Abstract

T he outbreak of pneumonia in American Legion conventioneers in the summer of 1976 has led to more than might have been expected at 9:15 A.M. on August 2, 1976, when Sidney Franklin, M.D. of the Veterans Administration Clinic in Philadelphia called Robert Craven, M.D. of the Center for Disease Control (CDC) to report fatal illness in four Legionnaires. The cases then, and each summer since, have provided the challenge for immediate investigations and the grist for winters’ studies of the bacterium, the disease it causes, and methods for treatment and prevention. The Philadelphia outbreak showed Legionnaires’ disease to be a generally severe, multisystem illness that affected 4 per cent of conventioneers, was associated with pneumonia in 90 per cent of those affected, and had an incubation period of two to 10 days and a casefatality ratio of 16 per cent [l]. The disease did not appear to spread from person to person but rather through the air. The first winter, McDade and his colleagues [2] found the agent to be a fastidious gram-negative bacterium, for which the name Legionella pneumophila has been proposed. They showed that L. pneumophila had caused an outbreak of pneumonia in 1965 in patients at St. Elizabeth Hospital in Washington, D. C. [3], confirming a prediction made in August 1976 by John V. Bennett, M.D. of CDC that the Legionnaires’ disease and St. Elizabeth outbreaks had been caused by the same agent. Quite unexpected, however, was the finding that L. pneumophila had also caused Pontiac fever, an explosive airborne outbreak of illness typified by myalgia, fever, chills and headache that had affected 95 of 100 employees in a health department building in Pontiac, Michigan, in 1968 [4]. Pontiac fever had an incubation period of 24 to 48 hours in most cases and, although very debilitating for two to seven days, was not associated with pneumonia or death. No differences (e.g., virulence for animals, presence of toxins) have been found in the bacteria that caused Legionnaires’ disease and Pontiac fever to account for the clinical and epidemiologic differences in the two conditions. The summer of 1977 confirmed the suspicion that Legionnaires’ disease was not rare. Outbreaks were identified in Columbus, Ohio; Kingsport, Tennessee; Burlington, Vermont: and Los Angeles, California, and scores of sporadic cases were confirmed from throughout the United States. The incidence of sporadic Legionnaires’ disease has since been estimated as 12 cases/lOO,OOO population/year (or about 25,000 cases a year in the United States) [5]. L. pneumophila was found to be an important cause of nosocomial pneumonia, especially in immunocompromised patients. Community-acquired sporadic cases occurred most commonly in men, cigarette smokers and heavy drinkers; proximity to construction or excavation and overnight travel were other significant risk factors. Data retrospectively collected from the Vermont epidemic showed chances of survival were significantly greater in those treated with erythromycin [6], corroborating experimental studies that indicated that erythromycin (and rifampin) were consistently effective against L. pneumophila. The availability of effective therapy heightened the need for methods for rapid diagnosis. Clinical clues were found to be of some value in differentiating Legionnaires’ disease from pneumonia due to other agents: very high fever, unexplained impairment of consciousness, hematuria, abnormal liver function, lymphopenia, negative routine bacterial cultures, and failure to respond to therapy with penicillins, cephalosporins and aminoglycosides. Direct immunofluorescent testing of secretions from the respiratory tract, or pleural fluid, offered a surer diagnosis. Early studies showed the specificity of the method: more recent data suggest that as many as 71 per cent of serologically confirmed cases may be positive by direct immunofluorescent testing if multiple specimens of respiratory secretions are tested [7]. Polyvalent antiserums should be used for direct im-

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