Black abalone in southern California are afflicted with chronic intestinal infections of a rickettsia-like organism that causes a debilitating and fatal withering syndrome. The hematology of withered animals indicated that cellular degradation and apoptosis occurred in tandem with the decline and catabolism of abalone tissues. Two types of hemocytes were found in the hemolymph. Type I and Type II Hyalinocytes were distinguished by subtle differences in their cytoplasmic vesicles. Densities of both types hemocytes declined in abundance, and small, presumptive stem cells increased in abundance with the progression of the disease. No circulating granulocytes were present in hemolymph; but serous cells were present as fixed granulocytes in hemal spaces. Cellular inclusions, dying cells, and vacuolate cells increased in abundance with the disease. An evaluation of cellular immunity resulted in disparate findings associated with serum levels and types of buffer used.  In the presence of micronutrients, and divalent metal ions, however, hemocytes from infected abalone showed increased degrees of phagocytosis (percent phagocytosis, and number of yeast particles per hemocyte) compared to hemocytes from uninfected animals.   Experimental transmission of the disease was effected in healthy, unexposed abalone held together with asymptomatic, exposed abalone.  Clinical signs of infection appeared after 180 days of cohabitation. The chronic nature of the disease progressed relatively unnoticed until 6 to 8 months infected abalone began to show signs of withering. The withered condition represented an end stage of the disease and probably resulted from starvation caused by rickettisial disruption of the digestive processes.