pyogenes strains from 44 patients at the time of initial onset and following treatment (after therapy without symptoms) and from those with recurrent pharyngitis. The emm genotypes found in the post-treatment samples corresponded with the genotypes of the initial strains in 38 of 49 of the clinical recurrent episodes (Fig. 1). Next, PFGE analysis was conducted to examine the differences among

the strains obtained at different time points. PFGE analysis exhibited a higher discriminatory power than emm genotyping and showed different patterns in cases in which both strains were found to have the same emm SD-208 price genotype (Fig. 2). Furthermore, speA, speB, and speC genotyping analyses were performed using post-treatment strains that corresponded with the emm genotypes and PFGE patterns isolated at the time of initial onset. The speA, speB, and speC genes were examined using PCR, followed by DNA sequencing in specimens with at least one of the genes present. Of the 38 tested cases, the speA, speB, and speC genotypes found in the post-treatment samples were different from the genotypes of the initial strains in nine (no. 4, 8, 9, 10, 18, 22, 25, 28, 39), three (no. 16, 25, 39), and four (no. 3, 5, 7, 35) cases, respectively (Table 1). In 49 cases clinically diagnosed as recurrent pharyngitis, more than half of the recurrent infections (27 cases) were caused by S. pyogenes strains that differed from those isolated during the Selleckchem Adriamycin initial

onset. The mean period from initial onset in 22 recurrent infection cases was 17.7±12.9 days (range, 7−58 days), all while that of 27 reinfection cases caused by different strains was 95.9±138.1 days (9−499 days). There was a significant difference between these

groups, as shown by the results of a Mann–Whitney U-test (P=0.019). Of the 93 strains tested in the present study, two were resistant to penicillin G (MIC>2.0 U mL−1), 58 to erythromycin (MIC >1.0 μg mL−1), 55 to azithromycin (MIC>1.0 μg mL−1), and 93 to clindamycin (MIC>1.0 μg mL−1), as shown in the results obtained using our broth microdilution method. Furthermore, 46, 39, and 49 of those resistant strains showed an MIC value >128 μg mL−1 toward erythromycin, azithromycin, and clindamycin, respectively (Table 4). In addition, 32 strains (72.7%) from initial onset, 17 strains (77.3%) from recurrent, and 12 strains (44.4%) from reinfection cases possessed ermB, while 11 (25.0%), 12 (54.5%), and two (7.4%), respectively, possessed mefA. In contrast, ermTR was not detected in any of the strains examined (Table 1). It is of considerable concern that antibiotic treatment failure has occurred in up to one-third of streptococcal pharyngitis cases reported in clinical practice (Macris et al., 1998; Kuhn et al., 2001). The current protocol recommends the administration of penicillin with no regard for bacterial factors. Thus, it is important to establish treatment guidelines based on molecular analysis of S.