Histological examination of moribund specimens of turbot grow-out facilities in northwest Galicia (Spain) revealed lesions severe enough to be responsible for the diseased condition and death of many fish. The lesions were caused by 2 agents, the microsporidian Tetrarnicra brevifjlum, already described from the same host farmed in the same region and a histophagous ciliate. Both agents were found In mlxed infections; the dominant role in pathogenesls was played by the histophagous ciliate which was tentatively assigned to the subclass Hymenostomata, order Scuticociliatida Small, 1967

No abstract

The turbellarian Urastoma cyprinae (Graff. 1882) Graff. 1903 was found inhabiting the mantle cavity between the lamellae of the demlbranchs of mussels Mytilus galloprovincialis Lamarck cultured in Galicia (NW Spain). Heavily infested mussels were recognized by the presence of white spots in the gills. The affected area exhibited disarrangement of the gill filaments. The space between 2 lamellae was considerably reduced and the blood sinuses were wider in the unhealthy area than in the healthy area. The turbellarian also induced a heavy lnflltration by blood cells and subsequent necrosis of the gill tissues. Routine parasitolog.ica1 stud~es showed that this parasite was first detected in the Galician region in early 1989. In 1993, U. cyprinae appeared to be present in the 3 main production rias in the Galician region, affecting both natural beds and rafted mussels. U. cyprinae could be considered a potential threat to mussel culture.

The development of turbot Scophthalmus maximus culture has resulted in an increase of pathological problems involving mainly bacterial infections. During 1990, mortalities were detected in some grow-out facilities in Galicia, Spain, and were attributed to the microsporidian Tetramicra brevifilum Matthews & Matthews, 1980. The outbreak lasted for 3Y2 mo. The start of the outbreak was associated with a drop in temperature. Affected fish showed an erratic swimming behaviour, swelling of different parts of the body, darkening of the dorsal surface, and overproduction of mucus on the surface of the body. Fish with a high intensity of infection had jelly-like muscles. Small xenomas formed by T brevifilum were found to be associated with regressive changes of the host tissue, with agglomerations of mature spores eliciting sometimes inflammatory reaction of the host. The agglutinin titers detected in naturally infected fish were low. There was a light host response. Electrophoresis of sera from naturally infected fish showed an additional protein band (molecular weight: 128 kDa) not found in uninfected samples. Results suggest that although turbot infected with microsporidians are immunologically impaired, the immunodepression does not increase the susceptibility of fish to vibriosis.

Haplosporidjum nelsoni (MSX) is an ascetosporan parasite that has caused heavy mortalities of oysters Crassostrea virginica (Gmelin) on the mid-Atlantic coast of the United States. Oysters in some areas have developed resistance to mortality, which involves an ability to restrict infections and tolerate parasitism for prolonged periods. Effects of such sublethal infections on gametogenesis and spawning were examined in native oysters in Delaware Bay, an estuary where the parasite is enzootic A comparison of infection levels with gonad state in histological sections of 2700 oysters demonstrated a clear inhibition of gametogenesis, in proportion to infection ~ntensity, during late spring when parasite levels were high. Subsequently, however, temperature-associated infection remlsslon occurred; many oysters recovered, developed mature gonads, and spawned before new or recurrent infections proliferated in fall. Inhibition of early gametogenesis was more severe in males than in females. There was no evidence that spawning 'stress' accelerated the development of infections. There was no correlation between year-to-year fluctuation in parasite abundance and oyster setting in Delaware Bay.