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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.
Mauel et al. (Wed,) studied this question.