Abstract. Alveolar echinococcosis was diagnosed in 12 cynomolgus monkeys (Macaca fascicularis) at postmortem examination within a period of 6 years. Besides consistent involvement of the liver, parasitic lesions were also present in mesenteric lymph nodes, pancreas, lung, and kidney. In the liver, various patterns of host's responses to parasitic tissue could be distinguished. Infiltration of macrophages, often multinucleated, around usually intact metacestodes was the main feature of one pattern. A second pattern was characterized by the presence of abundant, normally degenerate granulocytes in addition to macrophages surrounding collapsed laminated structures. Finally and as a third pattern, some cysts were surrounded by marked collagen deposition, which was usually not a significant feature of the other foci. Parasitic cysts with protoscolices were observed in foci with the first and third pattern but not in the second one. The simultaneous occurrence of all three patterns was observed in most animals. Type AA amyloid was identified either in the space of Dissé, macrophages or blood vessel walls in nine animals using immunohistochemistry. Identity of parasitic structures such as metacestodes of Echinococcus multilocularis was confirmed immunohistochemically. All animals that could be tested serologically (7/12) had detectable antibodies against the E. multilocularis-specific Em2 antigen. Liver lesions of six animals were additionally analyzed by polymerase chain reaction, yielding the amplification of a specific E. multilocularis DNA fragment in each case.
A 22-year-old female African elephant (Loxodonta africana) developed diarrhoea of unknown cause which lasted for two days. The animal was euthanased after it remained recumbent and refused to get up. Gross pathological changes were present mainly in the gastrointestinal tract. The intestinal contents were watery and dark brown. Several areas of the mucosa of the small intestine were covered minimally to moderately with fibrin and had a few 0.1 x 10 to 15 cm linear ulcerations. Microscopical lesions consisted of discrete areas of necrosis of the surface and crypt epithelium without overt inflammatory infiltrates. Culture of the small intestinal contents resulted in a moderate growth of Clostridium perfringens. No salmonella were found in the small or large intestine. PCR of the isolate of C. perfringens revealed the presence of the beta2-toxin gene cpb2 and the alpha-toxin gene cpa but no other known toxin genes. The expression of the beta2-toxin gene in vivo was demonstrated by the immunohistochemical localisation of the beta2-toxin to the microscopical lesions in the small intestine.
A captive 16-year-old male camel (Camelus ferus bactrianus) was euthanized after a prolonged period of inappetence leading to cachexia. At necropsy, there was a 7 cm large, tan, firm, well-demarcated nodule in the tunica muscularis and serosa of the distal region of C3. Histologically, a gastric adenocarcinoma was diagnosed. Numerous metastases were found in the liver and the hepatic lymph nodes, in the wall of the portal vein and the aorta, in the lung, heart, and pleura parietalis. Osseous metaplasia was found within the pleural and aortic metastases. In the mucosa of the glandular region of the C3 compartment a diffuse marked hypertrophy of rugae resembling cerebral convolutions was observed. The lesion was characterized by glandular hyperplasia and stromal inflammation and oedema. These changes closely resembled Menétrier's disease described in humans. To our knowledge, this is the first report of concomitant metastatic gastric adenocarcinoma and gastric hyperplasia in a camel.
Natural nocardial infection has been reported in many different species including mammals and fish, but reports in birds remain uncommon. Eight juvenile Black Crakes (Limnocoraxflavirostra) died unexpectedly at the Basle Zoo. Necropsy revealed disseminated white, firm nodules, 1-3 mm in diameter, throughout the lung parenchyma. Histologically, the lungs contained multiple, often confluent granulomas with central necrosis. Delicate, gram-positive, 0.5- to 1.0-microm-wide, branching, occasionally beaded, filamentous organisms were visible in necrotic centers. These organisms were acid fast when stained with Fite-Faraco. No histologic lesions were seen in other organs. Nocardia nova was isolated from liver, spleen, kidney, and lung. Granulomatous and necrotizing nocardial pneumonia with agonal septicemia was diagnosed, suggesting an aerogenous infection. To our knowledge, this is the first reported epizootic outbreak of nocardiosis in birds, which is additionally unusual because it was caused by N. nova.
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