Exposure to Neisseria meningitidis may result in either asymptomatic infection (carriage) or acute disease. Early studies indicated that acute meningococcal disease probably occurs about 2 wk after acquisition of the organism (1). Regardless of whether individuals become carriers or develop acute disease, they develop humoral antibodies to a variety of antigens, including the groupspecific polysaccharide (2, 3), the protein serotype antigen (STA), 1 and lipopolysaccharide (LPS) (4). Group-specific polysaccharide antibodies peak approximately 2 wk after onset of acute disease (5, 6), but the nature of the immune response to the STA and LPS antigens resulting from carriage or disease is unknown.There is no entirely satisfactory animal model simulating meningococcal disease in man, although several have been studied for their ability to predict the effectiveness of vaccines or serum therapy. The mouse-mucin model described by Miller and Castles in 1936 (7) and later standardized by Branham and Pittman (8, 9) was one of the first models for study of immune protection. Study of the immune response resulting from mouse infection is difficult because the effects of mucin on the immune response and clearance are unknown. The rabbit has also been used, but massive doses of organisms injected intracranially wererequired to cause meningitis-like disease (10). The chick embryo model was used to study passive protection against meningococcal infection (11-14), but active immunization is not possible.In these studies, the guinea pig implant model of Arko (15) was examined. This model proved useful because (a) the animals could be actively immunized, (b) useful amounts of serum from individual animals were obtained, (c) the induced meningococcal infections were not lethal, thus permitting rechallenge, and (d) localization of the infection permitted quantitation of organisms present. As long as no attempt is made to study the pathophysiology in relation to human disease, the guinea pig spring implant model is satisfactory.The purpose of our investigation was to examine the specificity and duration of the immune response to meningococcal infection and to determine the