抄録
Japanese flounder (Paralichthys olivaceus) were experimentally infected with the highly pathogenic scuticociliate Miamiensis avidus (syn. Philasterides dicentrarachi) using the immersion method to clarify/identify the possible neural invasion route and possible dissemination routes that enable rapid spreading of the scuticociliate into the fish body. Scuticociliates were observed on the skin and gills right from days 0–1 post-infection, muscle tissue on day 2 post-infection, reached the brain, and spinal cord on day 3 post-infection, and systemic infection was prominent afterwards. Brain infection was observed in most of the examined fish. The sudden increase in mortalities was considered to be due to severe brain lesions, which appeared frequently from days 3 and 4 post-infection. Affected fish showed varying degrees of tissue damage including severe epidermal and dermal necrotic lesions, necrotic myositis, encephalitis and myelitis. Scuticociliates were frequently observed along the optic and/or olfactory nerve in the fish which were accompanied by severe brain lesions but by minimum lesions in the gills and skin, suggesting that in addition to skin and/or gills, neural routes including periorbital and nasal routes may play a role in scuticociliate invasion to the brain. Scuticociliates were also observed in the peripheral nerve fibers in the muscle tissue, cranial and spinal nerves, cranial cavity and in the vertebral canal, suggesting that nerve fibers and/or cerebrospinal fluid circulation may be involved in the spread of the scuticociliate throughout the body in addition to the blood circulation and connective tissue.
