Areum Durey, et al. otics inhibited the growth of the bacteria. N. meningitidis is divided into 13 serogroups based on the immunological specificity of the capsular polysaccha- ride. It has been known that patient strains are encapsulated and five of these serogroups (A, B, C, W135 and Y) cause more than 90% of the invasive disease worldwide.16 In con- trast, 50% of the strains isolated from carriers lack a cap- sule and are therefore serologically not serogroupable.17,18 In our study, serogroups could not be determined by the slide agglutination method with polyclonal antisera because fre- quent non-specific reactions or cross reactions were frequent- ly observed. This was probably due to the lack of a capsule in the strains isolated from carriers or there could have been problems related to culturing the isolates. Claus, et al.19 com- mented that there are two essential reasons for the lack of capsule - the deletion of the capsule locus or down-regula- tions of the expression of the capsule, either temporarily or permanently, by one of a number of genetic mechanisms. Until recently, nongroupable isolates were thought to be non- pathogenic. On the contrary, it has become progressively clear that capsular expression is phase variable,20 and the loss of capsule may enhance the organism’s ability to colonize the nasopharynx. Caugant, et al.21 performed a comparative study of the expressed capsular antigens in a collection of 667 meningo- cocci isolated from patients and carriers in three European countries to better understand the relationship between car- rier and disease-causing strains. Serogroup B strains was predominant among both patient and carrier isolates. Al- though marked differences between countries were observed in the serogroup distribution of patient isolates, the sero- group distribution of the carrier isolates was similar between countries, with predominance of serogroup B among iso- lates expressing a capsular polysaccharide, followed by se- rogroup Y. In our study, serogrouping by PCR was per- formed for the detection and identification of serogroups A, B, C, Y, W135, X, Z and 29E. Of 16 total meningococcal isolates of the first culture, serogroup C was found to be the most frequent (31.3%) and serogroup B followed (18.8%). We could not determine a serogroup by PCR for 8 isolates (genetically non-groupable, 50%). The currently available meningococcal vaccines are based on the capsular polysaccharides of meningococcal sero- groups A, C, W-135 and Y. None of these vaccines provide protection against serogroup B meningococci, which is the prevalent serogroup in Europe, North America, South Ameri- ca, and Australia, because the capsular polysaccharide of meningococcal serogroup B is unable to stimulate a protec- tive immune response.22 Other alternatives for meningococ- cal outer membrane protein (OMP)-based vaccines have been investigated to prevent meningococcal disease, re- gardless of their serogroup.23 The PorA OMP, characterized by genosubtyping of the VR1 and VR2 of the porA gene, is highly immunogenic and is considered to be an important component in protein-based vaccines against meningococ- cal disease. However, PorA shows a high degree of anti- genic variation which is used for serologic differentiation of isolates.24 Consequently, newer PorA-based vaccines have to consider the prevalence of genosubtypes and contain mul- tiple antigenic variants of PorA.25 Our data revealed the di- versity of the PorA types of N. meningitidis, although the number of isolates analyzed was small. Moreover, PorA VR2 sequences were changed in 2 students during pro- longed carriage in our study, which is different from the re- sults of a group of military recruits in the UK.26 This sug- gests the possibility of either rapid mutation of the porA gene or horizontal exchange of genetic material between strains during the 4-week interval between cultures. It also reveals the difficulty in designing a useful OMP vaccine. This study was the first report of rates of carriage and ac- quisition of N. meningitidis among freshmen in a university dormitory in Korea, together with serogroups and genosub- types. The carriage rate is comparable with those reported from other studies. However, it did not significantly increase after four weeks, which is markedly different from previous studies in Western countries. This suggests that freshmen at this university may be at low risk of clusters of cases with meningococcal disease, and may therefore be at a low risk of outbreaks. Inversely, this low rate of carriage acquisition after one month might explain the low incidence of menin- gococcal disease in freshmen in Korea. As we mentioned, transmission dynamics in freshmen in Korea may differ from those in western countries. Therefore, it will be help- ful to continue follow-up swabbing in the same dormitory or to perform a longitudinal study at other universities on a large scale, to assess how it compares with Western studies. REFERENCES 1. Rosenstein NE, Perkins BA, Stephens DS, Lefkowitz L, Cartter ML, Danila R, et al. The changing epidemiology of meningococ- cal disease in the United States, 1992-1996. J Infect Dis 1999;180: 1894-901. 2. Harrison LH, Dwyer DM, Maples CT, Billmann L. Risk of menin- 746 Yonsei Med J http://www.eymj.org Volume 53 Number 4 July 2012