Characterization of a piscirickettsiosis-like disease in Hawaiian tilapia.

In 1994, tilapia (Oreochromis mossambicus and Sarotherodon melanotheron) in wild and farmed populations on Oahu, Hawaii, USA, began to die of an unknown disease that was similar but not identical to piscirickettsiosis in salmonids. Only tilapia were affected. Diseased tilapia often swam erratically and had trouble staying at depth. Scattered cutaneous haemorrhage and exophthalmia were often noted. In many cases, fish were found dead with no clinical signs. Gills exhibited epithelial hyperplasia with severe multifocal consolidation of secondary lamellae. Multiple granulomas were observed in the gills, spleen, kidney, choroid gland and testes, but not in the liver. Tilapia mortalities occurred only during the cooler months (October to April) of the year and were not recorded during the warmer months (May to September). The mortalities declined with each successive year, after the 1994 outbreak, and currently losses are sporadic. Oxytetracycline-medicated feed reduced mortality. Cytologic examination of blood smears revealed moderate to large numbers of Gram-negative, pleomorphic, intracellular bacteria in rare circulating monocytes. Histologically, some predilection for nervous tissue and brain was observed. When viewed with transmission electron microscopy, pleomorphic coccoid bacteria, measuring 0.56 +/- 0.14 x 0.7 +/- 0.20 microm, occurred free in the cytoplasm and within phagolysosomes. The organisms had a double cell wall, no defined nucleus and variable electron-dense and -lucent areas. Unlike Piscirickettsia salmonis, the agent of piscirickettsiosis, the Hawaiian tilapia Piscirickettsia-like organism (HTPLO) does not form craterform lesions in the liver and is active above 20 degrees C. HTPLO can be transmitted horizontally by cohabitation, and cold stress induces the syndrome in juvenile tilapia from farms where the disease is endemic.

Thymic hematoma in juvenile dogs associated with anticoagulant rodenticide toxicosis.

Ten cases of thymic hematoma in young dogs (9-24 weeks of age) were reviewed. Anticoagulant rodenticide toxicosis was confirmed in 5 cases. Histologically, hemorrhage caused variable expansion of thymic lobules and interlobular septa. The medulla appeared to be the primary site of hemorrhage. In areas of severe hemorrhage, normal lobular architecture was lost and lymphocytes were admixed in the hemorrhagic exudate. Vasculitis, necrosis of capillaries, and degeneration of the capsule were observed in infarcted areas. In 2 cases, angiofibroplasia indicated a longer interval between onset of thymic hemorrhage and death. The lesions are similar to those in 5 cases of idiopathic thymic hemorrhage. Appropriate samples were not available for anticoagulant rodenticide analysis in 3 of these 5 idiopathic cases. Lesions in confirmed cases of anticoagulant rodenticide toxicosis also are compatible with published descriptions of idiopathic and spontaneous thymic hemorrhage, but are inconsistent with normal thymic involution. Analysis for anticoagulant rodenticides is indicated in cases of thymic hematoma when an obvious cause is not detected at necropsy.

Congenital erythropoietic protoporphyria in a Limousin calf.

Bovine congenital erythropoietic protoporphyria is an uncommon genetic defect in Limousin and Blonde d'Aquitaine cattle that is characterized by severe photosensitization. Clinical signs include intense pruritus and exudative dermatitis involving the face, pinnae, and dorsal aspect of the thorax. Affected cattle have hematologic and serum biochemical values within reference ranges, and their teeth are normochromic. Definitive diagnosis of bovine congenital erythropoietic protoporphyria is accomplished by genetic testing. Affected cattle should be sent to a terminal market.