{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T01:32:26Z","timestamp":1787016746175,"version":"build-2736575974"},"reference-count":39,"publisher":"American Society for Microbiology","issue":"9","license":[{"start":{"date-parts":[[2002,9,1]],"date-time":"2002-09-01T00:00:00Z","timestamp":1030838400000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["J Clin Microbiol"],"published-print":{"date-parts":[[2002,9]]},"abstract":"ABSTRACT<\/jats:title>\n \n Erythromycin-resistant isolates of\n Streptococcus pneumoniae<\/jats:italic>\n from blood cultures and noninvasive sites were studied over a 3-year period. The prevalence of erythromycin resistance was 11.9% (19 of 160) in blood culture isolates but 4.2% (60 of 1,435) in noninvasive-site isolates. Sixty-two of the 79 resistant isolates were available for study. The M phenotype was responsible for 76% (47 of 62) of resistance, largely due to a serotype 14 clone, characterized by multilocus sequence typing as ST9, which accounted for 79% (37 of 47) of M phenotype resistance. The ST9 clone was 4.8 times more common in blood than in noninvasive sites. All M phenotype isolates were PCR positive for\n mef<\/jats:italic>\n (A), but sequencing revealed that the ST9 clone possessed the\n mef<\/jats:italic>\n (A) sequence commonly associated with\n Streptococcus pyogenes<\/jats:italic>\n . All M phenotype isolates with this\n mef<\/jats:italic>\n (A) sequence also had sequences consistent with the presence of the Tn\n 1207.1<\/jats:italic>\n genetic element inserted in the\n celB<\/jats:italic>\n gene. In contrast, isolates with the\n mef<\/jats:italic>\n (E) sequence normally associated with\n S. pneumoniae<\/jats:italic>\n contained sequences consistent with the presence of the mega insertion element. All MLS\n B<\/jats:sub>\n isolates carried\n erm<\/jats:italic>\n (B), and two isolates carried both\n erm<\/jats:italic>\n (B) and\n mef<\/jats:italic>\n (E). Fourteen of the 15 MLS\n B<\/jats:sub>\n isolates were tetracycline resistant and contained\n tet<\/jats:italic>\n (M). However, six M phenotype isolates of serotypes 19 (two isolates) and 23 (four isolates) were also tetracycline resistant and contained\n tet<\/jats:italic>\n (M). MICs for isolates with the\n mef<\/jats:italic>\n (A) sequence were significantly higher than MICs for isolates with the\n mef<\/jats:italic>\n (E) sequence (\n P<\/jats:italic>\n < 0.001). Thus, the ST9 clone of\n S. pneumoniae<\/jats:italic>\n is a significant cause of invasive pneumococcal disease in northeast Scotland and is the single most important contributor to M phenotype erythromycin resistance.\n <\/jats:p>","DOI":"10.1128\/jcm.40.9.3313-3318.2002","type":"journal-article","created":{"date-parts":[[2002,8,29]],"date-time":"2002-08-29T15:27:50Z","timestamp":1030634870000},"page":"3313-3318","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":73,"title":["Molecular Epidemiology of Erythromycin Resistance in\n Streptococcus pneumoniae<\/i>\n Isolates from Blood and Noninvasive Sites"],"prefix":"10.1128","volume":"40","author":[{"given":"Maria Rosario","family":"Amezaga","sequence":"first","affiliation":[{"name":"Department of Medical Microbiology, University of Aberdeen, Aberdeen AB25 2ZD, Scotland, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Philip E.","family":"Carter","sequence":"additional","affiliation":[{"name":"Department of Medical Microbiology, University of Aberdeen, Aberdeen AB25 2ZD, Scotland, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Phillip","family":"Cash","sequence":"additional","affiliation":[{"name":"Department of Medical Microbiology, University of Aberdeen, Aberdeen AB25 2ZD, Scotland, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hamish","family":"McKenzie","sequence":"additional","affiliation":[{"name":"Department of Medical Microbiology, University of Aberdeen, Aberdeen AB25 2ZD, Scotland, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1128\/AAC.43.9.2335"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1093\/jac\/44.1.133"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1002\/(SICI)1522-2683(19990801)20:11<2259::AID-ELPS2259>3.0.CO;2-F"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-2958.1996.01521.x"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0966-842X(00)88930-1"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1128\/JCM.40.3.774-778.2002"},{"key":"e_1_3_2_8_2","doi-asserted-by":"publisher","DOI":"10.1093\/jac\/45.2.167"},{"key":"e_1_3_2_9_2","doi-asserted-by":"publisher","DOI":"10.1128\/AAC.45.6.1721-1729.2001"},{"key":"e_1_3_2_10_2","doi-asserted-by":"publisher","DOI":"10.1128\/AAC.44.11.2979-2984.2000"},{"key":"e_1_3_2_11_2","doi-asserted-by":"publisher","DOI":"10.1099\/00221287-144-11-3049"},{"key":"e_1_3_2_12_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0966-842X(99)01609-1"},{"key":"e_1_3_2_13_2","first-page":"56","volume":"284","year":"2001","unstructured":"Gay, K., and D. 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