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A representative collection of meningococci was isolated from cases and healthy carriers in The Gambia between 1982 and 1988, during and after an epidemic of meningococcal meningitis. These bacteria were subjected to a clonal analysis. All serogroup A bacteria from both cases and carriers were of one clone (A IV-1). Several unrelated clones were observed among serogroup 29E and serogroup Y carrier strains. The serogroup A strains were uniform for serotype and subtype antigens (serotype 4, subtype P1.7) and antibiotic sensitivity pattern. Occasional strains varied in their lipopolysaccharide (LPS), DNA fingerprint pattern, and/or the quantitative expression of the class 1 protein. A high degree of strain-specific variation was found for the expression of class 5 proteins, pili, and sulfonamide sensitivity. The frequency of strains expressing reduced amounts of the class 1 protein, altered LPS, and/or increased amounts of capsular polysaccharide rose among case strains obtained after the epidemic had ceased. These strains seem to be generally resistant to antibody-mediated bactericidal activity.

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Typing of Neisseria meningitidis serogroup B disease isolates was carried out using a panel of serotype-and subtype-specific monoclonal antibodies (MAbs) in enzyme-linked immunosorbent assays (ELISA). Three hundred and sixty-two strains isolated from 1977 to 1986 were typed using five serotyping and seven subtyping reagents and outer membrane vesicles as antigens. Serotype 2b accounted for 30% of the disease isolates. The most common subtype was P1.2, which occurred on 18.5% of all strains or 48.6% of the serotype 2b strains. Of the 362 strains typed, 135 (37.3%) were serotyped and 122 (33.7%) were subtyped. Overall, 185 (51.1%) of the strains could be assigned a serotype and (or) subtype. Strains (221) isolated during the years 1987-1989 were typed using a panel of 6 serotyping and 12 subtyping reagents by whole-cell ELISA. Strains of serotypes 4 (21.7%) and 15 (20.8%) were the most common and carried a wide variety of subtypes. The most common subtypes were P1.2 (11.8%) and P1.16 (9.5%). Of the 221 strains analyzed, 132 (59.7%) were assigned a serotype and 123 (55.7%) a subtype and with all 18 MAbs, 192 (86.9%) of the strains were serotyped and (or) subtyped. Two different MAbs to the four epitopes 2a, 15, P1.2, and P1.16 gave discordant reactions of 0.3, 6.6, 2.6, and 2.2%, respectively, when used to analyze over 300 strains of N. meningitidis.

A system for typing Neisseria meningitidis has been developed which uses monoclonal antibodies against two separate classes of outer membrane proteins (class 1 and class 2/3) in addition to capsular polysaccharide serogrouping. It was shown that class 1 outer membrane protein subtypes are common to meningococcal reference strains of different serotypes. Application of the system to 50 group B meningococcal patient isolates revealed that 75% could be categorized as class 1 subtypes. The typing system has potential usefulness in epidemiological surveillance and vaccine development.

The subtypes of meningococci are defined by antigenic determinants on the class 1 outer membrane proteins. The established subtypes, designated by P1 and a number according to the prototype reference strain on which they were first recognized by monoclonal antibodies, includes P1.2, P1.9, P1.15 and P1.16. We have investigated more prototype reference strains, using new monoclonal antibodies, and identified the new subtypes P1.1, P1.6 and P1.1,16. The P1.1,16 epitope is found on both the P1.1 and the P1.16 reference strains, but not on all P1.1 and P1.16 strains and can occur independently from the P1.1 and the P1.16 epitopes. It appears that class 1 outer membrane proteins contain at least two independent subtype‐specific epitopes. For clarity, we now redefine P1.1,16 as P1.7, permitting thus the identification of strains of P1.1, P1.1,7, P1.7, P1.7,16 and P1.16 subtypes. It can clearly be expected that more class 1 outer membrane protein determinants will be recognized as more monoclonal typing antibodies are produced. The monoclonal antibodies now available to us can subtype 80–90% of group B and C meningococci; they also react with group A meningococci, but not with other Neisseriae. The immunological dissection of these subtyping antigens will improve our understanding of the relationship between components of the bacteria and the induction or prevention of disease.