by Kevin M. Cahill, M.D., D.T.M. & H. (Lond.), Head, Department of Epidemiology, Director of Tropical Medicine, U.S. Naval Medical Research Unit No. 3, Egypt and The Sudan. xiii + 225 pages, illustrated. J. B. Lippincott Company, Philadelphia and Montreal. 1964. $9.50
Parasitology Division and Statistical Activities, Bureau of Laboratories, and the Parasitic Diseases Division, Bureau of Epidemiology, Center for Disease Control, Public Health Service, U.S. Department of Health, Education, and Welfare, Emory University Student Health Clinic, and the Department of Ophthalmology, Emory University, Atlanta, Georgia 30333
Approximately 3 months after an outbreak of toxoplasmosis at a riding stable in Decatur, Georgia, 31 of 36 individuals who had had clinical symptoms or had shown specific serologic reactivity by immunofluorescence were tested for lymphocyte proliferative responsiveness. Whole blood was cultured in microtitration plates with the nonspecific mitogens phytohemagglutinin (PHA), concanavalin A (con A), and pokeweed, and with specific Toxoplasma gondii antigen. Patients with chorioretinitis due to T. gondii or with lymphadenopathy due to other causes were used to evaluate the assay. Healthy controls with and without a past history of toxoplasmosis were included in each set of assays. All patients from the toxoplasmosis outbreak showed increased responsiveness to T. gondii antigen with counts per minute (CPM), corrected for background, ranging from 588 to 39,943, with a mean of 8,421. The negative controls had a mean of 13 CPM. Responsiveness to mitogens was normal in patients in the stable outbreak. Control patients with infectious mononucleosis had markedly suppressed responses to PHA and con A during the early stage of infection, and return of responsiveness was observed on follow-up. All individuals in the stable outbreak were retested at least once and some as many as four times over a 3.5-month period. No marked changes in responsiveness to either antigen or mitogens were observed.