Diagnosis of suspected hypovitaminosis A using magnetic resonance imaging in African lions (Panthera leo)

Vitamin A deficiency is described in captive lions. Ante mortem diagnosis can either be made by serum analysis or liver biopsy, both of which may be problematic. This study utilised magnetic resonance imaging to identify vitamin A deficiency in lions with relatively mild clinical signs, which could otherwise be attributed to numerous other neurological conditions. Magnetic resonance imaging is a non-invasive, reliable diagnostic tool to demonstrate pathology typically associated with this condition. To accommodate varying lion ages and sizes, a number of cranium and brain measurements were compared with that of the maximum diameter of the occular vitreous humor. Occular ratios of the tentorium cerebelli osseum and occipital bone were most reliable in diagnosing the thickened osseous structures characteristic of hypovitaminosis A. The ratio of maximum:minimum dorsoventral diameter of the C1 spinal cord was also of value.     

Hyperostotic bone disease in red pandas (Ailurus fulgens).

Three adult red pandas (Ailurus fulgens) developed multiple periarticular exostoses in their elbow joints. Two of these animals also had extensive periosteal new bone formation and osteosclerosis of the ulnae and radii and mild periosteal new bone deposition on the femurs. One animal also showed extensive hyperostosis of the cranium and mandibles. Dietary concentrations of calcium and phosphorus were estimated to be adequate, but dietary vitamin A and D appeared excessive when compared with recommended levels for this species. Serum vitamin A concentrations were not elevated in the two most severely affected animals, but their liver vitamin A content was higher than what is considered normal for most domestic animal species. Serum 25-hydroxy vitamin D concentrations were within normal ranges for domestic species. A definitive diagnosis for the cause of the lesions was not established, but hypervitaminosis A was suspected.     

COMPUTED TOMOGRAPHIC ANALYSIS OF CALVARIAL HYPEROSTOSIS IN CAPTIVE LIONS

Osseous malformations in the skull and cervical vertebrae of lions in captivity are believed to be caused by hypovitaminosis A. These often lead to severe neurologic abnormalities and may result in death. We describe the characterization of these abnormalities based on computed tomography (CT). CT images of two affected and three healthy lions were compared with define the normal anatomy of the skull and cervical vertebrae and provide information regarding the aforementioned osseous malformations. Because bone structure is influenced by various factors other than the aforementioned disease, all values were divided by the skull width that was not affected. The calculated ratios were compared and the most pronounced abnormalities in the affected lions were, narrowing of the foramen magnum, thickening of the tentorium osseus cerebelli and thickening of the dorsal arch of the atlas. CT is useful for detection of the calvarial abnormalities in lions and may be useful in further defining this syndrome.     

RADIOLOGIC ABNORMALITIES OF THE APPENDICULAR SKELETON OF THE LION (PANTHERA LEO): INCIDENTAL FINDINGS AND MYCOBACTERIUM BOVIS-INDUCED CHANGES

Thoracic and pelvic limbs from 15 euthanized free-ranging lions (Panthera leo), ranging in age from 16 to 144 months, underwent standard radiographic evaluation. All lions had tested positive for Mycobacterium bovis by means of a modified intradermal tuberculn test. The radiographs of six lions were normal and nine had incidental findings of which six had more than one lesion. Seven lions had lesions suspected to be associated with tuberculosis, which was confirmed in specific joints in two lions. Incidental pathology was classified as traumatic injuries and degenerative or trauma-associated joint disease. The traumatic lesions were fractures of which the most remarkable was a femur malunion. Four lions had fibula and another three lions had metacarpal/tarsal and phalangeal fractures. Joint lesions included glenoid, humeral head, and accessory carpal bone osteophytes. There was evidence of a cranial cruciate ligament rupture in an 8-year-old male. Trauma induced joint lesions were seen in four stifles (fragmented or displaced sesamoid bones, fragmented meniscal ossicle, or mineralized fragments). Radiological abnormalities believed to be caused by M. bovis were present in one stifle, one radiocarpal three tibiotarsal, and one tarsometatarsal joints. These had evidence of septic arthritis with extensive bone formation and capsular mineralization. In one 20-month-old lion, changes typical of a bone abscess were found in a proximal tibia. Radiologic evidence of elbow hygromas were seen in three elbows, all believed to be caused by M. bovis. Lions appeared to cope fairly well with a variety of traumatic injuries and were also susceptible to some of the aging/incidental radiologic findings seen in dogs and cats. The suspected M. bovis osseous lesions were more likely to involve the joints, particularly the tarsal joint and were mainly proliferative.     

Needle biopsy for hepatic vitamin A levels in lions (Panthera leo)

Hypovitaminosis A (HA)-related skull malformations resulting in neurologic abnormalities and death have been, and still are, reported in captive lions (Panthera leo) worldwide. Liver vitamin A (VA) concentration is the most reliable indicator of animals' VA status, and its assessment is essential in prevention and treatment of HA in lions. A percutaneous needle liver biopsy using high-performance liquid chromatography ultraviolet retinoid analysis for VA concentration measurement was validated. It was first assessed in vitro using chicken liver. Later, the safety and feasibility of ultrasound-guided percutaneous needle liver biopsy was assessed in living lions. Hepatic VA concentrations in lion liver were measured using the above laboratory method. Mean chicken hepatic VA concentration in needle biopsy (NB) and wedge biopsy (WB) of the same liver lobes were 108.66 and 60.89 microg/g wet tissue, respectively, and were significantly (P = 0.03) correlated (r = 0.74). The calculated linear regression for predicting VA concentration in WB using NB VA for chicken liver was 25.194 + 0.3234x NB (microg/g). Four ultrasound-guided percutaneous needle liver biopsies were obtained from each of the four lions under general anesthesia. Mean hepatic VA concentration was 8.25 microg/g wet tissue (range 1.43-25.29 microg/g). Mean serum VA concentration, measured in these four lions was 1,011.1 nmol/L with a standard deviation of 337.91 nmol/L (range 590.26-1,077.2 nmol/L). The lions recovered uneventfully, and no complications were observed during a 4-yr follow-up period. In conclusion, the percutaneous needle liver biopsy technique is a reliable, practical, safe tool for obtaining liver tissue samples antemortem for assessment of the VA status in lions and can be used in future studies.     

Suspected inherited rickets in Corriedale sheep

A suspected inherited form of rickets was diagnosed in Corriedale sheep on a commercial sheep farm in Marlborough. Affected lambs were normal at birth but showed a reduced growth rate and a range of skeletal abnormalities, including both varus and valgus deformities and a characteristic dip in the shoulder region. Up to 20 affected lambs had been born on the property over the last two seasons. Skeletal lesions in affected lambs included swollen costochondral junctions, moderate to marked thickening of physes in long bones, and collapse of weakened subchondral bone, particularly in the proximal humerus. These lesions, together with the microscopic changes, strongly suggested a diagnosis of rickets. Affected lambs were hypocalcaemic and hypophosphataemic, consistent with a deficiency of vitamin D.

Vitamin D assays revealed significantly higher 1,25(OH) vitamin D concentrations in affected lambs than in controls, suggesting a defect in the vitamin D receptor as the likely mechanism. DNA testing revealed that 4/10 Corriedale rams used during the previous season had sired affected lambs. Studies aimed at confirming the genetic nature of the disease and the mechanism are continuing at Massey University.     

Evaluation of T lymphocytes in captive african lions (Panthera leo) infected with feline immunodeficiency virus

OBJECTIVE: To determine whether FIV infection in captive African lions is associated with changes in immune cell variables similar to those detected in domestic cats infected with FIV. ANIMALS: 5 captive African lions naturally infected with FIV (FIV+) and 5 lions not infected with FIV (FIV-). PROCEDURE: Peripheral blood samples were collected from FIV+ lions during annual examinations conducted during a 7-year period and at a single time point from the FIV- lions. From results of CBC and flow cytometry, lymphocyte subsets were characterized and compared. RESULTS: Flow cytometric analysis revealed that the percentage and absolute number of CD4+ and CD8+ T cells were significantly lower in FIV+ lions, compared with these values in FIV- lions. In FIV+ lions, severe depletion in the absolute number of CD4+ and CD8+ T cells was detected, although this did not correlate with clinical signs. Muscle wasting was the most consistent clinical sign of infection. CONCLUSIONS AND CLINICAL RELEVANCE: Results suggest that FIV+ African lions develop lymphocyte deficiencies, including significant decreases in the absolute number of CD4+ and CD8+ T cells; these findings of immune dysfunction are similar to those defined for FIV+ domestic cats. It is important to monitor the number of CD4+ T cells in infected animals as a measure of disease progression.     

Degenerative myelopathy and vitamin A deficiency in a young black-maned lion (Panthera leo).

Degenerative myelopathy and vitamin A deficiency were diagnosed in a 1-year-old, female, black-maned lion (Panthera leo). Diffuse white matter degeneration characterized by dilated myelin sheaths, Wallerian degeneration, and reactive astrocytosis was present at all levels of the spinal cord. With luxol fast blue-resyl echt violet stain, bilaterally symmetrical demyelination was observed in the fasciculus cuneatus of the cervical spinal cord and in peripheral white matter of cervical, thoracic, and lumbar segments. Additionally, the ventral gray columns and brain stem nuclei contained rare chromatolytic neurons with abnormal neurofilament accumulation. Leptomeninges of the cervical spinal cord were focally adhered to the dura and thickened by fibrosis and osseous metaplasia. Vitamin A deficiency was diagnosed based on hepatic vitamin A concentration of 1.71 microg/g dry weight. Adequate hepatic vitamin A concentration for yearling to adult domestic animals ranges between 150 and 1000 microg/g dry weight. Lesions were distinct from those previously described in young captive lions with vitamin A deficiency, which had thickened skull bones and cerebellar herniation. The pathogenesis of vitamin A-associated myelopathy in this lion may be similar to that described in adult cattle, which is believed to result from spinal cord compression secondary to elevated pressure of cerebrospinal fluid.     

Pathology of domoic acid toxicity in California sea lions (Zalophus californianus)

Over 100 free-ranging adult California sea lions (Zalophus californianus) and one Northern fur seal (Callorhinus ursinus), predominantly adult females, were intoxicated by domoic acid (DA) during three harmful algal blooms between 1998 and 2000 in central and northern California coastal waters. The vector prey item was Northern anchovy (Engraulis mordax) and the primary DA-producing algal diatom was Psuedonitzschia australis. Postmortem examination revealed gross and histologic findings that were distinctive and aided in diagnosis. A total of 109 sea lions were examined, dying between 1 day and 10 months after admission to a marine mammal rehabilitation center. Persistent seizures with obtundation were the main clinical findings. Frequent gross findings in animals dying acutely consisted of piriform lobe malacia, myocardial pallor, bronchopneumonia, and complications related to pregnancy. Gross findings in animals dying months after intoxication included bilateral hippocampal atrophy. Histologic observations implicated limbic system seizure injury consistent with excitotoxin exposure. Peracutely, there was microvesicular hydropic degeneration within the neuropil of the hippocampus, amygdala, pyriform lobe, and other limbic structures. Acutely, there was ischemic neuronal necrosis, particularly apparent in the granular cells of the dentate gyrus and the pyramidal cells within the hippocampus cornu ammonis (CA) sectors CA4, CA3, and CA1. Dentate granular cell necrosis has not been reported in human or experimental animal DA toxicity and may be unique to sea lions. Chronically, there was gliosis, mild nonsuppurative inflammation, and loss of laminar organization in affected areas.     

Light and Electron Microscopic Examination of Various Doses of Given Vitamin A on the Development of Cornea in Mice; Partly presented in ICEM 13-Paris

Vitamin A (0.2 μgr, 0.6 μgr, 1.2 μgr) was administered orally to the mice on days 8–11 of gestation. Fetuses were removed on day 17 of gestation. No external malformation of the fetuses was seen on the stereomicroscope investigation. Corneal degeneration was seen on the light and electron microscopic examination. As a result it was accepted that vitamin A taken during the critical periods of gestation affected the development of cornea.     

Morphological variation of "complex vertebral malformation" in Holstein calves.

A study was performed to investigate the morphological expression of the inherited syndrome "complex vertebral malformation" (CVM) in Holstein calves. A total of 107 late-term aborted, premature, or neonatal calves suspected of having CVM were necropsied and retrospectively analyzed for the causal mutation in the gene SLC35A3. Sixty-two calves were homozygous affected, 16 were heterozygous, and 29 were homozygous normal. Calves affected by CVM were growth retarded. Vertebral lesions identified by radiography were present in 61 cases, of which 58 also had costal malformation. Malformation of the head, primarily in the form of dysplasia or palatoschisis, was present in 15 cases. Bilateral symmetric flexion of the carpal and metacarpophalangeal joints was present in all cases, whereas posterior arthrogryposis was found in 54 cases. Interventricular septal defects occurred in 33 calves, often in combination with other cardiac malformations. A wide spectrum of additional malformations was found. Other congenital syndromes were in most cases distinguishable from CVM on a morphological basis. However, a calf with a prenatal infection with bovine virus diarrhea virus constituted a phenocopy. The study demonstrated that the morphological expression of CVM is wide, but certain aspects, i.e., growth retardation, vertebral malformation, and symmetric arthrogryposis, are almost constant findings. However, cases without vertebral defects and phenocopies constitute a diagnostic problem. A presumptive diagnosis of CVM can in most cases be based on necropsy findings combined with information on descent and paternal CVM genotype, whereas a definitive diagnosis requires genotyping.     

Hypovitaminosis A in feedlot cattle

Hypovitaminosis A was diagnosed in a group of feedlot cattle that had been fed a diet low in carotene for 18 months. The primary signs of disease in the cattle were poor weight gain, ataxia, convulsions, night blindness, and total blindness. Serum vitamin A concentrations were used to confirm the diagnosis. The cattle were treated orally and intramuscularly with vitamin A, and the less severely affected herd members recovered rapidly.     

Hypervitaminosis A in a cat.

A 10-year-old cat that was kept on a diet consisting largely of raw liver was evaluated because of lethargy, partial anorexia, and weight loss of several months' duration. The cat's head and neck were rigidly extended, and a hard mass was palpable in the ventral cervical region. Cervical and thoracic radiography revealed proliferative bony lesions of the cervical and thoracic vertebrae as well as of the sternum and costal cartilages. Serum vitamin A concentration was 4 times normal. For reasons unrelated to hypervitaminosis A, euthanasia and necropsy were performed 6 months after evaluation. The skull and the cervical and first few thoracic vertebrae were rigidly fused, and the vertebral architecture was altered by deposition of new bone. The sternum and costal cartilages were similarly affected. The historical, physical, radiographic, laboratory, and postmortem findings were consistent with the diagnosis of hypervitaminosis A. On the basis of findings in this cat, hypervitaminosis A should be suspected in any sick cat fed a diet consisting partly or completely of raw liver.     

High vitamin D3 requirements in broilers for bone quality and prevention of tibial dyschondroplasia and interactions with dietary calcium, available phosphorus and vitamin A

1. Two experiments were carried out to investigate responses in performance and bone compositional and structural characteristics in broilers fed diets containing 4 concentrations of vitamin D3 (5, 20, 125 and 250 microg cholecalciferol/kg) at different concentrations of calcium, available phosphorus and vitamin A. 2. In experiment 1, body weight and tibia breaking strength were maximised at 14d with 250 microg vitamin D3/kg, tibia ash was maximised with 125 microg vitamin D3/kg. A high incidence of tibial dyschondroplasia (TD) was decreased to very low levels with 125 microg vitamin D/kg. 3. At 42d, performance and bone characteristics showed no response to vitamin D3 concentrations above 20 microg/kg. 4. Dietary vitamin A within the range 2-4 to 4.5 mg retinol/kg did not show any interaction with vitamin D3 status at either age. 5. In experiment 2, responses to vitamin D3 were strongly influenced by dietary calcium/available phosphorus. With 13 g calcium and 5 g available phosphorus/kg, performance and bone characteristics responded to vitamin D3 concentrations up to 125 microg/kg but more was needed at less optimal concentrations of calcium and available phosphorus. TD incidence was minimised with 250 microg/kg. 6. This study shows that high dietary concentrations of vitamin D3 can prevent TD. It is concluded that the vitamin D3 requirement of broilers up to 14 d of age at optimal dietary calcium and available phosphorus concentrations may be in the range 35 to 50 microg/kg for cortical bone quality and up to 250 microg/kg for prevention of TD. The vitamin D3 requirement for cortical bone quality after 14 d is not higher than 20 microg/kg. These requirements are much higher than earlier estimates and may be related to higher calcium requirements of modern broiler genotypes. Current regulations limiting maximum vitamin D3 concentrations in broiler starter diets may need to be reviewed.     

Bent-limb syndrome in lambs raised in total confinement.

A bent-limb syndrome in lambs raised in total confinement was characterized by curvature of the forelimbs. Radiographic findings included flaring of the affected long bone and thinning of the growth plate. The main histologic change was endochondral dysplasia of the long bone. In feed samples, all trace minerals analyzed were within recommended concentrations except iron, which was much higher (400 ppm dry matter) than the normal requirement of lambs (70 ppm). All mineral concentrations in serum were normal except those of inorganic phosphorus and iron, which were higher. Results of soft tissue and bone mineral analyses were normal. Altering the ratio of calcium and phosphorus did not affect the incidence of disease, but intramuscular administration of massive doses of vitamin D3 and reducing the amount of dietary iron had a prophylactic effect. The increase in serum phosphorus was probably related to the dietary excess of iron, which probably decreased vitamin D metabolite formation in the kidney, which in turn could be prevented by massive doses of vitamin D3.     

Vitamin A deficiency in the captive African lion cub Panthera loe (Linnaeus, 1758).

Dietary, breeding and clinical histories and pathological findings are presented from 2 confirmed and 5 presumed cases of vitamin A deficiency in immature African lions. Five of the 7 animals were born in the wild while 2 were born in captivity. All animals were fed lean red meat sprinkled with a vitamin/mineral supplement. Salient clinical signs were incoordination, "star gazing", blindness and intermittent convulsions. Pathological lesions seen in 4 animals included severe thickening of the cranial bones, with consequent marked compression of the brain and partial herniation of the cerebellum. Vascular damage in the cerebellum and ensuing haemorrhages, resulting in acute increases of an already high intracranial pressure, were thought to be the cause of some of the clinical signs, particularly convulsions rather than direct pressure-necrosis and atrophy of nervous tissue.     

Domoic acid toxicity in Californian sea lions (Zalophus californianus): clinical signs, treatment and survival

Eighty-one Californian sea lions (Zalophus californianus) with signs of domoic acid toxicity stranded along the coast of California in 1998 when there were blooms of the domoic acid-producing alga Pseudonitzschia australis off-shore. In 2000, a further 184 sea lions stranded with similar clinical signs, but the strandings occurred both during detectable algal blooms and after the blooms had subsided. The clinical signs in these 265 Californian sea lions included seizures, ataxia, head weaving, decreased responsiveness to stimuli and scratching behaviour. Affected animals had high haematocrits, and eosinophil counts, and high activities of serum creatine kinase. They were treated supportively by using fluid therapy, diazepam, lorazepam and phenobarbitone. Fifty-five of the 81 sea lions (68 per cent) affected in 1998 and 81 of the 184 (44 per cent) affected in 2000 died despite the treatment. Three of the 23 sea lions which survived in 1998 were tracked with satellite and radiotransmitters; they travelled as far south as San Miguel Island, California, and survived for at least three months. Eleven of the 129 animals which were released stranded within four months of being released.     

BILATERAL ELBOW MALFORMATION IN A CAT CAUSED BY RADIO-ULNAR SYNOSTOSIS

A 9-month-old neutered male cat was referred because of left forelimb lameness. Physical examination, laboratory analysis, and radiographic examination of the entire skeleton were performed. The radiographic diagnosis was bilateral radio-ulnar synostosis with secondary elbow malformation. A comparison between clinical and radiographic findings of the cat and those described in children affected by radio-ulnar synostosis is reported. Correlations and differences are discussed.     

Inheritance of occipital bone hypoplasia (Chiari type I malformation) in Cavalier King Charles Spaniels

Occipital bone hypoplasia with foramen magnum obstruction and secondary syringomyelia (SM) is a common condition in the Cavalier King Charles Spaniel (CKCS) that is similar to human Chiari type I malformation. A worldwide family tree of more than 5,500 CKCSs spanning a maximum of 24 generations was established by obtaining pedigree information from 120 dogs diagnosed with SM secondary to occipital bone hypoplasia. The ongoing study showed 6 of 8 great grandparents of all affected dogs could be traced back to 2 female ancestors so that all 8 were descended from one or the other or both. The disease appears to be more severe and have an earlier onset with increased inbreeding, especially when breeding from affected dogs. The family tree of idiopathic epilepsy (IE) appears to be a different subset of the CKCS population, although some overlap was observed. Idiopathic epilepsy is more frequent in lines originating from whole-color dogs. Selection for coat color is believed to have influenced the development of both occipital hypoplasia with secondary SM and IE. In addition, breeding guidelines to reduce the incidence of mitral valve disease have placed further pressures on the gene pool.