Vitamin A deficiency
Vitamin A deficiency
Vitamin A deficiency manifests itself in a number of species but is most commonly seen in captive carnivores. Vitamin A deficiency has been reported in sea otters (Enhydra lutris),  and has been suggested as the cause of liver disease and hepatic neoplasia in captive polar bears (Ursus maritimus) . However, the most common manifestation of vitamin A deficiency is in captive lions cubs between 6 months and two years of age. A recent study suggests a species- and captivity-specific predisposition for lions to develop the condition . Confirmed cases of this deficiency in captive cheetahs fed deficient diets have also been reported
Free-ranging carnivores frequently consume the entire carcass of their prey including the liver which is by far the richest source of preformed vitamin A (retinol and retinyl esters). Most herbivores and omnivores convert ß-carotene from plants into retinol to meet their vitamin A requirements. This biochemical pathway is relatively inefficient in many carnivores. Felids being obligatory carnivores require preformed vitamin A in their diet. In captivity, carnivores are often fed beef, horse or chicken carcasses from which the internal organs have been removed. Muscle meat is extremely low in Vitamin A as well as several other important vitamins and minerals.
Vitamin A is required for several different functions including vision, growth, epithelial differentiation, reproduction, and osteoclast function. The clinical signs of a vitamin A deficiency therefore manifest differently in different species and animals of different ages. In young lions the most consistent clinical signs are progressive ataxia, incoordination, opisthotonus, star gazing, blindness, and intermittent convulsions that manifest particularly when they are chased. If not treated, these animals may die within a matter of two months
The presence of vitamin A deficiency in animals in captive breeding facilities may be associated with a concomitant decline in litter size and increased cub mortalities particularly at the perinatal stage. It should be noted that these animals are likely to suffer from a combined mineral/vitamin deficiency including those that cause metabolic bone disease, thiamine deficiency, and copper deficiency. The lesions and related clinical signs may therefore differ from case to case.
The cranial osseuos changes associated with vitamin A deficiency in lions have also been referred to in the literature as an Arnold-Chiari-like malformations. The opinion has been expressed that most of these cases, were the consequence of vitamin A deficiency 
The neurological deficits seen in vitamin A deficiency are considered to be the consequence of defective bone remodelling, and impaired resorption of the cerebrospinal fluid with consequent increased intracranial pressure
The consistent lesions seen at necropsy are severe thickening of the cranial and vertebral bones, with consequent marked compression of the brain and herniation of the cerebellar vermis through the foramen magnum. (Fig. 1). The occipital bones and those of the tentorium cerebelli ossseum are markedly thickened due to impaired remodelling of the bone due to low vitamin A levels, and may be more than double their normal thickness 
The herniation, and pressure caused by the thickened bones, result in impairment of the drainage of the cerebrovascular fluid, and a dorso-lateral flattening of the medulla oblongata. This compression may be accompanied by the development of syringomyelic cysts extending into the dorsal and latteral grey and white matter. There may also be symmetrical Wallerian degeneration affecting the dorsal white matter . Impairment of cerebrovascular fluid flow causes the development of an internal hydrocephalus, and distention of the central canal in the spinal cord. . The lesions in the spinal cord are more pronounces in the cervical section of the cord. 
The pressure on the cerebellum causes malacia and eventual atrophy of the folia, accompanied by haemorrhage that may be acute of or older duration. Additional lesions in the cerebellum include rarefaction of the molecular layer, patchy loss of Perkunje and granular cells and proliferation of Bergman glia. In advanced cases there was marked gliosis.
Distinct lesions that were different from those described above have been seen also a the consequences of vitamin A deficiency in a young lion. This lion also had low copper levels, which may perhaps be more relevant to the development of the nature of the lesions seen in this case. In this case there was diffuse white matter degeneration at all levels of the spinal cord. The ventral gray columns and brain stem nuclei contained rare chromatolytic neurons with abnormal myofilament accumulations. The leptomeninges of the cervical spinal cord were focally adhered to the dura and thickened due to fibrosis and osseous metaplasia
To confirm the diagnosis, it is necessary to determine vitamin A levels in tissues. Fresh liver is an appropriate specimen and normal values of lions in the wild are 5400 IU/g of tissue. In lions suffering from vitamin A deficiency, levels may be as low as 2 IU/g
The diagnosis can also be confirmed by magnetic resonance imaging. It is suggested that abnormal values of the vitreous humor diamater, tentorium cerebelli osseum, occipital bone, and cervical spinal cord measurements and ratios be used to assist in making the diagnosis.
Developmental defects in felids, such as, the Arnold-Chiari and the Dandy-Walker syndromes, may be considered as differential diagnoses in these cases. The occurrence of an Arnold-Chiari type 2 malformation has been diagnosed in a lion cub in captivity
It is imperative that diets in captivity should be supplemented adequately. It is difficult to prescribe a standard compilation of such a vitamin/mineral mix, since the type of food offered may differ substantially and it is advisable to determine the need for the individual supplements based on the prevailing feeding regime in each specific facility.
Animals that are in the acute phase of the deficiency, may respond rapidly to Vitamin A supplementation and may return to normal within a matter of two weeks. Usually animals that manifest advanced signs of deficiency start to respond to treatment within two weeks and are fully recovered after about three months
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