Twenty seven adult/sub-adult lowland leopard frogs (Rana yavapaiensis), two larval lowland leopard frogs, two adult Chirichahua leopard frogs (Rana chiricahuensis), and two adult canyon tree frogs (Hyla arenicolor) collected from populations experiencing mortality events at eight sites were found to have characteristic lesions of chytrid fungus infection (Batrachochytrium dendrobatidis). The mortalities occurred during December 1992 and between October and February in 1997-98 and December and February in 1998-99. Gross lesions varied from none to diffuse reddening of the skin of the abdomen, pelvic area, and legs. Microscopic lesions were characteristic of those previously reported for the disease and included diffuse epidermal hyperplasia, hyperkeratosis, and colonization of the keratinized layers of the epidermis by sporangia of the chytrid. Bacterial cultures did not yield a primary pathogenic agent. Virus isolation from frog tissues was negative. Batrachochytrium dendrobatidis was isolated from the skin of two of 10 R. yavapaiensis and one of two H. arenicolor cultured following necropsy. An additional nine of 11 clinically affected or dead R. yavapaiensis from the same locations, but not necropsied, were culture positive for B. dendrobatidis.
The chromosomal gene encoding the phospholipase D from Corynebacterium pseudotuberculosis (biovar ovis) isolate Whetten 1 was replaced with an allele containing a nonsense mutation. The virulence of the mutant strain (W1.31r1) and the isogenic parental strain were then compared by inoculation of goats. The wild-type strain caused abscessation at the site of infection, which then spread to the regional lymph node, while W1.31r1 had a reduced ability to establish a primary infection and was incapable of dissemination. Our results confirm that phospholipase D is a virulence determinant of C. pseudotuberculosis that increases the persistence and spread of the bacteria within the host.
An echogenic line in the outer zone of the renal medulla, paralleling the corticomedullary junction is described as the renal medullary rim sign. This renal ultrasonographic change is demonstrated in 4 dogs and 2 cats with a range of renal diseases. The renal medullary rim sign provides additional ultrasonographic criteria indicating primary renal disease in some patients. However the renal medullary rim sign may prove to be a poor correlate for prognosis across the range of differentials present in these clinical patients.
Three female sika deer from a single captive herd were submitted for postmortem examination over a 139-day period. The first 2 deer submitted were reported to have lost body mass for 20 days to 1 month before euthanasia. One of these deer had diarrhea, the other had a crusting dermatitis on the nasal planum and inner aspects of both pinnae. The third hind did not have any signs of disease before it was found seizuring and was immediately euthanatized. Microscopically, all 3 animals had a lymphocytic vasculitis typical of malignant catarrhal fever (MCF), with the most severe lesions in the brain. All 3 deer were polymerase chain reaction (PCR) positive for caprine herpesvirus 2 (CpHV-2) and were negative for ovine herpesvirus 2 (OHV-2). Two healthy goats that were housed adjacent to the deer were also PCR positive for CpHV-2 and PCR negative for OHV-2. The CpHV-2, PCR amplicons from the hinds, and the 2 healthy goats had an identical single base polymorphism. A male sika deer that was housed with the hinds and a fawn from 1 of the hinds remained asymptomatic and were PCR negative for CpHV-2. This represents the first report of mortality with MCF-like lesions in association with CpHV-2.
An in vivo model system for human campylobacteriosis has been developed in which colostrum-deprived newborn piglets are orally challenged with an invasive strain of Campylobacterjejuni. Piglets developed clinical symptoms and histopathological lesions similar to those observed in humans infected with C. jejuni. Gross lesion examination at autopsy revealed the presence of edema, hyperemia, and mucus. Histopathologic examinations by light and transmission electron microscopy demonstrated damage to surface epithelial cells
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