Disseminated microsporidiosis due to Encephalitozoon hellem in an Egyptian fruit bat (Rousettus aegyptiacus).

Disseminated microsporidiosis was diagnosed in an adult female Egyptian fruit bat that died unexpectedly in a zoo. Gross findings, which were minimal, included poor body condition, bilateral renomegaly, and mottling of the liver. Histopathological lesions, which were particularly pronounced in the urogenital tract and liver, consisted primarily of inflammation associated with intracytoplasmic microsporidian spores. Polymerase chain reaction -based methods were used to establish the identity of the microsporidian as Encephalitozoon hellem. E. hellem is an emerging cause of human and avian disease, manifested mainly as opportunistic infection in immunosuppressed patients. This report describes the first documented case of E. hellem in a non-human mammalian species.

Carboplatin for treatment of a Sertoli cell tumor in a mallard (Anas platyrhynchos).

A 13-year-old male mallard was diagnosed with a non-resectable Sertoli cell tumor involving the left testis. The duck was treated with four doses of single-agent carboplatin given at 4- to 5-week intervals. Heteropenia, 2 weeks after each treatment, was the acute dose-limiting toxicity. The tumor reduced in size by 25%, and the duck's clinical condition improved for 12 months. Sertoli cell tumors are rare in birds, and this is the first report, to our knowledge, of attempted chemotherapy treatment in the veterinary literature.

Modelling cortical cataractogenesis 21: in diabetic rat lenses taurine supplementation partially reduces damage resulting from osmotic compensation leading to osmolyte loss and antioxidant depletion.

The concentration of taurine and the amino acids, glutathione, cysteine, ascorbate and ATP were determined in the lenses of rats made diabetic with streptozotocin. In the clear lenses, prior to vacuole formation after 1 or 2 weeks of diabetes, the increase in concentration of sorbitol and the total decrease of all these osmolytes were not significantly different. The major components of the osmolytes lost were taurine and amino acids, which together accounted for over 75% of the total osmolyte loss. Since glutathione, ascorbate, taurine and cysteine have been reported to have antioxidant activity, it appears that their loss may potentiate damage occurring as a result of free radicals generated by nonenzymic glycation by the Maillard reaction. Amino acids also lost as a result of the osmotic compensation, are estimated to be responsible for almost half of the antioxidant activity lost. To test this hypothesis, normal and streptozotocin diabetic female Wistar rats were given taurine at 0.05% or 0.10% (w/w) in the diet. This treatment resulted in small only marginally significant increases in serum taurine levels. At the end of 6 weeks the rats were examined for weight gain or loss and at the time of killing, blood was collected for measurement of serum glucose. gamma-Crystallin levels were determined in vitreous and aqueous humours using a radioimmunoassay. A lens from each rat was homogenized in 8 m guanidinium chloride for adenosine triphosphate (ATP) analysis. In normal rats, a small amount of gamma-crystallin was found in the vitreous humour, and an even smaller amount in the aqueous humour. Diabetes caused a 4- to 5-fold increase in the vitreous humour and a 4-fold increase in gamma-crystallin in the aqueous humour. Diabetes also led to a significant worsening in general body condition, loss of body weight, formation of cataracts, and decrease in lens ATP levels. Addition of taurine to the diet of diabetic animals resulted in a significant decrease of gamma-crystallin leakage into the vitreous but not the aqueous humour. Taurine had no effect on the lens ATP levels. Neither streptozotocin diabetes nor taurine in the diet appeared to affect the weight of the lenses.

Cysteine and ascorbate loss in the diabetic rat lens prior to hydration changes.

PURPOSE: Glutathione (GSH) loss precedes vacuole formation in the diabetic rat lens, but the cause of this loss is not known. Cysteine availability is a rate limiting factor to glutathione biosynthesis in rat and human lenses but its concentration is not known; therefore free cysteine was measured prior to lens hydration in the diabetic rat lens. GSH can regenerate ascorbate from dehydroascorbate within the lens and potentially modulate the ascorbate pool; therefore ascorbate loss is also a possibility that has not been examined previously. METHODS: Diabetes was induced in Wistar rats to provide a slowly progressing model of cortical cataract. Age-matched control rats were injected with buffer vehicle only. Lens condition was monitored by binocular slit-lamp microscope after pupil dilation. Lens cysteine and glutathione were measured in the same lens, while ascorbate and total ascorbate (ascorbate + dehydroascorbate) of the contralateral lens were quantified by high performance liquid chromatography electrochemical detection. The 1- and 2-week periods of diabetes were chosen as they both preceded lens hydration changes and Na+/K+ changes, to avoid leakage due to ruptured cell membranes. RESULTS: Lens weights were not significantly different compared to controls at either the 1- or 2-week periods, and lenses were completely free of initial vacuole formation. Lens GSH concentration was diminished by 72% compared with controls after 1 week of diabetes and 74% after 2 weeks of diabetes. Lens free cysteine was decreased by 62% and 78% compared with controls after 1 and 2 weeks of diabetes, respectively. Total lens ascorbate concentration was decreased by 34% after 1 week of diabetes and 48% after 2 weeks of diabetes. Dehydroascorbate levels represented less than 10% of the total lens ascorbate pool in all experimental groups. GSH and ascorbate concentration were correlated after 1 week of diabetes (p < 0.005) and after 2 weeks of diabetes (p < 0.001). GSH and cysteine concentration were also correlated after 1 week of diabetes (p < 0.001) and after 2 weeks of diabetes (p < 0.001). CONCLUSIONS: Decreased free cysteine, in the diabetic rat lens, precedes hydration changes and vacuole formation, contributing to decreased glutathione content. While cysteine was not abundant in the lens, its concentration is greater than previously supposed. The lens ascorbate pool was also diminished prior to lens hydration.

Outbreaks of yersiniosis caused by Yersinia pseudotuberculosis in farmed cervids.

Yersiniosis, caused by Yersinia pseudotuberculosis, was diagnosed in 25 deer submitted to the Veterinary Diagnostic Laboratories of the Ontario Ministry of Agriculture and Food from 8 farms in Ontario, Canada, over the 4-year period of January 1990 to December 1993. The organism was cultured, usually in large numbers, from the intestines and, less frequently, mesenteric lymph nodes and/or the spleen of 13 red deer (Cervus elaphus), 6 elk (C. e. canadiensis), 4 fallow deer (Dama dama), and 2 red deer-elk hybrids. Outbreaks occurred almost exclusively in the fall (September-November) and affected recently weaned calves, 4-6 months old. Sudden death usually signalled the start of an outbreak. Outbreaks often occurred during inclement weather; usually a sudden cold snap, with or without rain, after a period of relatively mild fall weather. At necropsy, the animals were usually emaciated and dehydrated, and the perineum and tail were sometimes fecally stained. The small and large intestines were congested and filled with serofibrinous and/or seroanguineous fluid. Mesenteric lymph nodes were edematous and congested. Microabscesses surrounding large bacterial colonies in the lamina propria in the jejunum and ileum were typical lesions seen histologically. Peyer's patches were depleted and sometimes contained microabscesses. Purulent lymphadenitis associated with bacterial colonies was the prominent histologic lesion in mesenteric lymph nodes.

Tuberculosis in farmed rheas (Rhea americana).

Avian tuberculosis was diagnosed in two mature rheas on different ratite farms over a 2-year period. Both birds had died after progressively losing body condition. Caseonecrotic granulomas were scattered throughout the liver and spleen in both birds. Similar granulomas were in the lung of one bird and bilaterally in the subcutis cranial to the shoulder in the other bird. Smears of several granulomas from both rheas revealed large numbers of acid-fast bacilli. Histologically, the granulomas had caseonecrotic, non-mineralized centers surrounded by giant cells. Large numbers of acid-fast bacilli were seen free in the necrotic material and within inflammatory cells. Amyloidosis of the liver and spleen occurred in one rhea. Mycobacterium avium complex was isolated at a reference laboratory from hepatic granulomas submitted from one rhea.

Modelling cortical cataractogenesis. 13. Early effects on lens ATP/ADP and glutathione in the streptozotocin rat model of the diabetic cataract.

A possible contribution to cell toxicity in the diabetic lens due to early ATP loss is not well characterized prior to the appearance of vacuoles in the lens. Changes in lens ATP levels at longer periods of hyperglycaemia (6-8 weeks) have been reported. We used [31P]NMR analysis of lens extracts at three time periods, comparing diabetic to concurrent control groups at 1, 2 and 4 weeks of hyperglycaemia. With this design, significant alterations (> 10%) in the ATP/ADP ratio can be monitored. NMR analysis revealed a decreased ATP/ADP ratio at all time periods, averaging a 38% decrease. Luminescent determination of ATP levels indicates that this decrease is mainly caused by a decrease of 25% in ATP concentration. The early loss of GSH was large and not accompanied by an appearance of GSSG, as monitored by HPLC electrochemical detection. A 1-week experiment with animals receiving daily insulin treatment was carried out to control for effects of STZ on the lens. This treatment resulted in normal lens GSH levels and a near normal [31P]NMR profile.