Abstract

AbstractA disease affecting larval Pacific oysters (Crassostrea gigas) was observed during a 3‐year period at a hatchery in Washington State. It was also detected at 3 other hatcheries and in wild stocks. The clinical course of the acute phase of the disease in the hatchery varied from one to 3 days. Larvae that completed metamorphosis in less than 12 days survived the infection. Under intensive cultural conditions, the mortality rate exceeded 95%. The disease occurred at water temperatures of 20 to 30°C and salinities of 13 to 28 ppt.The earliest sign of the disease was the presence of numerous zoo‐spore‐like bodies on the cilia of the velum. These bodies progressively increased in number and the velum and mantle became eroded. Numerous thick‐walled spherical bodies, 4 to 24 μm in diameter, were found in the stomachs of apparently healthy and sick larvae that were at least 7 days of age. Moribund larvae regurgitated fascicular collections of zoospore‐like and thick‐walled spherical bodies from the stomach. The regurgitated masses became entwined on and were rotated by the velar cilia, further traumatizing the surface of the velum. The terminal stage of infection was characterized by severe velar erosion, numerous enlarged spherical bodies in the stomach, and dilated darkened intestines.Histologic and electron microscopic study of affected larvae revealed fascicular masses on velar and mantle epithelia associated with adjacent cellular destruction. Spherical bodies were impacted in the stomach and frequently obstructed the gastro‐diverticular opening. In some cases the intestines were dilated and ruptured.Based upon observations, a mycotic etiology is hypothesized. The etiologic agent exhibits similarities to the Dermocystidium group of organisms. The relationship between the wide distribution of the diseast and reported difficulties in culturing Pacific oyster larvae is discussed.

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