Intestinal atresia and ectopia in a bovine fetus.

A 2-year-old Red Holstein cow was presented with uterine torsion at 235 days of pregnancy. The fetus extracted by cesarean section had weak vital signs and marked abdominal distention. An edematous pouch that contained tubular structures with peristaltic activity was associated with the umbilical cord. Because of poor prognosis, both dam and fetus were euthanized. At necropsy, the fetus had severe distention of the forestomachs, abomasum, and proximal small intestine; absence of distal small intestine, cecum, and proximal colon; atresia of the 2 blind ends of the intestine; and atrophy of distal colon and rectum. The tubular structures associated with the umbilical cord were identified as the segments of intestine that were absent in the fetus. Intestinal atresia combined with ectopia may be caused by local ischemia during temporary herniation and rotation of the fetal gut into the extraembryonic coelom. The close connection between ectopic intestine and amniotic sheath of the umbilical cord in this case may have facilitated vascularization and allowed development and viability of the ectopic intestine.

A cluster of Chlamydia serpentis cases in captive snakes.

Following the occurrence of sudden death cases in a zoo reptile collection, histological analyses conducted on tissues from two common adders suggested an infection due to Chlamydia. The survey was extended to 22 individual snakes from the same collection and a PCR analysis targeting a conserved gene in Chlamydiaceae revealed bacterial shedding in six of them. The infection resolved spontaneously in one snake whereas another one succumbed one month later. The antibiotic treatment administered (marbofloxacin) to the remaining four PCR positive animals stopped the mortalities and the shedding. Analysis of the 16S and 23S ribosomal gene sequences identified C. serpentis, a recently described novel chlamydial species in snakes. A PCR tool for a quick and specific identification of this new chlamydial species was developed in this study.

Lymphocytic insulitis in a juvenile dog with diabetes mellitus.

Autoimmune diabetes has never been described in a juvenile dog, whereas serological evidence has established its development in adult dogs. Diabetes mellitus was diagnosed in a 3-mo-old Donge de Bordeaux dog suffering from persistent hyperglycemia and concurrent insulinopenia. Histological analysis of the pancreas revealed inflammatory lesions in 40% of the islets of Langerhans, with infiltration predominantly by T lymphocytes (more than 90%), either at the edge (peri-insulitis: 10%) or in the islets (insulitis: 30%). The remaining 60% of the islets showed a marked atrophy due to massive beta cell loss with no loss of alpha cells. This pattern is quite similar to that observed in humans in which a characteristic insulitis containing high numbers of T lymphocytes is found in 20% of the islets at diabetes diagnosis. By contrast, in rodent models, nearly 70% of the islets of Langerhans show inflammation at diagnosis and macrophages and dendritic cells predominate in the inflammatory lesions. This is the first report of lymphocytic insulitis in a juvenile dog exhibiting diabetes mellitus. Our observations suggest an autoimmune origin for the disease in this dog that is similar to human type 1 diabetes mellitus, for which there is no accurate spontaneous large animal model.

Microcystic meningioma in a dolphin (Delphinus delphis): immunohistochemical and ultrastructural study.

A wild common dolphin was found stranded on the French Atlantic coast. At necropsy, an intracranial grey- to tan-coloured mass (7 x 5 x 4 cm) was found at the right cerebellopontine angle, compressing the right cerebellar hemisphere, the brainstem and the occipital lobe of the right cerebral hemisphere. Microscopically, the tumour was composed of small lobules of polygonal to elongated neoplastic cells with multifocal areas of stellate and vacuolated cells. Neoplastic cells strongly expressed vimentin, S-100 protein and neuron-specific enolase. They were rarely positive for cytokeratin. Ultrastructurally, the neoplastic cells displayed all the diagnostic features of meningiomas and in some areas showed long cytoplasmic processes delimiting extracellular spaces. The immunohistochemical and ultrastructural features were consistent with the histopathological diagnosis of a microcystic meningioma. This is the first report of a meningioma in dolphins or in any other cetacean species.

Extranodal B-cell lymphoma in the urinary bladder with cytological evidence of concurrent involvement of the gall bladder in a cat.

A 15-year-old domestic shorthair cat was presented with severe haematuria, stranguria, anorexia and lethargy of 10 days' duration. Physical examination revealed a large painful urinary bladder and pain in the cranial abdomen. Abdominal ultrasound revealed severe generalised mural thickening of both the gall bladder and the urinary bladder. Lymphoma was diagnosed on cytology of urine sediment and fine-needle aspirates of the gall bladder. Despite a transitory clinical improvement and partial remission following chemotherapy, the cat was euthanased six weeks after initial presentation due to recurrent clinical signs. Post-mortem examination confirmed a B-cell lymphoma in the urinary bladder. This report is the first description of gall bladder and bladder lymphoma in a cat.

Clostridium perfringens beta-toxin targets endothelial cells in necrotizing enteritis in piglets.

Beta-toxin (CPB) is known to be the major virulence factor of Clostridium perfringens type C strains, which cause necrotizing enteritis in pigs, sheep, goats, calves, and humans. The exact mode of action, in particular the cellular targets of CPB in the intestine of naturally affected species, is however still not resolved. To investigate localization of CPB in naturally occurring necrotizing enteritis, we evaluated 52 piglets with spontaneously acquired C. perfringens type C enteritis and 14 control animals by immunohistochemistry. Our results consistently revealed binding of CPB to vascular endothelial cells in peracute to acute lesions of necrotizing enteritis. Subacute cases, in contrast, demonstrated reduced or no CPB staining at the endothelium, mainly due to widespread vascular necrosis. From these results we conclude, that the pathogenesis of C. perfringens type C induced necrotizing enteritis involves binding of CPB to endothelial cells in the small intestine during the early phase of the disease. Thus, by targeting endothelial cells, CPB might specifically induce vascular necrosis, hemorrhage and subsequent hypoxic tissue necrosis.