Common diseases of meat goats: Individual animal diseases (Proceedings)


Information on pregnancy toxemia, polioencephalomalacia, listeriosis, tetanus, scrapie, rabies, and anemia in goats.

Pregnancy Toxemia

Pregnancy toxemia (twin lamb disease, lambing or kidding sickness) is most common does with triplets, and/or are either thin or obese. Much of the abdominal space is occupied with multiple feti in the uterus during late gestation. Fat accumulation in the abdomen in obese animals also occupies space. Because of lack of space for the rumen, these females have difficulty consuming enough feedstuffs to satisfy their requirements. In late gestation, nutritional requirements increase to 150% of maintenance with a single fetus and 200% with twins. Late gestation is usually during the winter months, when less pasture is available, and as a general rule, poorer quality feeds are available. Pregnancy toxemia is also seen following anorexia secondary to other diseases (ex. foot rot, ovine progressive pneumonia, caprine arthritis encephalitis virus), or with stresses such as bad weather, transporting, etc. There is also a genetic predisposition in some individual animals.

Very early signs of pregnancy toxemia are mild depression, anorexia and possibly limb edema. If left untreated, goats become anorexic and depressed, and soon become recumbent. Neurologic signs including blindness, circling, incoordination, star-gazing, and tremors. Constipation and teeth grinding can also occur Icreased respiratory rate develops if acidosis occurs. If left untreated, does become recumbent.

Azotemia, both from dehydration and secondary renal disease, is a common finding. A urinalysis will be positive for both ketones and protein. Ketoacidosis is common in small ruminants. Hypocalcemia and hypokalemia may be present due to anorexia. They are not always hypoglycemic. Liver enzymes are usually found to be within normal limits, but occasionally may be increased.

Diagnosis is based on clinical signs, the presence of multiple fetuses, and typical clinicopathologic findings. Differential diagnoses include listeriosis, hypocalcemia, polioencephalomalacia, hypomagnesemia, and meningeal worm infestation.

In small ruminants, very early cases (prior to recumbency) may be treated with oral glucose or glucose precursors. 60-100 mls of propylene glycol orally twice a day, or oral corn syrup or glycerol can be tried. Oral high energy calf electrolytes with bicarb can also be given orally. Rumen transfaunation, vitamin B complex (including B12, biotin, and niacin) are also recommended treatments.

Once females show neurologic signs or become recumbent, treatment must be very aggressive. IV glucose, calcium borogluconate, and bicarbonate may be needed.

Glucocorticoids (15–20 mg dexamethasone) can help by causing gluconeogenesis, increasing appetite and inducing abortion. Prostaglandin (PGF2α) should also be used (5-10 mg) for induction of parturition in does. Flunixin meglumine (0.5-1 mg/lb) are indicated if endotoxemia is suspected from dead fetuses.

Removal of the fetuses is critical in these severe cases. Assessment of fetal viability with ultrasound helps with the decision to induce parturition or perform a C-section. Since a breeding date is rarely known, age of the fetuses is hard to determine. If the fetuses are alive, induction of parturition can be an option. However, if the fetuses are already dead, or the condition of the doe is severe, an immediate C-section is warranted. Fluid support during and after surgery is critical. Low birth weights of lambs, kids and calves at the beginning of the birthing season can indicate potential risk of pregnancy toxemia.

Prevention of this disease is through proper nutrition. Maintaining animals in proper body condition throughout the year, and making sure energy and protein levels are adequate in late gestation are important. For does in late gestation, hay should have protein content of at least 10%, and 1-2 lbs of concentrate should be fed per head per day. During periods of stress, particularly cold wet weather, concentrate may need to be increased to 2-3 lbs/head/day (divided in two feedings). Parasite control, disease prevention and decreasing stress are important.

Ultrasonography can help determine which females have multiple fetuses, and these animals separated into groups and fed accordingly. Addition of an ionophore in a feed or mineral mixture will enhance the formation of the glucose precursor propionic acid, and improve effeciency of feed utilization.

Neurologic Diseases

The most common diseases involving the brain that I see in adult goats are polioencephalomalacia (PEM) and listeriosis. PEM can be seen in any age animal, and is associated with disruption of normal diet or eating habits. High concentrate diets, sudden changes in diet, high molasses or sulfur content in the diet have all been associated with PEM. Any stressful situation (weaning, change in housing, introduction of new animals, bad weather) that causes a decrease in appetite can cause PEM. Signs associated with PEM are central blindness, depression, incoordination, head pressing, recumbency, opisthotonus, seizures, vocalizations, and/or dorsomedial strabismus. PEM and lead toxicity can both cause central blindness, and lead toxicity cases can transiently respond to thiamine treatment, so lead toxicity should be a differential diagnosis for PEM. Definitive diagnosis of PEM requires measurement of RBC enzymes that is not readily available in practice, so a diagnosis of PEM is usually made by response to treatment with thiamine. An attempt should be made to determine and correct the underlying cause. PEM can be treated with thiamine (5 mg/lb SQ, TID to QID). If caught early the prognosis is good. If no response to treatment is seen in 1-2 weeks, chances are the animal will have permanent deficits. Supportive care is important if animals cannot eat or drink. Transfaunation of rumen contents from a normal ruminant may help if GI disease is severe. Control of seizures can usually be accomplished with valium, but occasionally phenobarbitol is needed.

Listeriosis is most commonly seen in winter and early spring. Any damage to the oral mucosa (erupting teeth, introduction of hard feeds or browse) can predispose to listeriosis. It occurs in animals grazing close to the ground and eating wet, moldy hay. It is not commonly associated with silage feeding. Listeriosis in goats is characterized by depression and cranial nerve deficits. Circling is frequently seen, but listeriosis should be considered with any cranial nerve deficit, especially if multiple, asymmetric deficits exist, even if circling is not present. Progression of the disease can be quick, with many animals found recumbent. Migration of Paralaphostrongylus tenuis is also seen in goats and can present like listeriosis. Confirmation of this disease can be difficult. CSF tap shows elevations in protein and mononuclear cells, but this can also be seen with other diseases. CSF may also be normal in a small percentage of cases, especially if taken from the lumbosacral space. P. tenuis migration sometimes causes increased numbers of eosinophils in CSF. Listeria can be difficult to culture, and a negative CSF culture does not rule out listeriosis. If the clinical signs are consistent with listeriosis, antimicrobial therapy is indicated. Tetracyclines and penicillins are effective if instituted early. Some cases seem to respond to one but not the other of these antibiotics, and predicting which will work in a certain case is difficult. If no response is seen to either tetracycline or penicillin in 48 hours, therapy should be changed to the other drug. Since listeria can occur in multiple animals on a farm, historical response to therapy is important to note. Anti-inflammatory therapy (non-steroidal or steroidal) and supportive care are also very important. These animals may be unable to eat or drink, and can become acidotic due to excessive saliva loss.

Goats are very susceptible to tetanus. This disease should be suspected in nonvaccinated animals shoeing signs of lameness or stiffness. Signs progress to a stilted gait, raised tailhead, saw-horse stance and lockjaw. Retraction of the lips and hyperesthesia to sound and light are also seen. The disease eventually progresses to recumbency and death. Treatment if successful, is usually prolonged for months, and requires extensive supportive care. However, the small size of goats makes this easier than in other large livestock. Tetanus antitoxin (150-300 IU) and high doses of penicillin are needed to stop the progression of the disease. Fluid and nutritional support are imperative. If lockjaw is present oral fluids and feeding may be impossible. Fluids can be administered intravenously, and fluids and food can be administered through a rumenostomy. Acid base status should be monitored and baking soda can be added to fluids and food if necessary. A quiet, dark environment is important also. Sedation and muscle relaxants can also be administered. Many animals will be unable to rise, but will be able to stand and walk if lifted. Slings can also be made to help support weight and prevent decubital ulcers. Tetanus vaccines are highly efficacious and cheap. I recommend a toxoid in the first week of life, at one month of age, at weaning, and yearly after that. Older animals that have not been vaccinated should have an initial dose and booster according to the product label.

No discussion of neurologic diseases in small ruminants would be complete without mention of Scrapie and rabies. Scrapie is a transmissible spongiform encephalopathy, the cause of which is debatable. It's more common in sheep, but does occur in goats. It is transmitted both horizontally and vertically. Host genetics and stain of the infectious agent determine whether an animal will develop the disease. The genetics of susceptibility are well defined in sheep, but not in goats. The clinical signs are intense pruritis, ataxia, and wasting. The only antemortem test is immunohistochemistry of lymphoid tissue from the nictitating membrane. There is not treatment for Scrapie.

Rabies in goats can present with a variety of clinical signs. Sometimes the dumb form occurs where animals are depressed and progress to recumbency. Other times they are more aggressive, attacking people and other animals and sometimes becoming sexually excited. Any type of paralysis should be suspected to be rabies. Collection of CSF should be avoided if rabies is suspected or handled to prevent human exposure. Increased protein, mononuclear cells and neutrophils are seen. Rabies can be prevented through vaccination with products approved for sheep. Vaccination can start at 3-4 months of age with appropriate booster, then yearly after that.

Other diseases such as bacterial meningitis, brain abscesses, otitis, toxicosis and injuries that occur in other livestock species can occur in goats. The clinical signs, diagnosis and treatment is also similar to other livestock species. Organisms most often causing meningitis are E. coli, Pasteruella spp., and Mycoplasma spp. And are also implicated in otitis media and interna cases. Brain abscesses are most often caused by Actimomyces spp. Common toxicities include rhododendron (azalea), organophosphate, and lead toxicity. Salt toxicity/water deprivation can also occur.

Although much less common than bacterial meningitis/otitis, goat kids may also have neurologic disease due to enxootic ataxia and spinal abscesses, and the neurologic form of Caprine Arthritis Encephalitis virus (CAE). Enzootic ataxia, also called swayback, is caused by primary or secondary copper deficient diet in does. Signs of weakness and ataxia are seen within a few weeks of birth. Treatment is usually unsuccessful as damage to neurologic tissues is usually irreversible. Spinal abscesses usually present as acute spinal paresis/paralysis when the vertebral body fractures through the infection site. CAE most commonly presents as arthritis in adult goats, but can cause

Anemias other than Haemonchus

Lice infestations are common in goats, especially in the wintertime. Besides anemia, clinical signs of lice pruritus, hair loss, and weight loss. There are two types of lice; biting and sucking. Classically, only sucking lice cause anemia. However, mixed infections of both types are common. Sucking lice can be treated with injectable ivermectin or dormectin, or topical treatments, but only topical treatments are effective for biting lice. So, since mixed infections are common, topical treatments are preferred. Treatments (both topical and injectable) should be repeated in two to three weeks to kill any lice that have emerged from eggs or that were in the environment. All animals (of the same species) in contact with the infested animal should also be treated. There are several topical products approved for use in sheep and goats. An approved product should be selected, and proper meat and milk withdrawal times observed. Some of the pour-on products for cattle that are meant to be systemically absorbed for internal parasites are also labeled for lice control. However, many of these products have caused severe burning/dermatitis in small ruminants and should be avoided.

Blood loss anemia can also be due to trauma, especially from dog bites. Excessive bleeding following castration and dehorning can occur.

Excessive hemolysis of red blood cells (RBC) is uncommon, but can occur. Hemolysis can be classified as intravascular or extravascular, and the classification can help determine a diagnosis. Toxic plants and RBC parasites such as Anaplasma, Eperythrozoon and Babesia lead to destruction of RBCs by the reticuloendothelial system and thus extravascular hemolysis. Ingestion of bovine colostrum by neonatal goats can also sometimes lead to immune-mediated extravascular hemolysis. Ingestion of excess nitrates/nitrites and copper can cause intravascular hemolysis. Goats are not as sensitive to copper toxicosis as sheep, but it can occur. Bacterial toxins from some Clostridium and Leptospira species, and rapid changes in plasma osmolality due to rapid IV injection of hypotonic fluids or ingestion of large quantities of water following water deprivation or dehydration can also cause intravascular hemolysis.

Both intravascular and extravascular hemolysis can lead to pallor, weakness, icterus and bilirubinuria. Intravascular hemolysis will also be accompanied by hemoglobinemia and hemoglobinuria. Since hemoglobin is a pyrogen, fever is common with intravascular hemolysis, no matter the cause. Hemoglobin is also renotoxic, and secondary acute renal failure can occur due to severe intravascular hemolysis.

The most common causes of non-regenerative anemias are chronic diseases and iron deficiency secondary to chronic blood loss. Chronic blood loss is most commonly due to parasitism (either internal or external). Other nutritional deficiencies, such as copper and selenium, can also cause a non-regenerative anemia. ataxia/paresis/paralysis in goat kids from 1- 4 months of age.

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