Copper Deficiency in Animals
Deficiency of copper causes CNS disease in sheep, goats, and pigs. Swayback is the congenital form of copper deficiency in lambs and is characterized by degeneration and necrosis of the cerebrum. The acquired form, enzootic ataxia, affects lambs, kids, and pigs. Affected animals 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. Histologically, there is chromatolysis and loss of neurons and degeneration of axons, primarily in the spinal cord and caudal aspect of the brainstem. Animals may improve with copper supplementation; however, permanent neurologic deficits are likely in severely affected animals.
Hypervitaminosis A in Animals
Cats fed excess vitamin A, usually from diets consisting largely of liver, develop extensive exostoses, most prominent in the cervical and thoracic spine. Clinical signs include neck pain and rigidity and forelimb lameness. Vertebral lesions are evident on radiographs. Reduction of dietary vitamin A prevents further exostosis; however, it does not appreciably reduce the lesions already present.
Thiamine Deficiency in Animals
Thiamine (vitamin B1) deficiency is most common in cats; however, it has also been reported in dogs. 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. Pathological findings are polioencephalomalacia, most prominent in the midbrain. Diagnosis is based on clinical signs, dietary history, and response to thiamine administration (thiamine hydrochloride, 10–20 mg/cat or 25–50 mg/dog, IM, every 24 hours for 2–4 weeks or until clinical signs abate).
