At the Matlab Hospital of the International Centre for Diarrhoeal Disease Research, Bangladesh, the authors examined the blood groups of patients hospitalized between January and September 1979 for diarrheal disease due to a variety of bacterial and viral agents. A significant association was identified only for cholera, in which cholera patients were twice as likely to have blood group O and one-ninth as likely to have blood group AB as community controls. A follow-up study of family contacts of cholera patients, carried out between September 1980 and July 1982, indicated that blood group did not affect an individual's risk of having a culture-proven infection with V. cholerae 01 but was directly related to the severity of disease. Individuals with the most severe diarrhea compared with those with asymptomatic infection were more often of blood group O (68% versus 36%, p less than 0.01) and less often of AB (0% versus 7%, p less than 0.01). It was not possible to identify the molecular basis for this genetically related protection using biologic models of cholera that are currently available. The constant selective pressure of cholera against people of O blood group may account in part for the extremely low prevalence of O group genes and the high prevalence of B group genes found among the people living in the Gangetic Delta.

An outbreak of acute infectious nonbacterial gastroenteritis began among elderly patients in a convalescent hospital in Marin County in northern California in March 1978 and persisted through May 1978. The overall clinical attack rate was 51% of 187 residents and 12% of 180 employees. A 27-nm viruslike particle was observed by immune electron microscopy in stools obtained at or near the onset of illness from four of 32 patients. Seroresponses to the 27-nm particles were found by immune electron microscopy in 16 of 18 patients. In addition, serologic evidence of infection with this or a related agent was demonstrated in persons who developed illness in another large outbreak of acute infectious nonbacterial gastroenteritis which occurred in a nearby county. This agent is morphologically similar to but serologically unrelated to the Norwalk and Hawaii gastroenteritis agents and has been designated the Marin agent pending further classification.

Forty-nine cases of Legionnaires' disease were identified from May 1977 through July 1978 in patients and employees at Wadsworth Medical Center. Cases clustered in October and November 1977. Fifteen patients died. All Legionnaires' disease (LD) patients were in the hospital before onset of illness (median time from admission to onset, 17 days; range, 3 to 276 days). Twenty patients were immunosuppressed or compromised by malignancy. In 1977, six of 12 renal-homograft recipients acquired LD pneumonia in contrast to three of 22 during the preceding 3 years (P = 0.031, Fisher's exact test). In a prospective survey of 1658 consecutive hospital admissions, seven cases of Legionnaires' diseases occurred (0.4%), including six among 14 patients who seroconverted to the LD bacterium. Prevalence of a reciprocal titer of 128 or above in Wadsworth employees was significantly greater than in a nearby control population (P = 0.044, Fisher's exact test). Exposure to the external hospital environment may be an important factor, and soil may be a reservoir for the LD bacterium. Legionnaires' disease at Wadsworth may be a nosocomial pneumonia affecting a small group of patients with particular risk factors.