Of the 127 SPYS16.0026 isolates, 125 belonged to the emm12 type. The first isolate resistant to SmaI digestion was identified in central Taiwan in 1998 and was an emm33 type. The emm12:SPYS16.0026 strain was detected for the first time in 1999 [7]. Our previous studies indicated that the emm12:SPYS16.0026 strain is most likely derived from an emm12:SPYS16.0013 strain by an insertion of a large DNA fragment into the genome [7]. The large DNA segment could have carried the gene(s) responsible for DNA methylation and resistance to cleavage by SmaI. These
strains were analyzed with SgrAI. Clustering analysis of the PFGE-SgrAI patterns revealed diverse genetic relationships among the emm12:SPYS16.0026 strains (Figure 3). The high genetic divergence suggests that the emm12:SPYS16.0026 strains have derived from multiple origins. Recently, Ceritinib manufacturer Euler et al. [12] have shown that resistance to SmaI cleavage is due to the presence of a DNA methyltransferase gene, which is carried on a mobile chimeric element that has transposon- and bacteriophage-like HM781-36B characteristics. This mobile element may explain the high genetic diversity among the SmaI-resistant strains that emerged in such short period of time. The fluctuation of scarlet fever
cases between 2000 and 2006 may be partially explained by the shuffling of several prevalent emm clones. However, the dramatic drop in reported cases in 2003 is difficult to explain. In early 2003, Taiwan was badly hit by a severe SARS outbreak. The SARS epidemic in Taiwan had two distinct stages, with the beginning in the late-February (the 9th week) and the second ending in mid-June [13]. The not stage I epidemic occurred from late-February to mid-April (the 9th to 16th week) and consisted of only scattered, sporadic cases, with most of the patients
having recently traveled to China. In this stage, the disease did not cause much panic and the level of scarlet fever remained high. In stage II (from mid-April to mid-June or the 17th to 24th week), several clusters of infection occurred via intra-hospital or inter-hospital transmission. Enormous panic spread over the whole Country after an outbreak of nosocomial infection was confirmed on the 22nd of April. The disease was subsequently transmitted to several hospitals and spread from the North to the South. The number of scarlet fever cases dropped remarkably during this period. Because a large portion of the SARS infections was associated with hospitals, fear of SARS drove people out of hospitals and public places. This fear and the change of people’s behavior may have significantly reduced the number of outpatients and the transmission of many infectious diseases, including scarlet fever. In fact, the SARS outbreak had a long-term effect on the occurrences of scarlet fever. After the SARS epidemic, the number of weekly scarlet fever reports was often lower than the overall average until the first half of 2004.