Abdominal Distension
Description
Abdominal distension may be due to pregnancy, abnormal accumulations of food, gas or fluid in the abdominal cavity or herniation of the abdominal wall.
Important causes include:
bloat – frothy bloat or free gas bloat
advanced pregnancy – periparturient oedema and/or gravid uterus
vagal indigestion
oesophageal obstruction with a fruit, vegetable or milled feed
urethral obstruction and ruptured urethra
gastrointestinal obstruction or abomasal displacement
Clinical Signs and Diagnosis
A general physical examination should be performed including palpation, percussion, ballottement and paracentesis.
Differentiation is based on history (in particular the numbers affected, the suddenness of onset and feeding conditions) plus clinical examination and necropsy findings.
When viewed from the front or rear of the animal, distension may be unilateral, bilaterally symmetrical, asymmetrical or more prominent in the dorsal or ventral half, depending on the cause.
Passing a stomach tube, auscultation with percussion and ballottement to detect areas of gas and fluid, insertion of a trochar, rectal palpation (cattle) and examination of faeces may assist in deciding the cause and need for intervention.
Abdominal distension due to pregnancy is usually due to the presence of multiple foetuses or may be associated with pitting oedema due to fluid accumulation along the floor of the udder and adjacent tissues.
The rumen will distend after rapid engorgement on grain (grain overload) or slow accumulation over days of indigestible roughage (rumen impaction). If the distension is mainly gas, it will usually be due to free gas or froth in the rumen (gas cap or frothy bloat). If it is gas and fluid it may be due to a gastrointestinal accident such as torsion, obstruction or perforation of the abomasum or intestine. In goats, distension may be caused by intestinal tympany of enterotoxaemia.
Distension by fluid may be due to urine in a distended bladder or free in the abdomen after bladder rupture following urinary obstruction. Fluid may also be ascites if blood is chronically low in protein from parasites or undernutrition.
Hernias should be considered in sheep and goats because the abdomen is thin walled and easily traumatised.
Treatment
This will depend on the diagnosis. Pregnancy will require additional care and management and bloat is treatable. Most other causes have a poor prognosis under export conditions.
Prevention
Preventative measures will depend on diagnosis and risk factors.
Abdominal Hernia
Description
This is the protrusion of abdominal contents (mesentery or intestinal tract) through a defect in the abdominal wall, the skin remaining intact.
Size of the lesion depends on the extent of the defect and the amount of intestine or other content involved. Hernias may be congenital (umbilical hernias) or acquired such as traumatic, inguinal and scrotal hernias, and rupture of the pre-pubic tendon.
Hernias are unlikely in the animals selected for the live export process. They are mentioned because they may resemble haematomas, ruptured urethra, abscesses and peri-parturient oedema.
Clinical Signs and Diagnosis
A hernia may present as a soft, elastic, reducible swelling except when trapped gut is being strangulated or acute rupture causes haemorrhage and oedema. Umbilical hernias occur in the ventral abdomen, the result of the umbilical ring failing to close after birth. The sharp edge of the umbilical ring can be palpated. Traumatic hernias occur in the ventral or lateral abdomen and are the result of trauma from a horn or a fall. Acute and severe hernias may be associated with pain and distress. Hernia associated with rupture of the pre-pubic tendon occurs in older cows generally in late pregnancy due to failure of stretched and thinned abdominal muscles. Scrotal hernias involve herniation of abdominal content through the inguinal canal of males. The scrotum is unusually enlarged and strangulation is a real risk. Close external and internal (rectal) palpation may assist in confirming the diagnosis.
Treatment
Surgical and bandaging options are available but are unlikely to be practical or successful within the constraints of the export process. Animals in distress should be euthanased or sent for emergency slaughter. Pregnant animals with severe abdominal or pre-pubic herniation may be induced to abort or calve with corticosteroids (dexamethasone) and prostaglandins (cloprostanol, dinoprost trometamolin) and should be assisted as necessary at delivery.
Prevention
Low stress animal handling, well-designed facilities, and careful selection of animals prevent this condition in the live export process.
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.
PATHOPHYSIOLOGY
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
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
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
Abomasal Ulcer
Description
Abomasal ulcers are defects in the mucosal lining of the abomasum. They are difficult to diagnose unless there is perforation of the abomasal wall or erosion into a blood vessel. Even then, the leakage of ingesta or blood must be significant.
The causes of abomasal ulceration in cattle are not well understood. Prolonged inappetence resulting in sustained high acidity in the abomasum is considered an important risk factor. Stress, high dietary fibre in calves, and inadequate dietary fibre in adults are also believed to play a role. Rarely, in older cattle, ulcers are associated with tumours infiltrating the abomasal wall. Multiple shallow erosions and ulcers affecting the abomasum are also found at necropsy in viral diseases of cattle, such as bovine viral diarrhoea and malignant catarrhal fever. Prolonged treatment with high doses of non-steroidal anti-inflammatory drugs, antibiotics, or both may also cause abomasal ulceration.
Deaths from both perforated and bleeding abomasal ulcers have been recorded in cattle at sea.
Clinical Signs and Diagnosis
Cattle with ulcers may show signs of colic (lifting hind legs and looking at the flank) and grinding of teeth (bruxism). Chronically affected cattle may lose body condition.
Additional signs may be related to severity of blood loss (pale mucous membranes, weakness, elevated heart and respiratory rates), and black tarry faeces (melaena).
Animals may die suddenly if blood loss is extreme. Black tarry faeces also occur when blood from the respiratory tract is coughed up, swallowed and digested in the abomasum, therefore caudal vena cava syndrome should be considered as a differential diagnosis. When bright red blood is coating formed faeces, it is usually from the large intestine, in which case coccidiosis should be considered. Dull red blood is usually from the small intestine, and may indicate salmonellosis or intussusception. Haemorrhagic bowel syndrome (HBS) is a sporadic, acute, necrohaemorrhagic enteritis that has been reported in cattle in Australia and overseas, with signs similar to those described for abomasal ulcers.
Cattle with perforated ulcers may develop local peritonitis and recover fully if adhesions are not extensive, or they may develop acute diffuse peritonitis and die. The outcome depends on the amount of leakage into the abdomen and whether it is contained by the omentum. Animals affected with local peritonitis will have fever, inappetence, and a pain reaction to deep palpation of the right side ventral abdomen. Those with acute diffuse peritonitis will deteriorate and die quickly with sunken eyes, cold clammy skin and rapid, shallow breathing and pulse.
At necropsy, one or more ulcers will be present in the abomasal mucosa ranging from a few millimetres to 5 cm in diameter. They are easily missed. Examination under a good light following rinsing of the mucosa with water will assist detection. In cattle that have died from a bleeding ulcer, findings typically include pale mucous membranes, watery blood, shrivelled and empty intestines, black and tarry faeces, and blackened fluid within the abomasum. Washing of the ulcer may reveal an eroded blood vessel. Perforated ulcers are often associated with pockets of fluid and pus within the abdomen, possibly trapped within folds of omentum.
Death from other gastrointestinal accidents may resemble deaths from haemorrhage or perforation of the abomasum. If acute diffuse peritonitis is found at necropsy, it is important to determine the cause – the preventative measures against ulceration are different to those against traumatic reticulitis.
Treatment
If abomasal ulceration is suspected, minimise stress and stop any treatments with non-steroidal anti-inflammatory drugs. Feed animals increased roughage (hay or chaff) to keep the animal eating and also stimulate salivary production to counteract acid production within the abomasum.
Oral antacids such as magnesium hydroxide and sodium bicarbonate are ineffective because they are unlikely to reach the abomasum in adequate amounts to counter acidity.
For animals that are weak and lethargic as a result of anaemia from bleeding abomasal ulcers, the prognosis is poor, even if a blood transfusion is possible. A minimum of 4-6 L may be lifesaving, but there is a possibility that bleeding may continue.
Broad spectrum antibiotics (oxytetracycline, trimethoprim sulpha) are recommended for perforated ulcers because of the risk of infection, including localised peritonitis and adhesions.
For animals with acute diffuse peritonitis, the prognosis is grave, and euthanasia should be considered if the animal is recumbent, sunken eyed, the heart rate exceeds 120 beats per minute, and the skin is cold and clammy. If the animal does survive, it may suffer from chronic illthrift from adhesions.
Prevention
Minimise stress, feed roughage, and keep animals eating to avoid long periods of overly acidic conditions occurring in the abomasum.
Abortion
Description
Abortion is the early termination of pregnancy with expulsion of a dead foetus. A dead full term foetus is referred to as a stillbirth rather than an abortion. The normal gestation period for a bovine is 9 months. The gestational age of an aborted foetus can be estimated by measuring the distance in inches from the crown of the head to the tail head of the rump (inches=cm/2.5). This distance is multiplied by 2. The square root of this product gives the approximate gestational age in months.
Abortions may occur days, weeks or months after exposure to an infectious microorganism, toxin, stress or genetic fault that impacts the foetus or placenta. This means abortions may be the result of factors occurring before animals entered the export process. Abortions in up to 3 % of breeders per year are considered normal.
Aborting animals may have higher risk of retained foetal membranes and uterine infection (metritis) if aborting after 3 months of pregnancy, and development of the mammary gland may lead to mastitis.
Heat stress, mouldy feed, bovine viral diarrhoea virus and neosporosis are some of the agents potentially increasing abortion rates above background levels in the export process. Fever, severe trauma and administration of glucocorticoid drugs may cause abortion in individual animals. The sedative xylazine, used for minor surgical procedures at sea, may cause abortion in near term pregnancies.
Infectious diseases known to cause abortion and worth considering in investigation of outbreaks include trichomoniasis, campylobacter, bluetongue virus, akabane virus, salmonella, mycoplasma, Histophilus somni, leptospirosis, brucella, chlamydophila, listeria, neospora, infectious bovine rhinotracheitis and bovine viral diarrhoea virus. Non-infectious causes include plant poisonings and possibly heat stress.
There are three conditions occurring at sea that are sometimes mistaken for evidence abortion has occurred. First, mammary gland development and premature lactation occur commonly in heifers and cows (both pregnant and non-pregnant), without abortion or calving having occurred. Secondly, bloody vaginal discharge occurs commonly 2-3 days after oestrus. Third, coccidiosis in adult cattle at sea is common – these animals strain, have a raised tail and may have bloody faeces staining the tail and perineum.
Clinical Signs and Diagnosis
Signs of abortion include straining, raised tail, red to brown coloured vaginal discharge, protrusion of foetal membranes, mammary gland development, and the discovery of a foetus or foetal membranes in a pen. Rectal and vaginal examination of animals may be required to confirm abortion.
Specimens for laboratory diagnosis ideally include acute and convalescent maternal sera and the complete fresh (or frozen) foetal-placental unit. Otherwise submit sections of foetal and placental tissues in formalin plus foetal stomach contents for microbiology.
Treatment
Treatment is usually not required unless assistance to remove the foetus is necessary in which case antibiotics (procaine penicillin, oxytetracycline, or trimethoprim sulpha) may be recommended. Retained foetal membranes should be cut off level with the vulva and parenteral antibiotics (oxytetracycline, or trimethoprim sulpha) administered. Antibiotic pessaries are not effective at combating intra-uterine infection and are not recommended.
Prevention
Minimise stress (especially heat stress), avoid mouldy feeds, practice low stress handling and transport methods, avoid administration of glucocorticosteroids, protect feed from contamination and cull persistently viraemic pestivirus animals.
Abscess
Description
An abscess is an accumulation of pus surrounded by fibrous tissue. They may occur anywhere in the body where pyogenic (pus forming) bacteria can establish and multiply. Over time, pus is mostly replaced by fibrous tissue.
Abscesses of the lymph nodes in the head and neck region (often referred to as grass seed abscesses), and of the skin (skin abscesses), are commonly seen in the export process as a consequence of abrasions or penetrations of the oropharynx or skin from grazing prickly plants, seed penetrations or vaccination needles.
Golf ball to tennis ball size abscesses on the cheeks and jaw are probably due to skin penetration from thorns or other sharp objects during feeding or rubbing.
Subcutaneous abscesses (skin abscesses) may occur at vaccination sites when vaccination is performed under sub-optimal conditions (wet, dirty or blunt needles). Lumps on the side of the neck are usually vaccination site abscesses. Most cattle are vaccinated on the near side because of the way races and crushes are designed, hence most vaccination site abscesses in cattle are on the near side of the neck. Skin abscesses also occur more frequently with vaccines containing oily adjuvants.
Skin abscesses also may occur where calcium solutions have been injected under the skin when treating milk fever. Haematomas are large blood and serum filled lumps occurring on the bony projections of the hips and rump in cattle following trauma, and may become abscessed over time if contaminated with bacteria. This occurs if pyogenic bacteria infect them via the blood stream or via a contaminated needle inserted to drain them.
Clinical Signs and Diagnosis
In the early stages, abscesses may be accompanied by pain, heat and swelling. In later stages, they are cold and surrounded by a fibrous capsule. Rounded, tense swellings under the skin of the ventral neck, the cheek or under the ear are probably abscesses. However, there may also be cud stuck between the cheek and teeth, a blocked salivary duct, or oedema under the jaw (bottle jaw). Swellings on the side or top of the neck are almost always abscesses from vaccination. In goats, the abscesses of cheesy gland are common on the ventral neck and under the ear.
A burst abscess is recognised by discharging pus. If not burst, an abscess is confirmed by incising the swelling at its most fluctuant or raised point, or inserting a needle and finding pus. Culture of contents may reflect secondary bacteria rather than the primary cause.
Treatment
Antibiotics are ineffective as they don’t penetrate the abscess wall. If the abscess is not affecting the health of the animal and is not so unsightly that it might cause rejection at destination or slaughter, then taking no action should be considered. This is because incising and draining the abscess may cause it to become unsightly, or cause complications such as secondary infection and flystrike. In addition, incised abscesses may require ongoing flushing to ensure uncomplicated healing and healing may take some weeks.
Medical management may be considered if infection is spreading (or is likely to spread after incision) through the soft tissues around the abscess (i.e. cellulitis) or if the abscess is causing severe pain (i.e. the animal has a stiff neck and having difficulty feeding and watering). In these cases, anti-inflammatory drugs (flunixin meglumine, tolfenamic acid, meloxicam, ketoprofen), and antibiotics (procaine penicillin, erythromycin) should be administered.
Note that some abscesses may spontaneously shrink over time which may allow the animal to re-enter the livestock export process. However, shrinkage may take many weeks or even months.
Large abscesses of the lymph nodes of the head and neck (i.e. grass seed abscesses, cheesy gland abscesses) are difficult to treat successfully, may require excision of the node, and many weeks of antibiotic treatment, with no guarantee of complete healing. Affected animals should probably be sent for salvage slaughter.
A superficial abscess may be treated by incision and drainage. Before incising, double check that the swelling is fluid-filled, and not an indurated fibrous lump, hernia or haematoma. Restrain the animal (cattle may require a crush, sedation and even anaesthesia if fractious). Clean the area and use a sterile scalpel blade to make an incision at the most fluctuant or raised point of the swelling, or at the ventral most aspect of the abscess. Widen the incision sufficiently so that it won’t close over too quickly, otherwise the abscess may reform. Creating a ventral drainage hole may be helpful in large abscesses. Flush thoroughly with clean water under moderate pressure from a hose or syringe using a gloved finger to gently aid removal of pus.
Take personal hygiene precautions when dealing with abscesses as bacteria that may be present can infect humans and they may be resistant to antibiotics.
Prevention
Coarse, prickly and grass seed-containing feeds should be avoided if lymph node abscesses of the head and neck are a problem.
Source sheep and goats that are properly vaccinated against cheesy gland (caseous lymphadenitis or CLA).
Vaccination and other injections should be administered in compliance with manufacturer’s recommendations, including for cleaning and disinfecting equipment, the preferred injection site and gauge and length of needles.
Vaccinations should generally be administered into clean, dry skin of well restrained animals with a sharp, small gauge needle. This means vaccinating before dipping or spraying, avoiding wet or dirty conditions, and regularly changing needles (every 10 to 30 animals). The needles should preferably be 18g and not greater than 16g, and not exceed 0.5 inch in length for subcutaneous injections. It is important to rotate the needle on the syringe so that the bevel will be parallel to the skin during injection and the injection is administered at approximately a 45º angle as shown in Figure 4.1 above. Changing the angle of injection from perpendicular to 45º and adjusting the bevel as described has apparently reduced the number of vaccination site abscesses in problem enterprises (Fordyce G, personal communication 2011). It is recognized that other approaches may be successfully used for injection, including using a needle longer than 0.5 inch and inserting it at right angles to a skin tent fold elevated by the free hand (Manefield G, personal communication 2011).
Actinobacillosis
Description
This is a sporadic infection of the lips and cheeks (sheep) and tongue (cattle) caused by Actinobacillus lignieresii, a bacterium normally resident in the mouth.
Mucosal abrasion or injuries to the tongue allow bacteria to establish infection. Cases may be more likely to occur in dry periods or when feeding coarse or prickly feed. The tongue becomes progressively disabled by swelling and fibrosis, and affected animals suffer weight loss due to difficulty eating and drinking.
The infection is chronic and progressive. Early lesions may not be detected in pre-export inspections and may therefore present during export.
Clinical Signs and Diagnosis
Infection causes swelling associated with granulomatous abscesses in the tongue (cattle) or other oral tissues. Affected animals will have difficulty eating and generally lose weight.
Cattle will show drooling, tongue-lolling, chewing movements, protrusion of the tongue and bottle jaw. Finding a thick, hard, dry tongue is diagnostic.
Sheep will often show numerous small abscesses containing yellow granular pus in the soft tissues under the skin of the face. The abscesses often burst through the skin and thick pus can be expressed by squeezing. Spread to the nasal cavity may cause respiratory distress.
Differential diagnoses include oral foreign bodies such as a bone or stick, broken teeth or jaw, or a grass seed abscess affecting lymph nodes of the throat. At necropsy, affected areas contain numerous pus-filled yellow granules.
Laboratory confirmation requires a smear of pus from deep within the lesion for microbiology. Sections of skin and subcutaneous tissue may also be submitted in buffered formalin for histology.
Treatment
Treatment with sodium iodide or a course of antibiotics (procaine penicillin, oxytetracycline, or erythromycin) is usually curative. In advanced cases there may be irreversible fibrosis of affected tissues and cattle may not regain normal tongue function.
Prevention
The unpredictable and infrequent occurrence on farm or feedlot does not warrant special control measures. Awareness of the condition and systems for early detection are therefore important.
Alopecia
Description
Alopecia is the partial or complete loss of hair from skin. Its main impact in the live export process is not on health but on the aesthetic appearance of the cattle, and on hide value and acceptability at destination.
Clinical Signs and Diagnosis
Differentiating alopecic lesions as to whether they are discrete or diffuse, limited or extensive, and whether they are accompanied by changes in colour and conformation of the underlying skin will give clues as to the cause.
The main causes of alopecia in the export process include:
ringworm
urine and faecal scalding
dermatophilosis
stephanofilariasis
pseudolumpy skin disease
lice
Specimens for laboratory diagnosis include skin biopsy from the margin of active lesions for histology, hair and deep skin scrapings from the periphery of active lesions submitted dry for microbiology (including fungal culture), and insects for entomology.
Treatment
Choice of treatment will be determined by the diagnosis. With many skin diseases, letting them run their course is often the most practical and cost-effective treatment option. The use of injectable antibiotics, topical sprays or ointments is reserved for special circumstances.
Prevention
As with many diseases, providing a stress-free, uncrowded, dry, sunlit environment may reduce spread and expression of some skin diseases. A good inspection system applied at selection may prevent contagious animals entering the export process.
Annual Ryegrass Toxicity
Description
Annual ryegrass toxicity (ARGT) is a poisoning of livestock caused by ingestion of annual ryegrass (Lolium rigidum) that has been infected by a specific toxic bacterium. The bacteria are carried into the plant by a parasitic nematode and bacterial proliferation then creates the toxin. As plants mature and dry off (around hay making time), toxin levels may rise and peak.
ARGT occurs in the extensive sheep-wheat belts of Western Australia and South Australia, where many export sheep are sourced. The feeding of contaminated hay may cause disease during the export process.
Clinical Signs and Diagnosis
Signs include high stepping gait (hypermetria), staggering, collapse, trembling, terminal convulsions and death within one to two days. Affected animals may be found dead without observation of previous signs.
Signs appear from 4 days to several weeks after exposure and can persist intermittently for weeks after removal from the source. Mortality rates of 50 % in animals with clinical signs are typical.
At necropsy there is variable congestion, oedema and haemorrhage of many organs, and usually more obvious in the lungs, kidneys, liver and brain.
In suspect pastures, a yellow slime may be observed on infected ryegrass heads.
Laboratory confirmation requires formalin-fixed liver and suspect grass or grass seed showing bacterial galls.
Differential diagnoses include enterotoxaemia and polioencephalomalacia. Other stagger syndromes such as phalaris, perennial ryegrass and paspalum staggers can look similar but don’t have high numbers of acute deaths.
Treatment
No drug treatment is effective. Mildly affected sheep should be left undisturbed with access to water, feed and shade. Sheep in lateral recumbency should be euthanised.
Prevention
Deaths can be reduced by early recognition and removal from the source of the toxin.
Hay and seed heads can be tested using an ELISA to assess risks of using hay for feeding (contact your state animal health laboratory).
Arthritis
Description
Arthritis is an inflammatory condition of one or more joints and is often associated with bacterial or viral infection, although trauma may also be involved.
A wide range of bacteria may infect joints. Most are normal residents of skin, faeces or soil. Erysipelothrix and Chlamydophila are most commonly involved in Australian sheep. Erysipelothrix, a common dip inhabitant, enters the body via shearing cuts, marking and mulesing wounds, and grass seed penetrations. Chlamydophila are believed to be acquired by inhalation, ingestion or via the conjunctiva.
The arthritis of goats, known as Big Knee, is caused by Caprine Arthritis and Encephalitis (CAE) virus, and is common in dairy goats but very rare in meat goats of the type selected for export.
The infecting organisms may be disseminated through the blood stream and pass into many or all joint cavities. In some joints the infection may spontaneously resolve without permanent damage, while in other joints infection may persist and result in lameness and other changes.
Clinical Signs and Diagnosis
Signs include joint pain on movement and restricted movement. Pain and swelling around one or more joints in the early stages may subside in a few days, but usually persists in the knee and hock.
In early stages the joint fluid is increased, and less viscid than normal. It then becomes cloudy and clots form in recesses of the joint cavity. The lining of the joint is velvety and reddened. Persistent inflammation will lead to erosion of the normally smooth joint surface, especially about the margins. Thickening of the joint capsule enlarges the joint. Irregular small masses of bone and cartilage are attached at the joint margin. With chronic lameness there will be atrophy of the muscle of the affected limb.
Specimens required for laboratory determination of pathogens include aseptically collected joint fluid, chilled and unopened joints with the joint capsule intact, and acute and convalescent sera from affected sheep submitted chilled for chlamydial serology. It is often difficult to demonstrate the presence of organisms in chronic lesions.
Treatment
Chronic cases are likely to have irreversible joint changes and treatment is unlikely to be of benefit. Oxytetracycline antibiotics are recommended when treating earlier cases, although procaine penicillin or erythromycin may be more effective in some circumstances.
Prevention
Routine prevention is based on minimising risks of wounds and traumatic injury, and ensuring optimal general hygiene. A vaccine is available to prevent erysipelas arthritis in lambs.
Asphyxiation
Description
Asphyxiation is the condition or act of being deprived of oxygen. Strangulation implies compression of a tube such as the trachea (causing asphyxiation) or carotid arteries (causing interruption of blood supply to the brain). Smothering refers to crushing injuries (including strangulation and/or asphyxiation) when animals are trampled underfoot by pen mates. Misadventures causing compression of the chest, windpipe or carotid arteries occur occasionally in the export process, mainly on trucks during transport or in pens at sea.
Risk factors include overcrowding, poor yard or pen design, and use of excessive or inappropriate force in moving or restraining animals. These factors can create opportunities for animals to pile on each other, or be stuck under pen rails, and may make it difficult for fallen or downer animals to stand.
Situations where animals may pile on top of each other at sea include during very rough weather, when frightened, and during feeding when hungry animals may crowd at troughs, particularly if there is limited trough space.
Windpipe and carotid artery compression may occur when necks are stuck in horizontal gaps between pen rails or vertical gaps above gate chains. Ropes, wire, chain or baling twine sometimes used to suspend broken troughs are choking hazards.
Inadvertent injury to the windpipe and carotid arteries may result from the use of lassoes to catch and restrain animals and when cattle go down in a head bail, particularly one with a head locking device. Wild or frightened animals are particularly at risk because they may struggle when restrained and throw themselves down.
Clinical Signs and Diagnosis
Individual or multiple animals may be found down, dead, or standing but injured. Survivors have heaving respiration which eases over time. Animals may suffer neck, back or leg injuries trying to extract themselves from unusual positions. Hair coat or fleece on one side may be entirely covered in manure if stuck in lateral recumbency for a period.
At necropsy, bruising under the skin on the thorax or upper neck, congestion of trachea and lungs, or petechial haemorrhages on conjunctivae, are all changes consistent with trauma from smothering.
Treatment
Urgent reaction may be necessary to save stock from a life-threatening situation. The critical response is to remove the immediate cause of the asphyxia or strangulation. This may involve moving cattle or opening a head bail. In some cases it may require bending or cutting rails or ropes. Allow affected animals to recover to normal breathing before relocating to a less crowded pen for rest and confinement. Administer oral fluids and electrolytes if dehydration is present and the animal is unable to drink by itself. Inject non-steroidal anti-inflammatory drugs (tolfenamic acid, ketoprofen, flunixin meglumine, meloxicam) if soreness affects eating or walking.
Severely injured animals should be euthanised, particularly animals with limb fractures and irreducible dislocations.
Prevention
Be aware of codes of practice governing space allocation for animals during transport. Ensure crew members have training in stockmanship to either avoid or respond quickly to situations where animals may be suddenly alarmed or subjected to undue handling pressure during movements. Emergency rescue equipment should be easily accessible (knife, bolt cutter and pipe cutter).
Avoid disruptions to feeding that cause the animals to become hungry. Ad lib feeding is recommended to prevent hunger. Ensure there is sufficient feed for the voyage so that severe rationing is not required at the end of the voyage. Maximise trough space per head where possible.
Recumbent animals at the front of pens near feed troughs should be encouraged to stand before feeding.
Always monitor animals closely during feeding, especially if they are at risk of smothering, and have vigilant people on hand to deal with pile-ups if they occur.
If there is a risk of smothering, feed out to one pen at a time and have a team of people ready to prevent and disentangle pile-ups. Keep pens dry to prevent slipping and bogging. Livestock on trucks or at sea should be inspected regularly throughout the day and night for early detection of misadventures. Always allow sufficient room on trucks or in pens for animals to stand up easily if they fall or lie down.
Use non-tightening catching ropes or halters whenever possible to restrain cattle in pens. Head bails should have vertical bars and a quick release mechanism to avoid choking if an animal goes down. Crushes with head locking devices should have movable V-shaped side panels that squeeze, preventing animals lying down.
Check pens for hazards. Design low risk pens with special attention to removable and adjustable rails, hinges and latches on gates, and positioning and securing of troughs.
Big Head
Description
Big head is an inflammatory swelling of the head of sheep, usually young rams, caused by Clostridium novyi type A. Continual butting between young rams bruises the subcutaneous tissues of the poll and sets up suitable anaerobic conditions for entry and multiplication of pathogenic clostridia.
Clinical Signs and Diagnosis
The head, face and neck become swollen with oedema. Differential diagnoses include photosensitisation, bluetongue and possibly actinobacillosis.
Specimens for laboratory confirmation are smears or swabs of exudate for bacteriology collected from live or freshly dead animals. In dead animals, also aseptically collect sections of affected tissue to submit chilled for bacteriology and in buffered formalin for histology.
Treatment
Procaine penicillin.
Prevention
Vaccination.
Blackleg And Malignant Oedema
Description
Blackleg is an acute infection of heavy muscles caused by Clostridium chauvoei; malignant oedema is an acute infection of wounds usually caused by Clostridium septicum, although other clostridia may be involved.
Clostridia are present in the soil and gut of farm animals and are a constant threat to unvaccinated animals in the livestock export process. Once ingested, spores may be absorbed and then spread in the blood to various tissues in the body.
Blackleg can be caused by ingested spores that have lodged in muscle tissue, and possibly remained dormant there for a long time. Injury to muscle following vaccination, transport or rough handling may trigger germination resulting in extremely rapid bacterial multiplication and the production of toxins and gas. Multiple animals are usually affected. Most cases are found dead.
There is a risk of blackleg occurring in unvaccinated livestock in the livestock export process as a result of the intensive animal handling involved.
Malignant oedema occurs when skin wounds are infected by Clostridial sp. leading to bacterial proliferation and production of toxins. Specific risk factors may include shearing cuts, head butting or fighting behaviour in penned animals (particularly intact males), and possibly intramuscular injections.
Clinical Signs and Diagnosis
Affected animals are usually found dead or dying. Infected animals found alive will be severely depressed and have obvious swelling or lameness. The typical lesions are readily seen but may be obscured by rapid post-mortem decomposition.
In blackleg, there may be an area over the shoulder, back or rump that is swollen, and has darkened skin, and gas bubbles may be detected by gentle finger pressure. At necropsy, the affected muscle is black and dry, and gas bubbles will have spread between the muscles. The lesion may be in any muscle including tongue or heart and may be quite small.
In malignant oedema, tissues around the inciting wound will be soft, swollen, and pit on finger pressure. At necropsy, tissues surrounding the wound will be wet and large quantities of dark brown exudate will have spread out under the skin. Differential diagnoses include bloat and anthrax.
Specimens for laboratory confirmation must be taken from freshly dead animals. These include smears of affected muscle or wound exudate for bacteriology; sections of affected muscle, collected aseptically, and submitted chilled for bacteriology; and sections of affected muscle or tissue adjacent to an affected wound, in buffered formalin for histology.
Treatment
Treatment with antibiotics (procaine penicillin, or oxytetracycline) may be attempted but infection is likely to be overwhelming. To stop an outbreak, all susceptible animals in the mob should be vaccinated and treated with antibiotics (procaine penicillin, erythromycin, or oxytetracycline).
Prevention
Vaccination provides effective protection against clostridial diseases. Handle animals gently to avoid bruising and overexertion.
Bloat
Description
Over-distension of the rumen with gases of fermentation is termed bloat. If foam is present it is called frothy bloat, otherwise it is called free-gas bloat. Bloat causes compression of the thorax which in turn causes respiratory distress and death from asphyxiation or heart failure if severe.
Frothy bloat occurs after rapid engorgement of high protein, highly digestible feed that results in formation of excess amounts of stable foam in the rumen. Free gas bloat occurs when any physical (obstruction) or functional problem prevents normal eructation of rumen gas (burping).
When cattle gorge on feed, either because they are hungry or they are competing for feed, the rumen receives an oversupply of fermentable carbohydrates in a short space of time. Rapid consumption of pellets without roughage of an adequate fibre length means minimal production of salivary buffers when chewing feed and increased viscosity of the rumen contents. The influx of fermentable carbohydrates leads to the proliferation of certain bacterial species that produce slimy bacterial mucopolysaccharides (especially Streptococcus bovis). Bacterial slime can prevent bubbles of gas created during the fermentation process from coalescing resulting in frothy rumen contents. Gas bubbles held within frothy ingesta are unable to rise to the gas layer in the dorsal rumen. Frothy gas cannot be freely expelled by eructation and the presence of frothy ingesta means that the normal eructation sequence is not initiated by the presence of free gas in the dorsal sac of the rumen. In some cases, highly viscous rumen ingesta may block the cardia and completely prevent the animal’s ability to eructate.
Some observers have attributed frothy bloat at sea to ingestion of large quantities of rapidly fermented fine feed particles from pellets that have disintegrated during storage and handling. Lucerne hay may also cause frothy bloat. Free gas bloat at sea has been attributed to cattle eating plastic or string found in pens. On a ship, cattle may chew and swallow any foreign object that they can reach.
Clinical Signs and Diagnosis
Frothy bloat usually affects groups of animals within an hour of feeding. Free gas bloat occurs sporadically in individuals. Distension of the left flank is detected during pen inspection. The right flank will also be distended in severe cases, and there may also be respiratory distress (mouth breathing, tongue protrusion, outstretched neck).
Cattle with tetanus, rabies, oesophageal obstruction and ruminal acidosis may also develop bloat. With tetanus the animal is also stiff, with rabies there is aberrant behaviour, with oesophageal obstruction there is profuse salivation and bilateral nasal discharge, and with acidosis there is also dehydration and liquid, rich-smelling, brown faeces.
Cattle often develop bloat when lying down. This is because it is difficult for cattle to burp unless positioned almost exactly upright. When they become too uncomfortable they will reposition themselves or stand, belch and be okay. If they are unable to reposition themselves, for example if they get stuck under a pen rail, sat on by another animal, or if weakened by hypocalcaemia, they are in danger of bloating and asphyxiating.
Bloat is confirmed by the history and gross pathology. Cattle affected by bloat may die suddenly and are unexpectedly found dead during pen inspection. At necropsy there is intense congestion of the head and neck (especially the tongue, eyes and tonsils), relative pallor of the chest and abdomen, and moderate congestion of the hindquarters. The abdomen is hugely distended by the rumen which may still contain some froth in cases of frothy bloat. The sudden death and rapid decomposition can make differentiation from clostridial diseases difficult.
Note: well-conditioned animals dying of other causes can bloat quickly after death and develop signs resembling true bloat such as congestion of the head and neck, and an oesophageal bloat line (if post-mortem bloating occurs before blood coagulates).
Treatment
Cases of frothy bloat, if mild, can be treated by adding chaff or hay to the feed, or painting vegetable oil on the flank which is licked off by the patient. If severe, vegetable oils, mineral oils (paraffins) or antifoaming agents may be administered by oral drenching or via large bore needle directly into the rumen. The resulting free gas layer is then more readily eructated. Life threatening distension is treated by venting the rumen through a 10 cm stab incision with a knife targeting the middle of the left paralumbar fossa. Use a sharp pointy knife with a non-slip handle. Prepare the site so it is aseptic and use local anaesthesia and possibly sedation. Extend the stab incision to a minimum 5 cm and maximum 10 cm length, maintaining and rotating the knife in the hole during decompression to help the foam escape to outside the abdominal cavity. A trochar and cannula will usually have too small a bore to allow escape of the stable foam. The stab wound should not be sutured. Clean the wound area, administer antibiotics (procaine penicillin, oxytetracycline) for three days, keep flies away and hope for the best. If the stab incision and venting have been done properly, the wound will heal over in two to three weeks. If not, there will be peritonitis, a chronic festering wound and some animals will die.
In cases of free gas bloat, antibiotics (procaine penicillin, oxytetracycline) should be administered in case infection in or around the oesophageal groove is the cause. A stomach tube passed down the oesophagus into the rumen may dislodge an obstruction in which case it will be diagnostic and curative. It should at least provide temporarily relief. Severely distended cattle have been known to drop dead with this procedure due to further circulatory embarrassment as the tube passes the aortic arch. In severely affected animals, partial release of pressure via flank cannulation before passing a stomach tube may avoid risk of collapse while passing the tube.
If bloat keeps recurring, consider inserting a commercially available plastic, self-retaining cannula into the rumen. The accompanying trochar is not usually robust enough to penetrate the skin so it is best to make an incision with a scalpel at the intended place of cannula insertion. Make a vertical incision through skin and underlying fascia of a length equal to twice the diameter of the cannula body. With the trochar in place in the lumen of the cannula, sharply thrust through the abdominal and rumen walls. With the trochar still firmly in place, screw the cannula in so the spiral flange holds the rumen firmly against the abdominal wall. The trochar is then removed and the gas allowed to escape. Gas escape is best controlled in order to avoid a sudden fall in blood pressure accompanying the sudden fall in intra-abdominal pressure. The cannula can remain in place for as long as necessary. This may be as long as three to four weeks.
Prevention
Cattle areas must be kept free of rubbish, in particular plastic, string, rope and wire. This will help prevent free gas bloat and other cases of indigestion.
Prevention of frothy bloat is achieved by slowing the eating of high protein, highly digestible feeds and increasing salivary secretion, or by incorporating substances (alcohol ethoxylate teric) into feed to prevent rapid fermentation and foaming.
Options include provision of hard durable pellets, supplemental roughage and incorporation of ionophores such as monensin or lasalocid into pellets.
It is important to ensure the continuity of feed availability and feed composition by careful planning and close management of feeding regimens and fodder reserves. Avoid erratic feeding or creating undue competition at feed times. Roughage of adequate fibre length stimulates chewing and salivary production. A consistent supply of roughage will help to stabilise rumen fermentation, prevent ruminal acidosis, reduce the viscosity of the rumen contents and optimise rumen motility.
During routine inspection, animals that are lying in lateral recumbency or that have left flank distension should be forced to stand. Crew members should be trained to take such action and immediately report to the veterinarian or senior stockperson if any animal appears unable to stand.
Bluetongue
Description
This is a non-contagious viral disease spread by biting midges (Culicoides sp.), and that can infect sheep, goats, deer and cattle. Sheep are the most seriously affected species.
There are 25 serotypes of Bluetongue virus (BTV) worldwide. Some (but not all) strains are found in northern Australia (Northern Territory and northern parts of Queensland and Western Australia). Under conditions favouring southern spread of the vector, the virus may be found further south.
Infection of cattle with strains of BTV present in Australia has not been reported to cause any clinical symptoms. Clinical disease from BTV infection has also never been reported in sheep, goats or deer.
Clinical disease in livestock (particularly sheep) has been reported in other countries as a result of infection with virulent strains of BTV. Pathogenic strains damage blood vessels throughout the body causing them to leak or become blocked. This leads to oedema and haemorrhage, which if mild can result in full recovery and immunity, and if severe can cause rapid death and long term debilitation in survivors.
Pathogenic strains of the virus are not present in the sheep producing areas of Australia and exposure to infected midges is unlikely to occur at sea. The virus and the midge vectors are present in many countries to which Australia exports sheep. Clinical disease due to Bluetongue infection is therefore more likely to be seen in destination feedlots during periods of high insect activity, which is usually after rain in equatorial regions. Earliest cases occur about one week after being bitten.
Clinical Signs and Diagnosis
Bluetongue should be suspected if multiple animals are affected. Symptoms may be mild to severe, and if severe there are usually some deaths. Clinical signs include depression, fever, inappetence, swelling of the head, and lameness.
The head, including the eyelids and ears, will be swollen with oedema. The inside of the mouth and tongue may be congested, and erosions, ulceration and haemorrhages may be present on the gums. There may be nasal discharge and crusting around the nostrils. Lameness will be in all feet similar to laminitis, and the coronary band may be a purple red.
At necropsy there will be oedema and haemorrhage in organs and tissues, especially under the skin and in muscle. There may be haemorrhage at the base of the pulmonary artery and focal necrosis of the papillary muscle of the left ventricle, which if present should raise strong suspicions. There will be excess fluid in the pericardium, thorax and abdomen.
Differential diagnoses include photosensitisation, big head and possibly bottle jaw. However, these are likely to occur at the beginning of the export process rather than at the destination.
Laboratory confirmation requires whole blood (10-20ml) collected as early as possible from febrile animals into an anticoagulant and submitted chilled for virus isolation. Specimens from dead animals should include sections of spleen, lymph nodes, and red bone marrow collected as soon as possible after death and submitted chilled. Sections of heart, lung, liver, kidney, spleen, lymph nodes and red bone marrow should be submitted in buffered formalin for histology. In long standing cases or survivors, submit chilled serum for serology.
Treatment
There is no specific treatment other than nursing and provision of antibiotics (procaine penicillin, oxytetracycline, or trimethoprim sulpha) for prevention or treatment of secondary infections such as pneumonia. Animals that are unable to stand, eat or drink should be euthanised.
Prevention
Principles of control include controlling midges with insecticides, moving animals into sheltered areas during the evening to reduce the number of bites, and vaccination to increase resistance of animals.
Bottle Jaw
Description
This is the abnormal accumulation of clear oedema fluid under the skin of the lower jaw. It can be caused by an increase in local hydrostatic pressure such as from abscessed submandibular lymph nodes blocking lymph drainage or grass seeds blocking salivary ducts. Most commonly it is caused by reduced oncotic pressure as a result of systemic anaemia and hypoproteinaemia.
It is a feature of a number of diseases including chronic liver fluke, gastrointestinal parasitism, malnutrition, congestive heart failure, Johne’s disease, woody tongue and abscesses of the lymph nodes of the head and neck.
Severe bottle jaw is seen in chronic liver fluke infections and haemonchosis (Barbers Pole worm) because these parasites feed on blood. Usually in Australia, chronic liver fluke is seen in the winter and spring, while haemonchosis is seen in summer and autumn. More mild cases of bottle jaw are seen with other internal parasites and Johne’s disease where protein is lost from the body through the chronically inflamed bowel wall. It may also be seen with low protein diets. Bottle jaw is most likely to be observed in animals entering assembly points.
Clinical Signs and Diagnosis
Bottle jaw presents as cool, pendulous, pitting swelling under the jaw. With internal parasites and Johne’s disease there are usually multiple animals affected and there will be illthrift and diarrhoea. The oedema is generalised in the body but is most obvious under the lower jaw in grazing animals because gravity causes the fluid to pool in the loose tissue while animals have their heads down eating.
If haemonchosis or liver fluke are present there will also be profound anaemia evident as pale to white mucous membranes of the mouth and eye, exercise intolerance, and dark, dry faeces. At necropsy, liver flukes are found in the liver, and haemonchus worms are found in the abomasum.
Blockage of salivary ducts or lymph drainage from abscessed lymph nodes is likely to be sporadic and diagnosed by palpation and close examination for asymmetry.
Low protein in the diet is diagnosed by nutritional evaluation of the feed and exclusion of other causes.
Treatment
Internal parasite burdens including liver fluke will need to be removed by effective anthelmintics such as macrocyclic lactones, and flukicides such as triclabendazole. Johne’s disease is untreatable. Lymph node abscesses are best left untreated. Salivary gland blockages may be treated by massaging and removing any grass seeds found in the opening of a salivary duct under the tongue or in the cheek.
Prevention
Once the underlying cause is determined, known risk factors should be removed to prevent recurrence.
Bulling
Description
This is a problem of excessive riding behaviour. In cattle it can involve animals regardless of age, sex, pregnancy status or stage of the oestrous cycle.
It is a more common and serious problem in groups of bulls or steers. In sheep and goats it is more common in groups of entire or castrated males. The term for animals being ridden is bullers, the term for animals performing the mounting is riders. Riders persistently follow and mount bullers. Causes are unclear but may include sexual stimulation, establishing social hierarchy and relieving boredom.
Bullying can be a serious problem in shipments of male animals, particularly feral bucks.
Bullying may begin immediately after animals are penned and is a greater problem in pens with higher stocking densities. A buller may be relentlessly mounted by the rider(s). The problem worsens in groups of animals implanted with hormones or when pen densities increase. Bullers tend to be animals that are smaller, sick, look different (such as having a different coat colour), adopt the injured stance of a buller or are newly added to a pen. Usually one or a few animals in a pen are being mounted frequently by most of the others.
Pregnant heifers may display mounting behaviour at levels less likely to cause problems, though it may cause disputes with importers who think the animals are in oestrus and therefore not pregnant.
Clinical Signs and Diagnosis
Observation of behaviour will detect this condition. Bullers are readily identified as the animals being pursued and mounted by pen mates.
The bullers may suffer bruising, wounds, weight loss and are predisposed to pneumonia and other infections. They may have hair loss and swelling on the rump and tail head from bruising, and blood around the rectum. Their sides may be coated in manure from recumbency after falling or escaping. Animals may suffer partial paralysis associated with sciatic nerve damage, fractures and dislocations. In some cases animals may be so exhausted that they become recumbent. The riders may suffer heat stress or injuries from mismounting.
Riders that become injured or heat stressed may become bullers if pen mates sense an opportunity to change the social hierarchy. Affected animals may either die or require euthanasia.
Treatment
Remove bullers to a hospital pen and examine and treat for concurrent diseases or conditions. Haematomas and oedema should be left alone to heal.
Pulled animals can be reintroduced to the pen after they recover or after three days (whichever is longer), as pen mates often no longer find them attractive.
However, they should be monitored in case of relapse.
Removing bullers does not always fix the problem because sometimes others replace this role. Be aware that if a number of bullers are placed in a hospital pen, they may begin riding each other.
Prevention
Match animals in pens on size and looks, and maintain animals in their original social groups if possible.
Avoid high stocking densities. Regularly check for and remove bullers. Don’t place females near pens of entire males.
Installing overhead barriers to prevent mounting may be considered.
Caseous Lymphadenitis
Description
This is a bacterial disease (Corynebacterium pseudotuberculosis) featuring abscessation of lymph nodes and sometimes other organs. Bacteria enter the body through cuts and abrasions and spread via the lymph and blood to establish chronic infections in lymph nodes.
Infection spreads by direct contact between animals and by susceptible animals coming into contact with bacteria in contaminated yards or pastures.
The number and size of abscesses in affected animals will increase over time, and clinical disease is often more noticeable in older animals. The disease may be fatal.
In the export process, the abscesses are a common incidental finding at necropsy in animals dying of other causes. It is a significant potential cause of partial and whole carcase condemnation in overseas abattoirs.
Clinical Signs and Diagnosis
External abscesses may be detected as firm to fluctuant, non-painful rounded lumps, usually under the jaw or in front of the shoulder and thigh. Sometimes they will have ruptured and be discharging pus. Emaciation occurs when internal abscesses are numerous or large.
At necropsy, abscesses may be found anywhere in the body including brain, bone and mammary gland, and may be the explanation for unusual clinical signs. The most common sites are in the submandibular, prefemoral and prescapular lymph nodes (visible as subcutaneous abscesses), and internally in the lung, and bronchial and mediastinal lymph nodes. In sheep, the pus is pale green and becomes paler as it hardens with age. In goats, pus remains soft and pasty.
Laboratory confirmation requires a swab of pus submitted chilled for bacteriology.
Differential diagnoses include melioidosis, internal parasites, poor dentition, undernutrition, liver abscessation and Johne’s disease. An additional differential diagnosis in goats is infection with caprine arthritis-encephalitis virus.
Treatment
It is untreatable. Antibiotics are unable to penetrate the abscesses. Superficial abscesses tend to recur after surgical drainage or excision.
Prevention
A vaccine is available for sheep and goats but will not prevent all new infections nor cure existing infections. Effective control requires a range of biosecurity measures in addition to vaccination. Sheep for export should be sourced from flocks that have implemented effective control programs.
Coccidiosis
Description
Coccidia are protozoan parasites that invade the lower small intestine, caecum and colon, causing damage to the mucosa and submucosa of the intestine. Spore-like oocysts, highly resistant to environmental conditions and disinfectants, are shed in faeces. The disease is often subclinical but may cause enteritis, dysentery and straining in severely affected animals. There are many species of coccidia. Coccidia are host-specific, meaning that different species infect sheep, goats and cattle.
The life cycle of coccidia involves a multiplication phase in the intestinal lining. Cysts are passed in the faeces and contaminate pasture. Massive intake of cysts can occur where animals congregate at feeding and watering points.
Coccidia are probably present in many animals after weaning and often cause little or no disease. Disease is usually confined to young animals on heavily stocked wet pastures and may be exacerbated by stress or concurrent disease. Occasionally it is seen in older animals when subjected to stress and heavy challenge as may occur when animals are gathered in high density assembly yards in preparation for export.
Sporadic cases may be seen on ships if a coccidiostat has not been incorporated into pellets.
Clinical Signs and Diagnosis
When disease does occur, animals may show signs of tenesmus (straining to urinate or defecate), and acute scouring may occur for a few days. Diarrhoea is yellow-brown to black and may be stained with fresh blood. There may be loss of appetite, severe dehydration and weight loss.
Complete recovery from an acute disease episode may take several weeks during which affected animals may display varying levels of reduced appetite and poor weight gain.
Severe disease and death may occur under heavy exposures and when animals are compromised by other conditions such as heavy worm burdens.
Differential diagnoses include other causes of diarrhoea such as salmonellosis, gastrointestinal parasitism and bovine viral diarrhoea virus (cattle).
Laboratory confirmation requires a sample of faeces from affected animals for counting of oocysts. At necropsy, collect sections of small and large intestine in buffered formalin for histology.
Treatment
Sulphadimidine is effective either by injection or drench. Sulphadimidine may be added to the drinking water but it may be difficult to ensure animals drink enough to receive effective levels of treatment.
In older animals or where the clinical disease is less severe, animals may be left to recover spontaneously.
Prevention
In feedlots where coccidiosis has occurred repeatedly, feeds containing carefully measured concentrations of sulphadimidine or ionophores (monensin, lasalocid) may be used. Provide feed and water off the ground and minimise opportunities for animals to access surface water and spilt feed. There is no risk ofspread of infection from one species to another and therefore there is no value in separating sheep from goats as part of control or prevention measures. Rotation of pens, either between sheep and goats or to allow spell periods between successive uses, may help reduce build-up of oocysts.
Constipation
Description
The difficult or incomplete passage of dry hardened faeces.
Faeces becomes harder, drier and more difficult to pass the longer it stays in the colon. This may occur in animals suffering reduced water intake, temporary food deprivation, environmental or social stress making them reluctant to defecate, disrupted dietary and management routines, or painful pelvic disease.
In the export process, the condition is sometimes seen in the first week at sea. It is never life threatening. A typical circumstance where cattle may become constipated is after being fed a diet high in indigestible fibre in assembly points, and then being handled and transported for an extended period when dehydration and stress occur. The cattle do show signs of discomfort and straining.
Clinical Signs and Diagnosis
Usually multiple animals in a group are affected. Defecation may require severe straining for an extended period and eventually result in the passage of short columns of hard, dry faeces. This usually occurs in the first week at sea.
Treatment
Resumption of free access to good quality drinking water, rest and good quality hay, chaff or pellets will usually resolve constipation after a few days to a week. No further medical interventions are required.
Prevention
Regular, frequent access to good quality water, feed and rest is preventative.
Copper Deficiency
Description
Copper deficiency is common in Australian livestock. There are two main causes: low copper levels in soil and plants, and secondary copper deficiency caused by ingestion of excessive levels of molybdenum and sulphur in pasture or feed supplements.
Clinical Signs and Diagnosis
Cattle show loss of pigment in hair especially around the eyes, sudden heart failure, reduced growth, ataxia and falling, diarrhoea and anaemia.
Sheep and goats show ataxia especially in young animals, loss of pigment in dark coloured fleece or coats, steely wool (loss of crimp, hard feel to fleece), diarrhoea, anaemia and abnormal bone formation.
Specimens for laboratory confirmation are mainly liver samples (biopsy or necropsy), submitted chilled and unpreserved for copper estimation. Blood levels of copper are unreliable. Measurement of copper levels in pasture or feed may be indicative.
Treatment
Copper supplementation can be administered by oral drench, injection, in licks, feed and water, and by administration of fertilizer on to pasture. Good quality feed (lucerne hay) will contain copper. Be careful when supplementing animals with copper to avoid inadvertent overdosing which may result in copper poisoning.
Prevention
Copper deficiency is unlikely to develop while animals are within the export supply chain. However, it may be a factor when considering sourcing animals from areas that have a low availability of copper in the soil (sandy coastal areas of Western Australia, New South Wales and Queensland and some chalky soil areas of South Australia) or high levels of molybdenum and sulphur in pastures (western districts of Victoria and the South Gippsland).
Avoid over-supplementation of livestock with minerals that may lead to reduced copper absorption such as molybdenum, sulphur, iron, zinc and calcium.
Cyanide Poisoning
Description
Hay made from wilted forage sorghum and fed to hungry cattle in assembly points may cause cyanide poisoning. All sorghums have cyanide producing potential, especially after a check in growth. Once produced, the toxin will persist even after plant material has been harvested and baled into hay. After ingestion, cyanide is rapidly absorbed into and distributed around the body where it halts the use of oxygen at the cellular level. This causes oxygen retention in the blood where saturation levels give it an unmistakable cherry red appearance.
Cattle are more susceptible to poisoning than sheep.
Clinical Signs and Diagnosis
Signs usually appear within an hour of toxic feed being consumed. The prominent signs are respiratory distress, muscle twitching, staggering, cherry red mucous membranes and rapid death. At necropsy the blood is cherry red, later becoming dark red. The rumen content may smell like bitter almonds. The main differential diagnosis is nitrate-nitrite poisoning, which also causes respiratory distress and rapid death but the mucous membranes and blood are chocolate brown instead of cherry red.
Laboratory confirmation is by chemical demonstration of cyanide in the fodder or rumen contents. Specimens must be submitted frozen to prevent hydrolytic decline in concentrations during transit.
Treatment
Immediately prevent access to the suspect hay and offer an alternative low risk feed to dilute toxic feed already ingested. Handling must be minimal to reduce oxygen demand. Urgent treatment with intravenous sodium thiosulphate at 660 mg/kg may be life saving in severely affected animals. Follow-up oral dosing with 60 g in 600 mL of water at hourly intervals until full recovery is recommended to prevent relapse. Note that sodium thiosulphate is not registered in Australia for use in food-producing animals.
Prevention
Sorghum hay can be tested for dangerous cyanide concentrations. Potentially toxic sorghum hay can be diluted with other types of feed.
Decubital Ulcers
Description
Decubital ulcers are defects in the skin resulting from continuous pressure on a particular area leading to tissue ischaemia and necrosis.
In the livestock export process, it occurs in downers and animals that struggle when they get their head or legs stuck.
Ulceration may be accelerated by abrasive flooring, dirty skin, friction, skin maceration, urine scalding and loss of subcutaneous padding from undernutrition.
At sea, even minor skin sores and abrasions can quickly become infected and ulcerate.
Clinical Signs and Diagnosis
Lesions are usually located over bony prominences.
The skin over fetlock, carpus, hock, elbow and stifle joints is most commonly affected. The skin is initially red to purple then oozes, becomes necrotic and ulcerates. The ulcers tend to deepen quickly, become infected and may be slow to heal even under optimal conditions.
The prognosis for animals with deep decubital ulcers at sea is very poor, especially if joints are involved. Even if time and resources are available for a high standard of treatment, there may be insufficient time for recovery before arrival at the destination.
Treatment
Early treatment while the ulcer is superficial, is essential for survival. Relocate the affected animal to a hospital pen and provide a deep layer of dry absorbent sawdust. Sawdust provides padding, reduces friction and absorbs moisture and may help to prevent exacerbation of existing ulcers and development of new ones.
Treat ulcers similarly to any open wound – apply lavage, debridement and if on limbs, bandaging. The objectives are to keep pressure off the ulcer and allow healthy granulation tissue to rapidly fill in the ulcer.
Apply lavage using clean mildly salty water squirted under moderate pressure with a 35 mL syringe and 19g needle.
Apply debridement by cutting or scraping away necrotic tissue.
Apply topical antibiotic ointments or powders to help control surface infection, parenteral antibiotics (procaine penicillin, erythromycin, oxytetracycline, or tylosin) to control deep infection, and non-steroid anti-inflammatory drugs (flunixin meglumine, ketoprofen, meloxicam, or tolfenamic acid) to control pain and swelling.
Apply bandages that are close fitting, snug, long, firm and thick so they are like a cast. This can be achieved using rolls of gauze, cotton wool and elastic adhesive bandages. The objectives of bandaging are to stop bleeding, immobilise the area, prevent further trauma and contamination, keep the wound warm and prevent it drying out. Without bandaging, wound healing may be severely compromised.
An inexpensive, easily applied waterproof conforming bandage suitable for shipboard conditions can be made using rolls of plastic clingwrap, foam rubber and electrical or duct tape.
Encourage affected animals to stand as much as possible.
Prevention
Direct measures toward preventing downers and cattle getting stuck for prolonged periods – and reducing pressure and friction on skin if they do go down or get stuck.
Develop and implement a system for early detection and treatment of diseases, conditions and misadventures especially at sea.
Ensure pens are designed or modified to be free of hazards.
Provide bedding in the form of a thick layer of dry, absorbent sawdust in cattle and hospital pens.
Dermatophilosis
Description
This is a common infection of the skin caused by the bacteria Dermatophilus congolensis. The infectious agent requires skin damage from other causes in order to penetrate the skin and cause infection. Infection results in crusts at the surface of the skin with a characteristic lumpy appearance.
It is most common on the nose, ears and lower legs. In animals with reduced resistance from undernutrition or other stressors, skin infections may become generalised over the body.
The condition predisposes to flystrike, can make shearing difficult, and causes unsightly fleece damage.
It is usually seen in young animals because older animals have become immune from previous infections.
Favourable conditions for spread and establishment of infection are wet animals in close contact, such as yarding in heavy rain or high humidity, and during dipping for lice and fly control. It can then spread very quickly through a mob.
Clinical Signs and Diagnosis
Scabs in matted hair and wool on chronically wetted areas of the body should raise suspicions.
Alopecia develops if the scabs are pulled or rubbed off. Lesions occur on parts of body that are wet for prolonged periods. In wet weather, commonly affected areas include the dorsal and upper lateral neck and back. Animals grazing in long wet grass may be affected on the nose and pasterns. At sea, it may involve the lower legs and flanks, the areas which are continually wet when standing or lying down in slurry.
Laboratory confirmation is by microscopic identification of organisms from scabs and scrapings submitted chilled, or biopsy specimens submitted in buffered formalin.
Differential diagnoses include ringworm and scald, neither of which has matted hair and scab formation before alopecia appears.
Treatment
Animals will recover spontaneously. Treatment with antibiotics (procaine penicillin, oxytetracycline) is recommended only for severely affected animals, for sheep that must be shorn and where the shears are unable to pass beneath the scabs. It generally takes 6 weeks post antibiotic treatment for scabs to lift sufficiently and may be longer in stressed sheep in wet conditions.
Prevention
The spread and severity of the disease can be minimised by avoiding prolonged yarding of wet animals and minimising stressors such as undernutrition.
Diarrhoea
Description
Diarrhoea is the passage of fluid faeces. The immediate cause is generally an excess of fluid entering the intestinal tract, inability of the intestinal tract to absorb all of the fluid in the lumen, increased contractility of the intestines which reduces time for absorption to occur, or increased fluid secretion from the gut wall into the lumen.
Failure to absorb fluid may be caused by excess food material escaping from the small bowel to the large bowel and attracting water, as occurs with carbohydrate overload (ruminal acidosis). Atrophy or erosion of the large intestinal epithelium may also inhibit normal absorptive capacity.
Diarrhoea also commonly results from inflammation of the bowel that results in leakage or increased secretion of fluid from the bowel wall to the gut lumen. The main causes of inflammation are bacteria, protozoa or gastrointestinal worms.
The most likely causes of diarrhoea in the live export process include:
Indigestion associated with dietary changes.
Ruminal acidosis.
Bacterial enteritis.
Bacterial enteritis in sheep and goats in the export industry is usually due to salmonella and less commonly yersinia or campylobacter.
Bacterial enteritis in cattle may be due to salmonella and less commonly other bacteria such as clostridia, pseudomonas, proteus etc.
Bovine viral diarrhoea virus infection.
Coccidiosis.
Other bacteria and viruses, plant and chemical poisonings, parasites, and copper deficiency are less likely potential causes of diarrhoea.
Clinical Signs and Diagnosis
Diarrhoea may be accompanied by abdominal pain, tenesmus (straining), dehydration, loss of body condition and heavy faecal contamination of hindquarters depending on cause and severity. Speed of onset, the numbers affected, and the feeding conditions should be taken into account when determining the cause. See sections on specific diseases for more information.
Specimens from live animals for laboratory differentiation include chilled faeces for bacteriology, virology and parasitology, and serum for virology. Specimens from dead animals should additionally include sections of abdominal viscera chilled for bacteriology, and in buffered formalin for histology.
Because of the potential for acidosis to occur in export animals, it is advisable to have test strips readily available for measuring the pH of rumen fluid. Acidosis should be suspected if the pH is less than 5.5 (normal levels are >5.9). Rumen pH can change in the hours after death as rumen fermentation continues, so samples not taken close to the time of death must be interpreted with caution.
Treatment
Non-specific therapy for diarrhoea is based on ensuring access to plentiful clean water and providing fluid therapy (oral or intravenous), with electrolytes if necessary. Non-steroidal anti-inflammatory drugs may be useful if animals are febrile and also to counteract potential effects of endotoxin production associated with infectious enteritis. Replacing grain or concentrate diets with roughage (chaff or hay) helps to restore or maintain appetite and restore normal digestive function.
Additional medications may be appropriate depending on cause and clinical signs.
Dietary change to reduce concentrate and increase roughage is important if diet is thought to be contributing to diarrhoea. Alkalising agents may be administered for ruminal acidosis, and anthelmintics if parasitism is suspected.
The use of antibiotics in ruminants with diarrhoea is widespread but may not be very efficacious. Oral antibiotics are not recommended because they may disrupt normal populations of bacteria in the gastrointestinal tract and increase the risk of proliferation of pathogenic bacteria. Systemic administration of broad-spectrum antibiotics may be helpful in animals that are systemically ill and where septicaemia may be suspected.
Prevention
Choice of preventative measures is dictated by the diagnosis and risk factors predisposing to the current disease event.
Options available in the export process include providing adequate dietary fibre, changing diets incrementally, reducing faecal contamination of feed and water, and minimising stress. Ionophores such as monensin and lasalocid can be added to diets to prevent coccidiosis.
Pre-export testing and animal selection may reduce the risk of some diseases that cause diarrhoea such as Johne’s disease and bovine viral diarrhoea virus. Vaccines are available to protect against bovine viral diarrhoea virus and salmonellosis.
Downer
Description
In the livestock export process, ‘downer’ is the term applied to animals that cannot stand without assistance.
The diseases and conditions causing most cases of downers in the live export process include:
musculoskeletal injuries (including fractures or other severe injuries, footrot or sepsis in multiple feet).
toxaemia or septicaemia from overwhelming infection e.g. pneumonia or peritonitis.
weakness, dehydration and exhaustion associated with a range of conditions such as diarrhoea, ruminal acidosis, inappetence, and heat stress.
metabolic problems such as hypocalcaemia, hypomagnesaemia or ketosis.
ephemeral fever.
Clinical Signs and Diagnosis
Downers may be detected in lateral or sternal recumbency during pen inspections. Animals affected with localised and recent conditions such as musculoskeletal injuries may remain bright and alert. Animals affected with chronic or systemic conditions may be depressed.
Treatment
It is very important to examine the animal to try to determine why it is down. If there is a limb fracture, joint dislocation, ligament rupture or paralysing spinal cord injury, the decision to euthanise may be clear cut. If the animal looks bright, occasionally struggles to rise, and continues to eat and drink, recovery is a possibility and it is worthwhile persevering. However, if the animal deteriorates, loses interest in feed, or develops complications such as decubital lesions, consideration should be given to euthanising the animal.
Vigorous intervention is required to get recumbent animals standing before compressive musculoskeletal damage becomes irreversible. Specific treatment downers will be determined by the diagnosis, but in general they should receive antibiotics (procaine penicillin, oxytetracycline, ceftiofur, or tylosin), non steroidal anti-inflammatory drugs (flunixin meglumine, ketoprofen, meloxicam, or tolfenamic acid), calcium borogluconate, and magnesium sulphate solutions, together with supportive or nursing care. Try to provide the animal with a pen of its own by either relocating the affected animal or moving pen mates. Roll the animal from side to side every few hours and manipulate limbs where possible to reduce compression damage to limb muscles and nerves. Bandages may be applied to worn hooves to provide support and reduce the risk of infection.
Try to stand the animal up at least once daily. This can be done by encouraging the animal to stand with one or two people providing assistance at the tail head to lift at the same time as the animal tries to stand. Once the animal stands, one person can accompany the animal to provide lift and stability at the tail head until it appears more stable.
It is best to prepare for maximal effort on the first attempt to stand since animals may only try for one or two attempts. Move other animals out of the immediate pen area and, if appropriate, offer water to the animal, administer medications and allow a short period of rest in a sitting position before attempting to stand them up. Spreading sawdust in front of and around the animal, wrapping an absorbent paper towel around the tail to provide a better grip, removing pen rails in front of the animal (even if it means cutting them away), and ensuring two strong people are available to lift the tail or provide support, are measures that may be the difference between success and failure for the animal. Judicious use of an electric goad may be considered in cattle.
Once standing, weakened cattle may require the application of hobbles to prevent them doing the splits and dislocating a hip joint. Nylon straps around the cannon bones (metatarsi) allowing 0.5m distance between the legs should be used in preference to ropes.
Suspending the animal with ropes, slings or clamps is usually unrewarding unless managed carefully in an optimal environment and with purpose-designed equipment.
The prognosis is better for animals crawling or attempting to rise than animals remaining inactive. Strong consideration should be given to euthanising cattle that are unable to rise and show no improvement within a 24 hour treatment interval.
Prevention
Measures to prevent traumatic injuries and lameness such as low stress animal handling, non slip decks and hazard free pens and laneways will prevent some downers occurring. A system for early detection, accurate diagnosis and early treatment of health problems is also recommended. At sea it is recommended that all animals be stood up at least once or preferably twice a day, typically at the time of pen inspections. This is best done around feeding time when most animals are usually standing.
Electrocution
Description
Electrocution refers to death or injury resulting from electric shock. Common sources of electricity are electric fences, lightning and fallen overhead transmission lines in outside environments, and faulty wiring in inside environments.
With electric fences, usually individual animals are found dead with electrical wire wrapped around the neck or leg. With lightning, sometimes large numbers of animals are found dead under a tree or along a wire fence, during or after a thunderstorm. If overhead power lines are brought down by a storm, fallen tree, or disintegration of insulators, there may be deaths from animals directly contacting fallen lines, or animals may be found dead in water into which the lines have fallen. Faulty wiring and damage or loss of integrity of insulation or shielding may allow exposed wires to contact pipes (including water pipes), rails or other infrastructure. In some cases animals may be able to reach or contact an exposed wire directly.
Factors determining the severity of the shock, and life or death outcome include the strength of current, point of entry into the body, wetness and area of the skin contacted, and area of contact of the hooves with the wet ground (earthing).
Clinical Signs and Diagnosis
Livestock are usually found dead with no obvious signs. Some animals may show singeing of the hair coat and burnt skin. Some animals recover consciousness in a few minutes, others take hours, and affected animals may suffer permanent neurological deficits. The major differential diagnoses are nitrate-nitrite poisoning, blackleg and bloat.
Treatment
Administer non-steroidal anti-inflammatory drugs (flunixin meglumine, ketoprofen, meloxicam, or tolfenamic acid) if the animal appears sore, and provide general nursing care as required.
Prevention
Ensure power lines are maintained and do not fall into disrepair. Check for fallen power lines after storms or strong winds. Electrical fittings on ships should be regularly inspected and maintained with special inspections after rough weather.
Enterotoxaemia
Description
Enterotoxaemia occurs when specific bacteria (Clostridium perfringens) normally present in the gut, proliferate and produce toxins that are absorbed.
Conditions that favour excessive proliferation of clostridial organisms include carbohydrate overload, acidosis, higher flow of proteins and sugars from the rumen into the small intestine and motility disturbances that slow the flow of ingesta.
C. perfringens proliferates and produces toxins in the small intestine when intake of carbohydrate is high and there is overflow from the rumen and abomasum into the intestine. The epsilon toxin produced by type D bacteria causes increased vascular permeability with subsequent oedema. Development of oedema in the brain is associated with neurological signs. The beta toxin produced by type C has more direct effects on the intestinal epithelium, causing severe necrotic enteritis.
Classic enterotoxaemia due to C. perfringens type D is more common in the export process than type C. It may affect sheep, goats and cattle, but is most commonly reported in sheep. In feedlot situations it is seen in young, unvaccinated animals that are rapidly switched to high grain diets. A chronic form of enterotoxaemia occurs occasionally with the development of focal symmetrical encephalomalacia (FSE).
The proliferation of C. perfringens type C produces a different toxin (beta toxin) that causes necrotic enteritis with a high fatality rate in young animals and less commonly clinical disease in adult sheep, goats and cattle.
Clinical Signs and Diagnosis
Peracute and acute cases are more common in susceptible animals. These cases may be found dead or die rapidly after short episodes of excitement and convulsion, sometimes with opisthotonos (head arched back over the body). Affected animals may also vocalise (bleating), circle, head press, become recumbent and paddle or froth at the mouth. Profuse watery diarrhoea may also be seen (more commonly in goats than sheep).
Subacute and chronic cases also occur occasionally in sheep and goats. Chronically affected animals may deteriorate and die or may slowly recover.
Sheep that survive an initial acute insult appear to be likely to develop focal symmetrical encephalomalacia (FSE) due to chronic effects of toxins on the brain. Animals with FSE may show dullness, ataxia, incoordination, weakness and other neurological signs depending on the extent of damage, and progressive weight loss.
Goats may be less likely to show neurological signs in subacute and chronic cases and more likely to show signs of enteritis. Although they may also develop opisthotonos and convulsions shortly before death.
Diagnosis is typically made at necropsy. A full rumen and undigested feed in the lower intestines are evidence of overeating and should raise suspicions. Pulpy kidneys are an inconsistent finding and not specific to enterotoxaemia.
Sheep. If the necropsy interval is short, high levels of glucose are present in the urine and readily measured by dipstick (glucosuria may occur in ruminants that are stressed for any reason due to a low renal threshold for glucose). If necropsy is delayed, glucose is rapidly fermented by bacteria in urine and may not be elevated. The lungs are wet and heavy. The membranes on the surface of the heart (epicardium) and lining the heart chambers (endocardium) may be streaked with haemorrhages, and the pericardium often contains increased clear fluid with floating strands of protein.
Goats. In goats, post-mortem appearances resemble those in sheep but may be restricted to the gut, in particular, the coiled colon. The lumen of the coiled colon is empty, the wall thickened and contracted, and the mucosa is rough and eroded.
Specimens for laboratory confirmation include smears for bacteriology from inflamed and adjacent non-inflamed sites along the intestinal mucosa; intestinal content (40mL) especially yellow creamy material, for toxicology; and the whole brain and sections of liver and kidney in buffered formalin for histology.
Treatment
Treatment is not effective. In the face of multiple cases, surviving pen or paddock mates may be treated with antibiotics, non-steroidal anti-inflammatory drugs and vaccinated against clostridial diseases.
Prevention
Control depends on vaccination and management of feeding regimes to avoid overeating.
Exhaustion
Description
Livestock are susceptible to overexertion in the early phases of the export process. Animals may be at risk if they are big and fat, sick, very thin, very young, or heavily pregnant. Risk is exacerbated if animals are handled and transported over long periods without a break. They may suffer muscle soreness, sore feet, bruising, dehydration, low blood sugar, sleep deprivation and possibly hyper- or hypo-thermia depending on weather conditions and availability of shade and windbreaks.
Clinical Signs and Diagnosis
Exhausted animals may be reluctant to move or stand. Closer examination may detect closed eyes, unsteadiness and muscle tremors. Urine may be dark from myoglobin and dehydration. Differential diagnoses include hypocalcaemia, pregnancy toxaemia and transit tetany.
Treatment
Provide food, water and shelter and undisturbed time for rest. Administration of oral fluids containing electrolytes by stomach tube, and subcutaneous calcium borogluconate may accelerate recovery in very weak animals. Do not allow cattle to remain recumbent for more than an hour otherwise compressive muscle and nerve injury may occur.
Prevention
Provide periods for rest, feed and water during transport and handling especially during climatic extremes. Use low stress animal handling methods.
Eye Cancer
Description
This is a malignant growth on the surface of the eyeball, eyelid or third eyelid. It mainly affects Hereford and Friesian breeds in areas with prolonged exposure to sunlight.
Cattle at greater risk are older (>3 years), have protruding eyes, unpigmented eyeballs or lids, and are resident in higher latitudes (more sunlight hours), or areas with long dry seasons. Cancer eye is rare in the export process because cattle are generally young.
Clinical Signs and Diagnosis
Lesions always start on unpigmented areas of the eyeball or eyelids. Early lesions appear as discrete raised whitish areas on the third eyelid or corneoscleral junctions of the eye, or dark, crusty wart-like lesions on the margins of upper and lower eyelids. If they progress, lesions will grow, ulcerate, bleed, become friable and may smell foul from necrosis or infection. Without intervention, there can be progressive invasion of the eye and face, lymph nodes of the head and neck, and eventual spread to distant organs such as the liver and lungs. Affected animals will ultimately die from this condition if untreated.
Early lesions are easily missed because cattle tend to face observers side-on displaying the best functioning eye. Eye lesions in Herefords and Friesians should always be subject to close examination. Differential diagnoses include warts, foreign bodies and pinkeye.
Treatment
Options for treatment include surgical removal of lesions or the entire eye, possibly associated with cryotherapy (freezing) and irradiation. Choice of treatment will be influenced by extent of the lesion(s), time available for recovery, skill, resources and stage of the export process. Early stage lesions are more amenable to treatment. Larger and more chronic lesions have a higher risk of recurrence and consideration should be given to exclusion of affected animals from the export process, and organising salvage slaughter without delay. It may be an offence under relevant welfare acts to allow eye cancer to develop to advanced stages and animals may not be allowed to be processed for human consumption if the eye is discharging or if lymph nodes are involved.
At sea, removal of a cancerous third eyelid, using local anaesthesia and scissors, offers a quick, simple and permanent cure if adequate restraint is achievable.
Prevention
Both eyes should be systematically checked during selection for the export process and animals with suspicious lesions excluded.
Eye Discharge
Description
Eye discharges are the result of irritation to the cornea or conjunctiva, or both. They are commonly encountered in the export process, are usually very noticeable, and may raise concerns at health inspections.
Eye discharges are often initially serous and may then become purulent over time due to chronic inflammation and bacterial involvement. Unilateral discharge may be due to local inflammation, while bilateral discharge may be due to systemic disease or environmental irritants such as fodder dust or ammonia vapour. Eye discharge associated with closed, partly closed or excessive movement of eyelids, indicates pain in the eye from ulceration, foreign body or both. Conjunctival inflammation may result in prominent blood vessels, vascularisation, and reddening of the eye.
Corneal inflammation (keratitis) may result in increased vascularisation, ulceration and scarring, with more severe and chronic changes potentially interfering with normal eyesight.
Clinical Signs and Diagnosis
Animals with eye discharges should be examined, if possible, to determine the cause and particularly to look for foreign bodies.
Examination may require physical restraint, sedation, topical anaesthesia, and a light source.
Clues to diagnosis are whether single or multiple animals are affected and whether discharges are unilateral or bilateral, watery or purulent, and whether they are accompanied by other localised or systemic signs. Watery (serous) discharges are usually from dust, ammonia vapour and upper respiratory tract viruses. The hair on the face becomes wet and stained. Yellow, thick discharges are usually from foreign material such as grass seeds, chaff and sawdust or fodder fines. Severe inflammation and discharge on one side may be from listeriosis or middle ear infection.
Common causes of eye discharges in export livestock are ocular irritants, foreign bodies or trauma, pinkeye, and in cattle, infectious bovine rhinotracheitis (IBR) and malignant catarrhal fever. Excessive lacrimation may accompany many other systemic diseases including heat stress, bovine viral diarrhoea virus infection, bovine ephemeral fever and malignant catarrhal fever. These conditions should be associated with other characteristic signs or histories.
Treatment
If there is recent history suggesting grass seeds, chaff or other foreign bodies having entered the eye, each affected animal should be restrained and undergo examination of the eyes, especially of the conjunctival sacs. Removal of foreign bodies is made easier by use of topical anaesthesia and forceps.
Antibiotics (procaine penicillin, oxytetracycline, or trimethoprim sulpha) and non- steroidal anti-inflammatory drugs (flunixin meglumine, or ketoprofen) are commonly used to treat inflammatory eye conditions. Parenteral administration usually achieves therapeutic concentrations in the eye and tears. Topical treatments may be more problematic because of the effort required to restrain each animal to administer treatment and the need to repeat intra-ocular treatments frequently because they are rapidly washed away by tears.
Powdered formulations for topical use are contraindicated because they can scratch the eye and worsen the problem. Subconjunctival antibiotic injection (under the eyelid) may also offer an alternative approach to treatment.
Prevention
Controlling the factors contributing to corneal irritation such as flies, dust and fodder fines, as well as preventing aerial dispersion of sawdust and chaff, should lower the incidence of eye discharges.
Eye Foreign Body
Description
Ocular foreign bodies (grass seeds, feed material, bedding material, dust) may enter and irritate the eye, predisposing to inflammation and infection. Risk factors in the live export process include:
feeding unrolled round bales in assembly depots where cattle push their heads into the bale.
feeding chaff or spreading fluffy sawdust in windy conditions where it remains airborne for longer than normal.
high-pressure hosing of decks with the consequent risk of splashing airborne particulate matter into the eye.
Clinical Signs and Diagnosis
Affected eyes may be partially or wholly closed or weeping. A foreign body in the eye is usually located in the lower conjunctival recess and rarely in the upper recess. A proper examination requires good physical restraint aided by sedation, topical anaesthetic, and a light source (head lamp). Differential diagnoses include pinkeye and infectious bovine rhinotracheitis (IBR).
Treatment
Foreign bodies may be removed with forceps during the examination process, using appropriate restraint, sedation, and topical anaesthesia as required.
Topical antibiotics in the form of spray or ointment can be applied to the eye. However, parenteral administration of antibiotics (procaine penicillin, oxytetracycline, erythromycin, trimethoprim sulpha, or tylosin) will be easier, more effective and longer lasting.
Avoid applying antibiotic powders to the eye as they are irritating and may worsen the problem.
Prevention
Unroll round bales for feeding.
When feeding chaff or spreading sawdust, aim to minimise the risk of it becoming airborne in the vicinity of cattle.
Use large volume, low pressure hosing of cattle decks to avoid splashing manure or other matter into eyes.
Fleece Rot
Description
This is a superficial bacterial (Pseudomonas aeruginosa) infection of wooled skin that causes crusty, colourful lesions along the backline. Certain strains of bacteria act in moist conditions to stain wool close to the skin.
Young, shorn sheep are most susceptible, especially in wet, warm conditions. Affected sheep are also susceptible to fly strike.
Clinical Signs and Diagnosis
The skin and wool of the back are stained with hues of grey, green, yellow and brown but sometimes blue and orange, depending on the strain of bacteria present.
Diagnosis is usually by gross examination but a skin biopsy from an affected area may be submitted in buffered formalin if necessary.
Treatment
No treatment is necessary unless flystrike occurs.
Prevention
Preventative measures are usually unwarranted in the live export trade where fleece quality is usually unimportant.
Flystrike
Description
Flystrike occurs when larvae (maggots) of blow flies hatch on the skin and feed on tissues of live animals. Adult flies lay eggs in wool moistened from a range of causes such as urine or faecal staining, skin wounds, weeping from eyes, or the lesions of footrot, fleece rot or lumpy wool.
Affected animals may lose condition and be predisposed to secondary bacterial infections and septicaemia or toxaemia.
Warm, wet weather increases the likelihood of flystrike. If the weather is too hot or too dry, the eggs and maggots do not survive. Flystrike is rare in goats because they are hairy rather than wooly and have few skin folds. Fly strike in the live export process is uncommon because animals are crutched and shorn, conditions are usually dry, and they are closely monitored for much of the time.
Clinical Signs and Diagnosis
Affected animals may be first noticed showing signs of depression, anorexia, and separation from flock or herd mates. Affected animals may be irritated and attempting to bite or kick at the struck area. The animal may have a distinct smell coming from the struck area. Close examination reveals maggots burrowing or tunnelling under and into tissues.
Screw worm fly should always be considered where maggots are found in wounds. Specimens can be submitted in 70 % alcohol to the laboratory for identification.
Treatment
Cut away matted hair and wool, remove accessible maggots and apply insecticide or larvicide to kill remaining maggots. Individual animals showing signs of toxaemia should be treated with antibiotics (procaine penicillin, or oxytetracycline).
Humane euthanasia may be required for animals with extensive lesions.
Prevention
Reduce attractiveness of animals to flies by shearing, crutching, treating wounds and preventing diarrhoea and foot infections.
Under favourable environmental conditions, fly numbers can increase and lead to multiple animals being affected with flystrike. It is important to detect and treat affected animals promptly and consider applying prophylactic treatments (jetting or dipping) at strategic times to prevent further cases. A range of insecticidal and larvicidal preparations are available for individual or group prophylaxis during fly waves.
Foot Abscess
Description
Injuries to the sole of the foot or feet (abrasion, puncture wounds, bruising, abscess), are commonly associated with excessive wear of moisture-softened feet on rough and abrasive flooring. The conditions are painful and infection of the foot can lead to the development of abscessation and sometimes extension of the infection into the interdigital tissue, up the lower leg and into one or more of the joints of the foot.
Cattle that mount other cattle (riders) wear away the front part of the hind claws and may become lame from bruising and infection. Additional risk factors are cattle temperament, roughness of handling, concreted laneways with twists and turns, and sharp gravel on concrete yards (carried there on muddy feet).
Foot abscesses in sheep (and goats) usually involve one toe or one heel on one foot and cause acute lameness. The medial claw of the hind foot is most commonly affected. Toe abscessation is more frequent in young animals, involves front feet, and may follow horn cracks that provide an opportunity for bacteria to penetrate into the foot. Heel abscessation is more frequent in older, heavier animals, more frequently involving the hind feet and may occur as an extension from an interdigital dermatitis of the soft tissue at the back of the heel.
In cattle, foot abscesses may occur on any claw but are most common on the outside claws of the hind feet. They are thought to follow damage to the bottom of foot (sole), and particularly to the white line area (junction between the outer hoof wall and the sensitive part of the foot), allowing bacteria to penetrate into the foot. Damage most commonly follows abrasion of the foot on hard surfaces such as rough concrete flooring.
The highest risk groups are generally animals introduced to assembly points from high winter rainfall areas, but sole injuries may be acquired in pens that are muddy and soiled by faeces or when animals are competing for trough space at feeding.
Clinical Signs and Diagnosis
Affected animals are lame or reluctant to move or stand. Closer observation may detect swelling of the foot and discolouration of the sole with associated tenderness. Examination is aided by adequate restraint, good lighting, a sharp hoof knife, hoof testers, and double-action hoof cutters.
Cleaning the hoof followed by inspection and application of hoof testers to identify painful areas and then careful paring with a hoof knife will usually allow diagnosis. Sedation with xylazine may be helpful, particularly if a crush and head bail are not available.
Animals with foot abscessation are very lame, avoid weight bearing on the affected foot and rapidly lose body condition. The foot is hot and painful on pressure. Toe abscesses may extend to the coronet and heel abscesses will extend up behind the heel. When the abscess has ruptured or opened, usually as one or more sinusesabove the coronet, pus is discharged and pain is relieved. If infection has extended to the joint, damage and lameness may be permanent. Foot abscess is distinguishable from the under-run horn found in multiple feet in cases of footrot.
Necropsy finding may include discolouration, pus and foul smelling tissues within the claw, which may extend up the subcutaneous tissues of the leg.
Treatment
Cases should be treated early to prevent infection extending up the leg and to prevent the animal becoming a downer or developing other complications as a result of not being able to eat or drink normally. Lame animals are at risk of becoming non-competitive feeders, being smothered, becoming dehydrated, getting other secondary diseases, and developing heat stress if climatic conditions are marginal.
Treat solar abscesses and puncture wounds by paring the sole and wall around the injury to establish drainage. Care should be taken to avoid over trimming or indiscriminate digging with a hoof knife since this may exacerbate lameness and predispose to further injury.
Administration of antibiotics (procaine penicillin) and non-steroidal anti-inflammatory drugs (flunixin meglumine, ketoprofen, meloxicam, or tolfenamic acid) may be helpful.
With toe abscesses, paring of the hoof to allow drainage of pus may prevent the need for further antibiotics. Heel abscesses may not drain well when opened and may require a longer course of antibiotics (procaine penicillin, or oxytetracycline) to resolve the infection.
For severely affected cattle and if facilities and expertise are available, consider elevating the inflamed claw by applying a lift to the healthy claw in the form of a plastic shoe or a wooden or plastic block glued to the sole. This will provide dramatic pain relief and help keep the animal on its feet.
Isolate affected animals to provide comfort, ready access to feed and water and ease of monitoring and further treatment. Providing bedding will help to cushion the hoof-ground interface and reduce exposure to moisture.
Prevention
Avoid dirty, wet and rough ground conditions. Keep concrete yards free of sharp gravel especially for cattle with soles worn thin. At sea, provide soft, dry, non-slip flooring by distributing plenty of dry absorbent sawdust in pens and preventing water leaks.
Use low stress animal handling methods. Cattle worked on concrete yards over many days must be prevented from overwearing the soles of the feet by being allowed to walk and turn slowly and place feet carefully. Remove bullers from pens as soon as possible.
Footrot
Description
Footrot in sheep and goats is a different disease to the condition called footrot or interdigital necrobacillosis in cattle.
Sheep and Goats: Footrot is a contagious bacterial infection of sheep and goats caused by Dichelobacter nodosus, often in association with other bacteria. Initial infection involves the skin between the claws and may extend to cause separation of the horny hoof from the underlying soft tissue (corium). Footrot may be classified as benign, intermediate or virulent depending on the mix of bacteria involved, their virulence and the amount and location of tissue damage. In benign footrot, dermatitis (scalding) is confined to the interdigital skin and cannot be distinguished clinically from interdigital dermatitis. In virulent footrot, if conditions are suitable, the infection extends to under-run and detach the hoof. In sheep, the term footrot is usually only used to describe virulent footrot.
Note that in goats the clinical signs are not necessarily indicative of whether the bacteria are benign or virulent, unlike in sheep.
New infection can only establish in conditions that provide moisture and microtrauma to macerate the interdigital skin. Cases are more common in warm wet conditions.
Symptoms are more severe in Merino than British breed sheep. Goats vary in susceptibility.
Infection can persist for months in small pockets in the foot. Cases of mild or sub-clinical infection may slip through on-farm screening and enter assembly points. If prolonged wet conditions underfoot are then encountered at any point in the export process, the disease may flare up and outbreaks of lameness will occur.
Virulent footrot is a notifiable disease in some Australian states and is subject to control and eradication programs.
Cattle: Footrot in cattle is a painful bacterial cellulitis of the foot extending from the interdigital cleft, associated with infection with Fusobacterium necrophorum and other bacteria. Wet, boggy conditions macerate interdigital skin allowing entry of bacteria. Interdigital trauma from foreign bodies such as stones or straw also predisposes the area to infection. Footrot usually occurs sporadically but sometimes outbreaks are seen in poorly drained, muddy conditions. Suitable boggy conditions exist in assembly depots after rain. Occurrence is rare at sea despite pen floors being deep in slurry. This may be because gravel or other sharp material is not present to traumatise interdigital skin.
Dichelobacter nodosus infection can occur in cattle with foot lesions but in all cases investigated to date, it has been associated with strains of the organism that are benign in sheep.
Clinical Signs and Diagnosis
In sheep and goats, footrot should be suspected if multiple animals are lame in multiple feet. It should be strongly suspected if inspection of the feet reveals moist, red skin between the claws that is covered by a film of grey exudate, and there is slight to severe separation of the hoof horn from the underlying soft tissue. There should also be a characteristic odour similar to rotten cheese.
Clinical diagnosis should be sufficient for diagnosis. If laboratory confirmation is required, submit smears and swabs of interdigital exudate and necrotic tissue from multiple animals for bacteriology.
Differential diagnoses include foot abscess (typically restricted to one foot), toe abscess and founder (laminitis) resulting from an excessively carbohydrate-rich diet.
In cattle, footrot will present as sudden lameness in one or more animals, and one or more feet, with swelling of the interdigital space and coronet. Close examination of the foot will reveal a foul smelling, necrotic ulcer occupying the interdigital cleft.
If left untreated, the infection may spread to the interphalangeal joints and deeper structures of the foot, causing severe and chronic lameness. Differential diagnoses include a foreign body stuck between the claws, and solar abscess or other septic inflammatory process affecting the claw.
Treatment
In sheep, benign footrot should not require intervention. Intermediate and virulent footrot cases need attention to prevent large-scale outbreaks of affected sheep.
Systemic administration of antibiotics (procaine penicillin or oxytetracycline) and dry underfoot conditions usually resolve even severe lameness after a few days without the need to pare away dead horn. If antibiotics are injected, topical application of aerosol sprays of cetrimide or oxytetracycline is unnecessary.
Benign footrot may resolve if underfoot conditions are kept dry. Lameness in intermediate footrot may resolve just with paring to expose the affected area.
Foot bathing in formalin or zinc sulphate (with surfactant) is an option. However, the cost, chemical hazards and unpredictable results mean that injectable antibiotics are likely to be preferred. Affected cattle should be examined as part of the initial workup to confirm the diagnosis and any foreign bodies removed from the interdigital cleft.
Topical treatment and bandaging are unnecessary. Instead, treat with systemic antibiotics (procaine penicillin, florfenicol, or oxytetracycline) for three to five days. If treated early, recovery is usually rapid. If lameness does not resolve in a few days, check for extension of infection into deeper structures, interdigital foreign body, a solar abscess, or other lesion. In severe cases where joint or other deep structures of one claw are affected, amputation of the claw may be required. Note that this procedure may require prolonged time for recovery.
Prevention
Muddy conditions in assembly points and feedlots should be avoided. At sea, take precautions to ensure the pads that form on the floors of pens are not accidentally flooded.
Spelling contaminated areas for two weeks removes Dichelobacter organisms from soil, mud or pasture. There is a short-acting vaccine for footrot in sheep, however it does not cover all strains of D. nodosus. In addition, it needs to be used in conjunction with other control strategies, and reaction to the vaccine is common, often resulting in granulomas or abscesses.
Gastrocnemius Muscle Rupture
Description
This injury usually follows attempts to rise on a slippery floor in an animal already weakened by other disease.
Clinical Signs and Diagnosis
It presents as a markedly dropped (flexed) hock joint, sometimes reaching the ground, and a markedly flexed fetlock. It is particularly obvious in the standing animal. It is usually unilateral, and may become bilateral if the animal continues to struggle.
Treatment
These animals cannot walk and have major difficulty rising therefore prompt euthanasia is recommended once the diagnosis is confirmed.
Prevention
Low stress animal handling and non-slip flooring may reduce incidence of this and other traumatic injuries.
Gastrointestinal Obstruction
Description
Gastrointestinal obstruction can have many causes including foreign bodies, intussusceptions, volvuli and displacements affecting the abomasum, small and large intestines. Enteritis, abrupt dietary changes, high starch low fibre diets and access to indigestible feeds are just some of many factors likely to predispose to gastrointestinal obstruction. Unless relieved, complete obstruction will develop into a life threatening condition.
Clinical Signs and Diagnosis
Affected cattle may show signs of abdominal pain, be inappetent, and pass no faeces, or scant faeces covered in mucus or blood.
Rectal examination can be expected to reveal a completely empty rectum with a dry but sticky feel. A ping and sloshing of fluid may be detected upon auscultation and ballottement of a distended abomasum.
At necropsy there are large distended loops of bowel anterior to the obstruction and shrunken empty bowel distal to the obstruction. At the site of the obstruction there is usually red, purple or black discolouration if congestion, strangulation or necrosis are present. A twist may be palpable at the root of mesenteric, caecal and abomasal volvuli.
Treatment
With the exception of left displacement of the abomasum (LDA), bold and early surgical intervention and supportive care are required to save the animal. LDA is also often managed by surgical correction but there is less need for urgent intervention. If suitable facilities and equipment are not available, and with the possible exception of LDA, prompt euthanasia of the animal should be performed.
Prevention
Inciting causes are uncertain, however avoiding abrupt dietary changes, high starch/low fibre diets and very coarse feeds are recommended.
Gastrointestinal Parasitism
Description
Gastrointestinal parasitism is a major cause of scouring and poor growth, and may cause death in heavily affected animals.
Parasitism of export sheep is seen mainly in young animals that have not yet developed immunity and in older sheep in which resistance is diminished by poor nutrition. Goats do not develop immunity to parasites. Parasitism is significant in animals raised in winter rainfall regions that provide favourable conditions for hatching and survival of immature (larval) stages of the parasite on pasture. If disease occurs in export animals it will often present at or soon after entry to assembly points.
Heavy worm burdens can lead to reduced productivity in cattle, but most problems occur in calves and cattle less than 12 months of age. Brown stomach worm (Ostertagia ostertagi) can cause severe diarrhoea (winter scours) in older cattle, often in late winter and autumn. Worm-related disease may be an issue in animals up to two years of age, and in bulls, but is less common in adult cows.
Clinical Signs and Diagnosis
Parasitism should be suspected if there is inappetence, loss of condition, and reduced growth in young animals. Severely parasitised animals will develop a greenish-black scour soiling the tail area and back legs. In poor nutritional circumstances, weakness can lead to recumbency and death. Faecal egg counts can be confirmatory but may be deceptively low. Diagnostic drenching is warranted if there is a history of favourable conditions and suggestive clinical signs.
Necropsy may show pallor, bottle jaw and gelatinous changes in fat depots. The parasites, depending on species of worm, may be visible in contents of stomach, small intestine and large intestine. Many infections are due to a mix of different species of parasites and heavy burdens may not be apparent to the naked eye at necropsy. Laboratory confirmation of parasite burdens and species involved will provide useful information to inform control and preventive strategies.
Laboratory confirmation is generally based on submission of faecal samples from multiple (10 to 20) affected animals for egg count and larval culture. Most state animal health laboratories offer a pre-packaged WormTest kit as a convenient system for collecting and submitting faecal samples to the laboratory. In dead animals, if possible, submit the whole gastrointestinal tract, unopened, but tied off, either chilled or frozen for parasitological examination.
Treatment
Administration of effective anthelmintics to affected mobs. Administration of an anthelmintic effective against larval and adult worms on arrival at the assembly feedlot should eliminate the problem for the remainder of the export process. Assembly depots, shipboard pens and destination feedlots can be regarded as post treatment “clean pastures” where reinfection is unlikely to occur.
Prevention
Prevention revolves around strategic use of drenches and grazing management.
Haematoma – Cutaneous
Description
These are subcutaneous swellings filled with blood, and usually located around bony prominences that may be more prone to inadvertent trauma. Hazardous pathways and rough handling are predisposing factors. The bony prominences of the pelvis are most affected. Cases can be expected to occur during the export process because of the high number of handling and transport events occurring over an extended period.
Clinical Signs and Diagnosis
Soft, painless, fluctuating, fluid-filled swellings developing rapidly over bony prominences are probably haematomas.
Haematomas must be differentiated from abscesses and tumours which enlarge slowly, and hernias.
Treatment
Most haematomas are best left alone as usually they will heal spontaneously. Large haematomas may leave residual, sometimes unsightly skin folds. The temptation to insert a needle to determine contents or to lance and drain an intact haematoma should be resisted as the result is often an abscess or unsightly infected mess. Some will become abscesses and will need draining and flushing.
Prevention
Avoid rough handling and identify and remove projections into pathways.
Heart Failure – Congestive
Description
Cases of congestive heart failure may occur in the export process.
The three most likely causes are valvular endocarditis, traumatic pericarditis and ionophore poisoning. Determining cause is important because it may have implications for other cattle.
Valvular endocarditis develops most commonly on the tricuspid valve (right atrioventricular valve) in cattle. The condition is generally preceded by a bacteraemia resulting from an infection located in a distant tissue or area (skin wound or infection of lung, gut, tooth root, joint surface or mammary gland). Bacteria can then lodge on the tricuspid valve and develop into the classic vegetative lesion, interfering with valve function and resulting in valvular insufficiency.
Traumatic pericarditis develops most commonly when a nail, needle or piece of wire is swallowed in hay or chaff. Foreign bodies often lodge in the reticulum and digestive contraction may then result in penetration of the reticular wall, the diaphragm and the adjacent pericardial sac. The sac then fills with a fibrinopurulent inflammatory effusion or blood that compresses the heart (cardiac tamponade).
Ionophores like monensin and lasalocid are antibiotic feed additives that in toxic amounts, cause myocardial necrosis. Toxicity may occur as a result of errors in pellet formulations or uneven mixing of added premixes. Severe damage to the muscle of the heart interferes with normal contractions.
Clinical Signs and Diagnosis
Heart failure is associated with oedema of the brisket and submandible, marked distension and pulsation of the jugular vein, diarrhoea, laboured respiration, and reluctance to move. Affected animals may collapse and die if forced to move. At necropsy there is a large amount of fluid in the thorax, abdomen and pericardium, the liver is swollen and congested with an accentuated lobular pattern, and there is oedema around the kidneys and in the mesentery. Pericarditis is recognised distension of the pericardium with fibrinopurulent pus and a nail, needle or wire may be found in or near the reticulum. Valvular endocarditis is recognised by the presence of a vegetative growth on a heart valve. Ionophore toxicity is recognised by areas of paleness and pallor on the epicardium, especially of the left ventricle, extending into the myocardium.
Treatment
The damage to the heart and the debilitating symptoms are irreversible, hence salvage slaughter or euthanasia is indicated for all cases of congestive heart failure.
Prevention
Diagnosis of traumatic pericarditis or ionophore toxicity may require withdrawal of feedstuffs potentially contaminated with nails, wire or ionophores. Manufacturers should be notified in case other batches are affected. Valvular endocarditis is rare and impossible to predict. Systems of early detection and aggressive treatment of infections with antibiotics is good export practice to prevent this and other complications of infections.
Heat Stress
Description
The term heat stress describes a state where animals are responding to excessive heat load (EHL). Normal function of various tissues and organs within the body require that body temperature be maintained within a relatively narrow range. If body temperature is raised beyond the level that animals can tolerate then there is a risk of organ dysfunction, and even death. Heat stroke is a term used to describe the life-threatening condition of failure of an animal’s thermoregulatory system in response to EHL. Body temperature is the result of a balance between heat load and heat loss. Livestock normally maintain body temperature within a narrow range mainly by influencing metabolic heat production and evaporative heat loss through the respiratory tract, specifically the lungs and nose.
Endogenous heat production (physical activity, digestion and other processes such as inflammation) is a major source of heat accumulation. Animals may also take in additional heat from solar radiation (sun), from nearby structures that are releasing heat (pen fences, floor, ceiling etc) and from the air (if the temperature is higher than the animal’s body temperature).
On an export vessel, the metabolic heat production from the animals is the major source of heat below decks, accounting for a temperature differential between air inflow and outflow of up to 6°C. Other important heat sources on export vessels include the incoming air being blown out of outlets on each deck (incoming air delivered to the pens will be hotter than environmental air as a result of heat from the supply fans and turbulence and friction from supply ducting), and radiant heat from the vessel itself (particularly engine room bulkheads, fuel oil storage walls, the ceiling on the uppermost deck or the sides of the ship that are heated from solar radiation).
Animals dissipate body heat by convection (when air or water is warmed by contact with skin resulting in a loss of body heat), conduction (when heat is transferred from skin to a cooler surface in contact with the skin), radiation (movement of heat from the body into the surrounding atmosphere), and evaporation of water from the body surface (sweating or panting).
The major means of body heat loss are evaporative cooling through panting and sweating, and convective cooling due to air flow. Mechanical ventilation is used on export vessels to provide air flow and ensure removal of heated air. Panting provides increased airflow across the mucosa of the respiratory tract and allows for convective and evaporative cooling.
Environmental conditions that predispose to EHL include recent rainfall, high ambient temperature, high relative humidity, the absence of cloud cover or shelter with high solar radiation, minimal air movement over several days, and sudden adverse climatic conditions. Minimal airflow past the ship’s ventilation inlets will occur if there is little to no wind and the ship is not moving, or if the apparent wind is minimal, which can result in warm air being drawn from the ship’s exhaust fans back into the supply fans. An export ship must be kept moving wherever possible when faced with heat stress conditions. In feedlot situations, exposure to solar radiation is an important contributor to heat load. On export vessels, animals are typically not directly exposed to solar radiation. The impact of solar radiation is more through indirect heating of the air and the physical structure of the ship. The manure pad will hold moisture and contribute to humidity and wet bulb temperature.
Animal factors that may predispose to EHL include breed, coat type (dark and woolly coats may be more likely to accumulate heat), body condition (fatter animals accumulate more heat), lack of adaptation to heat, and concurrent illness. Bos indicus cattle have a greater natural heat tolerance compared to most Bos taurus breeds. Diet can also influence metabolic heat production, and diets that are high in readily fermentable carbohydrate or protein will generate more metabolic heat. Metabolic heat production will also rise during and soon after feeding and therefore feeding animals in the cooler parts of the day may help avoid excessive heat load.
Flow of heat away from an animal depends on temperature and humidity gradients. If the surrounding environmental temperature is lower than the animal’s body temperature then heat loss mechanisms such as convection, radiation and conduction can all operate to move heat from an animal to the environment.
Evaporative cooling is based on a loss of heat associated with evaporation of water from the body surfaces (skin or respiratory tract). Once environmental temperatures exceed about 21°C, evaporative cooling through sweating and panting becomes the major form of heat loss, and if the environmental temperature equals or exceeds an animal’s body temperature then evaporative heat loss is the only available heat loss mechanism for animals to regulate body temperature.
Heat loss from the skin through convection and evaporation (sweating) is more important in cattle than panting (assuming that a temperature gradient exists where body temperature is higher than the surrounding air temperature). In contrast, panting is the main form of evaporative heat loss for sheep. Mechanical ventilation provides an aid to evaporative heat loss by ensuring continual air flow over the animals. If animals are using evaporative cooling to regulate temperature then forced air flow ensures that the higher humidity air is moved away from animals and replaced with incoming air of lower humidity.
Evaporation of surface water is influenced by temperature and relative humidity of the air. As air temperatures rise, air can retain more water as water vapour, meaning that in hot dry conditions (low relative humidity) evaporative cooling offers important potential for heat loss. However, as relative humidity rises there is less potential for air to absorb more water vapour and when relative humidity is 100 %, the air is saturated and additional evaporation cannot occur.
As temperature and humidity rise, evaporative cooling from the skin is lost earlier than evaporative cooling from the respiratory tract. The reason for this is that air flow into the respiratory tract during panting will increase the temperature of the air slightly and this will raise the amount of water vapour that the air can retain (absolute humidity) and drop the relative humidity. As a result, evaporation may still occur, meaning that panting can function as a heat loss mechanism even when evaporative cooling from the skin is no longer occurring.
In many hot climates, animals may accumulate heat through the hottest part of the day and then dissipate heat in the cooler parts of the day and continue to function normally. In situations where the environmental temperature remains high for most of the day and night, animals have relatively little opportunity to lose heat and they may gradually accumulate excessive heat over time.
During export voyages, the conditions that favour heat stress are long periods where very high environmental temperatures are in place for much of the day and night (providing little or no period of respite where animals can shed heat), and periods where both temperature and humidity are high. Under these conditions, animals have very limited ability to lose heat and severe heat stress conditions may rapidly develop. The physical constraints of pens within the decks of an export vessel also mean that there is limited capacity for animals to use some strategies for dealing with EHL, such as moving to less dense or cooler areas.
Heat stress can result in reduced feed intake along with depression, increased heart and respiratory rate. Heat stress is a significant stressor that in turn may reduce resistance to other pathogens. Panting and open mouth breathing predisposes to pneumonia. A continued rise in body temperature will eventually result in respiratory and circulatory failure and death.
A range of factors other than environmental temperature and humidity may influence the risk of heat stress including physical activity, dehydration, ingestion of rapidly fermentable feed, febrile disease and concurrent diseases of the respiratory tract that interfere with evaporative heat exchange. In the export process, dangerous levels of heat stress occur occasionally in assembly points on extreme summer days, at sea when crossing the equatorial zone or when ventilation systems fail or struggle, and in summers in the Middle East. Export risk may be elevated in unacclimatised animals coming from an Australian winter into a northern hemisphere summer. Heat stress is one of the most important concerns of the livestock export industry. It must be prepared for, recognised, and carefully managed when it occurs in order to avoid mortalities either directly from heat stress or other complications that may result. This applies particularly to British and European breed cattle.
Clinical Signs and Diagnosis
Animals exposed to heat load will attempt to adapt by decreasing heat production and increasing heat loss.
Cattle will sweat, drink more water and increase their respiratory rate. Animals in feedlots or other environments exposed to sunlight may seek shade, spend more time standing, and generally be more restless. On board export vessels the symptoms are similar but animals may have less opportunity to move or change behaviour. They may move towards fans and away from the ship’s structures that radiate heat near pen areas.
Panting score used in the assessment of heat stress in cattle
| Breathing Pattern | Panting score (PS) | Respiratory rate (per minute) |
| Normal – No panting, difficult to see chest movement. | 0 | <40 |
| Slight panting, mouth closed, no drool or foam. Easy to see chest movement. | 1 | 40-70 |
| Fast panting, drool or foam present. No open mouth panting. | 2 | 70-120 |
| As for 2 but without occasional open mouth. Tongue not protruding. | 2.5 | 70-120 |
| Open mouth + some drooling. Neck extended and head usually up. | 3 | 120-160 |
| As for 3 but with tongue out slightly & occasionally fully extended for short periods. Excessive drooling. | 3.5 | 120-160 |
| Open mouth with tongue fully extended for prolonged periods + excessive drooling. Neck extended and head up. | 4 | >160 |
| As for 4 but with head held down. Cattle ‘breath’ from flank, drooling may cease | 4.5 | Variable – RR may decrease |
If heat load continues, animals will reduce feed intake in an attempt to reduce heat production due to rumen fermentation. Cattle on high concentrate diets may reduce feed intake by up to 25%. Animals will also show a rise in body temperature.
Provided heat loads are not excessive, animals may show the above signs for several days and then adapt and become more tolerant to hot conditions.
Failure of adaptation is more likely to occur when animals are suddenly exposed to excessive heat load or when conditions are beyond the capacity of animals to adapt. These conditions can result in severe disease and even death.
Animals that are failing to adapt to EHL will show progressively more severe respiratory signs. They will show increased respiratory rate that progresses from panting to open-mouth breathing and, if stress is sustained, to open-mouthed, laboured breathing with neck extended and tongue extruded. Animals may then collapse, become comatose and die.
Panting scores provide a better indicator of heat load in animals than respiratory rate and should be monitored during periods when heat stress may occur. In assessing cattle if more than 10% of animals have a panting score of 3.5 or higher, then there is a potential for serious losses if steps are not taken quickly to allow animals to dissipate heat.
Wet bulb temperatures of ~28ºC usually mark the onset of heat stress in Bos taurus cattle. Hot spots on cattle decks are detected during pen inspections by monitoring the level of panting among cattle, and the level of one’s own personal discomfort.
Panting score used in the assessment of heat stress in sheep
| Panting score | Description |
| 0 | No panting |
| 1 | Slight panting |
| 2 | Fast panting and open grin |
| 3 | Open mouth panting |
| 4 | Open mouth panting, tongue out |
Wet bulb temperatures approaching or exceeding 30ºC indicate environmental conditions that favour development of heat stress in small ruminants and preventive measures should be considered under these conditions.
The main differential diagnosis is advanced pneumonia which tends to affect individual animals in a group rather than whole pens. Heat stress and pneumonia may sometimes be difficult to differentiate while the animal is alive. At necropsy, pneumonia is diagnosed by feeling the lungs – firm solid tissue is indicative of pneumonia.
In heat stress, at necropsy the carcase is hot to touch, the eyes sunken, the lungs red to dark red from congestion (but still spongy), and the heart is small and hard from being in a state of strong contracture. The core temperatures require a cooking thermometer for measurement and are consistently greater than 43ºC. The muscles are pathognomonically pink (like cooked silverside) and dry rather than red-brown and moist. This latter change is thought to be a result of lactic acid leaching myoglobin from heat denatured cells. In a heat stress event, the first animals to die will be Bos taurus, and particularly animals that are fatter, with long hair coats covered in manure, and those suffering concurrent diseases such as lameness, pneumonia or diarrhoea.
Core body temperature normally elevates considerably after death in large, fat, hairy or otherwise well insulated cattle. However, it usually takes a few hours before the core temperature may reach the levels that may be seen immediately after death from heat stress. It is important to measure core temperature soon after death to avoid erroneously attributing post-mortem elevation of body temperature to heat stress.
Treatment
Outbreaks of heat stress must be treated as an emergency.
On land, options are to:
- Ensure there is unlimited access to clean, cool water for all animals.
- Minimise handling and disturbance of animals. Essential activities should be conducted at the coolest times of the day, usually early in the morning or late at night.
- Reduce stocking densities.
- Use low stress stock handling techniques.
- Erect shade that encourages air flow including over loading and unloading ramps.
- Consider moving affected animals to cooler pens with reduced stocking density, shade and better air flow.
- Remove barriers to wind.
- Provide fan-forced airflow.
- Temporarily reduce or cease feeding of concentrate and consider a higher roughage proportion in ration until other emergency measures are implemented.
Many of these options are applicable at sea. Additional options at sea include:
- Move animals from areas of the vessel that may be particularly prone to heat stress, e.g. areas where mechanical ventilation is less effective or pens are affected by heat radiation. This is best done in preparation for a heat stress event rather than when the conditions are already hot.
- Stow higher risk animals in lower risk areas of the ship.
- Reduce density in pens by spreading animals between more pens or opening dividers to create larger pens.
- Minimise disturbance of the animals – all unnecessary physical exertion must be avoided.
- Increase access to water by emptying feed troughs and filling with water.
- Add electrolytes to water (particularly for Bos taurus cattle) to ensure supplementation with sodium, potassium and bicarbonate to replenish electrolytes lost through evaporative cooling.
- Ensure ventilation systems are operating maximally, and check that intake and exhaust fans are unobstructed.
- Set up portable fans in poorly ventilated areas or on higher risk animals.
- Maximise the ability for animals to access fans by opening up pen areas or removing gates around fans.
- Shade top deck areas from direct sunlight.
- Change course to allow breeze to blow across the ship, especially if there are following winds.
- Ventilation of open decks is dependent on wind direction and speed. When there is a following breeze, effective ventilation in open decks may be very poor. In a following breeze, minor course deviations (up to 30°), may result in major improvements in effective ventilation with relatively little loss in overall progress. Course deviations may be carried out for days under extreme conditions with the ship zig-zagging around the intended course. If air speed can be increased from close to zero to around 1 m/second, the effect can reduce wet bulb temperature by as much as 4 to 5°C.
- Keep the ship moving where ever possible in a heat event, this will ensure that the airflow from the exhaust fan outlets is not being drawn back into the supply fan inlets.
- Temporarily reduce or stop feeding. Feed chaff in preference to shipping pellets to reduce heat produced by rumen fermentation.
- In preparation for a heat event, conduct a deck-wash down and spread absorbent bedding to reduce humidity.
In severe heat stress situations, there may be benefits in spray-wetting cattle. The following issues should be considered:
- The increase in humidity that will be caused by spray wetting.
- Only consider spray wetting if it will improve evaporative cooling rather than adding humidity.
- Set-up spray wetting equipment when weather forecast predicts risk conditions.
- Start spraying when 5% show panting score 3, i.e. open mouth breathing and drooling with neck extended.
- Spray only when there is discernible air movement.
- Sea or fresh water is ok.
- Apply spray to the head and neck for maximum benefit.
- Avoid cold water (<25oC) and high pressure.
- Don’t spray-wet if there is a ventilation system failure, otherwise dangerous increases in humidity may occur.
- Ensure minimal disturbance of cattle – all unnecessary physical exertion must be avoided.
- Continue spray-wetting until respiratory distress has eased.
Prevention
Livestock exports to the Middle East are subjected to heat stress risk assessment prior to export. This includes application of the industry’s heat stress risk assessment software which incorporates detailed information on predicted weather conditions, ship design and ventilation capacity, the type and bodyweight of livestock on board, time of year, and the route that will be taken by the vessel. Stocking densities can then be adjusted to minimise heat stress.
At sea, risk periods for heat stress may be anticipated from observations of local conditions and animal behaviour, and weather forecasts over the next several days. Preparations can then be made to implement some of the measures listed above, under Treatment, in order to minimise the risk of large scale heat stress occurring.
Hepatic Encephalopathy
Description
Hepatic encephalopathy refers to the nervous disease that follows severe liver damage. The liver has a large reserve capacity meaning that loss of three-quarters of liver capacity generally must occur before signs of liver dysfunction appear. As liver function reduces following extensive liver damage, toxic metabolites including ammonia that are normally detoxified by the liver, will accumulate in blood and tissues. Accumulation of ammonia and other toxins may then reach levels that cause deterioration of brain function.
Liver injury may occur in animals ingesting toxic plants that contain pyrrolizidine alkaloids such as heliotrope (Heliotropeum europeum) and Paterson’s curse (Echium plantagineum), or fungal-infected lupin stubbles that produce phomopsin. The liver damage may be exacerbated in the export process if animals consume feed (pasture, hay or pellets) contaminated with hepatotoxic plants, or drink from water sources containing blue-green algae.
Clinical Signs and Diagnosis
Affected animals will be dull, appear to be blind, stagger, and exhibit head pressing before becoming comatose and dying.
At necropsy the liver may be swollen and pale or misshapen and nodular. Laboratory determination of the toxin may be assisted by histological examination of sections of liver submitted in buffered formalin.
Polioencephalomalacia is the main differential diagnosis.
Treatment
There is no effective treatment. Regeneration of liver can occur, but only after a long delay. Severely affected animals should be humanely euthanased.
Prevention
Source animals from areas where toxic plants are controlled. Avoid further exposure to hepatotoxins in the export process.
Hypocalcaemia
Description
Hypocalcaemia is low blood calcium. Calcium is essential for many body functions especially muscle contraction, nerve conductivity and bone strength. Maintenance of normal blood concentrations is achieved by a combination of release from bone stores and absorption of dietary calcium from the gut.
Animals are at risk of hypocalcaemia when:
Bone stores are depleted – may occur with long term grain feeding or vitamin D deficiency (seen in low sunlight, vitamin A-rich grazing conditions of southern Australian winters).
Sudden reduction in intake and absorption from the gut – fasting associated with transport or yarding, sudden dietary changes, sudden climatic changes (hot or cold), and ingestion of plants containing oxalate.
Mobilisation from bones is too slow to meet an increase in demand – may occur in older, fatter animals.
Animals have high demand for calcium such as in early lactation and pregnant animals especially those with multiple foetuses.
The first three situations might occur in assembly points, the fourth at destination.
Clinical Signs and Diagnosis
Early signs include excitement and muscle tremors followed by staggering gait, recumbency, paralysis, coma and death. There is no fever.
Diagnosis is based on clinical signs, presence of risk factors and response to treatment. Fragility of bones and sometimes healing rib fractures may be present in sheep with prolonged dietary deficiency. Blood samples will have low calcium concentrations.
Before kidding/lambing/calving, pregnancy toxaemia is the main differential diagnosis. Some animals have both diseases. In pregnancy toxaemia, the onset is gradual over a few days and response to calcium is slight and temporary.
Laboratory confirmation requires 2 mL of serum submitted chilled for calcium and magnesium estimation. In dead animals submit aqueous humor for calcium estimation, taking care to minimise cellular contamination from the iris.
Treatment
Administer injectable calcium and magnesium solutions under the skin over the ribs. Massage well to speed absorption. Commercial solutions of calcium borogluconate are commonly used and should be warmed to body temperature before injection. A response is expected in a few minutes (burping, muscle tremors, voluntary movements) with full recovery usually within an hour. Treatment occasionally needs to be repeated. It is fatal if left untreated. Careful intravenous administration of calcium solutions may be considered for severe cases.
Prevention
Avoid selecting old, over-fat and pregnant females for export. Avoid interruptions to food and water availability. Feed roughage as hay, chaff or pellets high in fibre (to increase dietary intake and gut absorption of calcium) in high risk animals or conditions.
Illthrift
Description
Illthrift is the loss of body condition in the presence of ample feed. Illthrift may be the end result of a wide range of different causes including parasitism (of blood, skin or gut), infectious diseases, specific nutrient deficiencies such as copper, chronic conditions causing organ dysfunction or toxaemia, and conditions causing pain. Contributing causes may be difficult to diagnose such as indigestion, mild ruminal acidosis, depletion of rumen microflora, abomasal ulcer, pneumonia, liver abscess, local peritonitis, and mild laminitis in all four feet. Single or multiple animals may be affected. It is common for some cattle under shipboard conditions to have greater difficulty than pen mates in adapting to the unfamiliar environment, the type of feed and water and the way it is offered. Animals with persistent infection with pestivirus are usually excluded from the export process by testing or visual inspection or both.
Clinical Signs and Diagnosis
During pen inspection, a flank scan may detect affected animals due to a reduction in size of the abdomen (i.e. hollow flanks and a tucked up posture), and wasting of muscles of the back and rump regions. Different hair length, lustre, density and colour may stand out. Cattle may still appear healthy and bright.
The most likely causes of illthrift in shipboard cattle include:
Shy feeders.
Chronic toxemia or pain associated with conditions such as pneumonia, pleurisy, rumenitis, liver abscessation and abomasal ulceration.
Necropsy of unresponsive cases may reveal muscle wasting, empty rumen, depleted fat reserves and serous atrophy (jellying) of fat deposits especially mesenteric, renal and bone marrow fat. The pancreas, liver and gall bladder may be atrophied.
The choice of specimens for laboratory differentiation will be dictated by field observations. They may include faeces for parasitology, blood samples to test for trace element deficiencies, and samples from a range of body organs, including fresh sections for bacteriology and virology, and formalin-fixed sections for histology.
Treatment
Treatment will depend on the diagnosis. Animals with suspected infectious or painful conditions may be treated with antibiotics (procaine penicillin, erythromycin, ceftiofur, or oxytetracycline) and non-steroidal anti-inflammatory drugs (flunixin meglumine, ketoprofen, meloxicam, or tolfenamic acid). Response to initial therapy may be used to guide further treatment. It is possible that long and costly courses of treatment may be required to achieve improvement, and relapse may occur upon withdrawal of treatment.
Prevention
Preventative measures depend on a good understanding of and anticipation of risk factors likely to affect a consignment.
Inappetence / Inanition
Description
Inappetence refers to a reduction in appetite and feed intake (synonymous with shy feeders).
For more information regarding inappetence in cattle see Shy Feeders.
Inanition is defined as the state of exhaustion resulting from lack of food and water. Inanition is used to describe deaths in the export industry due to prolonged refusal of food or inability to eat. Starvation refers similarly to the prolonged effects of deprivation of food or food refusal. Prolonged inappetence may progress to inanition and also results in increased risk of other conditions, such as salmonellosis causing severe and sometimes fatal infections in compromised animals.
Inanition and salmonellosis are the most common causes of death in exported sheep and goats and may occur separately (one disease resulting in death without evidence of the other) or together in the same animal. The first week of a sea voyage appears to present an elevated risk of salmonellosis, while inanition tends to occur more in later stages of a voyage.
Causal factors contributing to inappetence in sheep and goats are not well described. Adult sheep that are fat, exported during the second half of the year and coming from a high plane of nutrition are at a higher risk. In addition, feral goats appear to be at an elevated risk. Inappetence may appear in individual sheep or in lines of sheep. There also appear to be farm-level factors contributing to risk of inappetence such that some farms may be at higher risk than others.
It is presumed the stresses of transition from pasture to feedlot conditions may contribute to the risk of inappetence, including transport, curfew periods without feed or water, and transition to water troughs and pelleted feed. The greater appetite of younger, growing sheep, and sheep coming from a lower plane of nutrition is thought to protect animals from inappetence.
Most sheep that are inappetent in the assembly feedlot will start feeding during the early part of a voyage. However, inappetence in the feedlot is considered to indicate a higher risk of prolonged inappetence continuing during the voyage and an elevated likelihood of inanition and death.
Mortality studies in the late 1980s and early 1990s (LIVE.0112, 2002) suggested that persistent inappetence was the single major initiating condition that then led to elevated risk of subsequent occurrence of either inanition or salmonellosis (each associated with high mortality risk). Further studies (LIVE.0123, 2008; W.LIV.0132, 2009) have suggested that inappetence and salmonellosis may occur separately or together and the initial occurrence of either condition can then lead to increased risk of the other. The unified causal web presented in W.LIV.0132 (2009) and depicted in Figure 4.2, describes a complex pattern of causal factors that may lead to one or the other condition or both. The point of this is that control and prevention efforts need to be directed at both inappetence and salmonellosis and not just at inappetence.
Clinical Signs and Diagnosis
Affected animals can be difficult to identify except by extended or careful observation. Animals may be noticed as not pushing forward to eat at feeding time, so called ‘non competitors’, and may show varying signs from hollowing of the left flanks to obvious emaciation.
At post-mortem the rumen is shrunken, containing light grey-coloured fluid (due to the loss of rumen microflora and lack of ingesta), and very little food material. The lining, normally papillated, will be smooth. The intestines are empty. The gall bladder may be enlarged, and there may be accumulation of fat in the liver, especially in fatter sheep.
Specimens for laboratory determination include serum for beta hydroxybutyrate estimation and heart, liver, kidney, pancreas, bone marrow and long bone diaphysis in buffered formalin for histology.
Treatment
Treatment is symptomatic and may not always be successful. Early recognition, separation, provision of adequate trough and floor space, and feeding of high quality chaff or fresh hay may encourage eating. Where multiple animals in a mob appear to be inappetent during the assembly feedlot, adding or resuming addition of chaff or hay to a pelleted diet may encourage animals to eat and facilitate transition to eating pellets in preparation for loading onto an export vessel.
Prevention
Ensure healthy livestock are sourced for export. Avoid stress or prolonged periods of feed and water curfew during transportation into the assembly feedlot, and while managing animals in the feedlot. Provide shelter so animals can avoid extreme weather during feedlotting.
Provide high quality feed and water, and observe reasonable standards of hygiene. Avoid pellet dust when feeding pellets, particularly on board ship when pellets may be delivered through automatic feeding lines. Consider adding additional trough space and providing troughs in the middle of feedlot paddocks and on the inside of pens on board ship, in an attempt to allow shy feeders increased opportunity to access feed.
There is conflicting evidence over the benefits of feeding sheep hay in the assembly feedlot including some evidence that feeding hay may actually contribute to inappetence, or delay the transition to pellets in some animals. Alternatives include feeding chaff with pellets as an initial introductory strategy, and introducing sheep to pellets that contain lower concentrations of starch in an attempt to avoid the risk of acidosis which may exacerbate inappetence.
Lines of sheep that have high levels of inappetence in the assembly feedlot may be pulled from the voyage because of the increased risk of mortality from subsequent inanition and possibly other conditions such as salmonellosis.
Indigestion
Description
The term indigestion is used to refer to alteration in the rumen environment as a result of dietary changes. The change in quantity and quality of feed disrupts rumen microflora, pH is altered and the result is temporary ruminal atony, inappetence and change of faecal consistency.
It is the most common cause of diarrhoea in shipboard cattle and is usually associated with the sudden feed change, from hay in assembly points to pellets at sea. Indigestion may also result in constipation in assembly points when cattle come from lush grass pastures on to coarse hay. It may also occur when a new batch of hay or pellets with a different concentration of nitrogen, starch or fibre are introduced into the diet.
Clinical Signs and Diagnosis
Cattle typically have fluid to watery faeces but can otherwise appear healthy with a normal to slightly depressed appetite. Multiple animals in more than one pen will be affected. The diarrhoea usually resolves in a few to several days as rumen flora adapt. The main differential diagnoses are ruminal acidosis, salmonellosis or vagal indigestion.
Treatment
Substituting chaff or hay for part of the pellet ration speeds recovery.
Prevention
Avoid uneven feeding regimes and introduce new diets gradually over several days. It is recommended that cattle be adapted to the shipboard ration before the voyage.
Iodine Deficiency
Description
Iodine deficiency may be due to inadequate dietary intake of iodine or consumption of feeds containing compounds that either interfere with iodine uptake by the thyroid gland or with normal synthesis of thyroid hormones (goitrogens). Iodine deficiency typically results in enlargement of the thyroid glands (goiter). The thyroid glands are located in the upper ventral neck on the trachea and produce thyroid hormone, important for controlling metabolism.
Goiter may be seen in animals sourced from high rainfall areas where there are iodine deficient soils, with elevated risk often following high rainfall in the autumn or winter. Goiter may also be seen in animals that have recently grazed certain white clover pastures or brassica crops that were high in goitrogens.
Clinical Signs and Diagnosis
Large firm, non-fluctuant, swelling of the ventral neck in an otherwise healthy animal is likely to be goiter. Differential diagnoses include bottle jaw and cheesy gland abscesses. Laboratory confirmation requires thyroid glands submitted in buffered formalin for histology.
Treatment
Pelleted feeds contain supplemental iodine and should be sufficient to prevent development of symptoms associated with iodine deficiency.
Prevention
Control exposure to iodine-deficient or goitrogen-rich conditions on farm, or ensure supplemental iodine is provided.
Itch Mite
Description
Itch mite, Psorobia ovis (formally Psorergates ovis), is a microscopic mite that lives in the skin. Heavy mite infestations cause skin disease and fleece damage from scratching. Infestations are usually subclinical and limited to sheep.
Widespread use of macrocyclic lactone drenches have greatly reduced the incidence of itch mites and the condition is now rare. In addition, itch mite populations build more slowly than lice and the mite does not tolerate hot, humid conditions or exposure to sunlight in short wool.
Clinical Signs and Diagnosis
Heavy mite infestation causes scratching, biting and fleece damage. Mites should be suspected when lice or grass seeds are not found.
Laboratory confirmation requires skin scrapings collected using a scalpel blade dipped in paraffin oil. A skin biopsy submitted in buffered formalin may assist in differential diagnosis.
Treatment
Macrocyclic lactones are highly effective.
Prevention
Specific preventative measures beyond the occasional use of macrocyclic lactone drenches are usually unnecessary.
Johne’s Disease
Description
This is a fatal mycobacterial infection affecting the intestines. Multiplication of bacteria and chronic inflammation slowly thicken the intestinal wall, preventing absorption of nutrients, and leading to wasting and diarrhoea. Affected animals show no signs for months or years after becoming infected until the extent of intestinal compromise causes progressive wasting. Eating and drinking continue normally until animals are too weak to move.
There are separate sheep and cattle strains of Mycobacterium paratuberculosis. Goats may be infected with either strain. Bovine Johne’s disease (BJD) is endemic in south eastern Australia. There are control and eradication programs in Australia for both Ovine Johne’s disease (OJD) and BJD. The disease is widespread in sheep and goats in Australia. Prevalence is lower in drier, lightly stocked areas.
Problems may occur in the export process if infected animals are sourced in the belief they have easily remedied problems such as internal parasites or undernutrition. Also, stressors within the export process may accelerate progression of the disease and onset of clinical signs. It takes six weeks to 3 months from the onset of signs to death so there is the potential for animals to die during export.
Clinical Signs and Diagnosis
Suspicions are often first raised when there is unresponsive or unexplained wasting and death in yearling and adult animals. Flocks may have a distinct tail of clinically affected animals. At necropsy, the important diagnostic lesions are found in the intestines which have thickened walls, enlarged lymph nodes and prominent lymphatics. Differential diagnoses include internal parasites, undernutrition, poor dentition, and internal abscesses from cheesy gland or following rumenitis. Caprine arthritis and encephalitis (CAE) is an additional differential diagnosis in goats. With many of these differentials there is often some level of inappetence.
Laboratory confirmation in live animals requires serum and faeces submitted chilled. In dead animals, recommended specimens include thickened gut, enlarged lymph nodes and liver chilled for microbiology and in buffered formalin for histology. In the absence of obvious gross lesions submit specimens of ileum, liver and ileal and caudal jejunal lymph nodes.
Treatment
It is untreatable, including with antibiotics.
Prevention
Prevention of infection occurs on farm by vaccination and management to avoid exposure of susceptible animals to infected stock. Prevention of onset of clinical signs in the export process is by sourcing younger, vaccinated animals from drier regions, or from flocks and herds in the Johne’s disease market assurance program. Minimising environmental and management stress will also reduce the likelihood of early infected animals developing clinical signs.
Ketosis
Description
The term ketosis is used to refer to a spectrum of conditions associated with low blood sugar and intense fat mobilisation resulting from reduced food intake. In conditions of persistent low blood sugar the liver attempts to produce sugar from fat. This process involves production of ketones, which in turn have the potential to result in suppression of appetite depending on the levels produced. The result may be persistent inappetence, inanition and death.
The trigger, persistent low blood sugar, is brought about by feed deprivation, inadequate energy in feed, or inappetence caused by stress or concurrent disease such as displaced abomasum, metritis or lameness.
Any class of animal in any physiological state may be affected. Animals that are older, fatter, pregnant or lactating, are at higher risk. Ewes and does that are pregnant with multiple foetuses are at higher risk. In heavily pregnant animals the disease is usually irreversible and fatal, while lactating animals may self-cure by reducing milk production. Some animals may become persistently inappetent and die from inanition. Depletion of rumen flora may be a complication in later stages in some animals and this may explain some treatment failures.
There are numerous potential stressors during the export process that may predispose animals to ketosis including mixing of cattle, introduction to unfamiliar environments, periods of feed or water deprivation during transport and handling, and dietary changes from farm to assembly depot to ship. Older, well-conditioned cattle entering the export process that become shy feeders at sea and at destination, may be suffering from ketosis.
Clinical Signs and Diagnosis
Inappetence, lethargy, weight loss and reduced abdominal size are often present. Pen inspection will detect sharp transverse processes, hollowing and woody appearance of skin (from loss of skin fat).
A strong reaction to ketones in urine or milk on a dipstick test strip is diagnostic. Ketosis causes the breath to smell sickly sweet. Incessant chewing and licking and sometimes other nervous signs occur in lactating cattle with ketosis. A chilled serum sample may also be tested for beta hydroxybutyrate (one of the ketone bodies produced from fat mobilisation in response to low blood sugar).
Differential diagnoses include those causing inappetence and weight loss, such as displaced abomasum and chronic inflammatory conditions such as liver abscess or low grade pneumonia. Hypocalcaemia is a differential for pregnant and lactating animals. The necropsy of animals that have not eaten for several days and where fat catabolism is occurring, may reveal livers that are enlarged, pale, yellow or orange, and friable. The kidneys may be similarly affected. The rumen and intestines may be shrunken and fat deposits (especially around the kidneys and heart), may appear jelly-like (serous atrophy). A smaller than normal liver and gall bladder may be present in animals suffering long term reduced food intake.
Treatment
Ketosis can be very difficult to reverse in pregnant and older, fat, non-pregnant cattle. Early detection and treatment is essential to avoid death or protracted recovery.
Isolate suspected cases, feed good quality hay to stimulate appetite and provide energy, and treat concurrent diseases.
Drench with propylene glycol or glycerol daily for 3 days. Follow the manufacturer’s dosage recommendations and avoid overdosing.
Administer calcium borogluconate under the skin – in the feedlot industry this is regarded as essential to reverse the ketosis and stimulate appetite.
Glucocorticosteroids such as dexamethasone are effective in reversing ketosis in lactating cattle. In other classes of cattle, the benefits are uncertain and it may be detrimental, exacerbating ketosis by stimulating breakdown of fat and muscle.
Glucocorticosteroids are contraindicated if infectious conditions are present.
Rumen inoculation of >3 L but preferably 8-16 L of rumen fluid from a healthy animal may benefit animals with depleted rumen microflora.
Prevention
Minimise periods of feed deprivation, rapid diet changes and avoid unpalatable or low energy feeds. Provide feed with adequate but not excess energy to meet physiological demand.
Avoid selecting older, fatter or heavily pregnant cattle for the livestock export process. Minimise the number and duration of stressors.
Knuckling
Description
Knuckling refers to flexion of the fetlock joint caused by damage to spinal cord, nerves, muscle or tendons. There may be partial flexion where the soles of the hooves are bearing weight, or extreme flexion where the front of the pastern is bearing weight.
Many injuries or conditions may cause knuckling. In the export process the main cause of knuckling in the hind leg is injury to the spinal cord, the sciatic nerve and its branches, or the gastrocnemius muscle or tendon. Knuckling in the forelegs is from injury to the radial nerve.
Clinical Signs and Diagnosis
Spinal cord injury may occur from being ridden by or riding other animals, or pulling and twisting the head or neck when it is stuck under a pen rail or over a gate chain. These animals stand weakly on the front and hind limbs with both hind fetlocks knuckling equally. The tail may have reduced muscle tone or be flaccid, and anal reflex may be absent.
Cattle with mild calving paralysis knuckle bilaterally in the hind limbs as a result of compression injury to nerves in the pelvic canal suffered during parturition. A pelvic fracture may cause similar signs.
In animals recumbent for a long time on hard or uneven surfaces, compression injury to a branch of the sciatic nerve (the peroneal nerve) as it crosses the lateral stifle can cause knuckling. Sometimes both hind limbs are affected, and this resembles calving paresis.
Unilateral knuckling in a hind leg may also be the result of injection site paresis affecting the sciatic nerve. Injection site paresis is where needle puncture or irritant injections in the gluteal region or caudal thigh result in injury to the sciatic nerve and branches. The risk is greater in animals with small muscle mass (young or very thin animals), and in any animal where large volumes of irritant medications or long large gauge needles are injected intramuscularly.
Knuckling in the forelimb is usually from injury to the radial nerve but can be due to rupture or severe trauma to the extensor tendon or its associated musculature. With these injuries, the elbow is dropped, the fetlock is hyperflexed, and the limb appears unable to bear weight. Radial nerve injury is typically seen in animals that have been stuck in lateral recumbency for long periods following blunt trauma to the shoulder area (striking a gate) or following avulsion injury, such as from struggling to free a stuck front leg.
A severely dropped hock in conjunction with knuckling indicates rupture of the gastrocnemius muscle or tendon (Achilles tendon).
Note that knuckling may also be caused by systemic diseases such as rabies, Aspergillus clavatus poisoning, cerebral babesiosis and Histophilus somni meningitis.
Treatment
Provide rest and confinement and administer non-steroidal anti-inflammatory drugs (flunixin meglumine, ketoprofen, meloxicam, or tolfenamic acid). Recovery from nerve damage may take weeks or months, and may not occur at all.
Bandage or splint fetlocks in the extended position to assist standing and walking, and to protect the anterior pastern. Provide non-slip flooring. Treat any underlying conditions leading to the injuries causing knuckling.
Prevention
Injections into the neck and subcutis are preferred if manufacturers’ directions allow. Roll downer animals from side to side every few hours to reduce compression damage to limb muscles and nerves.
Lacerations
Description
Lacerations generally involve wounds of the skin and possibly underlying tissues.
Lacerations may occur in animals striking sharp projections in ramps, gates or laneways during loading or unloading, or when moving between yards or pens. Lacerations due to shearing cuts may be detected in sheep shorn just prior to loading.
If lameness is present it is especially concerning, because more serious underlying damage to leg muscles, tendons, joints and ligaments carries a poor prognosis, particularly if flexor tendons and penetration of joints are involved.
Laceration and bruising may result in damage to local blood supply and further necrosis and sloughing of tissue.
Clinical Signs and Diagnosis
Diagnosis is based on clinical examination.
Treatment
Apply a pressure bandage if there is severe haemorrhage.
Relocate the affected animal to a hospital pen and provide a deep layer of dry absorbent sawdust to prevent decubitus ulcers should the animal spend a lot of time lying down during recovery.
The principles of treatment are to apply lavage, debridement and where appropriate, suturing and bandaging.
Manage grossly contaminated wounds as open (unsutured) wounds using lavage, debridement, and bandaging where appropriate.
An inexpensive, easily applied waterproof outer conforming bandage suitable for shipboard conditions can be made using rolls of plastic clingwrap, foam rubber and electrical or duct tape.
Apply topical antibiotic ointments or powders to help control surface infection, parenteral antibiotics (procaine penicillin, oxytetracycline, ceftiofur, erythromycin, or tylosin) to control deep infection, and non-steroidal anti-inflammatory drugs (flunixin meglumine, ketoprofen, meloxicam, or tolfenamic acid) to control pain and swelling.
Encourage affected animals to stand as much as possible.
Prevention
Use low stress animal handling methods to minimise the speed at which animals might hit sharp projections when being moved.
Identify and remove hazards from ramps, gateways and laneways before moving animals through them.
Lameness
Description
Lameness refers to changes in posture, stance or gait to relieve pain in the limbs or trunk. It must be differentiated from ataxia resulting from peripheral or central nervous system disease or muscular weakness from systemic conditions.
Lameness can be difficult to detect in crowded pen conditions. It is easier to diagnose when there are swellings, abrasions and non-weight bearing in single limbs. Floor design and management of pens greatly influence the number and severity of lameness cases.
Early detection and management of lameness is important. Any condition may become life threatening if it worsens to the point where an animal can no longer move effectively or becomes a downer. Most lameness in export cattle involves the foot (especially the lateral claws of the hind limbs) because they are subjected to the most wear from twisting and turning.
Clinical Signs and Diagnosis
Lame cattle can be identified by swollen and/or non-weight-bearing limbs, reluctance to move or prolonged recumbency. One or more feet and legs may be affected. Systemic signs occur when pain is severe or access to feed and water is affected. Inspect the limbs of recumbent cattle carefully because animals may spend more time lying down if they are lame, and particularly if multiple limbs are affected. Decubital ulcers and a tail with a depleted brush may indicate the animal has been down for prolonged periods.
The most likely causes of lameness in export cattle and other ruminants include:
Solar abscesses, bruised soles and decubitus ulcers from excessive wear on abrasive flooring
Traumatic injuries, from slipping, trampling or being mounted.
Footrot, when conditions underfoot are constantly wet and damaging to interdigital skin
Infectious arthritis caused by organisms such as Mycoplasma bovis, Histophilus somni and Chlamydiosis – joint swelling and lameness are part of the disease complex caused by these pathogens.
Other conditions such as scabby mouth (orf virus) and selenium deficiency may be unlikely causes of lameness in sheep and goats.
Treatment
Relocate the affected animal to a hospital pen and provide bedding and uninhibited trough access. Administer non-steroidal anti-inflammatory drugs (flunixin meglumine, ketoprofen, meloxicam, or tolfenamic acid) and antibiotics if appropriate (procaine penicillin, oxytetracycline, erythromycin, ceftiofur, trimethoprim sulpha, or tylosin).
Prevention
Lameness can often be prevented by quiet handling of livestock and matching pen mates on sex and size. Check flooring for hazards such as broken anti-slip mesh or holes, and abrasiveness. Avoid forced walking for long distances on abrasive surfaces. Design laneways in yards and on ships with minimal cornering.