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6 (95%?CI?1.2�C11.5; p?=?0.04) and 4.5 (95%?CI?1.6�C12.2; p?selleckchem There was no association of CRP level with poor outcome in the three groups. emm typing was carried out for 231 SDSE isolates and for 82 of the 97 S.?pyogenes isolates; capsular typing was performed for 123 of the 151 S.?agalactiae isolates. The incidences of emm types among SDSE isolates are shown in Table?3. Interestingly, emm type stG6792 in SDSE isolates, which was confirmed most frequently (n?=?55, 24%), was significantly associated with poor outcome of invasive SDSE diseases in comparison with other SDSE emm types, with an OR of 2.4 (95%?CI?1.0�C5.9; p?=0.04). Within the stG6792 type, most isolates showed emm type stG6792.3 (n?=?54), Selleck Lapatinib whereas PFGE of the isolates of the stG6792.3 type revealed similar profiles. On the other hand, among GAS isolates, emm type?1 was found most frequently (n?=?27, 33%). This type was also significantly related to poor outcome of invasive infections, with an OR of 3.4 (95%?CI?1.1�C10.5; p?0.02). Other emm types frequently found in GAS infections were 49 (n?=?12), 89 (n?=?5), 11 (n?=?4), 12 (n?=?4), and 75 (n?=?4), whereas emm types?12 and 6 predominated in our study of non-invasive GAS infections (T. Wajima, S. Y. Murayama & K. Ubukata, unpublished data). Capsular type?Ib in GBS isolates were not associated with poor outcome of invasive diseases. This type (n?=?39) was observed most frequently in adults. Other GBS capsular types, i.e. V (n?=?23), II (n?=?15), III (n?=?14), and Ia (n?=?11), were predominantly observed, showing distribution patterns different from those found in the study of non-invasive GBS infections. Antibiotic susceptibility testing was performed for all isolates of SDSE, GAS and GBS. Of 231 SDSE isolates, four had the mef(A) gene, and 13 and six isolates had erm(A) and erm(B) genes, respectively; the presence of the latter suggested a high level of resistance to clarithromycin (MIC?��64?mg/L). In addition, two SDSE isolates showed resistance to fluoroquinolones, such as levofloxacin S6 Kinase (MIC?��32?mg/L), based on substitutions in GyrA (Ser81 to Phe or Tyr) and ParC (Ser79 to Tyr). No penicillin or cephalosporin resistance was observed. To the best of our knowledge, this is the first nationwide surveillance regarding invasive infections caused by SDSE in Japan. The study demonstrates significant differences in clinical aspects, including prognosis, between disease entities caused by SDSE, GAS and GBS. The mortality rate of invasive SDSE diseases in our study (13%) was similar to those previously described in other countries (8�C18%) [1,5,14,15].
