Laminitis
Description
Laminitis refers to inflammation and failure of the soft tissues that suspend the distal foot bone from the inner hoof wall. It may occur in individuals after any toxic infectious condition such as pneumonia or metritis, or after ruminal acidosis.
In the livestock export process, it is most likely ruminal acidosis that will cause multiple animals to be affected. Laminitis may become chronic if a single bout is severe or if overfeeding of high-energy diets is continued.
Clinical Signs and Diagnosis
Acute laminitis begins with sudden onset of tenderness of one or more feet. In mild cases only the forefeet are affected. Usually, all four feet become hot and painful, especially the coronets. There will be reluctance to walk or stand, shifting of weight and walking on knees.
The differential diagnosis is footrot, which will have an established interdigital infection with under-running and a characteristic smell. Note that other problems like liver abscess and fungal rumenitis are also associated with ruminal acidosis.
Treatment
Place acute cases on soft flooring, an energy-restricted diet, and keep moving but not excessively.
Pain relief using non-steroidal anti-inflammatory drugs (flunixin meglumine, or ketoprofen) can be provided to severely lame animals to prevent permanent recumbency. Careful paring of overgrown horn may also help relieve pain.
Prevention
Preventing ruminal acidosis is the key to preventing laminitis.
Lice
Description
Lice are common parasites of sheep and less commonly of goats. Lice are usually host-specific meaning that different species of lice are found on sheep, goats, and cattle. Lice cause skin irritation and severely affected animals may exacerbate this by scratching and rubbing, further damaging skin and fleece. Transmission in a flock occurs when animals rub against each other.
Lice are very sensitive to heat, sunlight and humidity. Shearing and exposure to direct sunlight on short fleeces tend to discourage lice burdens, and lice are unlikely to be a problem in the export process unless the animal is otherwise debilitated. On goats, however, the louse population can increase explosively in stressed animals.
Clinical Signs and Diagnosis
Lice are small active insects that can be difficult to see in hair or fleece. Adult lice on sheep and goats are less than 2 mm in length with a red-brown head and cream coloured body. Lice may be seen under conditions of good lighting by quickly parting the hair or wool in or adjacent to irritated areas. They may be found anywhere on the body in heavy infestations, but may be localised to the head, neck, underbelly or ankles, depending on species, coat length and intensity of sunlight.
Grass seeds penetrating the skin is the main differential diagnosis when a number of animals in a mob are scratching and biting at themselves.
Treatment
There are a range of pour-on backline preparations available to control lice. Shearing and exposure to sunlight will dramatically reduce lice populations.
Prevention
Infested animals pose a risk of spread at assembly points. This is less common if animals are shorn, exposed to sunlight, and have been treated for lice on farm. Unnecessary chemical treatments during pre-export preparation should be avoided to prevent residues.
Lupinosis
Description
Lupinosis refers to the liver disease caused by ingestion of a fungal toxin (phomopsin) on stubble of lupin crops. The toxin is produced in increasing amounts on the stem after the plant dies over summer, especially after rain, dew or high humidity.
Animals most at risk are hungry sheep or goats, heavily stocked on lupin stubbles, with little else to eat. All lupin stubbles are dangerous. Animals intended for export could have recently grazed high risk stubbles and may develop clinical signs in the assembly point over ensuing weeks. The stresses of transport and handling in assembly points may exacerbate expression of disease and large numbers may die.
Clinical Signs and Diagnosis
Signs include depression, anorexia, jaundice, collapse and death in a large proportion of mobs. Survivors may have chronic illthrift and are susceptible to photosensitisation and chronic copper poisoning.
Necropsy findings in acute cases include jaundice, swollen yellow to orange livers, ascites and oedema of the mesenteries and gut wall. In chronic cases there are misshapen, hard, small livers.
Laboratory confirmation requires sections of liver and kidney in buffered formalin for histology.
Differential diagnoses include pyrrolizidine alkaloid poisoning from plants such as heliotrope and Paterson’s Curse, or copper poisoning.
Treatment
There is no effective treatment. Nurse mildly affected animals. Provide shade and hay. Ensure animals do not have access to other compounds that may be a problem if liver function is compromised, such as copper. Severely affected animals should be humanely euthanised.
Prevention
Avoid sourcing sheep or goats that have grazed lupin stubbles, especially after rain, dew or humid weather.
Malnutrition
Description
Malnutrition occurs when the diet fails to provide adequate energy and protein to meet needs for growth and maintenance of body weight. It predisposes animals to other conditions such as plant poisonings in drought and pregnancy toxaemia.
In some cases the diet may be adequate and other conditions may reduce appetite, interfere with normal digestion and absorption (parasitism), or increase metabolic rate and feed requirements (inflammation). Diets may also be deficient or unbalanced in particular elements such as energy, protein, minerals, or vitamins.
Clinical Signs and Diagnosis
Growth or weight gain may be diminished, especially in young animals. Inappetence, weight loss, pale mucous membranes (indicating anaemia), and bottle jaw (due to fluid accumulation under the skin) may be observed.
Diagnosis is generally by clinical examination and necropsy of affected animals to determine if underlying disease is present. Generally, fat depots will be reduced and wet or absent (serous atrophy), tissues will be pale (anaemia) and free fluid will be present in the abdomen (ascites), chest and heart sac (pericardium).
Differential diagnoses include parasitism, infectious diseases such as pneumonia and Johne’s disease, chronic conditions causing organ dysfunction such as pyrrolizidine alkaloidosis and arthritis, and deficiencies of copper, selenium or cobalt.
A full range of fresh and formalin fixed tissues plus faeces, serum and plasma may be needed for laboratory differentiation.
Treatment
Review the composition of the diet and the animal’s ability to access sufficient feed. Make any necessary corrections. Treatment of chronic conditions is unlikely to be economically justified.
Prevention
Prevention of malnutrition requires provision of adequate dietary energy and protein and resolving any underlying health problems.
Mastitis
Description
Mastitis is inflammation of the mammary gland (udder) often associated with bacterial or fungal infection.
Lactating and heavily pregnant cattle are usually excluded from the export process. However, sometimes on long haul voyages, non-pregnant and early pregnant cattle will develop swollen udders and some of these will commence lactation, evident by dripping or spraying milk. The condition has been termed premature lactation or spontaneous lactation. Some of these will develop mastitis.
Clinical Signs and Diagnosis
Affected animals will generally show heat, swelling, redness and pain in one or more quarters, with associated asymmetry of the udder. If milk can be stripped from the affected quarter, the presence of clots further confirms the presence of mastitis. Mild inflammatory disease may not be detected clinically.
More severe cases of mastitis may be associated with lameness or changes in gait, and systemic signs such as fever, inappetence, and depression.
Laboratory identification of pathogens, including sensitivity testing to antibiotics, requires 20 mL of milk collected aseptically into a sterile container prior to antibiotic treatment. The samples should be frozen if there is likely to be any delay before processing, or chilled if they are processed quickly.
Prepartum udder oedema may be mistaken for mastitis. Oedema occurs in the third trimester of pregnancy and presents as symmetrical swelling over the mammary gland and extending anteriorly along the ventral abdomen. The swelling is not hot or painful and will pit if a finger is pushed into it.
Treatment
Mastitis in prepartum heifers is difficult to treat and the prognosis for later milk production may be adversely affected. Parenteral antibiotics (florfenicol, oxytetracycline, erythromycin, trimethoprim sulpha, or tylosin) may be administered.
The use of commercial intramammary preparations is a last resort. At sea, there may be difficulty in restraining animals sufficiently to insert intramammary antibiotics aseptically. In prepartum heifers, the teats and teat canals are often underdeveloped adding to the difficulty of inserting intramammary antibiotics. Non-steroidal anti-inflammatory drugs (flunixin meglumine, ketoprofen, meloxicam, or tolfenamic acid) may assist to reduce pain, swelling and toxaemia in serious cases.
Stripping out of mastitic milk may be beneficial if time and facilities are available. Normal quarters should not be stripped. Animals with systemic disease associated with mastitis may require intensive therapies to combat septicaemia (intravenous fluids, antibiotics and anti-inflammatories).
Prevention
To prevent mastitis in the export process, measures must be directed at preventing premature lactation and providing a relatively clean dry environment should lactation occur.
The risk of premature lactation may be reduced by increasing the roughage component of the diet (more hay and fewer pellets), and by careful selection of animals (non-pregnant animals instead of pregnant; Friesians may have lower risk than Jerseys).
A relatively clean dry environment is created by having ample sawdust, conservative stocking rates, and well managed watering and drainage systems on cattle decks.
The application of long acting teat dip preparations to individual animals pre- embarkation, or spraying iodine-based teat dips on swollen udders during the voyage (using a backpack pressure sprayer and wand) is probably not practical or effective.
The administration of non-antibiotic paraffin-based teat-sealants has been tried. These are introduced into the teat canal and cistern to provide a physical barrier to entry of pathogens during the period of non-lactation. However, application may be associated with slow processing times in facilities at assembly points, difficulty in achieving adequate disinfection of the teat end in those facilities, and lack of patency or sufficient size of teat canals in some heifers to allow administration. In addition, if lactation does commence, the sealant is removed and the animal is then susceptible to entry of pathogens and development of mastitis.
Because subclinical infections may have established in cattle developing swollen udders or premature lactation during a voyage, farm managers at destinations receiving these cattle may need training in detection and treatment of mastitis at calving.
Meningitis
Description
Meningitis is inflammation of the membranes encapsulating the brain. In feedlot cattle in Australia, meningitis may occur following upper respiratory bacterial infection.
The bacterium most commonly involved is Histophilus somni. It can cause an acute, often fatal, septicaemic disease involving the respiratory, cardiovascular, musculoskeletal, or nervous systems, either singly or in combination. Affected cattle are usually found dead but may display premonitory nervous signs from thrombotic meningoencephalitis associated with septicaemic episodes.
Occasionally Mannheimia haemolytica and Pasteurella multocida, which usually cause a fibrinous pneumonia, may produce a localised fibrinopurulent leptomeningitis.
Listeria monocytogenes may proliferate under favourable conditions in spoiled silage or hay and then cause a pyogranulomatous meningoencephalitis in animals consuming the contaminated feed.
Clinical Signs and Diagnosis
Animals with meningitis will show signs of central nervous system disease that may vary depending on the location, extent and severity of damage. Signs may include head tilt, circling, ataxia, hyperaesthesia, neck rigidity, blindness, seizures, coma and death.
At necropsy, examination of the meninges on the ventral brain may detect a diffuse infiltration of pus and congestion of blood vessels. The cerebrospinal fluid may be cloudy.
Specimens for the laboratory should include swabs of cerebrospinal fluid and meninges for bacteriology, and formalin-fixed brain for histology.
Differential diagnoses include lead poisoning and polioencephalomalacia.
Treatment
Treatment of animals with signs of meningitis or encephalitis is often unrewarding and affected animals have a high risk of dying.
Treatments may include high doses of antibiotics (ceftiofur sodium, penicillin, florfenicol, oxytetracycline, erythromycin, or tylosin), and non-steroidal anti-inflammatory drugs (flunixin meglumine, ketoprofen, meloxicam, or tolfenamic acid).
Prevention
Prevention largely depends on reducing stress, preventing respiratory disease and providing unspoiled feed.
Metritis
Description
This is inflammation extending deep into the uterine wall, usually from infection of the uterus after calving, abortion, or as a complication of retained foetal membranes.
Only cattle up to 6 months pregnant are usually exported, hence metritis is more likely associated with abortion than calving in the export process.
Retention of foetal membranes after abortion (and calving) may increase the risk of metritis. In some cattle, metritis may develop into a systemic infection or septicaemia which can be rapidly fatal if untreated.
Clinical Signs and Diagnosis
Metritis is often associated with straining and a foul smelling brown watery discharge from the vulva. A recent history of calving (particularly dystocia with assisted delivery), abortion, or retained foetal membranes should identify animals at risk of metritis.
Differential diagnoses include dystocia with a dead calf, retained foetal membranes, and possibly salmonellosis and coccidiosis if there is straining and blood on the tail.
Treatment
Systemic antibiotics (procaine penicillin, oxytetracycline, trimethoprim sulpha, erythromycin, tylosin, or tilmicosin) should be administered as soon as metritis is suspected, to minimise the risk of septicaemia or toxaemia. Use of intra-uterine treatments, such as pessaries, is not recommended as they are likely to be ineffective.
Non-steroidal anti-inflammatory drugs (flunixin meglumine, ketoprofen, meloxicam, or tolfenamic acid) are recommended if the animal is continually straining or is not eating.
Prevention
Careful selection to avoid heavily pregnant animals that may be at risk of parturition and subsequent metritis during the export process. If vaginal intervention is required for assistance with aborting or calving animals, or in animals with retained foetal membranes, pay attention to hygiene, avoid manual extraction of retained foetal membranes, and observe animals closely for any signs of metritis.
Middle Ear Abscess
Description
An abscess in the middle ear occurs as a complication of ear mite infection or barley grass seeds. Usually only a single ear in a single animal is affected, but there may be multiple cases in sheep grazed on barley grass in summer. Signs are related to damage to the facial nerve as it passes through the middle ear.
Clinical Signs and Diagnosis
There will be a head tilt and a drooping upper eyelid, and if inflammation extends internally it results in circling and incoordination. Very rarely the infection extends to become a brainstem abscess, resulting in death.
Progression to death is not rapid like in listeriosis and an otoscopic examination may reveal pus from the abscess deep in the ear canal.
Treatment
Antibiotic (procaine penicillin, or oxytetracycline) and anti-inflammatory (flunixin meglumine, or ketoprofen) treatment may delay or stop progression of signs. However, resolution of head tilt and other nervous signs is usually not possible.
Prevention
The usually sporadic occurrence of this condition does not warrant specific preventative measures.
Monensin Poisoning
Description
Ionophore antibiotics such as monensin and lasalocid are commonly used feed additives for controlling coccidiosis, bloat and improving efficiency of weight gain in cattle. They are sometimes incorporated into pellets fed on ships.
Toxicity may result from mixing errors and consequent inadvertent over exposure of animals to these compounds. Affected animals suffer muscle damage leading to acute heart failure and possibly skeletal muscle effects (paresis and paralysis). Deaths in cattle can be expected to commence at intakes of 10 mg/kg bodyweight.
Clinical Signs and Diagnosis
There is usually sudden onset of feed refusal, recumbency, tachypnoea (fast breathing), ruminal atony, diarrhoea and brown urine. In the subsequent days to weeks, there may be development of illthrift and signs of congestive heart failure including submandibular and brisket oedema, and distended and pulsating jugular veins.
Necropsies performed on animals dying acutely may not reveal any gross lesions. In longer surviving animals there may be pallor of the myocardium, especially of the left ventricle reflecting areas of myocardial necrosis. There may also be signs related to congestive heart failure: pulmonary oedema, hydrothorax, ascites and hepatomegaly (enlarged liver).
Laboratory confirmation is based on specimens of myocardium and skeletal muscle submitted in buffered formalin for histology, and identification of toxic concentrations of an ionophore in samples of feed.
Treatment
No antidote or specific drug treatment is available. Nursing care and careful handling is required. Survivors should be marked for salvage slaughter once residue periods have passed. In an outbreak, decisive measures to replace, reduce or dilute toxic feed are required.
Prevention
Prevention relies on preventing mixing errors in formulated rations.
Nasal Bots
Description
The sheep nasal bot fly deposits larvae in the nostrils of its host. Once deposited, the larvae will grow and can move within the nasal cavity and frontal sinuses causing irritation, resulting in sneezing and mucopurulent discharge from the nostrils. They can lead to debilitating secondary bacterial infections. Animals may attempt to avoid flies by running with their head down and nosing into corners. Infection is very common in Australian sheep and goats. Fly activity typically peaks around spring and late summer with warmer weather. However, this varies between regions.
Clinical Signs and Diagnosis
Infected sheep may not show any obvious clinical signs. Some sheep may be seen sneezing, snorting, coughing and congregating in shade where flies are less active.
Wandering maggot-like larvae up to 20 mm long may be an incidental finding at necropsy when the nasopharynx is exposed during longitudinal craniotomy for brain examination.
Treatment
Anthelmintics are highly effective at killing larvae.
Prevention
Prevention is usually achieved incidentally with helminth control programs using macrocyclic lactones.
Nasal Discharge
Description
Nasal discharge is an excess of fluid material from the nasal cavity originating from either the respiratory or gastrointestinal tracts. Nasal discharge can be the result of the accumulation of normal respiratory secretions. However, excessive or abnormal discharge is usually an indication of upper respiratory tract disease.
Sheep breeds with convex facial profiles such as Suffolk and Border Leicester are reputedly more susceptible.
Clinical Signs and Diagnosis
Nasal discharge is detected during pen inspection. Discharges may be serous (thin, clear and colourless), catarrhal (grey, flocculent), purulent (thick, yellow), or haemorrhagic (red). A discharge may change in colour and consistency over time depending on the progression of underlying disease. Colour, consistency and content will often reveal the source. Presence of food or stomach content indicates obstruction of the oesophagus or gastrointestinal tract, respectively. This is generally accompanied by distress and severe systemic signs. Unilateral discharge indicates localised conditions involving the nose or sinuses, whereas bilateral discharge may indicate thoracic or systemic conditions.
The most likely differential diagnoses in shipboard cattle with nasal discharge include:
Infectious bovine rhinotracheitis (IBR).
Other respiratory pathogens (see Pneumonia).
Dusty feed causing irritation of nasal mucosa or respiratory irritants such as ammonia. Ocular discharge, sneezing and coughing may be seen but animals will be bright, alert, appetant, afebrile and the nasal discharge may be heavily discoloured by dust. Examination of the feed will assist diagnosis.
Systemic illness (sick cattle). Sick cattle tend to accumulate nasal secretions in the nares because they stop normal grooming behaviour, where the tongue is used to groom the nose. Abnormal nasal secretions may therefore be a generic sign of any underlying systemic disease.
Oesophageal or gastrointestinal obstruction may cause reflux to appear at the nares.
In sheep and goats, common causes of discharge in multiple animals include nasal bots, dusty feed, ammonia vapour, fly worry, and upper respiratory tract infections due to viruses or bacteria. Fly worry will occur on land, and other causes may occur at all stages of the export process. When single animals are affected, differential diagnoses may include tumours, foreign bodies, and facial trauma distorting the nasal passages.
Differentiation may be assisted by the presence of other signs, such as sneezing, coughing, eye discharge, attempts to hide the face, and whether the discharge is unilateral or bilateral. Unilateral discharge usually indicates local involvement of one nasal passage. Bilateral discharge may indicate systemic disease affecting the upper respiratory tract. Close examination for the presence of mucus, pus, blood or foreign material may offer clues.
Treatment
Choice of treatment is dictated by the diagnosis. Many animals with a nasal discharge will not require treatment. However, if nasal discharge is marked or it is associated with other clinical signs of infectious respiratory disease, the administration of parenteral antibiotics (ceftiofur sodium, florfenicol, tilmicosin, tulathromycin, procaine penicillin, oxytetracycline, erythromycin, or tylosin) is warranted.
With dusty feed, the problem may be related to a batch of feed, which when changed, resolves the problem.
With reduced grooming of the nose, feeding chaff or hay may stimulate appetite and rumen function. The animal will then start licking its nose. Treatment with glucocorticosteroids or other injectables purported to stimulate appetite are not recommended.
Prevention
Prevention relies on careful screening during selection and on controlling flies, dust and ventilation during the export process.
Vaccination of cattle against infectious bovine rhinotracheitis (IBR) and Mannheimia haemolytica have been reported to reduce risk of infectious respiratory disease in export consignments.
Dampening of dusty feed can be helpful. However, this may lead to mouldiness and palatability problems. Other preventative measures are determined by hazards and risk factors specific to the consignment.
Nervous Disease
Description
Disease processes affecting the nervous system may be infectious or inflammatory, toxic, metabolic, traumatic or vascular. There are others such as degenerative, genetic, and neoplastic conditions, but these will be extremely rare. Specific viruses and bacteria cause infectious conditions. Insecticides, fungicides and rodenticides cause toxicities. Hypoglycaemia, hypoxia, hepatic dysfunction, hypocalcaemia and hypomagnesaemia cause metabolic nervous diseases. Haemorrhage, oedema and direct physical damage to the central nervous system cause a range of focal or multifocal neurological deficits. Septicaemia and bacterial embolisation cause vascular lesions in the central nervous system. With inflammatory, metabolic and toxic processes, there will be evidence of disease in other body systems. With traumatic and toxic exposures, there may be obvious external signs or clues. Toxic and metabolic processes are unlikely to produce asymmetric deficits.
Diseases of the nervous system generally result in changes in posture and gait or mental state, depending on the location and extent of the pathology.
Clinical Signs and Diagnosis
Affected animals may display one or a combination of signs that include abnormal limb movement, swaying or staggering, head tilt, circling, recumbency, blindness, rapid lateral eye movements, convulsions, and coma.
Differential diagnoses in the live export process include:
Metabolic conditions (pregnancy toxaemia, hypocalcaemia or hypomagnesaemia).
Meningitis as an extension of bacterial pneumonia, i.e. thrombotic meningoencephalitis.
Listeriosis.
Hepatic encephalopathy.
Nervous ketosis.
Annual ryegrass toxicity.
Tick fever, especially Babesia bovis.
Trauma.
Grain poisoning.
Poisoning with lubricants, fumigants, exhaust gases or lead.
Polioencephalomalacia from dietary changes.
Salt poisoning (water intoxication).
Differentiation is by examination of history, clinical and necropsy findings.
Listeriosis and middle ear infection both cause circling and are likely to be recognised at assembly. Listeriosis is most commonly seen as outbreaks associated with feeding spoiled silage in cold weather. Middle ear infections are sporadic and can happen anytime and anywhere.
Annual rye grass toxicity (ARGT), hepatic encephalopathy, salt poisoning, and polioencephalomalacia (PEM) are convulsive diseases. Diseases such as pregnancy toxaemia and hypocalcaemia may terminate in convulsions or coma. Traumatic injuries should also be considered.
Complete necropsy of affected animals will help to rule out some causes. Laboratory samples likely to be of value include serum for biochemistry, brain in buffered formalin for histology, blood smears, spleen for haematology and rumen content for toxicology.
Treatment
Choice of treatment is dictated by the diagnosis.
Prevention
Careful screening for early stage disease during selection can prevent many of the nervous diseases from becoming a problem in the export process.
Specific preventative measures will depend on the disease(s) involved.
Nitrate – Nitrite Poisoning
Description
In the export process, nitrate-nitrite poisoning may occur in assembly points when hungry cattle gorge on hay containing high concentrations of nitrate. In ruminants it is the nitrite which is toxic. Rumen microbes convert nitrate to nitrite.
If absorbed into the blood stream in sufficiently high amounts, nitrite can reduce the oxygen carrying capacity of blood by altering haemoglobin, causing hypoxia and death.
Dangerous concentrations of nitrate may be present in hay made from pasture or crop fertilised heavily with nitrogen. High levels may also occur in hay made from plants wilting from water, cold or heat stress or herbicide poisoning at time of cutting, or improperly cured at the time of baling. Mouldy hay may have high levels of preformed nitrite which can be absorbed directly into the blood stream after ingestion and cause respiratory distress and death.
Clinical Signs and Diagnosis
Signs appear 6 to 24 hrs after toxic feed has been consumed. There will be weakness, ataxia, respiratory distress, and brown cyanotic mucous membranes. This is typically followed by collapse and death due to asphyxial convulsions. At necropsy the blood is initially a dark chocolate brown colour but fades rapidly to near normal colour a few hours after death.
In the field, on fresh cases, urine test strips are adequate to test body fluids for nitrite. Laboratory confirmation requires serum or aqueous humour submitted chilled for toxicology. Test strips are available for field and laboratory testing for nitrate in plant samples. Plant samples submitted to the laboratory must be fresh and chilled. They must be frozen if there will be delays in reaching the laboratory.
The main differential diagnosis is cyanide poisoning, which can be differentiated by the cherry-coloured blood at necropsy and history of feeding sorghum hay.
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.
Prevention
Avoid feeds that may be high in nitrates. Seek advice on feed selection and management. Consider submitting feed samples for nitrate testing if concerned.
Nutritional Myopathy
Description
This is a degeneration of skeletal and heart muscle as a result of selenium or vitamin E deficiency. Selenium and vitamin E prevent cell damage by oxidants produced during tissue metabolism, but have different sites of action.
It is usually a disease of very young animals, but can occasionally affect older animals. Myopathy associated with selenium deficiency usually occurs in young animals grazing lush spring pastures, in higher rainfall on lighter, acidic soils.
Affected animals may show signs on entry to assembly points. Myopathy associated with vitamin E deficiency occurs in young animals fed dry feed, hay or grain over extended periods, which may occur in the livestock export process.
Clinical Signs and Diagnosis
The disease is triggered by sudden exercise such as moving, yarding or transporting. Continued physical exertion is likely to worsen the condition.
Animals develop a stiff gait or die suddenly from heart failure. Others go down but remain bright and alert and are reluctant to stand. If they stand they have a hunched back and are reluctant to move. Urine is brown from myoglobin.
At necropsy, there are areas of muscle that are diffuse, pale, and dry, and others that contain well defined chalky white streaks or patches. These can be found in the heart and tongue, and are distributed symmetrically in muscles of the shoulder, back and thighs. The myopathies from selenium and vitamin E deficiencies cannot be differentiated, except by investigation of dietary history.
Specimens required for laboratory confirmation include heparinised blood (10 mL) submitted chilled (not frozen) for glutathione peroxidase (GSHPx) activity, from at least 5 animals in the group; at least 2 mL of serum submitted frozen for serum enzymology and vitamin E analysis; and sections of affected and unaffected skeletal muscle and cardiac muscle, in buffered formalin for histology.
Differential diagnoses include enterotoxaemia when there is sudden death, and arthritis when there is stiffness.
Treatment
Injections, oral drenches and rumen boluses containing vitamin E and/or selenium are available for treatment. The prognosis is good for mildly affected animals.
Selenium deficiency should be confirmed and care must be taken when treating so as not to overdose animals with selenium as the threshold for toxicity is low.
Prevention
Anthelmintic drenches, rumen boluses and vaccines containing selenium are available. However, the concentration of selenium in a vaccine may not be high enough to prevent disease in some areas. A small amount of green pick, even weeds, will avert vitamin E deficiency.
Oesophageal Obstruction
Description
Oesophageal obstruction may occur from feed impaction or following ingestion of a suitably sized object such as a fruit or vegetable. Predisposing factors may include low feed quality or quantity causing hungry cattle to bolt down feed, or problems with chewing as a result of injury or infection of the animal’s teeth or tongue.
Clinical Signs and Diagnosis
Bloat, profuse salivation and nasal discharge may be observed.
Treatment
Treatment options include sedation with acepromazine or xylazine to relax the oesophagus. Gentle passage of a stomach tube with or without administration of fluid may help to move the obstruction into the rumen.
An obstructing mass can sometimes be quickly and easily removed from the proximal oesophagus by an experienced operator reaching down the throat. Alternatively, an obstruction in the cervical oesophagus may be massaged up into the pharynx by pressing the fingers into each side of the ventral neck behind the mass. When at the pharynx, keep the fingers pressed into the oesophagus until the animal ejects the mass. If the mass is in the lower cervical or thoracic oesophagus, a carefully manipulated loop of 8-gauge fencing wire passed down the oesophagus by an experienced operator may allow the mass to be moved towards the pharynx.
Prevention
Spoiled feedstuffs from the galley such as turnips, potatoes and apples should not be fed to cattle or disposed of in a location accessible to the herd.
Animals recovering from teeth or tongue problems should be closely monitored.
Overgrown Hooves
Description
These are the result of inadequate or uneven wearing of the horn of the hoof. Any disease causing lameness may result in deformity or uneven weight bearing, or it can occur simply from constantly being on soft ground.
Clinical Signs and Diagnosis
The hoof is misshapen by overgrowth of horn of the wall and toe. Lameness may be present which may be a cause or a consequence of overgrowth.
Treatment
Re-establish the normal shape of the hoof by paring with secateurs to remove excess horn. Cases that are detected on board export ships should be kept on increased bedding with uninhibited trough access.
Prevention
Correct any underlying lameness problem. Running animals on abrasive surfaces such as concrete yards and bitumen roads from time to time may assist prevention.
Photosensitisation
Description
Photosensitisation is the clinical condition in which skin is damaged by photodynamic agents of dietary origin that react to sunlight.
Phylloerythrin is the most important of the light-sensitive pigments causing skin disease in grazing ruminants in Australia, but there are other agents that may also cause the same disease. Phylloerythrin is produced by fermentation of chlorophyll (that is present in all green plants) in the rumen. Phylloerythrin is absorbed and carried in blood and normally excreted in bile by the liver. Sunlight penetrating unprotected skin can cause fluorescence of pigment within superficial blood vessels and result in damage to tissues of the skin including the small blood vessels.
Phylloerythrin may be retained in the circulation by simple overload of the excretory capacity of the liver when young sheep and goats are exposed to succulent, immature forage such as early growth lucerne, perennial rye grass, clover or canola (rape). Outbreaks also occur secondary to liver damage from some other cause that impedes the excretion of even normal levels of the pigment.
Acute clinical cases of photosensitisation at assembly points would be unusual and dependant on exposure of animals in the period prior to assembly, but significant residual lesions on the skin can affect large numbers of animals. The highest risk is generally in late winter and spring when pastures are rapidly growing and there may be less cloud cover.
Clinical Signs and Diagnosis
Affected areas of skin become itchy, blisters develop, and scabs form. Non-pigmented skin areas and those with minimal wool covering are most likely to be affected, such as face, ears, and feet. Affected skin may become necrotic and ulcerate, and covering fleece may be ragged and lost along the back. Animals with short wool, especially with open fleeces, may be affected along the dorsal midline. Face and ears are swollen, ears droop, tears are excessive, and a bright band of redness is present on the coronet. Head shaking and shifting lameness may occur if the skin of the face and legs is involved.
Affected cattle may show skin damage along the back and on the sides of the udder, depending on where non-pigmented skin is located.
Clinical signs are usually adequate for diagnosis but must be differentiated from sunburn. Jaundice, if present, indicates liver disease.
Treatment
Protect from direct sunlight. Deny access to green feed. Secondary skin infections may require antibiotics. Prevent flystrike.
Prevention
Screen out animals with skin lesions during selection. Avoid grazing animals on hepatotoxic and phototoxic plants that may have emerged in holding paddocks at assembly points.
Pinkeye
Description
Pinkeye in sheep and goats is an infection of the eye caused by bacteria (Mycoplasma conjunctivae, Chlamydia organisms, and other Mycoplasma sp.), targeting the conjunctiva and cornea. In cattle, pinkeye is mainly caused by Moraxella bovis, but may be associated with other bacteria including Mycoplasma and Neisseria. Note that the bacteria primarily responsible for pinkeye in cattle (Moraxella bovis), has no role in pinkeye in sheep and goats.
Pinkeye generally requires a combination of causative bacteria in the eye and some form of irritation or trauma to the corneal epithelium from things such as dust, dryness or ultraviolet light.
The condition is contagious and can spread rapidly in susceptible groups of animals. Alternatively, it may present in individual animals in groups where most animals are immune.
The condition is painful and weight gains can be negatively affected. Animals left with corneal scars or blindness may have reduced sale value and suitability for purpose. Most cases, whether treated or not, recover within 4 to 6 weeks (cattle) or 2 weeks (sheep and goats). Recovered animals may have small white areas of residual scarring on the cornea. Occasionally the scarring is extensive, seriously reducing vision. Rarely the cornea ruptures and the eye collapses, causing permanent blindness.
British and European cattle breeds are affected more severely than tropically adapted cattle breeds. Goats are mildly affected compared to sheep.
Predisposing factors include:
Crowding allowing close contact and transmission of infection.
Hot, dry, dusty conditions and presence of flies.
Access to feedstuffs containing material that readily enters the eye such as grass seeds, chaff, fibrous stems or stalks, and fodder fines from disintegrating pellets at sea.
Stressors such as excessive handling, undernutrition, crowding, and climatic changes that reduce resistance.
In any export consignment, multiple animals are usually affected and pink eye may be cause for rejection of badly affected individuals. Most infections occur early in the export process. They are often acquired at the assembly point and are expressed in greatest numbers in the first week or two at sea. If infections are not severe, most will have healed by the end of a three week voyage. Animals still affected at destination, may have reduced vision and be difficult to move.
Clinical Signs and Diagnosis
One or both eyes can be affected. Signs include bloodshot eyes (hyperaemia), eye discharge staining the face, and closed eyelids.
The cornea may be red initially and then go through cloudy hues of red, blue, grey, and white during sequential stages of healing. Animals with unilateral lesions may be missed at pen inspection since they are likely to stand so their good eye is facing the observer.
Differential diagnoses include foreign body in the eye, salt water in the eye from high pressure hosing, and infectious bovine rhinotracheitis (IBR) in cattle. IBR can cause a severe conjunctivitis and oedema of the cornea at the corneoscleral junction, but corneal ulceration is absent. Trauma to the eye from ear tags of pen mates during trough feeding has been suspected to cause occasional eye problems at sea. Some cases of malignant catarrhal fever and ocular squamous cell carcinoma may be mistaken for pinkeye in cattle.
It is important to examine multiple affected animals to check for the presence of grass seeds or other foreign material in the eye. Outbreaks of grass seeds or chaff in the eye can behave like pinkeye, even though pinkeye bacteria may not be present. Exposing foreign material requires everting the eyelids, including the third eye lid.
Treatment
Most cases of pinkeye will heal without treatment and this will typically occur over the same time period as if treatment was administered. This must be considered when there are large numbers of animals affected, where catching and restraining animals is difficult, and where handling may stress animals and may predispose to other problems or increase the spread of pinkeye infection. There is a small risk of severely affected animals suffering long term effects or even permanent loss of eyesight.
However, correct treatment applied early in the disease when there is just epiphora and tear staining below the eye, may shorten the duration of disease and prevent the development of complications including permanent blindness and corneal scarring.
If there are concerns that grass seeds, chaff or other foreign bodies may be involved, then each affected animal should be restrained and undergo close examination of the eye, especially of the conjunctival sacs. Grass seeds and other foreign bodies are easier to remove if topical anaesthetic and forceps are used.
The treatment of choice for pinkeye is a parenterally administered course of antibiotics (oxytetracycline or trimethoprim sulpha) which should be repeated as necessary if signs persist. Injectable antibiotics are probably more effective than topical treatments because they are better able to achieve sustained therapeutic levels of antibiotic in the eye. Note that Mycoplasma are often involved in pinkeye in sheep and goats. Mycoplasma do not have a cell wall and therefore antibiotics that target bacterial cell wall synthesis (beta-lactam antibiotics such as penicillin and cloxacillin), are less likely to be effective.
A single topical application of long-acting, antibiotic eye ointment is commonly used in cattle. Both eyes should be treated even if only one eye is showing signs of disease. Animals may be re-treated at 48 hour intervals. These products often contain synthetic penicillins so may not be effective against Mycoplasma infections in pinkeye in sheep and goats.
Subconjunctival injection of antibiotic and anti-inflammatory drugs may be useful for individual animals with more severe disease and where good restraint is available to ensure safe administration of the treatment.
Severe cases must be handled carefully to prevent bumping the eye and the risk of corneal rupture. They may also benefit from applying an eye patch or suturing the eyelids closed for a period to provide protection while healing occurs.
Topical treatments with sprays and powders are not beneficial and may in fact be detrimental. The use of irritant chemicals in the eyes will cause damage to the cornea and will not help to treat or prevent infection. In large outbreaks, mass medication of drinking water with antibiotics may be attempted, but effectiveness is uncertain. This practice requires the installation of header tanks to achieve correct concentrations, the intake is variable with some animals not drinking enough, and it carries the risk of disrupting rumen function and feed intake.
Separate penning of severely affected animals with easy access to food and water may be warranted.
Prevention
Management changes can help to reduce the rate of spread and also to prevent cases. Reducing exposure to grass seeds and airborne feed particles, controlling flies in the local environment, and reducing dust, are all measures that can aid in preventing and controlling pinkeye. Source batches of feed pellets that do not disintegrate easily and produce dust. Minimise stressors such as excessive handling, crowding, and undernutrition.
At sea, avoid feeding chaff and hay in windy conditions, minimise splash into eyes during high pressure hosing of decks, and spread sawdust in pens carefully to prevent it getting into eyes.
A vaccine is available for cattle, but does not cover all strains of Moraxella bovis that are involved in causing pinkeye. It should be administered 3-6 weeks before the onset of a high risk period to provide protection. There is no vaccine available for sheep and goats.
Pizzle Rot
Description
Pizzle rot is an infection and inflammation of the prepuce that may lead to urine retention and severe inflammation. It is seen mainly in wether sheep, especially if castrated at an early age. It is a less common and milder disease in rams, bucks and wether goats.
Most cases are in wethers coming from high protein pastures like clover or lucerne, or animals fed high protein pellets. The high protein intake results in concentrated urea in urine. Bacteria present in the urinary tract such as Corynebacterium renale produce an enzyme (urease), that breaks down the urea and releases ammonia. Ammonia is highly irritating to the mucous membranes lining the prepuce and the skin around the preputial opening, causing inflammation and ulceration.
Wethers are predisposed because they tend to have a short penis and often collect urine in the prepuce, resulting in continual wetting of the preputial opening and adjacent abdominal wool or hair. Other animals are predisposed if urine-soaked organic matter builds up in long hair or wool around the prepuce.
Clinical Signs and Diagnosis
Clinical signs are usually advanced when noticed. There will be swelling, ulcers, scabs, and a strong smell of ammonia at the opening of the prepuce. The first sign is a small ulcer on the skin at the tip of the pizzle. Scabs will develop over the ulcer. If scabs extend around the opening of the pizzle, the passage of urine may be obstructed and allow infection and inflammation to extend deep into the prepuce and cause swelling. This may be confused with urolithiasis.
Non-progressive disease may occur in entire males as a small ulcer at the preputial opening of the sheath.
Treatment
Remove wool around the area and clean and debride necrotic tissue. An incision along the bottom of the prepuce may be effective to drain accumulated pus and urine. This combined with a course of antibiotics (procaine penicillin, oxytetracycline, or trimethoprim sulpha) usually results in a rapid recovery.
Prevention
During pre-export preparation, attention at shearing to remove hair and wool that might matt around the prepuce, and controlling dietary protein will be effective.
Pneumonia – Embolic
Description
Embolic pneumonia is the result of a showering of septic thrombi into the pulmonary arterial system from major veins such as the caudal vena cava, mammary, uterine and jugular veins. Septic thrombi result from bacterial infections in tissues, resulting in erosion into veins and release of thrombi into the circulatory system. Erosion into the caudal vena cava of hilar liver abscesses is a well known sequel to ruminal acidosis. Animals surviving the thromboembolic showering event may later develop pulmonary arterial aneurysms, which may rupture into a bronchus causing rapid blood loss and death.
Clinical Signs and Diagnosis
Animals are usually found dead from massive embolism of the lung, or rupture of a septic embolus into a bronchus and rapid blood loss.
In some cases, affected animals are noticed ante-mortem with sudden development of a cough, respiratory distress, and bleeding from the nose and mouth. A period of illthrift, followed by these signs, may indicate that sudden death is imminent.
At necropsy, there is severe widespread discolouration, abscessation, and haemorrhage affecting the lungs. Further dissection may find an abscess at the hilus of the liver that has eroded into the vena cava, or an infection of other organs and tissues that has entered other large veins.
Treatment
There is no treatment. Cattle showing sudden deterioration in strength and demeanour that are in respiratory distress should be euthanased without delay.
Prevention
Preventing ruminal acidosis will reduce formation of liver abscesses, the most common cause of embolic pneumonia.
Pneumonia – Sheep And Goats
Description
Pneumonia refers to inflammation of the lungs. It may be accompanied by inflammation of the larger airways (bronchioles) and referred to as bronchopneumonia, or by inflammation of the pleura (outer surface of the lung, adjacent to the chest wall) and referred to as pleuropneumonia. Pneumonia in sheep and goats is often caused by infectious agents, particularly by a combination of bacteria and viruses.
In sheep and goats, the important infectious agents associated with pneumonia include:
Viruses. Parainfluenza virus type-3 (PI-3), adenovirus, respiratory syncytial virus and caprine arthritis and encephalitis (CAE) virus (goats).
Bacteria. Manehimia haemolytica, Pasteurella multocida, Haemophilus sp., Chlamydia sp., Salmonella sp., and Mycoplasma sp.
Non-infectious causes of pneumonia include parasitic (lungworms) and aspirations from incorrect drenching.
Many of the causal pathogens (viruses and bacteria including Mycoplasma) are normal residents of the upper respiratory tract in most sheep and goat flocks in Australia. The most common sequence of events leading to pneumonia is thought to be initiated by stressors lowering the resistance of the animal and allowing an initial acute virus or mycoplasma infection to commence in the upper respiratory tract or lung. This compromises local defences sufficiently to allow invasion and multiplication of secondary bacteria.
Animals more at risk of viral and bacterial pneumonia are young animals subjected to a range of stressors that are common in the export process including transportation, mixing with new animals, crowding, inadequate ventilation, dust and sudden climatic changes.
Most viral and bacterial pneumonias develop acutely and are highly contagious in susceptible flocks with the potential to cause outbreaks of disease. Survivors are often chronically affected. In goats, pneumonia caused by caprine arthritisphalitis (CAE) virus is a chronic progressive pneumonia in adults. Lungworms may be acquired when grazing pastures in temperate climates before entering the export process.
Aspiration pneumonia is caused by incorrect drenching technique and might occur as part of fulfilling a pre-export protocol in an assembly point.
Animals with pneumonia may be more susceptible to heat stress and heat stress may exacerbate clinical signs and disease progression for animals with pneumonia.
Respiratory distress will occur if normal lung function is compromised. Progressive disease may also result in endotoxaemia and septicaemia. If the surface of the lungs and lining of the chest cavity become inflamed (pleurisy) there is severe pain. Death may occur when there is sufficient lung compromised to cause anoxia (usually when more than 70 % of the lung is affected), or from overwhelming systemic infection including toxaemia.
Clinical Signs and Diagnosis
Bacterial pneumonias are often first detected when an animal has died suddenly and is necropsied. Other animals may then be noticed to have signs, including reduced appetite, depression, rapid shallow breathing, coughing and nasal discharge. Dyspnoea (laboured or difficult breathing) may follow minor exertion or rise in temperature as respiratory reserve is reduced.
Nasal and ocular discharge may result from dust, ammonia vapour or fly worry. It can, however, be a result of viral infection of the upper respiratory tract and a prelude to pneumonia.
Pneumonias that cause persistent forced coughing in young sheep and goats can sometimes contribute to prolapse of the rectum.
Most lungworm infections are inapparent. Heavy infections may result in coughing that is reduced following anthelmintic treatment. They are susceptible to most modern drenches.
Necropsy changes have been described in Pneumonia – Cattle.
With bacterial pneumonias the anteroventral lobes are most affected. With viral and Mycoplasma pneumonias, all lobes may be involved with secondary bacteria invading the anteroventral lobes.
With lungworm, the lesions are grey to green nodules scattered throughout the caudal lobes. Sometimes tangles of white threadlike worms up to 5 cm long are found in mucus in the large airways. Lungworm lesions are usually an incidental finding in an animal necropsied for another disease.
Animals that aspirate usually develop severe pneumonia, decline quickly and die within a few days of the aspiration occurring. At necropsy, the anterior of one lung is usually more affected than the other. There is consolidation, liquefaction and involvement of the pleura. The aspirated material can be difficult to recognise.
In the pneumonia of goats, associated with CAE virus, the infection becomes clinical only in older goats. At necropsy, the lungs are grey and firm. Laboratory determination of pathogens requires nasal swabs in transport media for virus detection and isolation, and acute and convalescent sera for virus serology. In dead animals, portions of affected lung should be submitted fixed in buffered formalin for histology and chilled for microbiology and virology.
Treatment
When infectious pneumonia is suspected, treat sick animals with antibiotics (oxytetracycline, trimethoprim sulpha). Broad spectrum antibiotics are more likely to be effective than narrow spectrum antibiotics such as procaine penicillin. Non-steroidal anti-inflammatory drugs (flunixin meglumine, ketoprofen, tolfenamic acid, or meloxicam) may be warranted in valuable animals. Ensure ready access to feed and water which at sea may require separation from pen mates and movement to hospital pens. Severely affected animals should be euthanised without delay.
Use anthelmintic drenches where lungworm is suspected.
Prevention
Causative organisms are often ubiquitous and prevention generally involves management to reduce stressors that may increase the likelihood of disease. Options include avoiding mixing sheep of different origins, reducing crowding, ensuring good ventilation, and providing shelter against sudden climatic changes. Early detection, isolation and aggressive treatment with broad spectrum antibiotics may reduce the extent and severity of outbreaks of bacterial pneumonia.
Careful drenching on entry to assembly points will eliminate potential for lungworm problems for the remainder of the export process.
Poisoning With Lubricants, Fumigants Or Exhaust Gases
Description
This is a rare occurrence in well designed and maintained ships. However, bad weather, maintenance works, and inexperienced crew may create situations where these poisoning accidents occur. In bad weather, rolling, pitching and flexing of the ship can cause containers to relocate and pipes to break. Feed and water in bulk storage tanks may become contaminated with chemicals that have leaked from broken drums or pipes.
Maintenance may be performed by crew inexperienced in the ways of livestock. On ships, penned animals will lick and chew anything within reach and can turn on taps and move levers that seem out of reach. Hazards include unguarded or badly located pipes and valves, and containers of potentially poisonous chemicals (sealant, corrosion inhibitors) left laying around that might slide or roll into pens. Livestock may be temporarily penned in unusual and poorly ventilated locations with access or exposure to chemicals, paint, lubricant, and gas bottle storage areas or engine exhaust systems. Carbon monoxide and carbon dioxide poisoning may occur in poorly ventilated pen areas where portable combustion engines are being used for repairs or maintenance.
Clinical Signs and Diagnosis
Multiple animals in a pen or group of pens may be affected. Clinical signs will depend on the poison. Respiratory distress may be expected with fumigants and exhaust gases. Nervous signs or diarrhoea may be expected with lubricants. Animals may simply be found dull, down, dying or dead.
At necropsy, some of the ingested poisons may be detectable in the reticulum or rumen by sight or smell.
Specimens which might be submitted to a diagnostic laboratory include 100 g of rumen content and 500 g of suspect feed material submitted chilled for toxicology, and sections of liver, kidney and other organs showing lesions in buffered formalin for histology.
Treatment
Treatment options are dictated by cause or signs. These may include immediate relocation to sick pens for monitoring and to provide improved air quality and ventilation if there is respiratory distress. Affected animals should be provided with clean water and fed with chaff or hay if there are concerns about digestive system function or reduced appetite.
Prevention
Ships should be well designed and maintained, and crews made aware of the potential for inadvertent poisoning from exposure to these hazards. Bad weather, maintenance works and inexperienced crew are predisposing factors.
Polioencephalomalacia
Description
Polioencephalomalacia (PEM) refers to the nervous disease caused by degeneration (malacia) of the brain associated with thiamine (vitamin B1) deficiency or sulphur excess.
The thiamine deficiency of PEM is suspected to be caused by proliferation of bacteria in the rumen that produce thiaminase, which in turn breaks down thiamine.
Ruminal acidosis may create favourable conditions allowing proliferation of thiaminase-producing bacteria.
High sulphur intake is suspected to cause high concentrations of hydrogen sulphide (H2S) to be formed in the rumen, which is absorbed into the body. Feeds such as lucerne, canola (rape), and high protein pastures are rich in sulphur, as are some water supplies. Accelerated intake of sulphur can occur from high water consumption in hot weather, increased appetite after fasting, or sudden onset of cold weather to which the animal cannot adapt.
PEM is usually sporadic but can occur as an outbreak. Animals of any age can be affected, but it occurs more in young animals. The conditions of thiamine deficiency or sulphur excess described above can potentially occur at any stage of the export process.
Clinical Signs and Diagnosis
Ear twitching, incoordination, and hypersensitivity to any stimulus are the earliest detectable signs. Cases are often dull, apparently blind, and they may head press against fixed objects or stand with the head pulled back (star gazing). Sometimes they are found convulsing, comatose or dead.
Injections of large doses of thiamine (vitamin B1) at this stage may be diagnostic if they cause rapid recovery (within hours). If untreated they will become recumbent with retraction of head, arching of back, rapid eye movement, dog-sitting, convulsions and death.
Differential diagnoses in cattle include lead poisoning, water deprivation/salt poisoning, Histophilus meningoencephalitis, coccidiosis with nervous involvement, nervous ketosis and vitamin A deficiency.
At necropsy, flattening of the gyri of the brain and coning of the cerebellum may be suggestive. The whole brain should be submitted to the laboratory in buffered formalin for histology. Water and fodder may be tested in the laboratory for sulphur levels.
PEM in sheep and goats needs to be differentiated from salt intoxication/water deprivation, lead toxicity, and bacterial and viral brain infections.
Treatment
Injectable thiamine (vitamin B1) is highly effective at rapidly reversing signs, if given early and in massive doses. Intravenous products are available and should be administered slowly. Dexamethasone may be useful to decrease oedema and inflammation of the brain. Sulphur-induced PEM has a poorer response to thiamine treatment. In-contact animals may be supplemented with oral thiamine added to feed.
If cases continue to occur, feed more roughage, and reduce or replace water and feeds that contain sulphur.
Prevention
Adequate dietary fibre and gradual dietary changes are necessary to prevent acidosis or indigestion leading to thiamine deficiency. Avoid rations and water high in sulphur.
Pregnancy – Advanced
Description
Cattle in the last trimester of pregnancy may have a distended abdomen, especially if they are carrying multiple foetuses.
Heavily pregnant cattle do not travel well. They are prone to heat stress, metabolic diseases, are easily exhausted, and are at risk of aborting. Cattle more than 6 months pregnant at time of departure are usually excluded from the export process. Manual pregnancy testing by an experienced veterinarian is usually done to assist this. However, heavily pregnant animals may occasionally be mistakenly exported. This is typically as a result of errors in data recording (incorrect records of service dates or animal identity), errors in staging of pregnancy, following failed attempts to terminate pregnancy, or where animals are incorrectly recorded as having been ovariectomised and thought to be unable to get pregnant.
Clinical Signs and Diagnosis
Pregnancy of six months or more may be detected by ballottement through the right abdominal wall, or by rectal palpation. Differential diagnoses include vagal indigestion, bloat, gastrointestinal accidents, and naturally pendulous conformation of the abdomen. Premature lactation is seen in pregnant and non-pregnant cattle exported by sea and is not necessarily an indication of advanced pregnancy.
Treatment
Apply special care and handling.
Prevention
Apply accurate pregnancy testing and record keeping in initial selection screening. Follow this with assessment of abdominal profile and double checking the pregnancy status of any animal with a distended abdomen.
Prolapse Of The Rectum
Description
Rectal prolapse may be predisposed by conditions that increase intrapelvic pressure or abdominal straining, such as persistent riding behaviour, coughing, coccidiosis, and chronic diarrhoea. Vaginal prolapse in females and urinary tract obstruction in males may also predispose to rectal prolapse. Any partial, intermittent prolapse may lead to rectal mucosal injury and irritation, more straining, and eventually complete prolapse.
Once prolapsed, the blood supply becomes compromised and affected tissue will swell, become congested, oedematous and eventually necrotic. Without intervention there is a risk of peritonitis and death. Occasional cases may be seen in the livestock export process.
Clinical Signs and Diagnosis
A large cylindrical mass of dark, congested, friable tissue protruding from the anus will probably be prolapsed rectum, but should be differentiated from anal warts (which are hard, pale and nodular) and vaginal prolapse (which protrudes from the vulva).
Treatment
Treatment should not be delayed as swelling and necrosis will rapidly make manual or surgical correction more difficult.
Small, recent rectal prolapses with little swelling may be reduced manually under caudal epidural anaesthesia (to reduce straining), and using soapy water or lubricant to help with replacement. Insert a loose, anal purse-string suture to prevent recurrence while leaving a two finger opening to allow passage of faeces. Remove after one week by which time swelling will have disappeared if the underlying condition has been corrected.
If the prolapse is irreducible because of necrosis, size, or trauma, then submucosal resection or amputation should be attempted. Submucosal resection is preferred to amputation because there is less risk of rectal stricture. A field amputation method involving poly- or PVC pipe (about 2.5 cm in diameter) has been used effectively on export vessels (Manefield GW, Control and Therapy article number 4770, 2007). The pipe is inserted into the prolapsed rectum and rubber bands or suture material applied over the prolapse to form a tight ligature against the pipe, with the ligature placed close to the anal sphincter. The animal will defecate through the pipe during healing. At the site of the ligature, healthy proximal tissue will anastamose and the tissue distal to the ligature will necrose and fall away with the pipe after a week or so. A set of three different diameter pieces of pipe can be carried on board in case prolapses occur.
Alternative approaches to amputation have also been described. One approach involves placing a series of U-sutures around the base of the prolapse. A 23 cm Gerlach needle carrying two 30 cm lengths of heavy-duty absorbable suture (sutures 1 and 2) is inserted into the lumen of the prolapse and the prolapsed tissue penetrated from the inside to the outside. The Gerlach needle is then used to carry the inner end of suture 2 and a new suture 3 from the lumen to the outside about 3 cm from the first penetration. Suturing continues in this manner for the circumference of the prolapse until there is a series of U-sutures around the prolapse. Each suture is tightened and tied, then the prolapse excised about 2 cm distal to the sutures. No haemorrhage occurs due to the ligation of the tissues. Spontaneous retraction of the stump occurs.
Simultaneously treat any underlying cause such as pneumonia, urolithiasis or diarrhoea. Prompt euthanasia is recommended if the prolapse cannot be corrected or amputated.
Prevention
Prevention and treatment of predisposing underlying diseases and conditions such as pneumonia, riding behaviour or urinary obstruction are required to prevent rectal prolapse. If these diseases and conditions occur, then there must be awareness of the possibility of rectal prolapse occurring, and systems for early detection and intervention should be implemented.
Prolapse Of The Uterus
Description
Uterine prolapse describes the situation where the uterus everts through the birth canal to hang behind the animal with the interior surface (endometrium) visible.
Prolapse usually occurs immediately following calving while the cervix is still open and the uterus still flaccid. Prolapse may be predisposed by difficult birth or hypocalcaemia.
Uterine prolapse is followed by oedema, inflammation, swelling and risk of traumatic damage to the exposed organ. The uterine ligaments and associated blood vessels may stretch and tear, and there is a risk of serious and possibly fatal haemorrhage. In addition, involvement of the bladder and possibly intestines in the prolapse may result in urinary or intestinal obstruction.
Because heavily pregnant cattle are usually excluded from the export process, uterine prolapse will be rare.
Clinical Signs and Diagnosis
A uterine prolapse presents as a large mass of tissue hanging from the vulva, often past the level of the hocks. The amount of prolapsed tissue and the presence of large numbers of caruncles (the discrete mushroom-like lumps of uterine tissue which attach to the placental cotyledons), enables differentiation of uterine prolapse from retained foetal membranes, and prolapse of the rectum or vagina.
Treatment
Treatment should not be delayed. Affected cattle should be handled very gently as there is a high risk of blood loss and shock. If standing, they should be slowly walked to a crush with a head bail, and if recumbent, they should be tied up with a halter.
Wash the prolapsed tissue with warm soapy water, repair lacerations, and remove placenta carefully if still attached. If there is excessive bleeding, then stop trying to peel the placenta away from the caruncles. Apply glycerol to reduce oedema and lubricate in preparation for replacement.
Caudal epidural anaesthesia will prevent straining during replacement. If standing, use a tray or chaff bag held between two assistants to elevate the prolapse. If recumbent, position in sternal recumbency with hind limbs stretched backward to tilt pelvis forward and aid repositioning.
If bladder or intestines are contained within the prolapse, these should be repositioned first by pressure applied gently through the uterine wall. A urine distended bladder may need draining with a needle and catheter passed through the uterine wall. Ensure both horns are completely everted once the uterus is returned to the inside of the body. If this is done properly, there is usually no need for insertion of a perivulvar suture to prevent recurrence. Administer oxytocin and calcium borogluconate solutions to promote uterine contraction. Antibiotic pessaries inserted into the uterus are unnecessary. Instead, systemic antibiotics (procaine penicillin, oxytetracycline, or trimethoprim sulpha) should be administered daily for 3 to 5 days.
If severely necrotic or traumatised, the uterus may require amputation, or alternatively, euthanasia may be warranted on welfare grounds.
Prevention
Specific preventative measures are unwarranted in the livestock export process. Awareness of the condition, especially its occurrence at calving, and the need for prompt intervention is sufficient.
Prolapse Of The Vagina
Description
Increased pressure in the abdomen, straining, and hormonally-induced loosening of pelvic tissues approaching calving time may predispose animals to vaginal prolapse. Increased intra-abdominal pressure is most commonly associated with advanced pregnancy or excess fatness. Partial, intermittent prolapse of the floor of the vagina may initially occur when affected animals lie down. Over time, minor irritation and tissue injury may lead to further prolapse, and then affected animals may start to strain and further exacerbate the condition. The bladder and intestines may be trapped inside the prolapsed tissue. Prolapsed tissue is at increased risk of exposure, inflammation, and trauma leading to congestion, oedema, drying and necrosis.
Because overfat and heavily pregnant animals are usually excluded from the export process, occurrence of vaginal prolapse will be rare.
Clinical Signs and Diagnosis
A vaginal prolapse presents as a mass of tissue protruding from the vulva. Affected animals may be noticed with an arched back due to frequent straining. Vaginal prolapses are up to the size of a basketball, rounded, smooth and pink in the early stages, later becoming dry, hard and dark from congestion, sunburn, faecal staining and abrasions.
Differential diagnoses include rectal prolapse, which protrudes from the anus (and may occur concurrently), and uterine prolapse which occurs during or soon after calving. A prolapsed uterus will hang down further (to the level of the hocks), and is covered in caruncles (the lumps of tissue where the placenta was attached).
Treatment
Treatment should not be delayed. Progressive swelling, drying and necrosis can make it difficult to replace. The bladder and intestines may be trapped within the prolapse.
Replacing the prolapse is best done under caudal epidural anaesthesia to reduce straining. If glycerol or icing sugar are rubbed on the prolapse, oedematous swelling may be reduced, making replacement easier. If the bladder or intestines are present in the prolapse, manipulate these into the pelvis to make replacement of the prolapse easier. Insertion of a perivulvar Buhner’s suture, leaving a 3 to 4 finger hole, will help prevent prolapse recurring. The suture will need removing when calving is imminent.
Prevention
Avoid exporting fat, heavily pregnant cattle.
Respiratory Distress
Description
Dyspnoea refers to laboured or difficult breathing, often in association with evidence of general distress such as extended head and neck, sawhorse posture, and an anxious expression. Hypoxic animals will show signs of dyspnoea.
Clinical Signs and Diagnosis
Dyspnoea is most often associated with disease of the respiratory tract, such as airway obstruction, pneumonia, or other diseases of the airways or lungs. A range of other conditions may cause or exacerbate dyspnoea, including physical exertion, pain, trauma, severe systemic diseases, acidosis, and heat stress.
Dyspnoea accompanied by coughing is indicative of tracheobronchial disease.
The most likely differential diagnoses in shipboard cattle with respiratory distress include:
Pneumonia and other respiratory diseases.
Heat stress.
Bloat causing compression of the diaphragm.
Physical exertion.
Hypoxia from engine exhaust gases, or exposure to toxins in feed (nitrate/nitrite, cyanide).
Treatment
Choice of treatment will be dictated by the diagnosis. Animals that are dyspnoeic due to advanced respiratory disease should be humanely euthanased.
Prevention
The preventative measures implemented will depend on the hazards identified, the likelihood of mishap, and the cost of consequences should they eventuate.
Retained Cud
Description
Retained cud is the accumulation of feed between the cheek and molar teeth. Malocclusion of broken, worn or decayed teeth, or deformities of the jaw may be responsible.
Clinical Signs and Diagnosis
Unilateral swelling on one side of the face is noticed. External palpation and examining the inside of the mouth are used to make the diagnosis.
Treatment
Treatment is by carefully hooking the cud out with a bent finger, while holding the jaws open with the other hand. Recurrence is likely if malocclusion is present. Consider listeriosis as a differential diagnosis due to facial nerve dysfunction.
Prevention
Screen animals for dental problems during selection. Avoid damaging teeth and gums when administering oral drenches.
Retained Foetal Membranes
Description
If foetal membranes are not expelled within 24 hours after giving birth they are classed as retained. They are normally expelled within 3 to 8 hrs after birth, but may be retained for up to two weeks. Retained placenta is uncommon in beef cattle, may affect 5-15% of dairy cows, and is more common following early or abnormal parturition or abortion. Most cases require no treatment, but complications such as metritis and toxaemia may become life-threatening.
Clinical Signs and Diagnosis
Presence of visible membranes at the vulva are an obvious sign, but cows may have a retained placenta without any external signs. Diagnosis generally depends on physical examination, including rectal and vaginal examination.
Treatment
Manual removal is best avoided where possible because of the risk of trauma, haemorrhage, and subsequent infection of the uterus. Removing the exteriorised membranes by trimming under slight tension may be required.
Antibiotic pessaries inserted into the uterus are ineffective at reducing infection or preventing metritis and may also delay separation, which relies on bacterial action.
Animals with retained membranes that show systemic signs of illness associated with metritis should be treated with systemic antibiotics (procaine penicillin, oxytetracycline or trimethoprim sulpha).
Prevention
Specific preventative measures are not warranted because retained placenta is likely to be uncommon in the export process.
Ringworm
Description
Ringworm is an unsightly skin lesion, usually circular and hairless, caused by a fungal infection of the hair follicle and outer layer of skin Trichophyton verrucosum is the principal agent affecting cattle with other fungi less commonly involved. Ringworm is a zoonotic disease. Human infection is usually on exposed skin such as arms and neck, and is noticed when circular, itchy, red and exudative lesions appear after close contact with cattle.
Ringworm is rare in production sheep and goats. It can be a problem in young show sheep that have their skin and fleeces scrubbed clean. It is presumed this reduces the effectiveness of local protective barriers thereby allowing fungi to invade. It is unlikely to occur in production sheep and goats in the export process.
Tough, easily dispersed spores provide a source of environmental contamination. Transmission is via animals contacting infective spores in the environment or by close contact between animals.
Bos indicus breeds are less affected than Bos taurus breeds. Conditions in the export process are ideal for spread due to the combination of susceptible cattle, high humidity, reduced direct sunlight, and deck washing wetting the skin.
The presence of ringworm lesions can influence export market access and value. Affected animals may be rejected or have their market value downgraded if lesions are detected at destination.
Clinical Signs and Diagnosis
Lesions are typically circular, up to 3cm in diameter, with larger patches being the result of coalesced lesions. The head and neck are usually most affected, but lesions may occur on other parts of the body. Initially, the skin is moist and reddened; later it is dry, scaly and grey.
Laboratory confirmation requires deep skin scrapings or biopsy of lesions for microscopic demonstration or isolation of the organism.
Differential diagnoses include warts, bovine herpes mammillitis virus (bovine herpesvirus-2), dermatophilosis and stephanofilariasis. Lumpy skin disease, which is exotic to Australia, should also be considered.
Treatment
Ringworm heals with or without treatment in about 8 weeks.
Treatments may not shorten the time to complete healing of lesions. Not treating animals and letting the disease run its course is a common response to ringworm.
Treatment with imidazole spray may stop progression of lesions and slow the spread to other animals. Chlorine and iodine based compounds are much less effective.
Cationic alkyl dimethylbenzyl ammonium halides, appropriately diluted, may be blanket sprayed on affected cattle in pens at sea to minimise the spread of spores.
Prevention
Options include:
Prevent entry of cattle with active or extensive ringworm lesions into the export process and isolate any cases developing in assembly points.
Use cationic alkyl dimethylbenzyl ammonium halides to disinfect the cattle holding and handling facilities on land or at sea – this should be done between mass handling events.
Minimise mixing of animals in pre-embarkation confinement periods.
Process affected animals last through handling facilities and treat with imidazole spray at each yarding.
Highly effective cattle ringworm vaccines used for treatment and prevention are available overseas but not in Australia.
Rumen Acidosis
Description
Rumen acidosis is most likely to occur shortly after animals consume excessive amounts of grain starch. This is most likely to occur soon after animals are introduced to pellets, or when pellet feeding is re-commenced following an interruption. Limited or no access to roughage of an effective fibre length means that stock will spend less time chewing and will produce less saliva, which results in reduced ingestion of bicarbonate and phosphate buffers normally supplied to the rumen in salivary secretions. Rapid fermentation of starch causes high levels of lactic acid to form quickly in the rumen, killing essential gut microflora, damaging the mucosal lining, and drawing in body fluid. This leads to rumen stasis, dehydration, and diarrhoea. Severely affected animals may develop systemic acidosis, abdominal or systemic infections, and laminitis. Animals may die either acutely due to overwhelming acidosis or as a result of secondary complications.
Large, strong, young animals with excellent appetites are more at risk. Rapid engorgement of a ration due to hunger or competitive feeding will predispose stock to rumen acidosis. If a single animal is showing clinical signs of acidosis it will indicate a high probability of subclinical acidosis in the rest of the herd.
Clinical Signs and Diagnosis
Clinical findings and examination of feeding history and feed should raise suspicions. Bubbly diarrhoea can indicate acidosis, as it is a sign that feed is passing through undigested and there is fermentation occurring in the faeces.
Clinical findings and examination of feeding history and feed should raise suspicions.
Mild acidosis is associated with watery faeces accompanied by temporary inappetence. Increasing severity is evident by depression, dehydration, absence of ruminal movements, weak pulse, slow capillary refill, subnormal temperature, diarrhoea, and colic. Some animals may later develop laminitis or liver abscess.
Animals that survive the acute illness may still die within days due to kidney failure, fungal rumenitis or peritonitis.
At necropsy, the rumen is distended with pellets and fluid. Note that sloughing of the rumen mucosa is a normal post-mortem change occurring within an hour of death and should not be regarded as evidence of rumenitis or excessive grain feeding unless associated with inflammatory change.
Urine test strips or specific test strips may be used to test pH of rumen fluid. Normal rumen pH is >5.9 and acidosis should be suspected if the pH is less than 5.5.
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.
Laboratory confirmation requires sections of reticulum and ventral rumen in buffered formalin for histology.
Differential diagnoses include salmonellosis, gastrointestinal accidents, enterotoxaemia, and bloat.
Treatment
If acidosis is suspected, then high concentrate diets should be changed to increase intake of roughage of an adequate fibre length. On ships this involves replacing pellets with hay or chaff. Animals should be encouraged to maintain adequate fluid intake. Animals with mild to moderate acidosis will often recover within a few days following dietary change.
Infusion of alkalinising agents (magnesium hydroxide, sodium bicarbonate) into the rumen might be considered in early cases. Administration of antibiotics may provide protection against secondary infection. Transfer of >3 L, preferably 8 to 16 L, of rumen fluid from a healthy donor may be beneficial to reactivate the rumen and stimulate digestion and eating. Development of mycotic infection of the rumen wall may cause relapse over coming weeks and then the prognosis is grave.
Affected animals may also benefit from administration of antibiotic (procaine penicillin) to minimise the risk of complications associated with proliferation of gram-positive bacteria.
If feeding restricted fodder in a shipboard environment, consider feeding smaller feeds more frequently across the day.
Prevention
Introduce animals to higher carbohydrate diets incrementally over a period of two to three weeks, monitoring carefully for early signs of acidosis, such as reduced appetite, reduced rumen movement, and sloppy faeces. Avoid instances where animals might be allowed to gorge on concentrate diets, such as following a period of cessation or reduced feed availability (yoyo feeding).
Feed additives (ionophores, virginiamycin, sodium bicarbonate and sodium bentonite) may be considered in feedlot situations to minimise the risk of acidosis, particularly during the first few weeks of grain introduction.
Regular feeding of palatable roughage of an adequate fibre length will stimulate mastication and saliva production. Suggested fibre length for cattle is 5-10 cm, and an average fibre length of 2.5 cm is recommended for sheep.
Salivary Duct Blockage
Description
This is usually the result of a grass seed blocking a salivary duct under the tongue. This is followed by fluid accumulation and inflammation with variable swelling visible under the jaw.
Clinical Signs and Diagnosis
A grass seed awn can often be seen protruding from the duct opening under the tongue. Pus may be discharging around it. The distended salivary duct may be visible.
Major differential diagnoses include woody tongue and possibly lumpy jaw.
Treatment
Examination of the mouth is necessary to diagnose and relieve the obstruction. This will require good head restraint (halter, nose grips), lighting (head lamp), and possibly forceps and a scalpel.
The grass seed can usually be massaged out to relieve the obstruction. Sometimes an incision with a scalpel is necessary to access the grass seed with a pair of small alligator forceps. No further treatment is necessary once the grass seed is removed and patency is established.
Prevention
Preventative measures are unwarranted given its rarity.
Salmonellosis
Description
Salmonellosis is a bacterial infection of man and animals causing enteritis, abortion, and septicaemia.
Salmonella organisms may be carried by animals without any signs of illness, and are shed in faeces. Shedding rates may increase if carrier animals are stressed or if clinical infection develops. Organisms may also be spread by flies, rodents and birds. Animals are mostly infected by ingestion of organisms, although inhalation or conjunctival contamination may also result in infection.
The response of an animal to Salmonella challenge will depend on multiple factors including number of bacteria and virulence, specific immunity to Salmonella from vaccination or prior exposure to that strain, and a wide range of factors influencing general health (immune capacity, concurrent disease, nutritional state, and stress).
Within individually exposed animals, the outcome may range from resistance (no disease at all), to mild disease, to severe infection and possibly death. The export process is associated with a range of stressors (feed/water deprivation, change in environment and feed, transport, mixing of animals, exposure to other diseases, and climatic stress) that may increase the level of Salmonella shedding and make animals more susceptible to infection.
Cattle are at risk of exposure in assembly points, particularly if assembly points are continually populated with animals over time. Outbreaks of clinical disease may occur during assembly or at sea under favourable conditions (high density of stressed or susceptible animals and heavy exposure).
There is particular interest in salmonellosis in sheep in the export process because inanition and salmonellosis are the two most common causes of death in sheep exported from Australia to other countries.
The epidemiology of salmonellosis in export sheep is complex. A causal web for salmonellosis and inanition is shown in the section on Inappetence/inanition. Inappetence is recognised as a potential precursor that may predispose sheep to salmonellosis, but sheep may also develop salmonellosis without having inappetence. Salmonella are ubiquitous and many healthy animals will carry and shed organisms without disease. Many factors interact to influence the occurrence of disease, including Salmonella challenge (number of bacteria and virulence of a strain), specific immunity to Salmonella infection, as well as general health and immune capacity (influenced by innate immune response capacity, concurrent disease, nutrition, and stress).
The prevalence of sheep shedding Salmonella on entry to export assembly depots has been shown to be very low. Clinically infected animals and passive shedders are thought to be the major potential sources of Salmonella organisms for other susceptible animals, either directly, or indirectly through contamination of water, feed and the environment. Salmonella organisms can survive for months to years in the environment, and under favourable environmental conditions, Salmonella are capable of proliferation in the environment to increase the level of environmental contamination. Assembly feedlots that receive large numbers of sheep over many months for consecutive export voyages may become heavily contaminated with Salmonella organisms over time, leading to increased risk of exposure of new arrivals to infection.
Factors that are likely to be associated with increased risk of heavy shedding in sheep include mixing of animals in saleyards or dealer operations, frequent or prolonged transport movements, reduced feed access, inappetence, or other stressors.
Healthy sheep may be reasonably resistant to Salmonella exposure. Stressors such as transport, yarding, feed and water curfews or deprivation, inappetence, concurrent disease, and inclement weather can all reduce host resistance and increase the risk of salmonellosis. The outcome in individual infected animals may range from recovery, to acute, fulminant bacteraemia, endotoxaemia and death.
Compromised animals exposed to heavy levels of virulent organisms may develop acute disease and begin dying while still in the assembly feedlot. In other cases, animals may be exposed in the feedlot and develop disease during the early part of the voyage. In exposed and infected animals, the disease usually runs its course over 14-21 days.
Enteritis (mainly associated with salmonellosis), inanition, and the combination of both enteritis and inanition together, form the most common causes of mortality during export voyages (LIVE.0123, 2009).
Clinical Signs and Diagnosis
Animals with acute enteritis show fever, dullness, sunken eyes, and diarrhoea. Animals look ‘tucked up’ and miserable, may kick at the belly, and grind their teeth. The diarrhoea is watery and may contain blood or mucus. The diarrhoea has a putrid smell that may be suggestive of salmonellosis. Death can occur within a few hours in peracute cases, and these animals may die before developing diarrhoea or other severe clinical signs. Concurrent inanition is common. Pregnant animals may abort.
At necropsy, intestinal contents are watery and usually blood stained, intestinal walls are red and thickened, and the mucosal surface is coated with necrotic debris and fibrin. Mesenteric lymph nodes are large and wet, and sometimes red. Affected animals may or may not have concurrent evidence of inanition, such as very low or absent rumen contents, poor body condition and evidence of fat mobilisation (fatty liver, enlarged gall bladder and serous atrophy of fat stores).
Laboratory confirmation requires faeces submitted chilled for bacteriology. Additional specimens desirable from dead animals are sections of abdominal visceral organs, which should be submitted chilled and separated for bacteriology, and fixed in buffered formalin for histology. Samples from intestines may be stored in viral transport medium for polymerase chain reaction (PCR) testing to detect Salmonella genetic material.
Differential diagnoses include ruminal acidosis, clostridial enterotoxaemia, coccidiosis, and bovine viral diarrhoea virus (BVDV) infection in cattle.
Treatment
Fluid therapy is critical in the treatment of clinical salmonellosis to avoid severe complications associated with dehydration. Intravenous fluid therapy is likely to be important in individual high-value animals, but not in treating multiple cases in an outbreak situation during export.
Antibiotics are recommended by a number of publications and veterinarians, but the efficacy of antibiotic use in treating salmonellosis is unclear, and there are risks of adverse effects.
Several antibiotics, including potentiated sulphonamides, ampicillin and amoxicillin, have been recommended as effective treatments for salmonellosis in ruminants.
Antimicrobial use has also been associated with emergence of antimicrobial resistant Salmonella and increased duration of Salmonella shedding, and can actually interfere with normal digestive microflora, predisposing sheep to further gastrointestinal disease. Mass medication as prophylaxis in an attempt to prevent salmonellosis is not recommended.
Blanket administration of antibiotics via drinking water is not recommended. Sick sheep are unlikely to drink enough and the healthy sheep that do drink may become sick because of disruption to normal gut flora.
Prevention
Prevention of salmonellosis in the livestock export trade is based on maximising host resistance to infection and minimising exposure to Salmonella organisms.
Host resistance can be maximised by maintaining adequate nutrition and minimising stress. Management guidelines for achieving these goals throughout the export process are given in the Australian Standards for the Export of Livestock (ASEL).
The key to minimising exposure to Salmonella pathogens is to reduce environmental Salmonella contamination. Management procedures to reduce Salmonella contamination include paddock rotations, isolation of sick animals, feed and water management to prevent faecal contamination, and control of flies and rodents (LIVE.0112, 2002). Disease prevention and control strategies need to be tailored to each facility to account for differences in variables such as soil type, drainage, and environmental conditions.
It is important to use strategies to minimise the risk of inappetence and inanition since these conditions increase the risk of salmonellosis occurring. See the section on Inappetence/Inanition for more information. Spelling or rotating feedlot or assembly pens may be useful to avoid progressive build-up of environmental levels of pathogenic organisms and may reduce exposure risk. Scraping manure contaminated top-soil from assembly pens may also reduce environmental exposure. Changing flow patterns in assembly feedlots to move towards a one-way flow (separate receival yards and load out yards), and use of elevated sheds to house sheep are two examples of relatively high cost methods that may minimise exposure of livestock to Salmonella challenge.
Salmonella vaccines are available for use in cattle, mainly as an aid in preventing salmonellosis in calves. Efficacy of these vaccines in older cattle to protect against salmonellosis in the export process is unclear. Preliminary research trials on oral Salmonella vaccination in sheep appear promising, but commercial products are not yet available and further work needs to be done.
All people working with stock should be regularly reminded that Salmonella can be passed between animals and humans, and of the importance of personal hygiene, especially washing hands thoroughly with warm soapy water before eating.
Salt Poisoning
Description
Direct salt poisoning may occur following ingestion of excessive salt. Chronic salt poisoning may also occur when animals are ingesting normal levels of salt (or slightly increased levels) and are also experiencing decreased water intake. The pathogenesis generally involves a combination of water deprivation, variable levels of salt exposure, and then unlimited access to fresh water.
Excessive salt ingestion may lead to acute poisoning, with gastroenteritis resulting from local irritation to the mucosa of the stomach and intestines.
Chronic salt poisoning can result in accumulation of sodium ions in tissues, including the brain. If animals then gain unrestricted access to fresh water, fluid moves to tissues to restore normal salt-water balance. The presence of elevated levels of sodium can lead to excessive fluid retention and cerebral oedema with increased intracranial pressure and nervous signs. The disease is more serious if there is access to salt or salty water during the period of water deprivation. Intravascular haemolysis may occur during rehydration as water is drawn back into red blood cells.
Animals subjected to long transport in hot dry conditions and that are offered free access to water of low salt content at the end of the journey may be at risk of developing this condition. This may happen in the livestock export process.
Clinical Signs and Diagnosis
Within a few hours of the animals quenching their thirst, there is onset of acute nervous signs, similar to those of polioencephalomalacia. Affected animals are dull, blind, and head press, or they may stand with their head pulled back. Urine may be dark from haemoglobinuria caused by intravascular haemolysis. Collapse, convulsions, coma, and death follow development of nervous signs.
Elevated levels of salt in serum and cerebrospinal fluid samples are indicative of salt poisoning, especially if the sodium concentration in cerebrospinal fluid is greater than that of serum.
At necropsy there may be flattening of the gyri of the brain (from swelling associated with cerebral oedema), intense congestion of the abomasal mucosa, and hydropericardium.
Laboratory confirmation requires brain submitted in buffered formalin for histology.
The dark urine that sometimes accompanies salt poisoning may serve to differentiate it from the main differential diagnoses of polioencephalomalacia, lead poisoning, enterotoxaemia, and insecticide poisoning.
Treatment
There are no specific treatments and the condition is usually fatal, even if supportive treatment is attempted. Treatment with thiamine (vitamin B1) is not effective. Remove access to water and salt immediately.
Prevention
Prevent access to salt and salt water during periods of water deprivation. Following long periods of water deprivation, provide restricted amounts of water at frequent intervals, and aim to rehydrate animals over 24 hours.
Scabby Mouth
Description
Scabby mouth is a highly contagious viral disease that affects the skin of sheep and goats. It is caused by the orf virus, a member of the genus Parapoxvirus. Viral challenge is expected to be high during the export process from mixing of young sheep in close confinement. Higher stocking densities and feeding of pellets and hay that may cause small abrasions around the mouth, means the potential for outbreaks of scabby mouth in the export process is considerable.
Assembly facilities can become heavily contaminated as the virus is hardy and can survive in the environment for many years. Unvaccinated animals are susceptible, as are some heavily challenged or immunosuppressed vaccinated animals (although with mild, rapidly healing lesions).
Mainly young animals are affected, as older animals will have recovered from earlier infection. Australian goats appear to be considerably less susceptible than sheep.
The disease is seasonal in Australia’s sheep producing areas, occurring especially in summer and autumn when feed consists of abrasive stubbles, dry grass, seeds and burrs, and when flies are abundant and active. This should be a consideration when assembling sheep and goats for export.
If a significant number of animals have scabby mouth lesions on inspection at the destination, it could lead to rejection of the consignment.
Clinical Signs and Diagnosis
Reddened areas with clear, sticky exudates or hard brown scabs seen on the skin of sheep and goats, especially around the lips and nostrils, is probably scabby mouth. Coalescing of lesions can result in scabs covering a much larger area. As the disease progresses, the scab becomes a dry, cracked crust. Weight loss can be rapid if lips are swollen or the mucosa of the mouth is affected, however, most cases show few systemic clinical signs. Less commonly, lesions can affect other areas of exposed skin such as ears and feet.
Bacteria may infect the cracks and create purulent infections. If the crusts are dislodged, a granular surface is exposed and may show small amounts of pus and blood. Lesions will spontaneously regress over 3-4 weeks, but may persist for longer if there is secondary bacterial infection.
Laboratory confirmation requires scabs with underlying tissue scrapings for virus isolation or identification with electron microscopy.
Treatment
The disease must run its two to three week course as no effective treatment is available. Antibiotics are only warranted if secondary bacterial infection is present. Ready access to soft feed and clean water will encourage eating.
Prevention
There is an effective vaccine that should be administered before expected disease onset or as dictated by importing country protocols.
People handling infected sheep can become infected and should take precautions.
Shy Feeders
Description
See also Inappetance/Inanition for sheep.
Shy feeders are animals reluctant to eat pelleted rations. Shy feeders will often continue to eat roughage such as chaff or hay. Up to 15 % of cattle, especially if older, may become shy feeders at sea on pellet rations.
The cause is unknown but may be due to a rapid change in diet and the way it is offered. The change from pasture, to eating rolls of hay in assembly points, and then pellets in troughs on a ship can occur in a few days. A variety of other factors may be involved, including concurrent disease and stressors associated with the export process.
Reducing competition by separating affected animals to a hospital pen and feeding roughage in the form of hay or chaff is almost always successful in getting the animals to eat and maintain body condition.
Clinical Signs and Diagnosis
Affected animals are detected during pen inspection. Loss of condition from reduced feed intake results in the left flank being more hollowed and the short ribs more prominent than those of pen mates.
Differential diagnoses include chronic diseases and conditions affecting appetite such as liver abscess, low grade pneumonia, ruminal acidosis, displaced abomasum and ketosis.
Treatment
Shy feeders require special attention and management. The primary treatment is to separate affected animals to pens with fewer but similar age, size and sex animals, and feed roughage. From there, pellets can slowly be reintroduced to the ration and the number of animals in the pen eventually increased, if necessary, to relieve crowding elsewhere.
Additional treatments may be warranted depending on the results of examination of affected animals.
If ketosis is suspected, consider intravenous administration of dextrose and oral administration of propylene glycol. Transfer of rumen fluid from a healthy donor may be beneficial for animals where rumen microflora have been disrupted by inappetence, acidosis or oral antibiotics.
Antibiotics (procaine penicillin, erythromycin, or ceftiofur) and non-steroidal anti-inflammatory drugs (flunixin meglumine, ketoprofen, meloxicam, or tolfenamic acid) may be beneficial if infectious, septic, or painful disease is suspected or other efforts are ineffective. However, relapse at the end of a course of seemingly successful treatment may occur.
If apparent weight loss or reluctance to eat is becoming widespread, check the quality of water and feed, looking for any evidence of contamination or other changes that may affect intake.
A variety of injectable products are promoted as appetite stimulants (various combinations of vitamins often with other products), but efficacy is questionable. Glucocorticosteroids should be used with caution as they are immunosuppressive.
Although recommended in ketosis associated with lactation, they may be detrimental in other types of ketosis associated with pregnancy or over fatness.
Prevention
Measures available to reduce the number of shy feeders include:
Group according to size, age, sex and horn length to reduce competition.
Provide adequate trough space so most animals can feed at one time.
Ensure good quality feed and water.
Provide enough feed at each feeding so some is left for shy feeders after aggressive feeders have finished eating.
Adapt cattle to pellet diets in assembly points in preparation for full feeding of pellets at sea. This may be facilitated by feeding hay as a means of introducing cattle to trough feeding. Then begin feeding pellets on top of hay and increase pellets as a proportion of diet over time. Mixing rough cut chaff with pellets rather than feeding separately may also facilitate adaptation to pellets and create a more evenly balanced diet.
Feed a mixture of chaff and pellets on the first few days of a voyage if the fodder uptake is slow.
It may be necessary to put feed troughs on the inside of pen rails for some stock eg. some horned cattle may find it difficult to access feed troughs.
Skin Swellings
Description
A variety of diseases and conditions can cause skin swellings in a range of anatomical locations. The following table lists the main swellings occurring in the export process.
Causes of skin swellings in export livestock
| Type of swelling | Anatomical location and cause |
| Tumour | Abdomen and chest from various types of skin tumours; regional lymph nodes and body skin from lymphosarcoma. |
| Infection | Mandible and maxilla from lumpy jaw; lower legs following trauma. |
| Abscess | Side of neck from vaccination. |
| Haematoma | Pelvic prominences from trauma; penis and prepuce from ruptured penis. |
| Hernia | Ventral abdomen from trauma. |
| Oedema | Submandibular oedema from: woody tongue, blocked salivary duct and heart failure; brisket oedema from heart failure due to traumatic reticulopericarditis, valvular endocarditis, ionophore (i.e. monensin) poisoning. |
| Urine | Ventral abdomen and prepuce from urine leakage following urethral obstruction then rupture. |
| Gas | Over rump, back and shoulder from blackleg; over back and shoulder from sucking wounds of the armpit. |
Clinical Signs and Diagnosis
Swellings may be difficult to detect unless seen in profile in good lighting. The cause of most swellings may be differentiated by the location, extent, size, shape, surface, smell, contour and content. Inserting a needle or cutting into a swelling to determine its contents should be avoided in the export process because of the risk of iatrogenic infection.
Treatment
Choice of treatment will depend on accurate diagnosis.
Prevention
A good screening system will detect problems during selection, thereby preventing entry into the export process. Vaccination hygiene, low stress animal handling, and vaccination against blackleg, which are routine in the export process, should contribute to lowering prevalence. Awareness of the types of problems that may arise and having systems for early detection, accurate diagnosis, and effective treatment are important, particularly at sea.
Spinal Cord Injury
Description
In the export process, spinal cord injuries may occur as a result of being ridden by other animals or as a consequence of accidental injury (slipping or getting stuck between or under rails or other infrastructure).
Clinical Signs and Diagnosis
Affected animals show variable signs of ataxia and paresis, including bilateral knuckling of the lower hind limbs, staggering gait, and inability to stand or walk. Animals may stagger and fall if made to turn quickly or run. In some cases, the tail is paralysed and flaccid. Necropsy of severe cases requiring euthanasia may reveal bruising of the spinal cord where it was compressed, and even a vertebral fracture with or without osteomyelitis. Differential diagnoses include compressive injury to nerves of the limb acquired during recumbency, or rupture of the gastrocnemius tendon. These usually affect one rather than both hind legs.
Treatment
Administer non-steroidal anti-inflammatory drugs (flunixin meglumine, ketoprofen, meloxicam, or tolfenamic acid), isolate, and provide rest and non-slip floor conditions.
Prevention
Isolate animals that are riding or being ridden excessively, and match pen mates by size and sex. Design low risk pens and modify high risk pens. Use sawdust on ramps and loading areas when moving stock and ensure livestock are not slipping or falling when handled.
Squamous Cell Carcinoma
Description
These are neoplastic skin lesions commonly reported in older animals following prolonged exposure of skin to ultraviolet radiation. Squamous cell carcinomas are commonly found on the eye, and these are described separately under Eye Cancer. Cancer lesions are also found elsewhere on the body including the vulva, perineum, nose, lips, ears, and on the teats and udder (goats and dairy cattle).
Clinical Signs and Diagnosis
Lesions start as thickened areas of reddened, flaking skin that later become ulcerated, necrotic, bleeding masses. Flystrike is a common complication. Body condition is lost quickly once ulceration occurs. Scabby mouth lesions are the main differential diagnosis. Laboratory confirmation requires biopsy specimens collected in buffered formalin for histology.
Treatment
Animals with noticeable lesions should be excluded from the export process. If detected during export, they should be euthanased or salvage slaughtered without delay.
Prevention
Special attention should be paid to ensuring affected animals are screened out during selection. Lesions are easily missed when animals are grouped, hence a systematic inspection method is required.
Sudden Death
Description
Sudden death syndrome includes those cases found dead with no premonitory signs at last inspection, and those being treated and expected to recover that die unexpectedly.
Isolated cases of sudden death may occur as a result of a range of sporadic conditions that may be present at low levels in any population of animals. Sudden deaths in multiple animals at the same time is of great concern and may indicate point exposure to a poison or toxin, or an outbreak of a severe infectious disease.
Clinical Signs and Diagnosis
Determining cause requires necropsy examination.
Diseases and conditions to be considered include hypocalcaemia, clostridial diseases (enterotoxaemia, blackleg, malignant oedema), electrocution, asphyxiation, monensin poisoning, smothering, ruminal acidosis, chronic copper poisoning, pneumonia, and bloat.
Treatment
Not applicable.
Prevention
There are numerous potential causes of sudden death. However, the current processes of sourcing and transporting livestock for export provide a well-established and consistent approach to ensuring that exported animals are healthy and at low risk of unexpected or sudden death.
Swollen Legs
Description
See related information under Foot abscess and Lameness.
This is a loosely defined term given to swelling of one or more legs seen in cattle at sea. Swollen legs are generally the result of accidental injury with or without secondary bacterial infection. Swollen legs and lameness represent one of the most common conditions affecting cattle during export voyages.
Animals may be injured as a result of accidents during transport or loading, being stepped on by a pen mate, or from abrasion of the feet or lower limbs from contact with the deck or other hard surfaces. Anatomical areas that are commonly affected, and where initial swelling will be seen if detected early, are the fetlock, pastern or coronet region of the lower legs.
Deck surfaces can be rough and abrasive. As the voyage progresses and there is increased accumulation of faecal matter on the floor, abrasions and minor wounds, or injuries of the feet or lower limbs may easily become infected.
Cattle recumbent in crowded pens are always at risk of injury from being stepped on, especially the legs. All legs are at risk, but especially the hind legs, as they may be less likely to be tucked under a recumbent animal than the front legs. The number of swollen legs from this cause increases when pens are crowded with nervous, tired cattle. Cattle on slippery flooring or pens of cattle that push for feed are more at risk of developing skin abrasions or worn hooves creating an entry point for bacterial infection.
Initial injuries may be small and innocuous, but over time there is a risk of mild injuries being exacerbated by repeated insult, and contaminated from exposure to faecal matter on the floor. A localised cellulitis may develop and result in swelling and lameness. Infection may involve distal joints, depending on the site and extent of the initial abrasion or injury. If the cellulitis progresses, the swelling becomes extensive, there is incapacitating lameness or toxaemia, and the animal dies or must be euthanised.
Lame animals may have difficulty standing and moving and this, in turn, can lead to dehydration and inappetence, and may predispose animals to a range of other conditions, including heat stress.
Swollen legs may also be due to joint infection secondary to bovine respiratory disease (BRD).
Complications from swollen legs are one of the major causes of direct and indirect loss of animals at sea. The condition can result in death directly or lead to euthanasia. It can indirectly predispose animals to the development of other conditions. Leg complications can also result in rejection during health inspections at destination.
Clinical Signs and Diagnosis
During pen inspections, inspection of lower legs will detect enlargement of the coronet, pastern and fetlock regions when compared to other legs. Lameness may be mild or absent unless swelling is severe, although animals may be reluctant to stand on pen inspection. Lacerations are often not visible unless the skin is scrubbed clean, and then they may be very small.
Swelling of the coronary band and pastern may occur with diseases of the claw, such as excessive wearing of the sole, sole bruising, toe abscess, sole abscess, and white line disease; or diseases of the interdigital space such as foot rot. However, these conditions are accompanied by moderate to severe lameness and the claws are spread.
At necropsy, there is oedema and dark, mixed discolouration of subcutaneous tissues in the area of the swelling. A discharging skin wound may be present.
Treatment
Minor lacerations or swellings affecting legs of export cattle should not be ignored or treated lightly. Recovery without treatment is possible but unpredictable as the likelihood of wound infection is high for animals managed at sea. Without early treatment, uncontainable or irreversible cellulitis may occur.
Move affected animals to a hospital pen with fresh bedding to reduce environmental contamination.
Administer a course of antibiotics (procaine penicillin, oxytetracycline, or ceftiofur) and non-steroidal anti-inflammatory drugs (flunixin meglumine, ketoprofen, meloxicam, or tolfenamic acid) and once finished, recheck the animal for relapse.
Avoid long-acting penicillins and glucocorticosteroids.
Prevention
Avoid overcrowding during transport or in pens. Avoid situations where penned animals may rush and step on recumbent animals. Move quietly around the cattle decks when animals are settling into life on board, and make sure all cattle in a pen are standing before feed is put out into troughs.
Low stress handling practices during loading and discharge will reduce the incidence of injury.
Because early intervention saves lives, inspect cattle as soon as possible after loading and isolate and treat any animals that have lower leg wounds or swelling. During the voyage, all lower legs should be systematically scanned twice daily. This is best done immediately before or soon after feeding has commenced when most cattle will be standing up. Swollen legs are most easily detected after deck washing – ensure a scan of legs occurs immediately after deck washing and before spreading of sawdust when cattle will start to lie down.
Transit Tetany
Description
Transit tetany is a disease associated with transport stress. It is caused by hypocalcaemia, sometimes complicated by hypomagnesaemia. It is often associated with periods of food and water deprivation while being transported or held in yards, and may be precipitated by rough handling. The disease can occur in any animal, but those at greater risk are older, fatter, pregnant or lactating animals. The grazing of lush pasture, heavy feeding with grain or pellets prior to transport, and forced exercise immediately after transport also increase risk.
Clinical Signs and Diagnosis
Initially there is restlessness, incoordination and sometimes aggression. Knuckling of the hind legs and staggering may develop with the animal falling, becoming laterally recumbent, frothing at the mouth and grinding teeth. Without treatment affected animals may become comatose and die.
Diagnosis is made from history of transport and clinical signs. No specific lesions are present on necropsy.
Laboratory confirmation requires a serum sample submitted chilled for measurement of calcium and magnesium concentrations.
Differential diagnoses include exhaustion, polioencephalomalacia and lead poisoning – in the latter two diseases, animals appear blind.
Treatment
Administer subcutaneous injections of commercially available solutions containing both calcium borogluconate and magnesium sulphate, and rub in well to hasten absorption into the bloodstream. Slow intravenous administration may be required in severely affected animals, but this should be done under veterinary guidance to avoid risk of cardiac arrest if administered too quickly or in large amounts. As soon as possible, sit the animal upright if in lateral recumbency, to avoid inhalation of any regurgitated rumen contents.
Prevention
Feed cattle with adequate roughage and avoid prolonged feed curfews before transporting long distances. Avoid working cattle after long periods of transport until adequate rest, feed and water have been provided. Reduce periods of feed and water deprivation, especially in the above mentioned higher risk groups. Implement low stress handling methods.
Traumatic Injuries
Description
Traumatic injuries are generally accidents involving one animal injuring another, or when an animal falls or strikes the surrounding infrastructure (flooring, fence, gate). Injuries may be penetrating or non-penetrating, and usually fall into the categories of fractures, dislocations, bruising and wounds.
Physical injuries can occur throughout the export process. Slipping and being trampled or mounted during transport or yarding are probably the most common circumstances where traumatic injuries occur. Poorly designed or maintained facilities such as yards, laneways, fences, gates and flooring, may increase the risk of injury to animals while being housed or handled. Poor stockmanship, including rough handling and applying excessive pressure, may also contribute to risk of injury.
Individual animals may be injured by inappropriate restraint or handling such as dragging an animal by a front or hind leg.
See downer, gastrocnemius muscle rupture, haematoma – cutaneous, knuckling, lacerations, lameness and spinal cord injury for more information.
Clinical Signs and Diagnosis
An animal that is bright and alert with a sudden onset of inability to stand or walk properly is a strong indicator that traumatic injury may have occurred. At necropsy, fractures, dislocations, wounds, subcutaneous bruising, haematoma, and cellulitis or other forms of infection may be present.
Treatment
Animals with severe injuries (such as fractures) that interfere with walking, eating and drinking, should be euthanised without delay.
Animals with wounds should be isolated to a clean area and the wounds cleaned (see Lacerations). Topical treatment may be considered with antiseptic and fly repellent. Antibiotics (procaine penicillin, or oxytetracycline) should be administered if there is a risk of secondary infections, especially following biting or penetrating wounds. Administer non-steroidal anti-inflammatories (flunixin meglumine, ketoprofen, meloxicam, or tolfenamic acid) if animals are in pain.
Lame animals should be moved to a hospital pen with uninhibited trough access.
Dislocated joints require early intervention and expertise for successful reduction. Xylazine sedation or anaesthesia may be necessary to facilitate reductions.
Prevention
Handling facilities should be designed and constructed to minimise risk of injury to animals and people, and regularly checked for hazards. Personnel should be trained in low-stress animal handling to ensure that animals are handled in an appropriate way to minimise stress and injury risk. Group animals according to size, sex and horn length.
At discharge, sick and injured animals should be penned and unloaded separately from healthy animals so that they are not trampled. Use low stress handling and transport methods.
Traumatic Reticuloperitonitis
Description
Cattle are indiscriminate eaters and may inadvertently ingest wire, nails or needles if present in feed. If these sharp metal objects are longer than 2.5 cm, they may become trapped in and penetrate the reticulum. The leakage of gut contents into the abdominal cavity then causes traumatic reticuloperitonitis (TRP). Compression of the abdomen during advanced pregnancy, coughing, and mounting behaviour are thought to increase the likelihood of penetration.
Complications of TRP include reticular abscesses, splenic and liver abscesses, reticular fistula formation, and vagal indigestion. If the penetrating metal migrates into the diaphragm it may cause diaphragmatic hernia, thoracic disease (pleurisy, pneumonia) and pericarditis (traumatic reticulopericarditis – see Heart Failure).
Some animals may die suddenly from heart failure associated with traumatic reticulopericarditis.
Clinical Signs and Diagnosis
Inappetence, fever and an arched stance with abducted elbows should raise suspicions of acute localised peritonitis. There may be a painful grunt when the animal is forced to move. Muffled heart sounds, jugular pulse, and brisket oedema indicate pericarditis has developed. Many animals will suffer from illthrift.
Differentiating abomasal ulceration, pleuropneumonia, and indigestion from TRP is tricky, but may be possible using manual pressure to localise pain response. With an abomasal ulcer there is mid-ventral abdominal pain, with pleurisy there is thoracic pain, with indigestion there is no pain, and with TRP there is anterioventral abdominal pain. History of the cow having been administered an oral magnet in the past, or identification of a magnet in the reticulum (by using a compass), decreases the likelihood of TRP.
At necropsy, there may be fibrin, pus and adhesions involving the abdominal surface of the reticulum. The diaphragm and the contents of the abdominal, thoracic or pericardial cavities may be involved. A wire, nail or needle may be found in the lumen or wall of the reticulum.
Treatment
Oral administration of a magnet may immobilise the penetrating metal if it migrates or falls back into the lumen of the reticulum. A 3-7 day course of systemic antibiotic therapy (procaine penicillin, ceftiofur, or oxytetracycline) should be administered. If signs persist, a laparotomy and rumenotomy may be required to remove the metallic penetrant. Non-steroidal anti-inflammatory drugs (flunixin meglumine, ketoprofen, meloxicam, or tolfenamic acid) may be required for pain relief and to get animals standing and eating.
Prevention
Ensure feedstuffs are not contaminated with nails, needles or short pieces of wire.
TRP may be prevented by oral administration of magnets which eventually lodge in the reticulum and may then prevent metal from penetrating the reticulum. Manufacturers of processed feed may use large magnets on production lines to remove metallic contaminants.
Urinary Tract Obstruction
Description
Uroliths (urinary stones) are common in cattle, sheep and goats. Urolithiasis is an important disease in feeder animals but may also be seen in breeders. It occurs in both sexes, but partial or complete obstruction of the urinary tract tends to be more common in castrated males because of the relatively narrow urethra.
It is primarily a nutritional disease. Mineral salts from feed and water that are normally dissolved in urine may form small stones (calculi) that lodge in and block the urethra, usually in the sigmoid flexure or the urethral process. The bladder distends and eventually the bladder or urethra ruptures. Death occurs after a few days from uraemia or septicaemia or both.
Risk factors that favour formation of uroliths include diets low in roughage or high in phosphorus, calcium, magnesium, oxalate or silicates; prepubertal castration; mineral-rich, inaccessible or unpalatable water; and conditions that favour dehydration and reduced urine output. Obstruction is usually at the sigmoid flexure of the penis. The possible outcomes of complete obstruction will be spontaneous dislodgement and passing of the urolith(s) in the urine, perforation of the urethra (urine escapes subcutaneously), or bladder rupture (releasing urine into the abdominal cavity). Bulls may incur rupture of the urethra when mounting other cattle.
Clinical Signs and Diagnosis
Signs include reluctance to move, legs stretched out, straining to urinate, and little or no urine flow. If the bladder and urethra are still intact, the back will be arched and there may be bruxism (grinding of teeth), stretching and kicking at the abdomen. Affected animals may develop prolapse of the rectum from straining to urinate.
Rectal palpation in cattle will detect a hugely distended bladder. If the bladder has ruptured, there will be urine accumulation in the abdominal cavity. This results in moderate abdominal distension and ballottement may induce a fluid wave at the opposite paralumbar fossa. Rectal palpation may detect a collapsed bladder.
If the urethra has perforated, there will be subcutaneous swelling along the prepuce and ventral abdomen (known as waterbelly).
The ammonia smell of the urine distinguishes it from other types of ascitic fluid. Calculi may be impacted in the urethral process at the tip of the penis in sheep and goats.
At necropsy the site of obstruction is identifiable by discrete calculi or granules compressed into a section of discoloured and necrotic urethral mucosa. If rupture of the urethra has occurred, there will be urine in the tissues around the site of obstruction. If the bladder has ruptured, there will be urine and possibly blood clots in the abdomen. Hydroureter and hydronephrosis may also be present.
Laboratory analysis of uroliths may assist in determining aetiology.
Treatment
Treatment is based on establishing a patent urethra to allow urination to occur and restoring fluid and electrolyte balance.
If the blockage is in the urethral process in sheep and goats, amputation of the blocked tip of the process with scissors may resolve the condition. Care should be taken to ensure there are not additional stones further back along the urethra or in the bladder.
If there is a complete obstruction and the bladder is still intact, perineal urethrostomy may be lifesaving. This can be performed under caudal epidural anaesthesia while the animal is standing, if skills and resources are available.
Sometimes a ruptured urethra may resolve without intervention if a patent urethra is established. Incisions may be made into the subcutaneous tissues adjacent to the prepuce to facilitate drainage of urine. A 10 cm incision is made on each side of the prepuce, about 10 cm from and parallel to, the midline. It may also be necessary to perform a perineal urethrostomy to help drain the bladder and avoid further urine flow through the urethra while the rupture heals. Animals with a perineal urethrostomy may then be transported for salvage slaughter.
Animals with a ruptured bladder and urine accumulation in the abdomen may be salvaged with a perineal urethrostomy and drainage of urine from the abdomen using a trocar or teat cannula. This may allow the bladder to heal spontaneously. If facilities and expertise are limited or salvage slaughter is difficult then these animals should be euthanised.
Prevention
Analysis of the uroliths is essential before adjustments to dietary mineral balance are made in order to ensure that appropriate changes are made.
Prevention of formation of urethral calculi is mainly dependent on providing a calcium to phosphorus ratio of 2:1 in the complete ration, and ensuring animals have ready access to good quality water supply. Additional measures may be useful in some cases, such as supplemental sodium chloride (up to 4 % of the total ration) to increase urine output, and urinary acidifiers that may prevent formation of some crystals.
Where a small number of cases have occurred, it is important to implement dietary changes and check water quality as soon as possible to try and prevent further cases from occurring.
Warts
Description
Warts are hairless, normally benign growths on skin or mucosa caused by a papilloma virus. The virus enters skin and mucosal abrasions after direct contact with infected animals, and fomites such as contaminated feed troughs, ear tagging pliers and rectal palpation sleeves. The papilloma viruses causing warts in cattle do not cause warts in humans.
Typically, the condition affects young adult cattle under two years old. Lesions appear suddenly and proliferate rapidly. The disease is self limiting, but the timing of regression is unpredictable and ranges from one month to over one year. Animals with warts should be excluded from the export process if they are likely to become the subject of negotiations during health inspection at destination. Warts reduce value of hides and may bleed, become infected or flyblown, and affect reproduction if they occur on the penis and prepuce of bulls, or the udder and vulva of cows.
Clinical Signs and Diagnosis
Warts can occur anywhere on the body, including the oesophageal groove and reticulum, but they are most frequently seen on surfaces prone to abrasion such as the head (especially around the eyes, ears and lips), neck, shoulder, and brisket. They vary in form and size from 1 mm diameter to large, broad-based masses hanging from the neck or brisket. Warts have a hard surface, may be smooth and rounded, have finger-like projections, or have a rough cauliflower appearance. They may have a dry or crusty surface.
Laboratory confirmation requires a biopsy specimen submitted in buffered formalin for histology.
Differential diagnoses include chronic ringworm, dermatophilosis, cutaneous lymphosarcoma, solar keratosis, stephanofilariasis, and squamous cell carcinoma.
Treatment
Treatment of warts is rarely necessary. In most cases it is best to let the disease run its course. Surgical removal of large, awkwardly located or ulcerated warts is sometimes necessary, as may be the case in breeding bulls with penile warts. However, removal may be followed by recurrence or stimulation of growth. Ligation of pedunculated warts may affect removal. Autogenous vaccines have been used to treat warts, but effectiveness is uncertain because self cure is common.
Prevention
Autogenous vaccines and anti-viral compounds/disinfectants can be used to control the disease in problem herds. Vaccination must commence at a very young age. Infected animals may be isolated from herd mates, but the long incubation period means other animals are likely to have been exposed. The virus is enduring in the environment so the premises and equipment may remain infected for over one year.