The major emm types were further discriminated into a number of PFGE types, and clustering analysis of the PFGE patterns suggests that the emm1, emm6 and emm4 strains belong to a single clone. The emm12 strains belong to two major clones and two singletons, and emm22 strains belong to one major clone and one singleton (Figure 2). Thus, six emm clones caused most (96.5%) of the scarlet fever cases in central Taiwan during the seven year time period. The fluctuation of scarlet fever cases was associated with the shuffling of the prevalent emm clones (Figure 4). The
finding that only a few prevalent M (emm) types caused most occurrences of scarlet fever in a specific location in a given year period, as well as the shuffling selleckchem of predominant M types, has LOXO-101 chemical structure been observed in many epidemiological studies in the early 20th century . During major epidemics of streptococcal infections in previous years, only a few serotypes
predominated, and the strains were rich in M protein, encapsulated and were highly virulent . Type-specific immunity was important for preventing re-infection with the same M type. It is thought that the shuffling of predominant M types is due to the type-specific immunity, leading to the decline of infections with certain M types and the emergence of other virulent M types. In the present study, the prevalence of the emm12*, emm1 and emm6 clones both increased and decreased within one year. In contrast, the emm12 and emm4 clones persisted throughout the seven year period. This phenomenon may be due to the fact that the emm12 and emm4 clones produced less M protein and were less virulent than the emm12*, emm1 and emm6 clones. The PFGE study also indicates that each of the six emm clones has one predominant PFGE type, except for the emm4 clone, which has two major PFGE types (Figure 2). The less prevalent PFGE genotypes of each emm clone emerged and quickly disappeared. Even some major PFGE genotypes, such
as SPYS16.0026 of the emm12* clone, SPYS16.0020 of the emm6 clone and SPYS16.0022 of the emm1 clone, remained prevalent for only 2–3 years before declining. However, the SPYS16.0013 genotype of the emm12 clone did not follow Adenosine triphosphate this trend, as it was prevalent throughout 2000–2006 and was most prevalent in 2006. If a newly emerging strain can only prosper in a specific location for a few years, then the emm12:SPYS16.0013 strains isolated during two different time periods should be different. These differences may not be detectable by PFGE analysis. Whether bacterial isolates that prevail for two periods become genetically diversified is an interesting subject and may be studied by other genotyping methods, such as single nucleotide polymorphism, by virulence gene detection and by antimicrobial susceptibility mTOR inhibitor testing. The SPYS16.