Copper Deficiency
Copper deficiency causes CNS disease in sheep, goats, and pigs. Swayback is the congenital form of copper deficiency in lambs and is characterized by cerebral degeneration and necrosis. The acquired form, enzootic ataxia, affects lambs, kids, and pigs; this results in permanent myelin degeneration in the spinal cord, leading to progressive incoordination and paralysis.
Animals with copper deficiency appear normal at birth; however, they develop progressive paraparesis with hyporeflexia and muscle atrophy within the first few months of life. Other clinical signs include diarrhea and unthriftiness and, in lambs, abnormal fleece.
Differential diagnoses include caprine arthritis and encephalitis virus infection in young kids. Copper content of the ration should be evaluated. Histologically, chromatolysis and loss of neurons and degeneration of axons are observed, primarily in the spinal cord and caudal aspect of the brainstem.
Affected animals might improve with copper supplementation; however, permanent neurological deficits are likely in severely affected animals.
Hypervitaminosis A
Hypervitaminosis A (also known as vitamin A toxicosis or retinol toxicosis) is a nutritional disorder caused by excessive intake of vitamin A that primarily affects the skeleton and can result in vertebral abnormalities. Exostoses involving the vertebral column can cause spinal cord or nerve root compression and associated neurological deficits.
Affected species include cats, dogs, birds, and reptiles. Hypervitaminosis A is rare in ruminants.
In mammals, excess vitamin A inhibits intramembranous and endochondral ossification, resulting in dystrophic calcification and abnormal bone formation. Clinical abnormalities typically develop only after several months of excessive vitamin A intake.
Cats and dogs fed diets consisting largely of liver are at risk of chronic hypervitaminosis A. Cats are more susceptible than dogs.
Pearls & Pitfalls
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Affected cats and dogs develop extensive exostoses, most prominent in the cervical and thoracic spine. Clinical signs include neck pain and rigidity and forelimb lameness.
Affected animals typically have a history of chronic dietary intake of primarily raw liver or liver oil supplementation and may also have lethargy, anorexia, and weight loss. Vertebral lesions are evident on radiographs. Serum vitamin A concentration can be measured to support the diagnosis.
Decreasing dietary vitamin A prevents further exostosis; however, it does not appreciably decrease the lesions already present.
Thiamine Deficiency
Thiamine (vitamin B1) deficiency in animals is a nutritional disorder that primarily affects the brain but can also cause spinal cord dysfunction, particularly paraparesis.
Thiamine deficiency is most common in cats; however, it has also been reported in dogs (1). Causes include inadequately formulated commercial diets, vegetarian diets, food preserved with sulfur dioxide (which destroys thiamine), and raw fish diets (which contain thiaminase).
Affected cats typically exhibit brain dysfunction characterized by vestibular signs, head tremor, ataxia, depression, severe ventroflexion of the head, seizures, and death. Clinical signs in dogs include anorexia, depression, paraparesis, seizures, coma, and death. Polioencephalomalacia, most prominent in the midbrain, is a pathological finding in thiamine deficiency. Thiamine deficiency can also cause polioencephalomalacia in ruminants.
Diagnosis is based on clinical signs, dietary history, and response to a therapeutic trial of thiamine administration.
Treatment consists of thiamine supplementation. Recommended doses vary widely but a typical regimen is 50–100 mg, every 12 hours for cats and 100–600 mg every 12–24 hours for dogs (1). Initially, thiamine is administered by IM injection for 3–5 days; this is followed by oral dosing. Parenteral administration is especially important if vomiting or GI disease is present because oral absorption of thiamine may be inadequate.
References
Markovich JE, Heinze CR, Freeman LM. Thiamine deficiency in dogs and cats. J Am Vet Med Assoc. 2013;243(5):649-656. doi:10.2460/javma.243.5.649
