Minchinia nelsoni (Haplosporida) Disease Syndrome in the American Oyster Crassostrea virginica

SYNOPSIS. Minchinia nelsoni disease was studied in 3 populations of oysters from Marumsco Bar, Pocomoke Sound, Maryland. The native population was sampled regularly beginning in 1961 shortly after the disease invaded this area. Two populations of healthy year‐old oysters were introduced (one in 1965 and one in 1966) into Pocomoke Sound and studied concurrently with the native population to determine the course of development of the disease and epizootic differences in populations. Gross and microscopic examination of oysters showed progressive stages of infection. Initial infection occurred in epithelia of the filtering organs (gill, palp, water tubes) and spread into connective tissue where hyaline hemocytes infiltrated. Intermediate infection was characterized by local infection and infiltration of connective tissue in and adjacent to epithelia of gill, palp, esophagus, stomach, gut, diverticula, and gonadal alveoli. Advanced infection was recognized by the general invasion and infiltration of connective tissue and the circulatory system by hyaline hemocytes. Terminal infections showed histologically massive pyknosis of nuclei and necrosis of tissues before outward signs of death were apparent. Remission of the disease was recognized by diminution of infection intensity and infiltration; localization of parasites near external epithelia; increased pigment cell formation; and diapedesis and deposition of necrotic parasites and tissue against the shell, followed by external conchiolinous encapsulation. Death from M. nelsoni disease may be attributed in part to seasonal environmental or physiologic stresses, which infected oysters, weakened and in poor condition due to the pathologic manifestations of the disease, are unable to tolerate. The gross pathologic signs of disease were: pale digestive gland, poor condition, mantle recession, weakness, and conchiolinous shell depositions. The microscopic signs were: diapedesis, relative decrease in numbers of phagocytes; relative increase in numbers of hyaline hemocytes; phagocytosis, fibrosis, cellular infiltration, abscess, ulceration, excessive pigment cell formation, mechanical disruption, pyknosis, and necrosis.