Since 1986, serogroup B Neisseria meningitidis has caused approximately 80%Yv of the meningococcal disease in Brazil. In 1988, an epidemic caused byN. meningitidis B:4:P1.15 was recognized in the greater Sio Paulo area of Brazil. The Sfio Paulo state government decided to vaccinate children from 3 to 83 months of age with a vaccine consisting of serotype 4 outer membrane protein and group C meningococcal polysaccharide that was produced in Cuba. About 2.7 million children were vaccinated during two immunization campaigns conducted in 1989 and 1990. Because of this, a case-control study was designed to determine vaccine efficacy against group B meningococcal disease. The purpose of our study was to compare the antibody response with the protection from disease estimated from the case-control study. We measured the immune responses of vaccinees by enzyme-linked immunosorbent assay (ELISA), immunoblot, and bactericidal assay. The development of bactericidal antibodies was age dependent and in good agreement with the results of the case-control study. Only 40%o of vaccinees showed fourfold or greater increases in bactericidal antibody titers after vaccination. A poor correlation between antibody levels detected by ELISA and those by bactericidal assay was found. Immunoblot analysis showed that about 50%o of the serum samples with bactericidal titers higher than 1:4 were reactive with class 1 outer membrane protein. We conclude that the bactericidal assay is a good, laboratorybased, functional assay for the study of vaccine immunogenicity and that an effective solution to group B meningococcal disease remains to be demonstrated.

Beginning in 1988, the incidence of meningococcal disease in the area of greater São Paulo began to surpass the upper confidence limit of an 8-year average incidence (from 1979 to 1986), thus characterizing a new epidemic in the region of greater São Paulo. This epidemic, which extended to 1990, was different from previous epidemics in that it was caused by serogroup B. The increased incidence of meningococcal disease was paralleled by an increased prevalence of a single group B clone, B:4:P1.15, of the ET-5 complex. ET-5 strains have been present in the greater São Paulo area since 1979; however, they have been associated with a high percentage of the group B disease only from 1987 to the present. On the basis of the increased incidence of group B disease in São Paulo, a mass vaccination program with a serotype 4:P1.15 meningococcal protein vaccine was undertaken. The impact of this vaccination program is under analysis.

Serogroup C isolates of Neisseria meningitidis recovered from 121 patients with meningitis or septicemia in Greater Sao Paulo, Brazil, between 1976 and 1990 were analyzed with respect to serotype and multilocus enzyme genotype. The distribution of serotypes has changed since 1989 when serotype 2b started to replace serotype 2a. There were 48 distinct multilocus genotypes (electrophoretic types [ETs]) and 13 distinct complexes. Among the 41 serotype C:2b:-strains analyzed, 38 (93%) were found in complex 11. The percentage of complex 11 increased from 8% in 1988 to 50 and 66% in 1989 and 1990, respectively. Although we have been in an epidemic situation due to serogroup B:4:P1.15 ET-5 complex since 1988, the appearance and increase of a new unrelated strain, C:2b:-of ET-1l complex, in 1989 and 1990 provide enough data to conclude that the presence of two different complexes, ET-5 and-11, of N. meningitidis were responsible for the high levels of meningococcal disease in Greater Sao Paulo during this period.

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