Mixed bacterial infection of the lung is an increasingly common problem in the manage ment of many chronic diseases. The lower respi ratory tract frequently becomes populated with a mixed bacterial flora (1, 2), and several potentially pathogenic strains may be found together in the bronchial secretions. Yet, in acute infective states it is generally only one of these several strains that multiplies to be come the pathogen (3, 4). This observation suggests that there are selective mechanisms within the lung that determine or regulate the emergence of a single strain as pathogen from a mixed bacterial inoculum. Knowledge of such selective mechanisms would advance the under standing of infective events in the lung and might help to explain the sequences of bacterial superinfections that commonly complicate the therapy of pulmonary infections. Previously published studies in a laboratory model of pulmonary infection have shown that antibacterial defenses of the lung are more effective against some bacterial strains than others (5). Furthermore, agents that de press this host resistance are more likely to induce infection when certain strains of bac teria are inoculated than when others are used, despite the fact that all such strains are non pathogenic in the healthy animal. Data are
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Green et al. (1968) studied this question.
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