion pipette is introduced vaginally and the seminal fluid is aspirated using a 12 ml syringe.
Semen Evaluation
The major problem in interpreting semen analysis in the camelid is the lack of standard methods for collection and for examination.
Volume
Ejaculate volume varies greatly depending on the method of collection used, duration of copulation, and male variation.
Ejaculate volume ranges from 0.4 to 12.5 ml.
Vaginal aspiration yields volumes ranging from 0.25 ml to 5 ml.
Color
The color of semen varies according to sperm concentration.
It is predominately milky white whether it is collected by electroejaculation or by other methodology, but can sometimes be creamy white.
Ejaculate may be heterogeneous with some translucent material mixed with cloudy areas.
Ejaculates collected by vaginal aspiration may be pink or red because of contamination with blood from the cervix.
Consistency and Liquefaction
Camelid semen is viscous and requires some time to liquefy.
The degree of viscosity depends on the individual male and on the proportion of seminal gelatinous fluid and tends to decrease with number of ejaculates.
The time required for liquefaction varies from one male to another and from one ejaculate to another.
Viscosity is attributed to the presence of mucopolysaccharides from secretions of the bulbourethral glands or the prostate.
Liquefaction of camelid semen can be obtained by addition of trypsin or collagenase to the ejaculate.
Sperm Concentration
Concentration of semen is best estimated using a hemocytometer technique after liquefaction.
Sperm concentration is highly variable (82,000 to 250,000/mm3) and is affected by age, method of collection, and ejaculate rank.
pH
The pH of semen varies between 7.5 and 8.1.
Semen pH is affected by method of collection and rank of ejaculate.
Semen Motility
Motility of semen is appreciated on nondiluted samples (mass activity) and on diluted samples (individual sperm motility).
Mass activity is generally poor in camelidae semen unless the ejaculate is constituted exclusively by the sperm-rich fraction.
In fresh nondiluted samples, only oscillatory movements are observed.
Initial motility is very low (5%) and increases as the ejaculate liquefies.
Progressive motility can only be estimated after liquefaction and dilution with a suitable extender.
Semen Morphology
The head of camelidae spermatozoa is described as elliptical as opposed to ovoid in other species.
Lengths of the head and middle piece are shorter than those of other animals.
Morphology of the spermatozoa can be evaluated on smears stained with eosine-Nigrosin Hancock stain or Diff Quick (Giemsa) stains.
A total of at least two hundred sperm cells from different fields should be evaluated from each sample.
Morphological evaluation is done under phase contrast microscopy as for other species.
The morphological abnormalities should be reported according to type and location.
Effect of various types of abnormalities on fertility has not yet been determined.
Total abnormalities should not exceed 50%.
The most common abnormalities are proximal droplets, knobbed or swollen acrosome and tail, and midpiece reflex.
Endocrine Evaluation
Information on endocrinological evaluation of the infertile male camelid is completely lacking. The only practical use of endocrine evaluation is in the differential diagnosis between cryptorchidism and castration.
Presence of testicular tissue can be ascertained if there is at least a twofold increase in serum testosterone level within 8 to 24 hours after IV administration of hCG (3000 IU for alpacas, 5000 IU in llamas, 10,000 IU in camels).
Testicular Biopsy
Indications
Testicular biopsy is not a routine procedure for the evaluation of the breeding soundness in the male.
Testicular biopsy should be considered in males that have low fertility, testicular asymmetry, and abnormal testicular ultrasonography that is not consistent with hematoma or orchitis.
This technique is useful for diagnosis of spermatogenic arrest, oligospermatogenesis, hypogonadism, inflammations, and neoplasm.
Techniques
Wedge biopsy: an incisional or open biopsy requires general anesthesia. After surgical preparation of the scrotum, an incision (0.5 cm) is made over the skin, parietal vaginal tunic, and the exposed tunica albuginea avoiding vascular areas. Testicular tissue allowed to protrude from the rent in the tunica albuginea is ablated using a scalpel blade. The tunica albuginea, parietal vaginal tunic, and scrotal skin are closed with absorbable suture.
Trucut: use under sedation or anesthesia. After surgical preparation of the testicles, the scrotum is incised using a sterile #10 surgical blade (alpacas) or #11 scalpel (llamas). The trucut (14-gauge self-firing) biopsy needle is inserted in the testicle through the tunica albuginea. The scrotum is closed with two skin sutures using 2-0 Vetafil. Results obtained with this technique are more reliable but hemorrhage at the biopsy site is more frequent.
“Core” biopsy: A needle “core” biopsy can be performed using a 1 1/2 in., 16-gauge needle after heavy sedation of the animal. After surgical preparation of the scrotal skin, the needle is introduced into the testicular parenchyma and redirected by a gentle push-pull movement into two different sites. The needle is retracted from the tissue while a finder is placed over the hub to maintain the core sampled. A direct smear is prepared from the sample obtained.
Fine needles aspirate: Fine needle aspirate cytology is a commonly used technique for the evaluation of azoospermia and testicular neoplasm in humans. It is rapid, simple, and inexpensive. Testicular tissue is aspirated with a 20-gauge needle and 12 ml syringe. A puncture is made and aspirates are taken in three to four directions making sure not to include the epididymis. Cytological smears stained with Diff Quick are interpreted based on the different types of spermatogenic cells.
Interpretations
Interpretation should be done by an individual familiar with the technique and histology of camelid testes.
Fine-needle aspirates are very difficult to interpret. The relative frequency of cell types provides a differential diagnosis between hypospermatogenesis, spermatogenic arrest, and normal spermatogenesis. A fine-needle aspirate from azoospermic animals consists of Sertoli cells alone, a few mature spermatozoa, and scant cell material or spermatid but no spermatozoa.
“Core” biopsy provides more cellular material than fine-needle biopsy.
Trucut or self-firing biopsy instruments are safe and provide a good amount of tissue for examination of seminiferous tubule spermatogenic activity.
Presence of normal spermatogenic activity in cases of azoospermia may suggest the presence of segmental aplasia or other forms of obstructive azoospermia.
Atypical spermatogenic cells are usually associated with testicular neoplasm (seminoma).
No spermatogenic cells are obtained from atrophic testicles.
Complications
Hematoma or hemorrhage
Adhesions and inflammation
Autoimmune reactions (development of antisperm antibodies)
Degeneration of germinal epithelium and tubules
Transient decrease in sperm output that lasts for several months
Wedge biopsy is the most unsafe of all methods
Complication risk increases if the technique is not performed correctly and quickly
Reproductive Disorders in the Male Camelid
Inpotentia Cuendi
Inability to complete mating may be due to poor libido, erection or ejaculation failure.
Poor libido may be associated with endocrinological disorders, systemic diseases or diseases of other organs (including megaesophagus!) and high ambient temperature.
Young male may be too shy to perform particularly in clinic setting.
Erection failure may be due to neurological disorders, painful conditions, or preputial stenosis.
Incomplete mating may be due to obesity or abdominal pain.
Impotentia Gerandi
Inability to achieve fertilization
May be due to azoospermia or severe oligospermia of testicular (hypoplasia, degeneration) or epididymal (stenosis, segmental aplasia) origin
Asthenozoospermia (lack of motility)
Teratospermia (increased rate of abnormalities)
Diseases of the Penis and Prepuce
Infections of the prepuce and the penis are relatively rare in camelidae because they are well protected due to their anatomic position.
Preputial swelling is due to local inflammation caused by contact with chemical or physical irritants, parasitic infestation, or rupture of the urethra.
Preputial swelling can also be part of a large ventral edema in some animals suffering from heat stress.
Preputial prolapse is often seen in alpacas. It may require surgical correction.
Paraphymosis can become complicated by the presence of dirt in the preputial opening and lead to a balanoposthitis, sometimes with necrosis of the tip of the penis.
Early detection of paraphymosis and treatment will avoid these complications.
In llamas, paraphymosis and balanoposthitis can be due to the presence of “hair rings” if the females are not clipped before breeding.
Urolithiasis: most calculi occur at the level of the distal part of the urethra or at the level of the sigmoid flexure. Relief of the condition can be attempted via urethrostomy. Recurrence of obstruction is common even after urethrostomy.
Diseases of the Testis
Scrotal trauma
Bites from other males are a common complaint in the male camelid.
Prognosis for the reproductive life of the individual male depends on the extent of the injury and the time elapsed until detection.
The affliction should be differentiated from orchitis or hydrocele.
Deep lacerations are frequently complicated by testicular hemorrhage, infection, and development of schirrous cord and require urgent surgical intervention (castration).
Hydrocele
Due to an inflammatory or noninflammatory process.
The scrotal sac becomes pendulous and increased in size.
Initial diagnosis is based on palpation of the scrotum and its content.
The scrotum is not painful and the testes are usually free within the scrotal sac and fluid can be isolated in one area.
Confirmation is done by visualization of the fluid by ultrasonography.
Moderate hydrocele is sometimes observed in summer. The condition resolves progressively with decreasing ambient temperature.
Hydrocele can develop following obstruction of the normal blood flow in the spermatic cord.
Hydrocele may be due to the presence of an abscess at the level of the external inguinal ring.
Long-standing hydrocele affects the thermoregulation of the testes and decreases the quality and quantity of semen.
Orchitis
Usually caused by hematogenous route.
Systemic antimicrobial therapy is indicated but is generally not efficacious.
Castration of the affected testicle in valuable males may increase the chance of salvaging the nonaffected testicle and the reproductive life of the animal.
Testicular degeneration
The most common cause of infertility in camelids.
The degenerated testicles are smaller than normal and either soft or hard and fibrous.
Semen shows increased abnormalities and the presence of spheroid (round) germinal cells.
Partial or total testicular hypoplasia or atrophy
Testicular hypoplasia is common in camelids.
Differential diagnosis between hypoplasia and atrophy requires histopathological techniques.
Semen may show increased abnormalities and poor concentration.
Cryptorchidism
Relatively rare in camelids.
Can be unilateral or bilateral and is suspected when inspection of the perineal region shows a flat or absent scrotum.
The undescended testicles are usually found close to the internal inguinal opening but could also be found intra- abdominally, caudal to the kidney, or within the inguinal canal.
Cryptorchidism was reported in related vicuñas, which suggests that the affliction may be hereditary.
Should be differentiated from anorchism (absence of a testicle), which is generally accompanied by absence of the kidney on the same side.
Differential diagnosis: endocrinology, laparoscopy, laparotomy.
Testicular tumors
Rare
Seminomas are the most common
Sertoli cell tumors and teratomas are possible
Testicular cysts
Found in 15% of all males examined by the author.
Can be detected ultrasonographically.
They can be located in the rete testis, seminiferous tubules, head or tail of the epididymis.
The effect on fertility varies from complete sterility (azoospermia) to subfertility depending on the size and location of the cysts.
Some males with small testicular cysts have normal fertility.
Diseases of the Epididymis
Epididymitis is usually associated with orchitis.
Epididymal cysts are common in alpacas and llamas.
Cysts are found on the anterior aspect of the head of the epididymis and near the ventral border of the testis.
Cysts vary in size between 1 mm and 50 mm.
Large cysts may be due to segmental aplasia of the epididymal duct.
Subfertility or Infertility of Unexplained Origin
Decreased fertility may be due to overuse or senile changes.
The author has seen cases of infertility/sterility with normal seminal parameters and behavior.
Molecular factors (immunologic or genetic) may be involved in males with unexplained infertility.
Males have different abilities to induce ovulation (lack or reduced activity of the ovulation inducing agent present in seminal plasma).
MISCELLANEOUS ASSOCIATED CONDITIONS
It is very important to define exactly the problem(s) to be addressed: existence of visible lesions, suspicion of infertility due to many unsuccessful breeding attempts, or a change in the reproductive behavior (reduced libido).
AGE-RELATED FACTORS
Penile attachment to the prepuce is normal in young, prepuberal animals but can signal the presence of adhesions in the mature male. In llamoids, the penis should be completely free at 3 years of age.
ZOONOTIC POTENTIAL
Brucellosis, though not common in camelids, is a zoonotic disease worth concern.
PREGNANCY
N/A
RUMINANT SPECIES AFFECTED
Camelids and camels
BIOSECURITY
N/A
PRODUCTION MANAGEMENT
N/A
SYNONYMS
N/A
SEE ALSO
BSE: Bovine, Ultrasound
ABBREVIATIONS
BSE = breeding soundness exam
HCG = human chorionic gonadotropin IU = international units
IV = intravenous
Suggested Reading
Bravo, P. W., Flores, D., Ordonez, C. 1997. Effect of repeated collection on semen characteristics of alpacas. Biol Reprod. 57:520-24.
Flores, P., Garcia-Huidobro, J., Munoz, C., Bustos-Obregon, E., Urquita, B. 2002. Alpaca semen characteristics previous to a mating period. Animal Reproduction Science 72: 259-66.
Heath, A. M., Pugh, D. G., Sartin, E. A., Navarre B., Purohit, R. C. 2002. Evaluation of the safety and efficacy of testicular biopsies in llamas. Theriogenology 58(6):1125-30.
Tibary, A., Anouassi, A. 1997. Pathology and surgery of the reproductive tract and associated organs in the male camelidae. In: Theriogenology in Camelidae: anatomy, physiology, BSE, pathology and artificial breeding, ed. A. Tibary. Actes Edition, Institut Agronomique et Veterinaire Hassan II, Morocco.
Tibary, A., Anouassi, A., Memon, A. M. 2001. Approach to infertility diagnosis in camelids: retrospective study in alpacas, llamas and camels. Journal of Camel Practice and Research. 8:167-79.
Author: Ahmed Tibary

BREEDING SOUNDNESS EXAM: BEEF BULL
BASICS DEFINITION

A breeding soundness exam (BSE) is an evaluation of a bull’s reproductive soundness based on a physical examination of the reproductive tract and semen evaluation.
The primary focus is on the reproductive system but the musculoskeletal system and ophthalmic systems must be evaluated as well.
Some examiners will include libido or serving capacity tests as part of a BSE.
The BSE is not meant to be a general health exam.
PATHOPHYS IOLOGY
N/A
SYSTEMS AFFECTED
Reproductive, musculoskeletal, ophthalmic, behavioral
GENETICS
Genetics play an important role in the onset of puberty.
Large breed differences exist in age and weight at puberty and testicular size (scrotal circumference).
INCIDENCE/PREVALENCE
N/A
GEOGRAPHIC DISTRIBUTION
Worldwide
SIGNALMENT
All bulls should receive a BSE prior to the breeding season.
A BSE is particularly important in young bulls prior to their first breeding season.
SIGNS
N/A
CAUSES
The causes of poor fertility that can be detected during a BSE are numerous and include:
Late maturation
Small testicles
Poor semen quality
Injuries to the penis, prepuce, or testes
Lameness
Poor or excessive body condition
Infectious processes involving the testes or accessory sex glands
Eye injuries
Congenital reproductive anomalies
RISK FACTORS
N/A
DIAGNOSIS DIFFERENTIALDIAGNOSIS
Infertility
Deficiencies: iodine, manganese, vitamin A, zinc
Environment: cold weather infertility, heat stroke
Hereditary: Bulls cotwin with freemartin heifer, chromosomal abnormalities, inbreeding, segmental aplasia of reproductive tract
Lameness
Malnutrition
Penis/prepuce: balanoposthitis; bovine herpes virus-1; dermatophilosis; hematoma, hematocele; loss of penile sensation; micropenis, hypoplasia; papillomatosis, warts; paraphimosis; penile deviation; penile hair ring; penile preputial adhesion; persistent penile frenulum; prolapsed prepuce; trauma
Psychologic impotency
Scrotum: abscess, dermatophilosis, frostbite, inguinal scrotal hernia
Seminal vesiculitis
Sperm: abnormalities of spermatogenesis, hemospermia, infectious bovine rhinotracheitis (IBR), bovine viral diarrhea (BVD) contaminated semen, sperm granuloma
Testicles: cryptorchidism, degeneration, hypoplasia/atrophy, orchitis, trauma, tumors
Urethra and erectile tissue: corpus cavernosum vascular shunts, urethral fistula, urolithiasis
Varicocele
Vertebral spondylosis
Lack of Libido
Epididymitis
Iodine deficiency
Lameness
Malnutrition
Orchitis
Penis/prepuce problems: trauma-hematoma, prolapsed penis, loss of penile sensation, corpus cavernosum vascular shunts, persistent penile frenulum, posthitis
Psychogenic impotency
Vertebral osteophytosis/spondylosis
Zinc deficiency
Sexual Malfunction
Penile/preputial problems: balanoposthitis; deviation; herpes vulvovaginitis; infectious bovine pustular vulvovaginitis; papillomatosis; paraphimosis; penile/preputial adhesions; penile hair ring; persistent penile frenulum; phimosis; ruptured urethra; trauma, hematoma, abscesses; urethral calculi
Prepuce: abscess/cellulitis, foreign body, preputial stenosis, prolapsed prepuce, trauma
Testicles, spermatic cord, and scrotum: brucellosis; cryptorchidism; epididymitis; segmental aplasia; sperm granuloma; spermatocele; testicular degeneration, hypoplasia, atrophy; testicular trauma; testicular tumors; varicocele; zinc deficiency
CBC/BIOCHEMISTRY/URINALYS IS
N/A
OTHER LABORATORY TESTS
Culture and sensitivity may be indicated when disease is suspected.
IMAGING
Ultrasound examination may be a helpful adjunct.
DIAGNOSTIC PROCEDURES
Physical Soundness
Careful attention must be paid to the structural correctness of the feet and legs of a potential breeding bull.
A bull must be able to cover large distances to search out and find cows in estrus.
Pain in the limbs and/or back may prevent a bull from successfully servicing cows.
Breeding bulls should be free of heritable abnormalities such as post-leggedness, sickle hocks, and corkscrew claw.
The eyes should be examined since a bull primarily uses eyesight to detect cows in estrus.
Evaluation of the Scrotum and Testes
Visual inspection of the scrotum reveals information about the symmetry, size, and shape of the scrotum.
The scrotum should have a distinct neck above the testicles to allow adequate thermoregulation.
Appraisal of the scrotal skin allows detection of scrotal dermatitis or frostbite, which may affect semen quality.
The testicles should be equal in size, shape, and consistency and be freely moveable within the scrotum.
Palpation of lumps, soft spots, or any other abnormality of the testicles should alert the examiner to the possibility of an abnormality that may affect semen quality.
Scrotal circumference (SC) should be measured.
Changes in SC from year to year may be evidence of problems within the testes.
Most breed associations have established minimum SC measurements in order for yearling bulls to pass a BSE.
Some variability exists between breed associations but most have a minimum SC of at least 32 cm for bulls 12-15 months of age.
SC is measured by grasping the neck of the scrotum and firmly pulling the testes down into the scrotum. The thumb and fingers should be on the sides of the scrotum rather than between the testicles. The measuring tape should be looped around the greatest diameter of the scrotum.
Each epididymis should be evaluated by palpation.
The head of the epididymis can usually be palpated on the craniodorsal aspect of the testicle.
The body of the epididymis can be palpated on the medial aspect of the testicles. Abnormalities of the body are rare.
The tail of the epididymis can be palpated at the base, or ventral aspect, of the scrotum.
Each epididymis should be evaluated for side-to-side differences, swellings or masses, firmness, warmth, or pain.
Palpation of the Penis and Prepuce
Palpation of the penis and prepuce should be performed.
The penis should be palpated through the skin from the base of the scrotum to the glans. Detection of any swellings along the penis should alert the examiner to the possibility of an injury that may affect the bull’s ability to service cows.
The prepuce should be palpated from the preputial orifice to the reflection onto the glans. Special attention should be paid to the reflection of the prepuce onto the glans, as this is a very common site of preputial injury.
Transrectal Examination of Accessory Sex Glands and Inguinal Rings
Transrectal examination of the accessory sex glands and inguinal rings should be performed.
The urethra is usually the first structure palpated. It is a firm tubular structure and usually becomes pulsatile upon palpation.
The prostate is usually encountered next and can be palpated as a firm transverse ridge at the cranial aspect of the urethra.
The vesicular glands, or seminal vesicles, can be palpated craniolateral to the prostate. These glands vary in size between bulls but should be uniform in size, lobulated, turgid, and moveable.
The ampullae may be difficult to identify by palpation but they lie on the pelvic floor cranial to the prostate. Disease of the ampullae is rare.
The ampullae can be followed to the ductus deferens, which enters the abdominal cavity through the internal inguinal rings.
The internal inguinal rings can usually be palpated 15-20 cm ventral to the brim of the pelvis and 5-15 cm lateral to midline. One to three fingers can usually be inserted into the internal rings. Enlarged rings may predispose a bull to scrotal hernia.
The bulbourethral glands are imbedded in the urethralis muscle and cannot be palpated.
The most common abnormality found on rectal examination is enlargement, excessive firmness, or loss of lobulation of the vesicular glands.
Seminal vesiculitis occurs most commonly in young bulls.
Adhesions, abscessation, and development of a draining tract may occur in chronic cases.
Purulent material may be grossly evident in a semen sample or neutrophils may be seen upon microscopic examination of specially stained smears.
Samples for culture and sensitivity may be obtained by passing a long, sterile catheter up the urethra and massaging the vesicular glands per rectum.
After completion of the rectal exam, the pelvic urethra should be massaged to prepare the bull for semen collection.
Collection and Evaluation of Semen Sample
Collection and evaluation of a semen sample is an integral part of a BSE.
The nature of the bull, available facilities, response of the bull to previous collection attempts, and examiner preference should all be considered when attempting to collect a semen sample.
Semen may be collected by transrectal massage of the pelvic urethra, by electroejaculation, or by use of an artificial vagina.
Transrectal massage usually works well in calm bulls but requires at least two people, often does not result in protrusion of the penis, and is tiring to the person performing the massage.
Numerous types of electroejaculation equipment are available.
When using electroejaculation, a bull must be properly restrained.
The amount of stimulation should be determined by the bull’s response.
Stimulation should be low at first and gradually increased until the bull gains an erection and ejaculates. If maximal stimulation is reached without ejaculation, the bull should be allowed to rest for a few minutes and the collection attempted again. If collection is unsuccessful after two to three attempts, the bull should be retested on another day or by another means.
Some bulls will not ejaculate in response to electroejaculation and other means must be used.
A caudal epidural prior to collection attempts may reduce discomfort for the bull.
The semen sample should be obtained when the ejaculate becomes cloudy.
Semen collection by use of an artificial vagina (AV) is primarily used in artificial insemination centers.
Safety for the bull, the mount animal, and the collection personnel must be considered.
Collection of semen using an AV may be useful for bulls that fail to ejaculate in response to electroejaculation.
It is important that a bull achieve erection and protrusion of the penis so that the penis and prepuce can be carefully evaluated.
Semen Sample Examination
The semen sample should be examined microscopically as soon as possible after collection.
Equipment used in semen evaluation should be kept clean and warm in order to prevent a reduction in sperm motility.
Contamination of a semen sample with urine, blood, pus, or chemicals may reduce sperm motility.
The semen sample should be evaluated for both gross and individual motility.
Gross motility is evaluated according to the following: Very good-rapid dark swirls
Good-slower swirls and eddies
Fair-no swirls but prominent individual cell motion Poor-little or no individual cell motion
Individual motility is evaluated by preparing a wet mount by placing a drop of semen on a warm slide and placing a warm cover slip over it.
Individual motility is determined based on an estimate of the percentage of progressively motile cells. Very good-80-100%
Good-60-79% Fair-40-59% Poor-< 40%
Sperm morphology is evaluated by mixing a drop of semen and a drop of stain on a slide and preparing a smear.
Live-dead stains are most commonly used. With these stains, live cells appear clear while dead cells are stained pink.
Sperm cell morphology has historically been evaluated based on the percentage of normal cells versus the percentages of primary and secondary abnormalities.
Primary abnormalities have their origin in the testes during spermatogenesis while secondary abnormalities originate in the epididymis.
Some variability exists in the classification of primary versus secondary abnormalities. Generally speaking, abnormalities of the head or midpiece are considered primary while those of the tail are considered secondary. There are exceptions to this rule of thumb and the reader is referred to the Suggested Reading list at the end of the chapter for a more detailed description of these abnormalities.
Some authors question the validity of this classification system and propose a differential count of all abnormalities instead.
Primary abnormalities are not more important than secondary abnormalities as both types will reduce the viability of the cell.
Under most circumstances, a minimum of 30% progressively motile sperm and 70% morphologically normal cells are adequate to pass a BSE.
Bulls are classified as satisfactory potential breeders or unsatisfactory potential breeders, or classification may be deferred.
Bulls with poor semen quality but without obvious physical abnormalities should be deferred and retested.
Detection of a heparin binding protein known as fertility-associated antigen in bull semen may be an indicator of fertility. This test may be useful in further identifying subfertile bulls among bulls that pass a standard BSE.
Serving Capacity/Libido Test
A serving capacity/libido test may be included as part of a BSE.
Bulls are exposed to restrained, estrus cows for specified time periods and are observed for sexual behavior and mating activity.
Bulls may also be exposed to a small number of estrous cows in a small pen and be observed for mating activity.
Most standard BSEs do not include a serving capacity/libido test.
A rough estimation of serving capacity/libido can be obtained by observing the activity of bulls in a natural mating situation.
Classification Systems and Evaluation Forms
Different classification systems and evaluation forms are available but the most commonly used evaluation form is produced by the Society for Theriogenology.
PATHOLOGIC FINDINGS
N/A
TREATMENT CLIENT EDUCATION
Reproductive efficiency is the most economically important aspect of beef production.
Scrotal circumference is closely related to age of puberty and fertility in daughter progeny.
Each gram of testicular tissue produces roughly the same number of sperm cells so bulls with larger testicles produce a larger volume of semen.
MEDICATIONS
FOLLOW-UP
MISCELLANEOUS ASSOCIATED CONDITIONS
N/A
AGE-RELATED FACTORS
N/A
ZOONOTIC POTENTIAL
Infectious orchitis caused by Brucella spp. poses some zoonotic risk to humans.
Animals diagnosed with infections caused by these organisms should be culled.
Brucellosis is a reportable disease.
PREGNANCY
N/A
RUMINANT SPECIES AFFECTED
Beef bulls
BIOSECURITY
Quarantine all new bulls and those returning from shows for a determined period of time to protect herd health.
PRODUCTION MANAGEMENT
All bulls should receive a BSE prior to the breeding season.
A BSE is particularly important in young bulls prior to their first breeding season.
SYNONYMS
N/A
SEE ALSO
Beef bull behavior
Beef bull management
Body condition score bovine
Testicular anomalies
Ultrasounding bovine reproductive tract
ABBREVIATIONS
AV = artificial vagina
BSE = breeding soundness exam
BVD = bovine viral diarrhea
cm = centimeter
IBR = infectious bovine rhinotracheitis
SC = scrotal circumference
Suggested Reading
Bellin, M. E., Oyarzo, J. N., et al. 1998. Fertility associated antigen on bull sperm indicates fertility potential. Journal of Animal Science 76:2032-39.
Morrow, D. A. 1986. Current therapy in theriogenology 2. Philadelphia: W. B. Saunders.
Van Camp, S. D., ed. 1997, July. Bull infertility. In: Veterinary clinics of North America, food animal practice. Philadelphia: W. B. Saunders.
Youngquist, R. S. 1997. Current therapy in large animal theriogenology. Philadelphia: W. B. Saunders.
Author: John Gilliam

BRUCELLOSIS
BASICS DEFINITION
Brucellosis is a reproductive disease of cattle, bison, elk, yaks, sheep, and goats caused by a gram-negative, facultative, intracellular bacterium.
PATHOPHYS IOLOGY

Brucella abortus, B. melitensis, and B. ovis can be shed in the blood, urine, milk, semen, placenta, fetus, and vaginal discharges of infected animals.
Susceptible animals that come in contact with these fluids, either through ingestion, contact with mucous membranes, or skin abrasions, can develop a septicemia and abort if pregnant, deliver weak-born animals, and/or become a chronic carrier.
SYSTEMS AFFECTED
Reproductive in all ruminants, musculoskeletal (arthritis) in cattle affected with B. abortus.
GENETICS
N/A
Incidence of brucellosis varies between countries.
In the United States, since the implementation of the Bovine Brucellosis Eradication Plan in 1934, infection rate is less than 0.25% in two states (Class A status) as of May 2004.
More than 50% of the bison and elk herd in Yellowstone National Park and Grand Teton National Park have tested positive for brucellosis.
GEOGRAPHIC DISTRIBUTION
Can be found worldwide
B. abortus has been eradicated from Japan, Canada, Northern Europe, Australia, and New Zealand.
B. melitensis does not occur in northern Europe, southeast Asia, Australia, or New Zealand and is rare in the United States.
B. ovis is seen in Australia, New Zealand, and the United States and is endemic in other sheep-raising regions of the world.
SIGNALMENT
Species
Cattle, bison, water buffalo, sheep, goats-B. abortus
Sheep-B. melitensis, B. ovis
Goats-B. melitensis
Breed Predilections
N/A
Breed Predilections
N/A
Mean Age and Range
Reproductively active animals are susceptible, so age can vary depending on species.
Predominant Sex
N/A
SIGNS HISTORICALFINDINGS
In cattle, weak or stillborn calves, abortions during the second half of gestation, and decreased milk production may be the only clinical signs.
In sheep, late-term abortions and retained placenta. Rams may develop orchitis, epididymitis, and impaired fertility.
In goats, abortions can be noted during the fourth month, as well as mastitis and lameness. Bucks may develop orchitis and epididymitis.
PHYSICALEXAMINATION FINDINGS
Most often, systemic signs are rare with brucellosis infection.
Upon physical exam, retained placenta, decreased milk production may be noted in females.
Male sheep may have decreased sperm counts and swollen testicles.
CAUSES
Susceptible animals that come in contact with contaminated blood, urine, milk, semen, placenta, fetus, and vaginal discharges from infected animals, either through ingestion, contact with mucous membranes, or skin abrasions, can develop brucellosis infection.
RISK FACTORS
Contact with infected herd mates or wildlife.
DIAGNOSIS DIFFERENTIALDIAGNOSIS
In cattle, BVD, IBR, leptospirosis, listeriosis, neosporosis, mycotic abortion, trichomoniasis, campylobacteriosis, chlamydiosis, epizootic bovine abortion (in California), bluetongue, parainfluenza-3, Ureaplasma, Mycoplasma, Haemophilus somnus, Salmonella, and Arcanobacter pyogenes.
Noninfectious causes include heat stress, ponderosa pine needle ingestion, locoweed, broomweed, and mycotoxins.
In sheep and goats, vibriosis (primarily sheep), enzootic abortion (Chlamydia psittaci), toxoplasmosis, listeriosis, salmonellosis, and leptospirosis in goats.
Noninfectious causes are similar to those of cattle.
CBC/BIOCHEMISTRY/URINALYS IS
N/A
OTHER LABORATORY TESTS
Serology can be used to diagnose brucellosis infection (B. abortus, B. melitensis) by card and plate agglutination (buffered
Brucella antigen tests).
ELISA tests can be used to detect B. abortus in milk and B. abortus and B. ovis in serum.
The milk ring test can be used to detect B. abortus in bulk milk samples in cattle but not in small ruminants.
Complement fixation can be used to identify B. abortus and B. ovis.
IMAGING
N/A
DIAGNOSTIC PROCEDURES
Brucella abortus can often be cultured from fetal membranes, vaginal discharge, milk, semen, or aborted fetuses.
PATHOLOGIC FINDINGS
Aborted fetuses can be normal or autolyzed with evidence of bronchopneumonia.
Placentitis in cattle and sheep consists of edema and necrotic cotyledons.
In cattle, the cotyledons could also be normal, red, or yellow in color. The intercotyledonary area is leathery and thickened and has a wet appearance in cattle and sheep.
Goats have a normal placenta.
In the case of joint involvement, inflammatory lesions may be seen.
Granulomatous lesions may be found upon slaughter in the reproductive tract, supramammary lymph nodes, and the mammary gland.
TREATMENT APPROPRIATE HEALTH CARE
All cases of brucellosis need to be reported to the state or federal veterinarian and the animals need to be eliminated from the herd.
No treatment is effective.
ACTIVITY DIET
N/A
CLIENT EDUCATION
Veterinarians should educate cattle owners regarding their state’s recommendations regarding vaccinating young stock in keeping with the eradication program in the United States.
SURGICALCONSIDERATIONS
N/A
MEDICATIONS DRUGS OF CHOICE
No treatment is recommended for cattle.
In the case of valuable breeding rams, prolonged antibiotic therapy based upon culture and sensitivity can be used. However, fertility may never return to normal.
CONTRAINDICATIONS
N/A
POSSIBLE INTERACTIONS
N/A
ALTERNATIVE DRUGS
N/A
FOLLOW-UP
PATIENT MONITORING:
N/A
PREVENTION/AVOIDANCE
Vaccination of female calves against B. abortus with RB-51 from 4 to 12 months of age in endemic areas increases resistance to infection.
Adult cattle can also be vaccinated but only with permission of the state, provincial, or federal veterinarian. RB-51 is currently being used experimentally in bison, and disease status is being monitored to assess efficacy.
Goats and sheep can be vaccinated with live, attenuated Rev-1 B. melitensis in various parts of the world, but it is not available in the United States.
Rams have been immunized against B. ovis in New Zealand with some success; not available in the United States.
POSSIBLE COMPLICATIONS
Brucellosis leads to abortions in ruminant species with fertility ramifications in sheep and goats.
Contact with fetal fluids in infectious and carrier animals can spread the disease to all susceptible animals in a given herd/flock or geographic location.
EXPECTED COURSE AND PROGNOSIS
Ruminants typically abort only during their first gestation, 80% in late gestation.
Fertility can be permanently impaired in rams and bucks.
Death is uncommon in adult animals.
MISCELLANEOUS ASSOCIATED CONDITIONS
Arthritis in goats
AGE-RELATED FACTORS
Breeding-age animals most susceptible
ZOONOTIC POTENTIAL
Humans are susceptible to B. melitensis and B. abortus infection through direct contact with infectious fluids from animals and absorption across mucous membranes or breaks in the skin.
Brucellosis infection can also result from consumption of unpasteurized milk or cheese products from endemic areas.
There is concern with aerosolized particles being used as a bioterrorism agent and causing widespread disease in humans.
Disease can range from asymptomatic infection to chronic complications such as arthritis, endocarditis, orchitis, osteomyelitis, and other bone lesions.
PREGNANCY
Naïve animals abort late gestation in cattle and sheep and fourth month in goats.
RUMINANT SPECIES AFFECTED
Cattle, bison, elk, camels, water buffalo, yaks, sheep, goats
BIOSECURITY
Ensure newly purchased cattle have been vaccinated against brucellosis if they are coming from endemic areas. Do not introduce animals directly into the herd for at least 3 weeks.
Perform breeding soundness examinations on all sexually active males to make sure they are clear of disease and abnormalities.
PRODUCTION MANAGEMENT
Vaccination of female calves against B. abortus with RB-51 from 4 to 12 months of age in endemic areas increases resistance to infection.
Adult cattle can also be vaccinated but only with permission of the state, provincial, or federal veterinarian. RB-51 is currently being used experimentally in bison, and disease status is being monitored to assess efficacy.
Goats and sheep can be vaccinated with live, attenuated Rev-1 B. melitensis in various parts of the world, but it is not available in the United States.
SYNONYMS
Bang’s disease Contagious abortion Enzootic abortion SEE ALSO
Arcanobacter pyogenes Bluetongue Broomweed
BVD
Campylobacteriosis Chlamydiosis
Enzootic abortion (Chlamydia psittaci) Epizootic bovine abortion
Haemophilus somnus
Heat stress IBR
Leptospirosis Listeriosis Locoweed Mycoplasma Mycotic abortion Mycotoxins Neosporosis Parainfluenza-3
Ponderosa pine needle ingestion
Salmonella Salmonellosis Serology Toxoplasmosis Trichomoniasis Ureaplasma
Vibriosis (primarily sheep)
ABBREVIATIONS
BVD = bovine viral diarrhea
ELISA = enzyme-linked immunosorbent assay IBR = infectious bovine rhinotracheitis Suggested Reading
Aiello, S. E., Mays, A., ed. 1998. Merck veterinary manual. 8th ed. Whitehouse Station, NJ: Merck & Co.
Animal and Plant Health Inspection Services, Veterinary Services Division, United States Department of Agriculture.
Brucellosis in cattle and bison. Accessed at http://www.aphis.usda.gov/vs/nahps/brucellosis/cattle.htm on May 8, 2004. Corbel, M. J. 1997, Apr-June. Brucellosis: an overview. Emerging Infectious Disease 3(2):213-21.
Cutler, S., Whatmore, A. 2003, Nov 22. Progress in understanding brucellosis. Vet Rec. 153(21): 641-42.
Development of new/improved brucellosis vaccines: report of WHO meeting with participation of FAO and OIE, Geneva, Switzerland, December 11-12, 1997. Accessed at
http://www.who.int/emcdocuments/zoonoses/docs/whoemczdi9814.pdf on May 11, 2004.
Fosgate, G. T., Adesiyun, A. A., Hird, D. W., Johnson, W. O., Hietala, S. K., Schurig, G. G., Ryan, J. 2002, Nov. Comparison of serologic tests for detection of Brucella infections in cattle and water buffalo (Bubalus bubalis). Am J Vet Res. 63(11): 1598-605.
Metcalf, H. E., Luchsinger, D. W., Ray, W. C. 1994. Brucellosis. In: Handbook of zoonoses: section A, bacterial, rickettsial, chlamydial, and mycotic zoonosis, ed. G. Beran, J. Steele. 2nd ed. Boca Raton, FL: CRC Press.
Author: Danelle Bickett-Weddle

BURN MANAGEMENT
BASICS OVERVIEW

Burns in livestock are not common but may occur by several mechanisms:
Thermal-fire (barn, brush, forest), heat (heat lamps, heating pads), hot solutions
Electrical-lightning, electrocution
Frictional-rope burns, abrasions
Chemical-caustic agents, topical medications
Ultraviolet-sunburn
Radiation
Freeze “burns”
Burns in livestock commonly occur over back, face, udder, and teats, and over ventrum with brush fires.
Classification of burns is based on depth to which burn penetrates skin and extent of body surface involved.
First-degree burn: involves superficial layers of epidermis; characterized by erythema, transient edema, and pain, and generally heals without complication or extensive scarring, prognosis good
Second-degree burn: partial-thickness burns involving all epidermal layers but spare hair follicles and sweat glands; characterized by erythema, pain, and vesicles (blisters), necrosis, and sloughing with superficial and eschar with deep second-degree burns; usually re-epithelialized with proper care, some scarring
Third-degree burn: full thickness burns involving entire epidermis, dermis, and appendages and exposing deeper structures, local blood vessels and hair follicles destroyed; characterized by necrosis, ulceration, anesthesia, eschar, and extensive scarring, require extensive wound care ± skin grafting
Fourth-degree burn: involve entire skin, subcutis, underlying fascia, muscle, and tendon
The full extent of the thermal burn is difficult to predict immediately after injury.
Burns are usually complex with body areas being affected to different degrees.
The development of blisters, fluid separation of epidermis and dermis and eschars may not appear for several days.
Thermal injuries caused by fire associated with more than skin pathology
Fluid shifts, hypovolemia
Electrolyte abnormalities
Hypoproteinemia (loss of plasma is maximal in first 12 to 24 hours)
Extreme stress
Smoke inhalation
Immune suppression
Extracutaneous complications of burns may be cardiopulmonary, ocular, hematologic, renal
Animals suffering burns and/or smoke inhalation need to be closely monitored and repeatedly examined as signs and lesion development may be delayed.
Wound or burn infection is common in cattle and Pseudomonas aeruginosa is the most common organism to establish infection.
Infection under eschars is a common problem.
Animals with second-degree and third-degree burns over 50% of their body usually die.
Poor prognosis if second-degree and third-degree burns affect more than 10% to 15% of body surface
Sequelae to burn injuries
Hypoproteinemia from protein exudate from wounds
Progressive edema
Hyperkalemia
Burn-induced immunosuppression
Progressive anemia
Secondary infections; pneumonia, skin infections
Multiple system involvement, i.e., renal shut down, eye damage
Scarring
Damage to eyelids, conjunctiva, cornea, anterior uveitis, exfoliation of lens capsule
Sunburn
White and light-skinned animals, lateral aspects of teats, ears, nose, areas covered with little hair are most susceptible to ultraviolet light, 290-320 nm.
White-faced sheep, especially ears and face
Exposure to sunlight is associated with skin tumor development especially on udder of white goats.
Erythema, pain, swelling, blisters, erosions
Complications of teat burns include obstruction of teat orifice, distorted teats, mastitis
SIGNALMENT
No age, sex, or breed predilection
Sunburn: light-skinned or white animals, white-faced sheep
SIGNS
Severity of burn determines signs present, maybe mild erythema and superficial scabbing to extensive tissue damage and necrosis with severe protein exudation
Wool is fire-retardant; burns on sheep most commonly found on legs and around face
Goats and cattle are likely to have burns on any part of body.
Signs of sunburn
Erythema, swelling, crusting of skin
Headshaking, pruritus
Discomfort during milking or nursing if udder or teats burned
Teat burns
Mild burns: erythema, sloughing of outer, white, paper-thin tissue; areas of sloughing, crusting, and discoloration of tissue; milk is apparently normal; teat pliable on palpation
Severe burns: teats tend to be dull brown or black, dry, and often corrugated; thick layer of tissue is sloughed, underneath is red hemorrhagic tissue; teat is leatherlike and lacks pliability ± distorted.
Healing lesions may be very pruritic causing animals to scratch or lick at affected sites.
CAUSES AND RISK FACTORS
Symptoms can be acute or subacute
Nondermatological signs occur about 7 days prior to onset of skin lesions: pyrexia.
DIAGNOSIS
Diagnosis is based upon history and clinical signs.
DIFFERENTIALDIAGNOSIS
Differentiate sunburn from photosensitivity.
CBC/BIOCHEMISTRY/URINALYS IS
N/A
OTHER LABORATORY TESTING IMAGING
N/A
DIAGNOSTIC PROCEDURES
N/A
TREATMENT
Initial overall assessment of survivors-recumbent, obviously badly burned, suffering animals should be euthanized.
Evaluation of animal’s systemic and local injuries is essential.
Repeat examination is necessary to determine response to therapy and development of delayed signs and lesions.
Treatment is aimed at care of initial injuries, cardiovascular support, respiratory support, and prevention of secondary infection
Goal of treatment is epithelialization of wound.
First-and mild second-degree burns should heal well by epithelialization.
Severe second-degree and most third-degree burns require skin grafts.
Cool affected body areas to reduce heat retention and limit necrosis.
Hosing with cool water for 15 minutes
Wet cool towels
Hosing also removes burnt hairs, crust, and debris.
Blisters allowed to remain in place for 1-2 days on second-degree burns
Burn wound care
Thorough cleaning with irrigation or dilute chlorhexidine solution (controversial); repeat two to three times daily
Daily hydrotherapy
Topical antimicrobial; use water-soluble emollient antimicrobial cream, silver sulfadiazine (Silvadene)
Use of hydrogel and nonadherent, absorbent dressings, which are not constrictive, may be indicated in some cases, must be kept clean and changed at appropriate intervals.
Avoid occlusive dressings, which produce closed wound with bacterial proliferation and delayed healing.
Eschar over large second- or third-degree burns should be left undisturbed until natural sloughing occurs or if infection develops under eschar.
Wound debridement after 24 to 36 hours if necessary
Wound allowed to heal by granulation
Systemic antimicrobials fail to penetrate local burn wound infections, may permit growth of resistant organisms.
Systemic antimicrobials reserved for use when documented site of infection (i.e., pneumonia)
Analgesia as needed-nonsteroidal anti-inflammatory drugs (concern these may delay healing)
Correct hypovolemia: rule of thumb-give 3 to 4 ml/kg of body weight for each percentage body surface involved.
Maintenance of electrolyte and acid-base balance
Plasma administration if severe hypoproteinemia
Keep animal in clean environment.
Provide adequate nutrition.
Tetanus booster if indicated
Prevent delayed healing and self-mutilation from scratching and licking as lesions heal (pruritus), sedation may be required.
Eye damage
Cornea and eyelid damage are of particular concern.
With burns on face, cornea should be treated with artificial tears.
Gently remove debris from eye with saline-soaked cotton swab.
Inspect and fluorescein stain eye for ulcers.
Apply topical antibiotics with atropine.
Third eyelid flap if necessary to protect eye
Teat burns
Soothing, softening burn ointments, lanolin ointments, aloe vera
Antimicrobial ointment if skin surface sloughs
Maintain open teat orifice.
Healing is slow, takes many weeks to months.
Sunburn
Remove from exposure to sunlight.
Provide shelter.
Soothing burn ointments, topical human sunburn medications, or aloe vera, topical steroids
Application of pigmented teat dips
Contamination of milk should be avoided.
For secondary bacterial infection, use topical or systemic antimicrobial agents.
Prevention recommendations: see Production Management
MEDICATIONS
N/A
DRUGS OF CHOICE
N/A
CONTRAINDICATIONS /POSSIBLE INTERACTIONS
Appropriate milk and meat withdrawal times must be followed for all compounds administered to food-producing animals.
FOLLOW-UP
Lesions can persist for up to 12 weeks.
Recovered cattle have immunity for months.
MISCELLANEOUS ASSOCIATED CONDITIONS
Smoke Inhalation
Involves carbon monoxide toxicity and smoke toxicity
Three Mechanisms of Injury to Respiratory System
First stage: heat damage to upper respiratory tract, injury from toxic chemicals in smoke and carbon monoxide toxicity; usually signs within first 6 hours
Inflammation, edema, and necrosis of nasal passages, pharynx, and larynx lead to airway obstruction ± laryngospasm
Bronchoconstriction of lungs; inhalation of soot, noxious gases
Carbon monoxide toxicity: hypoxemia and tissue hypoxia in all organs, especially brain; level above 10% carbon monoxide is consistent with toxicity
Shock
Second stage: formation of pulmonary edema
Within 12 to 72 hours after exposure
Damage due to inflammatory mediators (cytokines, proteolytic enzymes, oxygen free radicals)
Obstruction of small airway from deposition of smoke material and inflammatory debris
Third stage: bronchopneumonia
Result of impaired immune system and exposure to pathogens
May occur within 24 to 48 hours or 1 to 3 weeks after initial injury
Clinical Signs
Many signs may not be apparent for 1 to 2 days after fire.
Oral burns, nasal mucosal swelling, pharyngeal swelling, laryngospasm, conjunctivitis
Hoarseness, expiratory wheezes, cough, stridor, tachypnea
Tachycardia
Bright mucous membranes with carbon monoxide toxicity may mask cyanosis.
±Cyanosis
Signs of hypovolemia
Signs of shock
Depression, disorientation, irritability, ataxia, or even comatose
± Signs of septicemia or pneumonia
Treatment
Depends on stage and severity of injury
Oxygen support
Maintenance of airway
Tracheotomy if upper airway obstruction
Keep airways clean.
Bronchodilators to counteract bronchoconstriction
Diuretics and anti-inflammatory agents (nonsteroidal anti-inflammatory drugs) to reduce edema and inflammation
Use of corticosteroids is controversial.
Analgesics
Fluid therapy if hypovolemic, electrolyte imbalances, or acid-base derangements
Caution not to fluid overload if ongoing protein loss through burns or from vasculature
Plasmas therapy if hyperproteinemia
Strict hygiene, nursing care, and optimal nutritional support
Prophylactic antimicrobials are not recommended.
Appropriate antimicrobials based on culture and sensitivity from documented site of infection
ZOONOTIC POTENTIAL
N/A
RUMINANT SPECIES AFFECTED
Cattle
Goats
Sheep
Camelids
Wild ruminants
BIOSECURITY
N/A
PRODUCTION MANAGEMENT
Recovery time is prolonged with teat burns and extensive burns.
Need to determine which animals to be euthanized or culled due to poor prognosis for successful recovery
Animals with second- and third-degree burns over extensive area
Burnt teats that will not withstand milking; mastitis is inevitable.
Badly burned feet may slough claws.
Facial burns involving cornea may lead to permanent stromal opacities.
Teat burns
Mild lesions have good prognosis.
Severe lesions prognosis variable; may have mastitis, occlude, or heal distorted
Mature adult cows are more likely to return to full function than heifers.
Prevention of sunburn
Gradual acclimation to exposure to sunlight
Provide shade
Application of sun blocking screens or ointments; use sunblocks with highest SPF available and those that are suitable for use in children; avoid PABA as it is not recommended as safe in children and little is known about its safety in animals.
Iodophor teat dips
Pet animals may wear fly nets on ears, hats, or bonnets.
SYNONYMS
N/A
SEE ALSO
Frostbite Lightening strike
Wound care, euthanasia
ABBREVIATIONS
PABA = para-aminobenzoic acid
Suggested Reading
Knottenbelt, D. C. 2003. Management of burn injuries. In: Current therapy in equine medicine 5, ed. N. E. Robinson. Philadelphia: W. B. Saunders.
Marsh, P. 2002. Smoke inhalation. In: Large animal internal medicine, ed. B. P. Smith, 3rd ed. St. Louis: Mosby. Pugh, D. 2002. Diseases of the integumentary system. In: Sheep and goat medicine. Philadephia: W. B. Saunders. Rebhun, W. C. 1995. Skin diseases. In: Diseases of dairy cattle. Baltimore: Williams and Wilkins.
Scott, D. W. 1999. Environmental skin diseases. In: Current veterinary therapy 4: food animal practice, ed. J. L. Howard, R. A. Smith. Philadelphia: W. B. Saunders.
Smith, M. C., Sherman, D. M. 1994. Environmental insults. In: Goat medicine. Philadelphia: Lea & Febiger.
Authors: Susan Semrad and Karen A. Moriello

CACHE VALLEY VIRUS
BASICS OVERVIEW

Cache Valley (CV) is a viral infection afflicting a wide variety of domestic and wild ruminants as well as humans.
Cache Valley virus (CVV) belongs to the genus Bunyavirus in the family Bunyaviridae, the latter being the largest single family of animal viruses with more than 350 members.
CV is endemic throughout the United States, Canada, and Mexico. Several CVV subtypes, such as E4-3484, CbaAr 426, and Fort Sherman, that are indistinguishable by neutralization tests from CVV, have been isolated in Central and South America.
CVV transmission to vertebrates occurs through bites of infected mosquitoes, including several species of Aedes, Psorophora, Anopheles, Coquillettidia, Culex, and from Culiseta inornata.
The majority of infections are subclinical, but embryonic mortality, fetal teratogenesis, and stillbirth may be common in sheep.
In the southwestern United States, lambs born in December, January, and February are more likely to show CVV-induced teratogenesis. This period coincides with increased rainfall and mosquito activity.
Fetal susceptibility to CVV-induced pathology is higher during the first 2 months of pregnancy.
SIGNALMENT
Infection by CVV has been reported in humans, sheep, goats, cattle, horses, pigs, deer, mouflon, caribou, raccoons, foxes, black-tailed jackrabbit, woodchuck, and turtles.
In sheep there is a positive relationship between seropositivity to CVV and age. This reflects the likelihood of exposure as the age of sheep increases.
In pregnant ewes, the CVV can cross the placenta causing embryonic death, mummification, or fetal malformation.
SIGNS
In most animals, CVV infection is subclinical.
In pregnant ewes, CVV infection may result in embryonic mortality, fetal mummification, and various degrees of musculoskeletal or central nervous system (CNS) abnormalities.
Experimentally, CVV-induced fetal malformation occurs when the virus infects the fetus between days 27 and 54 of pregnancy.
After the second month of pregnancy, fetal infection results in the production of fetal neutralizing antibodies that control and eliminate CVV without apparent consequences to the fetus.
Dystocia may be a sequela in ewes that deliver full-term malformed offspring.
Ewes that are CVV seropositive at the time of breeding are resistant to reinfection with CVV.
There is no cross-protection against other related bunyaviruses.
DIAGNOSIS DIFFERENTIALDIAGNOSIS
Main Drain, La Crosse, and San Angelo bunyaviruses induce similar fetal pathology.
Bluetongue virus of vaccine origin and border disease virus also may result in fetal infection and CNS malformations in sheep.
Akabane, Rift Valley fever, Nairobi sheep disease, and Wesselsbron viruses are exotic to North America but may cause similar fetal pathology in sheep.
Other causes of teratogenesis and pregnancy loss, such as genetic defects and teratogenic plants, need to be included in the differential diagnosis of CV.
DIAGNOSTIC PROCEDURES
CVV can be isolated from blood during the acute viremic phase by intracranial inoculation of suckling mice or infection of susceptible cell lines such as Vero cells. Because viremia is short-lived, in most cases results are negative.
CVV serum antibodies are more often demonstrated by serum neutralization, but ELISA, complement fixation, and hemagglutination-inhibition tests also have been used. In adult animals, serum antibodies are indication of previous exposure, but do not provide information regarding the infectious status of individuals.
Malformed fetuses that survive in utero for some time develop neutralizing antibodies and eliminate the virus. In these cases, assaying precolostral fetal serum for the presence of CVV neutralizing antibodies does the diagnosis.
In full-term malformed fetuses or newborns, virus isolation is always unsuccessful.
Lack of CV antibodies in sera of ewes lambing malformed fetuses rules out CVV as the cause.
PATHOLOGIC FINDINGS
Macroscopic
In sheep, CVV intrauterine infection during pregnancy may result in embryonic mortality, fetal teratogenesis, stillbirth, and/or oligohydroamnion.
Congenital abnormalities include arthrogryposis, hydranencephaly, hydrocephalous, microcephalous, porencephalia, cerebellar hypoplasia, scoliosis, torticollis, and lordosis.
In multiple pregnancies, the degree and type of fetal pathology may be different in each fetus. In some cases, one fetus may be normal while the others may show malformations.
In other ruminants, fetal abnormalities as a result of natural CVV infection during pregnancy happen sporadically.
Microscopic
Histologic lesions are more frequently observed in the brain, spinal cord, and skeletal muscle of malformed fetuses. In the CNS, microscopic lesions are consistent with the gross lesions. Some of the brain cavities contain blood, and evidence of neutrophil rarefaction and malacia may be present. In moderately affected lambs, muscle fibers are small, but in more severe cases, fibers are narrow and short with few nuclei and no cross striations.
Affected lambs often have meconium in pulmonary alveoli as a result of intrauterine stress.
Perivascular infiltration of neutrophils in placentas of affected ewes has been observed in some cases, but this is more likely an incidental finding and not a hallmark of CVV infection.
TREATMENT
There is no treatment for CVV infections.
MEDICATIONS
N/A
CONTRAINDICATIONS
N/A
POSSIBLE INTERACTIONS
N/A
FOLLOW-UP
N/A
PATIENT MONITORING
N/A
PREVENTION/AVOIDANCE
There are no vaccines available to protect animals against CVV infection.
Ewes that are seropositive to CVV at the time of breeding are protected from subsequent infection with CVV and its adverse effects on pregnancy, but they are susceptible to infection by bunyaviruses of different serogroups, some of which may induce similar fetal pathology.
Insect control is difficult because of the wide range of mosquito vectors and vertebrate hosts. Application of insecticides may not be ecologically admissible. Other insect control methods such as tire removal may greatly reduce the abundance of the vector.
Breeding ewes after the first frost of the fall reduces the risk of fetal infection.
MISCELLANEOUS ASSOCIATED CONDITIONS
The majority of infections are subclinical, but embryonic mortality, fetal teratogenesis, and stillbirth may be common in sheep.
AGE-RELATED FACTORS
The prevalence or CVV antibodies in sera of animals increases with age. This is a reflection of the likelihood of exposure in older sheep and not related to increased susceptibility of this particular age group.
ZOONOTIC POTENTIAL
CV is an indirect zoonotic in which humans may get infected through the bite of infected mosquitoes but not directly from infected vertebrate animals. Infection also can occur through accidental puncture with infected needles.
The great majority of CVV infections in humans are subclinical. However, fever, myalgia, chills, headache, vomiting and death have been reported in a few cases.
There is no conclusive evidence that CV virus in humans causes fetal malformation or pregnancy loss.
Further research is necessary to determine the role of CVV in human disease, particularly in human immunodeficiency virus (HIV)-infected individuals and those affected by other types of immune deficiencies.
PREGNANCY
Pregnancy loss and/or fetal malformation are common in CVV-infected sheep.
In pregnant ewes, CVV infection may result in embryonic mortality, fetal mummification, and various degrees of musculoskeletal or central nervous system (CNS) abnormalities.
SYNONYMS
N/A
SEE ALSO
Akabane Bluetongue virus Border disease virus
Nairobi sheep disease Rift Valley fever
Teratogenic plant consumption. Wesselsbron disease ABBREVIATIONS
CNS = central nervous system
CVV = Cache Valley virus
ELISA = enzyme-linked immunosorbent assay
Suggested Reading
Chung, S. I., Livingston, C. W., Jr., Edwards, J. F., Crandell, R. W., Shope, R. E., Shelton, M. J., Collisson, E. W. 1990.

Evidence that Cache Valley virus induces congenital malformations in sheep. Vet Microbiol. 21: 297-307.
Chung, S. I., Livingston, C. W., Jr., Edwards, J. F., Gauer, B. B., Collisson, E. W. 1990. Congenital malformations in sheep resulting from in utero inoculation of Cache Valley virus. Am J Vet Res. 51: 1645-48.
Chung, S. I., Livingston, C. W., Jr., Jones, C. W., Collisson, E. W. 1991. Cache Valley virus infection in Texas sheep flocks. JAm Vet Med Assoc. 199: 337-40.
de la Concha-Bermejillo, A. 2003. Cache Valley virus is a cause of fetal malformation and pregnancy loss in sheep. Small Rum Res. 49:1-9.
Edwards, J. F. 1994. Cache Valley virus. Vet Clin North Am-Food Anim Pract. 10: 515-24.
Edwards, J. F., Karabatsos, N., Collisson, E.W., de la Concha-Bermejillo, A. 1996. Ovine fetal malformations induced by in utero inoculation with Main Drain, San Angelo, and LaCrosse viruses. Am J Trop Med Hyg. 56: 171-76.
Author: Andrés de la Concha-Bermejillo

CALF DIPHTHERIA
BASICS DEFINITION

Fusobacterium necrophorum infection of the larynx and pharynx of calves
The organism is an opportunistic pathogen that causes numerous necrotic conditions (necrobacillosis), such as bovine hepatic abscesses, ruminant foot abscesses, and oral infections.
Because of the unavailability of suitable immunoprophylaxis, the control of F. necrophorum infection has depended mainly on the use of antimicrobial compounds.
PATHOPHYS IOLOGY
Injury to the mucosa of the pharynx and larynx allows Fusobacterium necrophorum, an oral commensal bacteria, to invade and infect the tissues. Inflammation can constrict the larynx, causing dyspnea.
Fusobacterium necrophorum is a gram-negative, non-spore-forming anaerobe and is a normal inhabitant of the respiratory and alimentary tracts of animals.
Two types of F. necrophorum, subspecies necrophorum (biotype A) and funduliforme (biotype B), have been recognized. These two biotypes differ morphologically, biochemically, and biologically.
The pathogenic mechanism of F. necrophorum is complex and not well defined.
Several toxins, such as leukotoxin, endotoxin, haemolysin, haemagglutinin, and adhesin, have been implicated as virulence factors. Among these, leukotoxin and endotoxin are believed to be more important than other toxins in overcoming the host’s defense mechanisms to establish the infection.
F. necrophorum is encountered frequently in mixed infections and, therefore, synergisms between F. necrophorum and other pathogens may play an important role in infection.
SYSTEMS AFFECTED
GI/respiratory N/A
INCIDENCE/PREVALENCE
Low incidence
GEOGRAPHIC DISTRIBUTION
Worldwide
Epidemiology
Occurs most commonly in calves up to 18 months of age, but can occur in older animals.
Abrasive feed, trauma to mucosa during oral medication, or other damage to the mucosa allows infection by the bacteria. Housed cattle and feedlot cattle are at higher risk.
SIGNALMENT
Species
Bovine
Breed Predilections
N/A
Mean Age and Range Three to 18 months. Predominant Sex N/A
SIGNS
GENERALCOMMENTS
Clinical signs are associated with edema and inflammation of the pharynx and larynx, making swallowing difficult and painful. Obstruction of the larynx causes dyspnea and may lead to death.
HISTORICALFINDINGS
Rough or abrasive feeds, unsanitary feeding areas, recent oral bolus medication
PHYSICALEXAMINATION FINDINGS
High fever (106°F); inspiratory dyspnea; difficulty swallowing; salivation; moist cough; anorexia; depression; swollen, painful pharynx
Visual observation of the pharynx and larynx reveal inflamed and necrotic mucosa.
CAUSES
Fusobacterium necrophorum infection through abraded or damaged mucosa in the larynx and pharynx
RISK FACTORS
Rough or abrasive feeds, unskilled workers giving oral medications
DIAGNOSIS DIFFERENTIALDIAGNOSIS
Foreign bodies or traumatic pharyngitis
Aspiration
CBC/BIOCHEMISTRY/URINALYS IS
N/A
OTHER LABORATORY TESTS
Culture and sensitivity are indicated in economically valuable animals. The most common sites or conditions from which members of this genus are isolated are abscesses, the respiratory tract, and pleural and peritoneal cavities.
Most specimen cultures contain a single Fusobacterium species. The most commonly isolated species is Fusobacterium necrophorum. Almost all of the specimens contain other obligate anaerobes together with facultative and obligate aerobes.
IMAGING
N/A
OTHER DIAGNOSTIC PROCEDURES
Bacterial culture of lesions
GROSS AND HISTOPATHOLOGIC FINDINGS
Swelling and edema of laryngeal-pharynx area, sometimes with necrosis of the mucosal tissue
TREATMENT
Cases with severe swelling and dyspnea may require tracheostomy.
CLIENT EDUCATION
Minimize abrasive materials such as sticks and cockleburs in hays and pastures. Keep feed areas, mangers, and feed equipment clean.
MEDICATIONS DRUGS OF CHOICE
Broad-spectrum systemic antimicrobial therapy for several days. Early recognition is essential for successful therapy.
Anti-inflammatory drugs such as corticosteroids or NSAIDs may be useful to reduce the swelling and dyspnea.
CONTRAINDICATIONS
Oral bolus medications
Appropriate milk and meat withdrawal times must be followed for all compounds administered to food-producing animals.
PRECAUTIONS
N/A
POSSIBLE INTERACTIONS
N/A
ALTERNATE DRUGS
N/A
FOLLOW-UP PATIENT MONITORING
Ability to breath and swallow without difficulty should be monitored.
PREVENTION/AVOIDANCE
Sanitary feed areas and equipment; avoid rough feeds.
POSSIBLE COMPLICATIONS
Toxemia
EXPECTED COURSE AND PROGNOSIS
Recovery if treated early before chronic damage to epiglottis occurs.
MISCELLANEOUS PREVENTION
Avoid rough feeds and maintain clean feed areas.
ASSOCIATED CONDITIONS
Necrotic stomatitis
AGE-RELATED FACTORS
Appears most commonly in calves 3 to 18 months old, but can occur in older animals.
ZOONOTIC POTENTIAL
N/A
PREGNANCY
N/A
SYNONYMS
Necrotic laryngitis Oral necrobacillosis SEE ALSO
Necrotic stomatitis
ABBREVIATIONS
NSAIDs = nonsteroidal anti-inflammatory drugs
Suggested Reading
Jang, S. S., Hirsh, D. C. 1994, Feb. Characterization, distribution, and microbiological associations of Fusobacterium
spp. in clinical specimens of animal origin. J Clin Microbiol. 32(2): 384-87.
Langworth, B. F. 1977, Jun. Fusobacterium necrophorum: its characteristics and role as an animal pathogen. Bacteriol Rev. 41(2): 373-90.
Radostits, O. M., Gay, C. C., Blood, D. C., Hinchcliff, K. W., eds. 2000. Veterinary medicine: a textbook of diseases of cattle, sheep, pigs, goats and horses. 9th ed. London: W. B. Saunders.
Smith, G. R., Barton, S. A., Wallace, L. M. 1991, Apr. Further observations on enhancement of the infectivity of
Fusobacterium necrophorum by other bacteria. Epidemiol Infect. 106(2): 305-10.
Tan, Z. L., Nagaraja, T. G., Chengappa, M. M. 1996. Fusobacterium necrophorum infections: virulence factors, pathogenic mechanism and control measures. Vet Res Commun. 20(2): 113-40.
Author: James P. Reynolds

CALVING-RELATED DISORDERS
BASICS DEFINITION

Calving-related disorders (CRD) occur during the transition period of dairy cows (21 days before expected parturition to 21 days postpartum).
The most important CRDs are hypocalcemia, retained fetal membranes (RFM), metritis, displacement of abomasums (DA), ketosis, fatty liver, and udder edema.
Other conditions such as lameness and mastitis are also related to the transition period but they can occur at any time during the production cycle.
PATHOPHYS IOLOGY
The transition period is a very dynamic stage in the production cycle of the cow.
During the prepartum, the fetus grows exponentially and cows start to decrease dry matter intake (DMI), especially during the last week of gestation. As a response, cows start to mobilize fat from body reserves. The result is an increase of nonesterified fatty acids (NEFA) in the blood. This is especially true in obese cows, and fatty liver may occur.
Calving is a stressful process that results in metabolic and hormonal changes that contribute to immunosuppression and a subsequent decrease of host resistance to diseases. Mammary gland tissue starts to extract elevated levels of calcium from the blood supply. Therefore, there is a more intense negative calcium balance with development with a concomitant hypocalcemia.
If calving is complicated, hypocalcemia worsens affecting uterine and gastrointestinal motility.
Retained fetal membranes may occur, with consequent metritis if preventive measures are not considered.
Displacement of abomasums may be also a consequence.
When lactation advances, energy requirements increase dramatically and DMI recovers slowly. This creates a typical negative energy balance during the first weeks of lactation. In addition, mammary glands extract large amounts of glucose from the blood for lactose synthesis. Hypoglycemia may develop and ketosis may be established.
SYSTEMS AFFECTED
Systems affected will depend on the calving-related disorder: mammary, hepatic, cardiovascular, gastrointestinal, respiratory, reproductive, nutritional, and production management
GENETICS
Some CRDs may have a hereditary component (ketosis and somatic cell count).
INCIDENCE/PREVALENCE
Incidences of CRDs are extremely variable and depend on factors such as season, geographical location, breed, type of housing, environment, and management.
Reported incidences for some CRDs include clinical hypocalcemia 0.2%-2%, retained fetal membranes 8%-14%, metritis 6%-12%, ketosis 2%-6%, displacement of abomasums 2%-6%.
GEOGRAPHIC DISTRIBUTION
Worldwide where dairy farming occurs
SIGNALMENT
Related to the periparturient period of dairy cows; there may be breed predispositions for some CRD (Jersey cows and hypocalcemia).
SIGNS
Retained fetal membranes (visible membranes after 24 h postpartum), metritis (fever, foul-smelling discharge), hypocalcemia (musculoskeletal compromise), ketosis (decrease in milk yield, high ketones in blood, urine, or milk), displacement of abomasums (high-pitch sound at auscultation on left flank, last two rib spaces).
CAUSES
Inadequate management of the prepartum, calving, and postpartum period; improper nutrition, environment, and management
RISK FACTORS
Management, breed, genetic potential, nutrition, season, herd size, geographical location
DIAGNOSIS DIFFERENTIALDIAGNOSIS
Hypocalcemia
Retained fetal membranes (RFM)
Metritis
Displacement of abomasums (DA)
Ketosis
Fatty liver
Udder edema
Lameness
Mastitis
CBC/BIOCHEMISTRY/URINALYS IS
Important tools for ketosis diagnosis (ketones in urine, blood, or milk). CBC/biochemistry can be useful in determining hydration, calcium and potassium levels, liver function, and infection level.
Urine pH should be monitored to evaluate anionic salts during prepartum period for the prevention of hypocalcemia. Urine pH should be between 6.5 and 7.0.
Serum Ca, Mg, P, nonesterified fatty acids (NEFA), beta hydroxy butyrate (BHBA), glucose, insulin, T3 and T4, liver enzymes, and urea nitrogen all can be monitored depending on differential diagnosis.
OTHER LABORATORY TESTS
Liver biopsy can be helpful with the diagnosis of hepatic lipidosis.
IMAGING
Ultrasound imaging can be a useful adjunctive tool.
DIAGNOSTIC PROCEDURES
N/A
PATHOLOGIC FINDINGS
N/A
TREATMENT APPROPRIATE HEALTH CARE
N/A
NURSING CARE
N/A
ACTIVITY
N/A
DIET
Proper transition diet. Moderate energy and protein levels. Prepartum diet with a negative cation-anion difference. Appropriate amount and particle size of fiber.
Fresh cow rations should be intermediate between the close-up and the high group rations.
Cows should be fed ad libitum-that means a 5% to 10% feed refusal. If concentration of energy and protein are somewhat low in the ration fed right after calving, it is important not to leave the cows in this group for too long of a time.
Rations should have at least 21% neutral detergent fiber (NDF) from forage and enough particle size to support good chewing activity and rumen fill.
Diets should have 8% to 10% of particles on the top screen of the Penn State Particle Size Separator for both prefresh and fresh cows. Researchers suggest feeding 3 to 5 lb of high-quality long forage to maintain rumen function.
Forage quality is very important in the transition period.
As for the close-up group, it is important to feed adequate levels of copper, zinc, manganese, selenium, and vitamin E.
Researchers suggest 2000 IU of vitamin E per day for fresh cows.
CLIENT EDUCATION
Proper nutrition and general management in transition cows is important.
SURGICALCONSIDERATIONS
Considered important for displaced abomasum
MEDICATIONS DRUGS OF CHOICE
N/A
CONTRAINDICATIONS
N/A
PRECAUTIONS
N/A
POSSIBLE INTERACTIONS
N/A
ALTERNATIVE DRUGS
Feed additives to improve energy and mineral balance such as propylene glycol, niacin, calcium propionate, vitamin E, selenium
FOLLOW-UP PATIENT MONITORING
Monitoring of body condition score during dry period; cows should not lose condition or gain excessive weight during the transition period.
Urine pH should be monitored to evaluate anionic salts during prepartum period for the prevention of hypocalcemia. Urine pH should be between 6.5 and 7.0.
PREVENTION/AVOIDANCE
Proper general and nutritional management
POSSIBLE COMPLICATIONS
Decreased milk production, infertility, and death
EXPECTED COURSE AND PROGNOSIS
N/A
MISCELLANEOUS ASSOCIATED CONDITIONS
Calving-related disorders are intimately related to each other. Cows with hypocalcemia are more likely to develop retained fetal membranes. Cows with RFM are more likely to develop metritis. Cows with metritis are more likely to develop ketosis and cows with ketosis are more likely to develop displacement of abomasums.
AGE-RELATED FACTORS
Older cows are more likely to develop clinical hypocalcemia, ketosis, and displacement of abomasum.
ZOONOTIC POTENTIAL
N/A
PREGNANCY
Prepartum management is critical for prevention of calving-related disorders. Enough feed bunk space, adequate shade, and comfortable environment are essential for prepartum dairy cows.
RUMINANT SPECIES AFFECTED
Dairy cattle
BIOSECURITY
N/A
PRODUCTION MANAGEMENT
Nutrition and feeding, housing, management
Dry cows (7 to 9 month pregnant nonlactating cows) need adaptation to their next lactation diet. Preparation for parturition and avoidance of calving-related disorders is an important component of this program.
Consequently, dry cows need to be moved to a prepartum transition pen (close-up pen).
Three weeks prior to freshening is sufficient for adult mature cows. However, 5 weeks should be considered for pregnant heifers because they are still growing and they have not experienced the challenges of calving and lactation before.
Close-up heifers and cows should be handled in different pens.
Prepartum transition animals need a comfortable environment with adequate shade, bunk space, and good-quality water.
Prepartum transition pens must be situated in a strategic location of the farm, with easy labor access and planned handling.
Transition pens must be monitored twice daily for cows showing signs of udder edema development and signs of impending parturition.
Calving may occur either in the same prepartum transition pen or in the maternity pen, depending on management criteria.
The calving environment must be quiet, clean, and easy to access if calving assistance is needed.
Major concerns of the prepartum transition period and calving are udder edema, dystocia, and hypocalcemia.
Udder edema must be addressed through proper nutritional management. Excess nutritional sodium and potassium are related to this metabolic condition.
Dystocia is a multifactorial problem where proper assistance is the key. Good knowledge of parturition physiology and obstetric intervention are basic and needed.
For the postpartum transition cow, the same recommendation of a good environment applies. The postpartum pen also should be in a strategic location.
Cows need to be monitored for retained fetal membranes, metritis, ketosis, and abomasal displacement.
A strategic plan should include monitoring cows during the first 10 days postpartum for fever development and ketone bodies either in urine or milk.
If cows are either febrile, positive to ketones, or both, they should be separated and evaluated through a complete physical examination.
Body condition of cows is important. On a scale of 1 to 5, they should be between 3.25 and 3.75.
Overconditioned animals are more likely to experience dystocia and calving-related disorders. Therefore, energy density of dry cow diets must be consistent and adequate.
Mineral content is important to the prevention of hypocalcemia and other related disorders.
Typical prepartum diets are rich in cations (sodium and potassium). Therefore, the difference in mEq/kg between (Na+K) – (Cl+S) should be positive (~+150 to +350 mEq/kg). This diet institutes an alkaline environment, which favors the development of hypocalcemia.
Receptors for parathormone and vitamin D are altered structurally by alkaline environments.
If the cow’s acid-base status has shifted to a more acidic level, these receptors work more efficiently with a better bioavailability and absorption of calcium.
A goal should be a urine pH between 6.0 and 7.0. This pH level has been associated with a lowered incidence of hypocalcemia.
Dietary ingredients of the prepartum diet should be exactly the same as the postpartum lactation diet to insure a better rumen microbial adaptation.
The diet should contain a higher level of effective fiber (NDF, neutral detergent fiber) with adequate particle size to stimulate rumination, avoid acidosis, improve rumen fermentation, and avoid abomasal displacement.
Close-up Cows
Feeding strategies needed during the close-up period to achieve these goals are:
Condition should be maintained during the dry period. Excessive body condition at calving can increase incidence of ketosis and fatty liver.
Increase grain feeding to 0.5%-0.75% of body weight.
Target 35%-40% nonfiber carbohydrates as a % of DM.
Feed high-quality forages with sufficient effective fiber.
Limit fat to 1/4-1/3 lb per day.
Feed low-potassium forages; balance for potassium concentration less than 1.5% of diet DM (get as close to 1% as possible).
Provide adequate magnesium (0.4% of diet DM) and calcium (1%-1.2% of diet DM).
Feed adequate selenium (0.3 ppm) and vitamin E (2000 IU per day).
Supply extra trace minerals such as copper, manganese, and zinc to account for decline in feed intake.
Feed adequate crude protein (cows need 12%-13%, heifers 15% of diet DM).
Fresh Cows
Calving and the change to lactating status are very stressful in the life of a cow. They need a lot of care. Assign your best employee/person to monitor this group of cows.
Maternity facilities must be clean, dry, well lit, well ventilated, and comfortable. After leaving the maternity pens, cows should ideally be moved to a fresh cow group. There is also benefit in having a separate heifer group, because heifers are smaller and do not compete as well at the feed bunk.
The first 1 to 2 weeks after calving set the stage for the entire lactation. Studies have shown that for each 1 lb increase in peak milk, there is a 220 lb milk production increase for the entire lactation.
Monitoring Progress
After calving, it is important to optimize dry-matter intake as soon as possible.
Monitor feed intake by rating how the cow consumes fresh feed on a scale of 1 to 4 (1 = 0%-33% consumed; 2 = 33%- 66% consumed; 3 = 66%-90% consumed; 4 = all consumed). Cows off feed require special treatment. Observe chewing and rumination activity.
Rumen movements should be monitored using a stethoscope-healthy cows have about 1.5 to 2 rumen movements per minute.
Body temperatures should be recorded daily. The goal is to be below 103°F for mature cows and 102.5°F for heifers.
Uterine discharges should be checked and a ketone test on the cow’s urine or milk is recommended.
SYNONYMS
Diseases of peripartum Periparturient disorders SEE ALSO
Body condition scoring: dairy cattle Displacement of abomasums Hypocalcemia
Ketosis Lameness
Mastitis Metritis Milk fever
Postparturient paresis Retained fetal membranes Transition management ABBREVIATIONS
CRD = calving-related disorder DA = displacement of abomasums DMI = dry matter intake
NDF = neutral detergent fiber NEFA = nonesterified fatty acids RFM = retained fetal membranes WBCs = white blood cells Suggested Reading
Melendez, P., Donovan, A., Risco, C. A., Littell, R., Goff, J. 2003. Effect of calcium-energy supplements on calving- related disorders, fertility and milk yield during the transition period in cows fed anionic diets. Theriogenology 60:843- 54.
Metabolic disorders of ruminants. 2000. In: Veterinary clinics of North America, food animal practice. Philadelphia: W.
B. Saunders.
National Research Council. 2001. Nutrient requirements of dairy cattle. 7th ed. Washington, DC: National Academy Press.
Risco, C. A., Melendez, P. 2003. Periparturient disorders. In: Encyclopedia of dairy science. H. Roginski, J. Fuquay, P. Fox(ed). Burlington, MA: Academic Press.
Author: Pedro Melendez

CAMELID TOOTH ROOT ABSCESSES
BASICS DEFINITION
Tooth root abscess is a localized osteitis, pulpitis, and/or alveolar periostitis around one or more tooth roots, often draining purulent exudates by a fistulous tract through the skin overlying the abscess.
PATHOPHYS IOLOGY

The adult camelid dental formula is: (I 1/3, C 1/1, PM 1-2/1-2, M 3/3) × 2 for 30 to 32 teeth.
The upper incisors are actually found caudally in the region of the canine teeth.
Cheek teeth can be numbered from 1 to 5 (rostral to caudal), or labeled according to the dental chart (PM 1&PM 2,M 1to M 3).
The upper premolars have three roots each; lower have two roots each.
The upper molars have four roots each; lower M 1 and M 2 have two roots, M 3 has three roots, but two are fused.
Tooth fracture, gingival penetration, or infundibular decay and infection can result in tooth root abscess. Often the source is unknown.
Periostitis and osteitis of the mandible secondary to tooth root abscess can spread along the mandibular canal.
SYSTEMS AFFECTED
Gastrointestinal
Musculoskeletal
GENETICS
None
INCIDENCE/PREVALENCE
Unknown
Mandibular molars 1 and 2 are most often affected
Maxillary teeth are rarely affected
Canine teeth may be affected: incidence appears to be decreasing with change in methods for trimming fighting teeth.
GEOGRAPHIC DISTRIBUTION
Worldwide
SIGNALMENT
All camelids can be affected.
Rarely seen in very young animals, usually >12 months of age
Median of 5 years
SIGNS
Firm swelling of the jaw
Drainage of exudates from mandible or maxilla
Reluctance to eat
Dropping food
Strange chewing habits
Nasal discharge if sinus affected.
Quidding
CAUSES
Gingival penetration along alveolus
Infundibular decay
Tooth fracture or trauma
Mandibular/maxillary fracture
DIAGNOSIS DIFFERENTIALDIAGNOSIS
Mandibular osteitis
Subcutaneous abscess/cellulites
Fracture
Sinusitis
Tumor
Actinomycosis
Osteomyelitis
Salivary gland disease
CBC/CHEMISTRY/URINALYS IS
Not usually useful
May see slight elevation in WBC count in chronic periostitis/osteitis
OTHER LABORATORY TESTS
Culture of exudates may sometimes indicate the bacteria involved, but is rarely necessary as tooth removal and flushing resolves the problem in most cases.
IMAGING
Radiology is essential for diagnosis of tooth root(s) involved.
Multiple oblique open-mouth views are often necessary, so sedation or anesthesia is usually required.
Mandibular abscesses are easier to image than maxillary abscess.
Contrast agent may be injected into a draining tract if the affected root is not obvious.
Extent of osteitis/periostitis can be determined from radiographs also
Bone lysis
Loss of lamina dura
Periodontal sclerosis
Periosteal reaction
Fistulous tracts
DIAGNOSTIC PROCEDURES
None
PATHOLOGIC FINDINGS
If seen at necropsy, localized purulent exudates, necrotic bone and alveolus, fistulous tract, loose teeth, and bony proliferation may be seen around the affected tooth roots.
TREATMENT APPROPRIATE HEALTH CARE
Tooth root abscesses require surgical care (nonemergency) and subsequent medical treatment.
Extraction is generally required.
Teeth can be removed by several methods in the anesthetized camelid.
Oral extraction may be appropriate for premolars, canines, and incisors.
Elevation from the alveolus may be difficult by oral approach due to the limited excursion of the jaws in these species.
Ensure all roots are removed.
Some curettage of alveolus will help remove necrotic bone.
Repulsion of the cheek teeth has been recommended by some.
Extreme care must be taken due to the fragility of the mandible and maxilla, which can be easily fractured.
Trephine openings are made as in horses-landmarks are described in references.
Motorized burr has been very successful for removal of an affected tooth, especially mandibular teeth.
Incision is made along the ventral or ventrolateral aspect of the mandible, resecting draining fistula if possible.
Periosteum and overlying musculature are elevated along the lateral aspect of the mandible to the level of the gingival attachment.
If a draining tract is present, it can be followed to the tooth using the burr to remove the overlying bone on the lateral aspect.
If no draining tract is present, the affected tooth is identified by oral palpation and an approach is made through the lateral alveolar plate to the tooth.
Following removal of the overlying bone, the tooth and roots are carefully elevated and removed.
Care must be taken not to damage adjacent normal tooth roots. Knowledge of anatomy and study of radiographs are essential.
In some cases, resection of the single affected root using the burr can be effective in resolving the problem without complete extraction.
A ventral opening in the incision is left for drainage, closing the remainder of the incision.
The empty alveolus can be packed with gauze or acrylic if desired, and may be necessary in the maxilla. In the mandible, it is not deemed to be necessary.
NURSING CARE
Following surgery, daily or twice daily flushing of the tract with dilute chlorhexidine solution to remove food particles
Flush until closed completely.
ACTIVITY
No restriction
DIET
No change required
Animals will usually begin eating within hours of anesthetic recovery.
CLIENT EDUCATION
Early signs of dental disease should be investigated immediately.
Subcutaneous infection can occur.
Osteitis prolongs treatment.
Packing of cavity with food will promote infection and prolong healing.
Proliferative bone may remain present for the life of the animal.
Animals are often chronic at the time of presentation because the masses are difficult to detect if heavy face fleece is present.
Palpation or close observation of jaw lines when handling may allow for earlier recognition.
SURGICALCONSIDERATIONS
None
MEDICATIONS DRUGS OF CHOICE
Flunixin meglumine 1.1 mg/kg IV q24h for postsurgical pain; rarely required for more than 48 hours
Procaine penicillin G 20,000 U/kg IM q12h for 7-10 days or longer if required by infection severity
Other antibiotics can be used if cultures indicate.
Oxytetracycline-18 mg/kg SC q 48 hours
Postoperatively-5-10 days of treatment
Medical treatment-14-30 days treatment
Ampicillin-2.5 mg/kg IM q 12 hours
Postoperatively-5-10 days of treatment
Medical treatment-14-30 days treatment
CONTRAINDICATIONS
None of the drugs listed are approved for use in camelids and do not have established withdrawal times associated with their use.
PRECAUTIONS
None
POSSIBLE INTERACTIONS
None
ALTERNATIVE DRUGS
Any broad-spectrum antibiotics effective against A. pyogenes and common oral bacterial inhabitants
FOLLOW-UP PATIENT MONITORING
Daily monitoring for cavity flushing will be required.
Further follow-up care is rarely required unless another abscess occurs.
PREVENTION/AVOIDANCE
Not much can be done
Avoiding stemmy hay and foxtail may be helpful.
POSSIBLE COMPLICATIONS
Ongoing osteitis and drainage
Damage to adjacent tooth roots
Infection of alveolar packing material
Electrolyte loss and/or dehydration if salivary drainage through ventral drainage opening is excessive
EXPECTED COURSE/PROGNOSIS
Healing will occur over several weeks, preferably healing from the inside out.
Prognosis is excellent; good if bony infection is severe.
Bony proliferation may be permanent.
Surgical Tooth Removal-Excellent
Short term (<30 days)
Decreased size of facial swelling within 1 week postoperatively
Long term (>30 days)
Resolution of facial swelling
Additional abscesses at adjacent teeth possible if extent of disease not identified at initial exam
Medical Treatment-Excellent-Good
Short term (<30 days)
Decreased size of facial swelling
Progression of disease possible in minor number of patients
Long term (>30 days)
Resolution of disease in most
Recrudescence possible: may respond to additional round of medical therapy
MISCELLANEOUS ASSOCIATED CONDITIONS
Retained tooth root
Fracture
Recurrence at adjacent teeth
Medical Treatment
Failure to respond
Recurrence
AGE-RELATED FACTORS
Rarely seen in animals < 12 months of age
ZOONOTIC POTENTIAL
None
PREGNANCY
N/A
RUMINANT SPECIES AFFECTED
All camelids
BIOSECURITY
N/A
PRODUCTION MANAGEMENT
N/A
SYNONYMS
None
SEE ALSO
Body condition scoring: camelids, anesthesia and analgesia
ABBREVIATIONS
C = canine teeth I = incisor teeth
IM = intramuscular M = molar teeth
PM = premolar teeth SC = subcutaneous WBC = white blood cell Suggested Reading
Cebra, M. L., Cebra, C. K., Garry, F. B. 1996. Tooth root abscesses in New World camelids: 23 cases (1972-1994). J Am Vet Med Assoc. 209:819-22.
Fowler, M. E. 1998. Digestive system. In: Fowler, M. E., ed., Medicine and surgery of South American camelids, 2d ed.,
pp. 305-59. Ames: Iowa State University Press.
Fowler, M. E. 1998. Surgery. In: Fowler, M. E., ed., Medicine and surgery of South American camelids, 2d ed., pp. 108-

Ames: Iowa State University Press.
Kock, M. D. 1984. Canine tooth extraction and pulpotomy in the adult male llama. J Am Vet Med Assoc. 185(11): 1304- 6.
Long, P. 1989. Llama herd health. Vet Clin Food Anim. 5(1): 227-32.
Authors: Jennifer M. Ivany Ewoldt and Dusty W. Nagy

Piramid Pemakanan Ternakan Lembu: Keutamaan Nutrisi untuk Prestasi Maksimum

6 Kesilapan Lazim yang Perlu Dielakkan dalam Penternakan Ternakan

Kematian Embrio dan Fetus, Keguguran (Abortion), serta Perkembangan Fetus yang Tidak Normal dalam Lembu

Perbezaan antara jerami/hay dan silage/silaj

Pengurusan Postpartum Anestrus dalam Lembu Pedaging

Faktor kehilangan berat badan pada kambing dan biri-biri