A hypothetical model of the epidermic behavior of Neisseria meningitidis, based upon the induction of susceptibility to disseminated disease by circulating IgA, is presented. The model is based on the assumption that epidemic susceptibility is acquired as a result of induction of serum IgA by cross-reacting enteric bacteria, the priming organism. Co-colonization with the appropriate strain of N. meningitidis then may result in disseminated disease. Colonization by either bacterium in the absence of the other results in reinforcement of the commensal relationship. Slow, silent, fecal-oral transmission of the priming organism determines the time/space characteristics of an epidemic; interruption of fecal-oral transmission aborts it. Aerosol transmission of the meningococcus determines the magnitude of an epidemic. Independent, age-related acquisition of both capsular polysaccharide and lipopolysaccharide antibodies provides immunity in the absence of aberrantly high levels of co-specific serum IgA.