Economic losses associated with disease outbreaks threaten the sustainability of the fish farming industry. Recently, we discovered a new nidovirus infecting farmed rainbow trout (Oncorhynchus mykiss) in Northern Israel named Trout Granulomatous Virus (TGV). While TGV causes characteristic granuloma lesions in the liver, it can also infect other trout organs such as the gills, spleen and heart. Interestingly, fish infected TGV were also reported to experience anemia. However, the specific impacts of TGV on the gill morphology and immune function are currently unknown.
The aim of the current study was to evaluate and characterize the histopathological damage and immune response in the gills of TGV infected rainbow trout. We sampled eight infected fish from a natural outbreak from a rainbow trout farm in Israel. We used four control uninfected rainbow trout from the Salinas laboratory at the University of New Mexico as baseline controls.
Histopathological scoring of TGV infected fish revealed a diversity of pathologies including hemorrhagic lesions, edema, lamellar fusion, infiltration of eosinophilic granular cells (EGCs) and goblet cell hyperplasia (Table 1). Interestingly, gill pathology scores were poorly correlated with TGV viral copies in the gills (Figure 1). Immunological staining using anti-trout MHC-II antibodies and anti-trout IgM antibodies revealed different staining patterns in TGV infected compared to control fish. Specifically, three out of the eight infected fish showed high MHC-II expression levels in the endothelial cells at the base of the secondary lamella, a potential indication of vascular dysfunction in the gills due to infection. Other fish showed high MHC-II expression in immune cells, putatively EGCs in the primary lamella. Current efforts are focused on evaluation of IgM, IgT and pIgR expression changes in the gill of TGV infected trout. These results indicate that TGV infection, directly or indirectly, results in severe gill tissue damage and disrupts the gill immune