Lymphocystis disease is a unique, typically chronic, viral infection of wild or captive marine and freshwater fish. The causal agent is an icosahedral DNA virus ~300 nm in diameter, of the Iridoviridae family. Infection may be manifest by benign cauliflower-like lesions typically located on fins. The disease affects a wide range of fish and is generally considered global. Within the aquarium trade, painted glass fish are commonly infected. Presumptive diagnosis is based on the presence of enlarged fibroblasts (up to 1 mm), which are easily visualized with a light microscope. Microscopic examination typically reveals the appearance of grape-like clusters of virus-laden cells. Diagnosis is confirmed histologically. Feulgen-positive cytoplasmic inclusions and a hypertrophied nucleus are pathognomonic. The disease is usually self-limiting but is of aesthetic concern.
Viral erythrocytic necrosis is an OIE-notifiable disease. It has been reported in >20 species of marine and anadromous fish (both cultured and free ranging) and is characterized by erythrocytic degeneration. Affected species include Pacific herring, Atlantic cod, and Pacific salmonids (chum, pink, coho, and chinook), steelhead trout, and cultured eels in Taiwan. The disease is chronic, and external signs may be subtle or nonexistent. Sick fish are anemic, which may result in pale gills and internal organs. Severity of the disease is related to age and species of fish, with juveniles <1 g most severely affected. The characteristic lesion is a single eosinophilic cytoplasmic inclusion body in the circulating erythrocytes of anemic fish. The inclusions are best visualized from Giemsa-stained fresh blood smears. Transmission electron microscopy has demonstrated hexagonal virus particles, presumptively classified as an iridovirus, in the cytoplasm of cells containing inclusions. To date, the agent has not been successfully isolated. Histologically, increased hematopoietic activity may be evident in the kidney, and round cytoplasmic inclusions (0.8-4 µm) are found in circulating RBC. Inclusions stain pink or magenta with Giemsa. Other degenerative changes may be evident in RBC, including cytoplasmic vacuolation and margination of nuclear chromatin. Hemolytic anemia with concurrent hemosiderosis and erythroblastosis has been reported in moribund Pacific herring. Multinucleated giant erythroblasts may occasionally be seen in peripheral blood, and macrophages may phagocytize abnormal erythroblasts. A presumptive diagnosis is based on the presence of typical cytoplasmic inclusions in circulating erythrocytes of anemic fish. Confirmation requires visualization of hexagonal virus particles in cytoplasm of affected erythrocytes using transmission electron microscopy. A marine reservoir is suspected but has not been identified. Vertical transmission is suspected due to the high prevalence of infection in fry from infected broodstock.
The ranaviruses are an important group within the family Iridoviridae that affect fish. One of these, epizootic erythropoietic necrosis (EHN) is listed as a notifiable disease by OIE. It was first reported in redfin perch in Australia in the spring of 1984, but has also been shown to cause disease, albeit less severe, in rainbow trout. Similar viruses have been reported in sheatfish in Germany and black bullhead catfish in France and Italy. EHN is endotheliotropic, producing necrotic lesions in the endothelium of blood vessels and some visceral lesions. Behavioral signs include lethargy, darkening, and erratic swimming. Mortality occurs after 4-5 days. The most consistent lesion associated with EHN is focal necrosis of hematopoietic tissue in the anterior kidney and liver. Necrotic hematopoietic cells may be visible within blood vessels. Presumptive diagnosis is based on clinical signs and isolation of the suspect agent in cell culture. Bluegill fry (BF-2) is the cell line of choice. Detection may also be accomplished using ELISA, immunofluorescence, or electron microscopy. Epizootics of EHN in redfin perch are most common in the spring and summer and almost exclusively involve juvenile fish. Survivors seem to be resistant to future infection. There is no evidence of vertical transmission of EHN, and redfin perch carriers have not been detected. An unidentified reservoir and carrier host is suspected. Fomite transmission of EHN has been demonstrated, and birds have also been shown to carry infected material.
Largemouth bass virus is a ranavirus that was isolated from moribund largemouth bass in South Carolina in 1995. It was previously isolated from largemouth bass in several Florida lakes but had not been directly associated with disease. In recent years it has been found in largemouth bass in most southeastern and many midwestern states. The disease is not well understood because the virus is commonly isolated from tissues of clinically normal fish. In the 1995 fish kill, ~1,000 fish died over a 2-3 mo period in an area that encompasses >66,000 hectares. Lesions were nonspecific and are still poorly described. Fat-head minnow (FHM) is the cell line of choice for isolation of virus.
Several other iridoviruses have been described in ornamental fish. Two of these were initially reported as being closely related to largemouth bass virus, but more recent work indicates that the isolates from guppy and doctor fish are not as closely related as originally thought. An iridovirus has been described in freshwater angelfish ( Pterophyllum scalare ) showing signs of systemic disease, but the agent has not been isolated. An iridovirus has been isolated from gouramis in the genus Trichogaster using a tilapia heart cell line. This virus does not grow on FHM cells or other common cell lines used for isolation of fish viruses. The gourami virus has been associated with systemic disease and mortality of Trichogaster spp gouramis. Efforts to fulfill River’s postulates were supportive though not conclusive. Clinical disease with largemouth bass virus and the gourami iridovirus seems more severe at water temperatures ≥30°C, based on very limited information.