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Zebrafish has become a popular research model in the last years, and several diseases affecting zebrafish research facilities have been reported. However, only one case of naturally occurring viral infections was described for this species. In 2015, infectious spleen and kidney necrosis virus (ISKNV) was detected in zebrafish from a research facility in Spain. Affected fish showed lethargy, loss of appetite, abnormal swimming, distention of the coelomic cavity and, in the most severe cases, respiratory distress, pale gills and petechial haemorrhages at the base of fins. Cytomegaly was the most relevant histopathological finding in organs and tissues, sometimes associated to degenerative and necrotic changes. ISKNV belongs to the relatively newly defined genus Megalocytivirus, family Iridoviridae, comprising large, icosahedral cytoplasmic DNA viruses. This is the first case of naturally occurring Megalocytivirus infection in zebrafish research facilities, associated with morbidity. The virus has been identified based on both pathologic and genetic evidence, to better understand the pathogenesis of the infection in zebrafish and the phylogenetic relationship with other iridoviruses. Given the ability of megalocytiviruses to cross-species boundaries, it seems necessary to implement stringent biosecurity practices as these infections may invalidate experimental data and have major impact on laboratory and cultured fish.

Electron microscopical and histopathological investigations were carried out on the anterior kidney often 1-year-old farmed rainbow trout naturally infected with the external signs of viral haemorrhagic septicaemia (VHS). The histopathology of the liver and the haematology of peripheral blood were also examined. The presumptive virus of VHS was directly demonstrated for the first time in the anterior kidney. All diseased fishes showed necrotic changes in the kidney and the liver. The melano-macrophage centres of the anterior kidney showed a partial destruction accompanied with a loss of melanin. A progressive destruction of the erythrocytes was observed. The liver exhibited moderate to extensive necrosis (karyorrhexis and karyolysis with lymphocytic invasion in the necrotic areas). Neither intranuclear nor intracytoplasmatic inclusions were observed. In the peripheral blood diverse stages of erythrocytic degeneration, amitoses of the erythrocytes and a five-fold increase in lymphocyte numbers were observed.

Histopathological studies on natural and experimental infections of nineteen microsporidian species from fishes distinguished two types of tissue reactions. The first type is characteristic of infections with xenoma-inducing microsporidian species and comprises three successive stages: a weakly reactive stage, a productive stage with the formation of granulomas and a stage of granuloma involution. Following the first stage, tissue reactions are directed towards the isolation of the parasite and result in its complete elimination and host tissue repair. The extent of pathological changes probably depends on the number of parasite cells which initiated the infection. The second type is represented by Pleistophora species infecting muscles or oocytes. Host tissue reaction is surprisingly slight during the schizogony and sporogony and does not tend to isolate the invaded muscle fibres. A slight lymphocytic infiltration of myosepta indicates the first stage of tissue reaction. The tissue reaction only reaches the productive stage when mature spores completely fill the contents of the infected muscle fibre. A thick wall of fibroblasts may be formed to demarcate the parasite mass as soon as it undergoes necrotic changes. The extent of pathological changes probably depends on the ability of early developmental stages of the parasite to spread the infection within the host. In both types of tissue reaction, the spores are destroyed by complete digestion within host phagocytic cells.