A total of 488 persons were included in the study; >96% were seen at each respective visit. Eighteen percent of the population carried a meningococcus at least once during the study. All genogroupable isolates could be serogrouped. The 152 meningococcal isolates were attributed to serogroups NmW135 (n = 28), NmX (n = 5), NmY (n = 3), and nongroupable, autoagglutinable, or polyagglutinable Nm (n = 116). No NmA, NmB, or NmC were found (Table 1).

Among the 151 meningococcal isolates submitted for serotyping, most could not be serotyped or serosubtyped with existing antibodies (n = 98, 65%). Serotype 2a:P1.5,2 (n = 17, 11%) and 15:P1.6 (n = 16, 11%) were the most frequently found serotypes, followed by NT:P1.5,2 (n = 11, 7%), NT:P1.5 (n = 6, 4%), and 14:P1.5,2 (n = 3, 2%) (Figure 3, Table 1).

Among the 151 isolates analyzed by MLST or PFGE, most were ST-192 (n = 96, 63%), followed by ST-11 (n = 19, 13%), ST-198 (n = 13, 9%), and ST-2881 (n = 8, 6%, including 1 strain with the single locus variant ST-4151) (Table 1). Other STs represented <5% of the carriage strains and included ST-4426 (in the clonal complex ST-198), ST-751 (including the single locus variant ST-4376), ST-4375 (in the clonal complex ST-23), and ST-4377.

Serogroup W135 was mostly found in combination with serotype 2a:P1.5,2 and genotype ST-11. Serogroup X was found with NT:P1.5, ST-751, and serogroup Y was found with 14:P1.5,2, ST-4375 (Table 1).

This longitudinal carriage study in a healthy young population in the African meningitis belt describes the diversity of carried meningococcal serogroups, serotypes, and genotypes during a nonepidemic meningitis season. Eleven STs and 4 serogroup categories (including nongroupable strains) were identified. Parallel culture- and PCR-based meningitis surveillance in this population during 2003 showed a high incidence of endemic meningococcal disease (annual rate = 77/100,000 among persons <5 years of age and 5/100,000 among persons >14 years of age). During February–April 2003, 9 cases of NmA meningitis and 28 cases of NmW135 meningitis were found in urban Bobo-Dioulasso (435,000 inhabitants), as well as sporadic cases caused by serogroup X and nongroupable meningococci (Table 4) (5,17).

Despite frequent serogroup A disease, no serogroup A meningococcal carriage was found. NmA was likely circulating at low levels during our study but not found because of low transmission density or short duration of NmA carriage, together with sample size limitation. Our study thus provides evidence for low prevalence of serogroup A carriage in nonepidemic conditions, which is similar to results of a study in Nigerian schoolchildren (18). This finding is useful for assessment of group A conjugate meningococcal vaccines by carriage studies. To show a reduction in NmA carriage prevalence after vaccination, as was recently reported from the United Kingdom for group C conjugate vaccine (19), studies need to include several thousand persons to achieve appropriate statistical power.

Apart from NmA, all phenotypes and genotypes isolated from meningococcal meningitis cases in this population from 2000 to 2005 (Table 5) were represented in this 4-month carriage study of 488 persons. This finding supports the use of carriage studies in nonepidemic conditions for surveillance of meningococcal strains of specific serogroups. For surveillance of new genotypes expressing a group A capsule, however, disease surveillance will be more appropriate. For example, ST-2859, a new genotype that expresses group A capsule, has become a major meningitis agent in Bobo-Dioulasso since 2002 (17). Our carriage study did not detect this development. In addition, results from localized carriage studies should not be generalized to West Africa and the African meningitis belt as a whole because only 4 of 7 serogroups and 5 of 15 genotypes found in meningococcal meningitis cases in the region during 2000–2005 were represented in our carriage study.

During bacterial meningitis surveillance in the Bobo-Dioulasso population in 2004, we observed 2 invasive strains whose genotypes had been associated with different serogroups and serotypes in our carriage study 1 year earlier (Table 5). ST-11, which is usually associated with phenotype W135:2a:P1.5,2 in invasive strains, had phenotype Y:14:P1.5,2 (seen in ST-4375 carriage strains), and ST-4375, which is usually associated with phenotype Y:14:P1.5,2, had phenotype W135:NT:P1.5,2 (seen in ST-11 carriage strains). These findings could be evidence for a capsular and serotype switch between co-colonizing meningococci, as described by Swartley et al. (23). However, that report described only gene conversion for capsule expression, not for outer membrane protein (PorB) expression. The potential capacity of meningococci to exchange capsular plus subcapsular genes needs to be further evaluated.

Our study and previous studies of meningococci in sub-Saharan Africa have shown a similar number of different serogroup categories, including nonserogroupable strains (18,24–26). However, assessing whether the genetic diversity we found is a new phenomenon is difficult because most studies do not report genotypes of all isolates. Five ST strains expressed group W135 capsule in this population that was followed up over a 4-month period. This variation has not been reported for other meningococcal serogroups in sub-Saharan Africa but is consistent with results of a report on increasing genetic diversity of W135-encapsulated strains in France since the Hajj-associated outbreak in 2000 (27). In contrast to NmW135, NmA has a relatively low genetic diversity, with only 6 genotypes found to express the A capsule over the past 30 years ([1]; http://pubmlst.org/neisseria). This difference between the 2 serogroups suggests that NmW135 may not replace NmA as the major epidemic agent in the future. Nevertheless, the easy adoption of a W135 capsule by various genotype stains, in combination with infrequent immune induction by NmW135 carriage (7), may cause regular NmW135 outbreaks to occur.

Nongroupable strains were predominant in our study and other carriage studies during nonepidemic conditions in Burkina Faso, Ghana, Europe, and the United States (20,24,28–31). In our study, nongroupable and nontypeable isolates were predominantly ST-192, which represented 63% of all carried meningococci. Data from the Neisseria MLST website indicate that ST-192 isolates were present in The Gambia and Niger in the 1990s, but no published data are available on the dimension of prevalence of this strain in these or other countries. This strain deserves closer observation because in Bobo-Dioulasso during 2003 and 2004, 3 persons were found with disease caused by nongroupable ST-192 isolates. Unencapsulated strains rarely cause invasive disease and usually only among complement-deficient persons (32). This may have occurred in the 3 patients, whose complement status was not determined. However, the isolates from Bobo-Dioulasso also showed enhanced capacity to escape human immune defenses (33), which would enable these isolates to cause invasive disease in immunocompetent persons.

In our study, carriage of the NG:NT ST-192 strain increased from the early phase of the meningitis season to just past its end, as did carriage of N. lactamica in children. This finding may be an annual phenomenon that is associated with a decreasing meningitis incidence by late April (Figure 4), which would be caused by a reduced risk for infection or disease by virulent meningococci, given the increased carriage prevalence of nongroupable meningococci (34). However, our data were from a small sample and only 1 population during 1 meningitis season. A more systematic evaluation by longitudinal carriage studies in several African sites is needed to further explore this hypothesis.

Carriage during this study was dynamic and short-lived compared with other studies in Europe (15,30,35). This finding emphasizes the need for a large sample size in cross-sectional carriage studies and the need for multiple assessment points over short intervals for studies on carriage association with risk factors or immune status. Estimated carriage duration was longer for less virulent nongroupable strains than for NmW135. This could be due to a more accentuated immune response to carriage of encapsulated strains, although serologic evaluation during the same study suggested that the immune response to NmW135 carriage does not occur frequently (7).

In the context of hyperendemic NmW135 and NmA disease in Bobo-Dioulasso in 2003, we found a large diversity of phenotypes and genotypes in carried Nm strains (including all strains, except for serogroup A) that caused meningococcal meningitis in this population. NmW135 showed substantial prevalence and high genetic diversity. These features distinguish this serogroup from NmA and indicate that, in combination with poor immune induction by carriage, this serogroup may be a potential epidemic agent. The absence of NmA during this nonepidemic meningitis season and the pronounced dynamics of meningococcal carriage emphasize the need for large samples and a longitudinal design for most carriage studies. By decreasing the risk for infection with a virulent clone, expansion of a nonvirulent clone in carriage toward the end of the meningitis season may be 1 of the mechanisms causing a seasonal decrease in the incidence of meningococcal disease.