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Treating meat goats for neurological ills
Practitioners provide veterinary care for a growing number of meat goats in the United States - animals known to develop neurological disease.
Practitioners provide veterinary care for a growing number of meat goats in the United States — animals known to develop neurological disease.
Such conditions can be frustrating to treat. Many neurological diseases can present with similar signs, and diagnostics are limited. But because some neurological diseases have herd implications or are zoonotic, practitioners must attempt to list the most likely diagnoses so treatment and/or preventative measures can be taken.
Take a history
Due to the limitations of physical examinations and diagnostics for neurological diseases, a thorough history is extremely important. Many times, a management or feeding change has taken place that leads to neurological disease. Remember: Many neurological signs are not caused by diseases of the nervous system but are secondary to other systemic diseases.
Brain or spinal cord?
A thorough physical examination is important. Injury to the animal and personnel must always be considered when trying to restrain diseased goats for examination, especially large males. Because many neurological signs stem from other systemic diseases like pregnancy toxemia, a complete general physical examination should be performed before concentrating on the neurological examination. Trying to observe the animal in its surroundings before restraint is key. Mentation, head posture, gait abnormalities, tremors and head tilt should be noted. Blindness can be difficult to prove because animals can avoid obstacles using their other senses.
The main objective is to classify the disease as a brain disease or a spinal- cord disease. Although multi-focal diseases can occur, they are less common. Gait abnormalities, especially ataxia, can be present with brain and spinal-cord disease. Also, generalized weakness from other diseases can be difficult to differentiate from true neurological ataxia. Cerebral disease should be suspected if changes in mentation, head pressing, blindness, bizarre behavior or seizures are observed. Cerebellar diseases usually cause hypermetria and intention tremors. Circling, ataxia, proprioceptive deficits and/or cranial nerve signs are seen with brain-stem disease. Blindfolding might worsen cerebellar or brain-stem disease signs.
Once the animal is observed at a distance, the practitioner often has an idea if the disease involves the brain or spinal cord. Cranial-nerve examination must be performed to help further differentiate brain disease, or if no brain signs are seen from distant observations, to rule out brain disease so spina-cord disease can be the focus. Localization of spinal-cord disease is the same as in other species.
A goat's size makes it a candidate for diagnostic procedures commonly used in small animals, such as plain and contrast radiography, computed tomography and magnetic resonance imagery. However, the cost of these procedures might be prohibitive.
Cerebrospinal fluid (CSF) is collected easily from the lumbosacral space and can provide valuable information. A 20-gauge, 1.5-inch needle is used for neonates and an 18-gauge, 1.5-inch needle for adult goats. Ambulatory patients can be tapped standing. Non-ambulatory patients should be placed in lateral recumbency or in sternal recumbency in a dog-sitting position with the rear legs forward on either side of the animal. The pelvis must be straight and level. Light sedation and a local anesthetic will help with restraint. The lumbosacral area should be clipped and surgically prepared. Wearing sterile gloves, the indention of the lumbosacral junction should be palpated. A needle is inserted into the deepest part of the indention, directly on midline. Keep the needle perpendicular to the spine from the side view, and straight up and down from the rear view. If bone is encountered, redirect the needle slightly cranial or caudal until the needle drops into the lumbosacral space. Advance the needle slowly until a slight pop is felt. The animal usually jumps slightly when the needle punctures the dura mater. CSF should flow from the needle or can be gently aspirated with a syringe. If the needle is in the lumbosacral space and advanced until bone is encountered again, back the needle out 1 mm to 2 mm, and try to aspirate. Place the fluid in an EDTA tube for fluid analysis and a plain tube if cultures are desired.
Normal, non-traumatically obtained fluid should be perfectly clear with no discoloration, sediment or turbidity. It is best to have the sample analyzed locally within one hour. If this is not possible, place half of the sample in an equal volume of 40 percent ethanol to preserve the cells (inform the laboratory that this has been done), or centrifuge half the sample to concentrate the cells and prepare slides to be sent with the rest of the fluid.
The most common brain diseases that I find in adult goats are polioencephalomalacia (PEM) and listeriosis. PEM can inflict animals at any age. In cattle, it usually is associated with high-concentrate diets, sudden dietary changes or high molasses or sulfur content in the diet. My experience with goats, however, is that these predisposing factors usually are not present, and the condition appears stress-induced (weaning, housing changes, new-animal introductions, bad weather). Signs associated with PEM are central blindness, depression, incoordination, head pressing, recumbency, opisthotonus, seizures, vocalizations and/or dorsomedial strabismus.
PEM and lead toxicity can cause central blindness, and lead toxicity cases can respond transiently 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 usually is made by response to treatment with thiamine. 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 one or two weeks, the animal likely will have permanent deficits. Supportive care is important if animals cannot eat or drink. Transfaunation of rumen contents from a normal ruminant might help if GI disease is severe. Control of seizures usually can be accomplished with Valium, but phenobarbitol occasionally is needed.
Listeriosis affects goats more often than cattle and sheep. It commonly appears in winter and early spring but can occur any time during the year. 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.
The most likely differential diagnosis for listeriosis is brain and/or spinal cord disease due to migration of Parelaphostrongylus tenuis (meningeal worm), which is common in some areas of the country. Confirmation of a diagnosis of listeriosis and meningeal worm infestation can be difficult. With listeriosis, a CSF tap shows elevations in protein and mononuclear cells, but this also can be observed with other diseases. CSF might 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 administered early. Some cases seem to respond to one but not both antibiotics, and predicting which one will work is difficult. If no response is seen to either antibiotic within 48 hours, the drug therapy should be changed.
Because listeriosis can occur in multiple animals on a farm, historical response to therapy is important to track. Anti-inflammatory therapy (non-steroidal or steroidal) and supportive care is crucial. These animals might be unable to eat or drink and can become acidotic due to excessive saliva loss, so fluid and nutritional support are indicated.
Goats are susceptible to tetanus. This disease should be suspected in non-vaccinated animals showing signs of lameness or stiffness. Clinical signs and treatment are similar to other species.
Scrapie and rabies
No discussion of neurologic diseases of small ruminants would be complete without mentioning scrapie and rabies. Scrapie is a transmissible spongiform encephalopathy more common in sheep, but it does manifest in goats. It is transmitted 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 pruritus, ataxia and wasting. There is no treatment for scrapie. The only antemortem test is immunohistochemistry of lymphoid tissue from the nictitating membrane or rectal mucosal biopsy.
Rabies in goats can present with a variety of clinical signs. Sometimes the dumb form occurs where animals are depressed and progress to recumbency. Others are more aggressive, attacking people and animals and sometimes becoming sexually excited. Rabies can be prevented via vaccination.
Bacterial meningitis, brain abscesses, otitis, toxicosis and injuries that occur in other livestock species can occur in goats. The clinical signs, diagnosis and treatment also are similar to other livestock species. Organisms most often causing meningitis are E. coli, Pasteruella spp., and Mycoplasma spp. and also are implicated in otitis media. Brain abscesses most often are caused by Actimomyces spp. Common toxicities include rhododendron (azalea), organophosphate, and lead toxicity. Salt toxicity/water deprivation also can occur.
Though much less common than bacterial meningitis/otitis, goat kids also might 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 deficiency in does. Signs of weakness and ataxia are seen within a few weeks of birth. Treatment usually is unsuccessful because damage to neurologic tissues usually is 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 ataxia/paresis/paralysis in goat kids age 1 month to 4 months.
Dr. Navarre works as an extension veterinarian with Louisiana State University's Department of Veterinary Science.