Clinical and pathological findings associated with congenital hypovitaminosis A in extensively grazed beef cattle.

OBJECTIVE: To determine the cause of exceptionally high mortality (41.4%) in perinatal calves on a beef cattle property 50 km south-west of Julia Creek in north-western Queensland. DESIGN: Investigations were based on clinical assessment of affected calves and laboratory analysis of pre- and postmortem specimens taken from 12 calves aged from 6 to 36 h of age. METHODS: Associations between gross and histopathological findings and biochemical analyses conducted on serum and tissue samples were examined in relation to clinical observations. RESULTS: Clinical signs varied, but commonly included mild to severe ataxia, difficulty finding a teat and sucking, blindness (partial or complete, as judged by avoidance of obstacles) and depression with prominent drooping of the head. Gross and histopathological findings included herniation of the cerebellar vermis through the foramen magnum, squamous metaplasia of interlobular ducts in the parotid salivary glands and Wallerian degeneration of the optic nerves. Biochemical analysis of serum and liver samples available from four of the calves revealed low or undetectable levels of both vitamin A and vitamin E. CONCLUSION: Although vitamin E is known to have a sparing effect on vitamin A, the role (if any) played by deficiency of this vitamin was uncertain. The combination of clinical signs, postmortem findings, histopathological features and biochemical findings indicate that gestational vitamin A deficiency was highly likely to have been an important contributor to perinatal calf mortalities in this herd.

Juvenile mortality in captive lesser kudu (Tragelaphus imberbis) at Basle Zoo and its relation to nutrition and husbandry.

Since 1956, when the Basle Zoo (Switzerland) initiated the breeding of lesser kudu (Tragelaphus imberbis), 43% of the lesser kudu juveniles died before reaching an age of 6 mo. In this study, the objective was to obtain the pathological findings, nutritional history, and family tree information in order to evaluate the influence of husbandry on juvenile mortality in these animals. The main cause of death was white muscle disease (WMD), diagnosed in 14 cases (26%) of the deceased juveniles. Although enclosure size had remained constant and animal accessibility to the public was constantly high, both herd size and juvenile mortality had increased from 1956-2004. The diet consumed by the whole group in 2004 had deficient levels of vitamin E and selenium. The increasing linear trend of the mortality rate since the 1960s was significant, and there was a significant correlation between herd size and overall juvenile mortality. In contrast, there was no correlation between herd size and the occurrence of juvenile mortality associated specifically with WMD. Other investigated factors (sex, inbreeding, and season) had no significant effect on overall mortality up to 6 mo of age or on mortality associated with WMD. These results characterize both a dietary and a husbandry problem, and are supported by a lack of similar juvenile mortality in another facility where the diet was supplemented with vitamin E, animal numbers were kept low, and the enclosure structure offered more retreat options for the animals.

Field investigation of perinatal mortality in friesian cattle associated with myocardial degeneration and necrosis.

Perinatal mortality and stillbirths were investigated in an extensively managed herd of Friesian cows and heifers calving over a 2-year period: 504 cows were calved and 215 heifers. Cows were bred to Friesian and Jersey bulls using natural service. The perinatal fetal mortality rate was 7.5% for cows and 30% for heifers. An experienced stockman managed these calvings and veterinary assistance was required only on nine occasions. All stillborn fetuses were examined post-mortem by the Veterinary Laboratories Agency, Carmarthen and no infectious agent was identified on any occasion. Thyroid hyperplasia was found in two fetuses. In blood samples taken from 10 late pregnant heifers, mean glutathione peroxidase values were 7.9 +/- 1.7 IU/ml Packed Cell Volume (PCV). Tissues from eight fetuses were submitted to the University of Liverpool for histopathological examination; all presented lesions consistent with myocardial degeneration and necrosis of the left ventricle. Following treatment of 205 late pregnant heifers with sodium selenite and vitamin E, the overall perinatal mortality rate in these cattle fell to below 11%.

Mortality in captive wild-caught horned puffin chicks (Fratercula corniculata).

Sixteen horned puffin (Fratercula corniculata) and six parakeet auklet (Cyclorrhynchus psittacula) chicks of various prefledging ages were caught in Alaska and transported to the North Carolina Zoological Park (USA) in August 1995. Six of the 16 puffin chicks died within a 5-day period beginning 2 days after their arrival into quarantine at the zoo. The birds that died were collected at a young age, weighed 45.4-65.7 g, and had been fed a diet of thawed frozen ocean silversides (Atherinidae) that was not supplemented with vitamins. Clinical signs were nonspecific, and gross necropsies, insecticide toxicology screens, and bacterial cultures were unremarkable. Microscopic examination of tissues from five of the six birds showed myocardial necrosis and degeneration suggestive of vitamin E deficiency and intestinal protozoa resembling Microsporidia. The mortality pattern and histopathologic lesions observed in this case support the use of selective age capture and vitamin supplementation for wild alcid chick collection.

Selenium-vitamin E deficiency in swine fed peas (Pisum sativum).

An experiment was conducted to study the effects of feeding a 96.8% cull pea basal ration, low in selenium (0.061 ppm) and vitamin E (7.0 IU alpha-tocopherol/kg of ration), to growing pigs with and without supplementation of selenium, vitamin E, or both. The basal ration was high in crude protein (25.2%) and contained no supplemented fat. Nine of 10 pigs fed the unsupplemented basal ration had lesions attributed to selenium-vitamin E deficiency, and 8 of these pigs died during the 160-day experiment. The deficiency was usually characterized by sudden death (with no prior signs of illness), massive hepatic necrosis, hemoglobinuric and to a lesser extent cholemic nephrosis, degenerative myopathy of cardiac and skeletal muscles, edema, icterus, and acute terminal congestion and hemorrhage. Clinical signs, deaths, or lesions attributed to selenium-vitamin E deficiency were not observed in any of the pigs fed the basal ration supplemented with as little as 0.01 ppm selenium as sodium selenite or 100 ppm alpha-tocopherol. Pigs fed the unsupplemented basal ration gained more slowly (P less than 0.01) and less efficiently and had higher serum glutamic oxalacetic transaminase (SGOT) levels (P less than 0.01) than pigs fed the basal ration supplemented with selenium, vitamin E, or both. There was no difference (P greater than 0.05) in albumin-to-globulin (A/G) ratios among dietary treatment groups. Using the criteria of this study, the minimum selenium requirement of growing pigs fed a low tocopherol cull pea diet was determined to be between 0.06 and 0.07 ppm.

Alleviating mortality associated with a vitamin E-selenium deficiency by dietary ascorbic acid.

Adding ascorbic acid to a practical ration deficient in vitamin E and selenium for the growing duck substantially reduced associated mortality. The continued appearance of various myopathies but absence of vascular faults supported implication of a reduced de novo ascorbate synthesis as part of the syndrome. Presumably, alleviation of this induced secondary inadequacy with its more lethal pathology was the primary reason for the lower death rate.