The potential role of IgA antibody to Neisseria meningitidis, which blocks bacteriolysis by IgG and IgM, in producing the susceptible state in military recruits, a population at greater than expected risk, was investigated in 28 patients with meningococcal disease. IgA was removed from acute-phase sera by immunoadsorption; IgG was separated by ion-exchange, and IgM by gel-filtration chromatography. The bactericidal activity of acute-phase sera, before and after removal of IgA, and of IgG and IgM fractions from the sera, was tested against each of the homologous infecting strains. Bactericidal activity, the correlate of protective immunity, was deficient in 24 of 28 unabsorbed sera, but uniformly present after the removal of IgA in a median titer of 1:16. IgM accounted for all or nearly all of the bactericidal activity. IgG was largely inactive. Susceptibility to meningococcal disease may be affected by the blocking of bactericidal IgM by circulating IgA.
Acute- and convalescent-phase sera from 34 children and 10 young adults were studied to determine if, at what age, and to which antigens of Neisseria meningitidis they respond during disseminated disease. Seven children older than two years of age who were infected with group C or Y strains developed significant increases in both binding and bactericidal antibody. Children infected with group B strains infrequently (eight [31%] of 26) had measurable increases in serum antibody to this capsular polysaccharide; response was meager when it did occur, was unrelated to age, and was considerably poorer than that of young adults, of whom 80% responded. Convalescent-phase sera from all children contained bactericidal antibody. Binding capacity for group B polysaccharide accounted for only 35% of the bactericidal activity in convalescent-phase sera of children infected with group B strains. Bactericidal antibody in the sera of children who did not respond to capsular polysaccharides was often to a lipooligosaccharide antigen.
Three collections of strains of Neisseria meningitidis that caused meningococcal disease during nonepidemic periods were serotyped to determine whether serotypes that cause endemic disease are more heterogeneous than those responsible for epidemic disease. Thirty-four strains isolated from pediatric patients in Houston, Texas, from February 1977 to March 1978 were of three separate serogroups and 11 serotypes; 27 contemporary (1977-1978) strains from predominantly military populations, obtained nationwide, were of six serogroups and six serotypes, while 11 strains isolated at military posts in the southwest United States from 1970 through 1976 were of four serogroups and five serotypes. Between 9% and 20% of the strains were nontypable, while type II strains which were responsible for the epidemics in the Northern and Western Hemispheres earlier in the 1970's, accounted for only 20%-44% of the strains. In contast to epidemics, which appear to be caused by a single serotype, endemic meningococcal disease appears to be caused by a broad, heterogeneous distribution of serotypes. Thus, development of a serotype-specific vaccine may have limited application to the prevention of endemic meningococcal disease.
An in vitro bactericidal assay that utilized a set of 20 typing antisera to Neisseria meningitidis was developed to distinguish differences in strains of Neisseria gonorrhoeae based on patterns of killing. When test conditions were rigidly standardized, the method was sensitive and reproducible. Strains of gonococci from 20 unrelated patients had 20 different patterns of killing. Sets of strains of N. gonorrhoeae that were likely to be identical on the basis of clinical histories were examined. Organisms isolated from consorts reacted in an identical fashion in seven of nine instances. The two nonidentical sets of strains from consorts were also different in their antibiotic sensitivity patterns. The case history of one patient suggested that one of these strains was obtained from a source of infection other than the named consort, and a second patient was reinfected with a strain from her partner four months later. Four sets of strains were cultured at different intervals after appropriate therapy. On the basis of bactericidal patterns, the strains from one patient were the same, a finding that suggested treatment failure; the strains from other patients were not identical, a fact that suggested that patients were reinfected.
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