Blackwell Publishing Journal Backfiles 1879-2005
An annual disease problem with high levels of mortality in Atlantic salmon, Salmo salar L., on a freshwater farm was investigated. In 2000, mortalities began early in October and peaked in December, being unevenly distributed between tanks. Histopathological changes included severe hyperplasia of gill epithelium, with fusion of secondary lamellae, and extensive necrosis of the haematopoietic centres in the kidney and spleen, the latter being consistent with a diagnosis of phagocytolytic syndrome (PCLS). Moribund fish were anaemic, with multiple, circular basophilic inclusion bodies, 1–2 μm in diameter and suggestive of erythrocytic inclusion body syndrome (EIBS), being observed on blood smears. Thin section electron microscopy (EM) revealed primarily membrane-bound aggregates of non-enveloped virus particles (73 ± 7 nm) with an electron dense core (35 ± 3 nm) in spleen, kidney and gill tissue and the erythrocytes therein. These particles had morphology and distribution consistent with those previously described separately for both EIBS and PCLS. Virus isolation attempts in a wide range of cell lines were unsuccessful. In the absence of suitable alternative infectious or environmental explanations, it is postulated that the aetiology was primarily viral, with possible contributory secondary environmental factors. It is further hypothesized that the agents of EIBS and PCLS may be the same or closely related viruses.
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