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Journal of Clinical Microbiology, September 2002, p. 3313-3318, Vol. 40, No. 9
0095-1137/02/$04.00+0     DOI: 10.1128/JCM.40.9.3313-3318.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Molecular Epidemiology of Erythromycin Resistance in Streptococcus pneumoniae Isolates from Blood and Noninvasive Sites

Maria Rosario Amezaga, Philip E. Carter,,{dagger} Phillip Cash, and Hamish McKenzie*

Department of Medical Microbiology, University of Aberdeen, Aberdeen AB25 2ZD, Scotland, United Kingdom

Received 3 April 2002/ Returned for modification 28 May 2002/ Accepted 25 June 2002

Erythromycin-resistant isolates of Streptococcus pneumoniae 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 mef(A), but sequencing revealed that the ST9 clone possessed the mef(A) sequence commonly associated with Streptococcus pyogenes. All M phenotype isolates with this mef(A) sequence also had sequences consistent with the presence of the Tn1207.1 genetic element inserted in the celB gene. In contrast, isolates with the mef(E) sequence normally associated with S. pneumoniae contained sequences consistent with the presence of the mega insertion element. All MLSB isolates carried erm(B), and two isolates carried both erm(B) and mef(E). Fourteen of the 15 MLSB isolates were tetracycline resistant and contained tet(M). However, six M phenotype isolates of serotypes 19 (two isolates) and 23 (four isolates) were also tetracycline resistant and contained tet(M). MICs for isolates with the mef(A) sequence were significantly higher than MICs for isolates with the mef(E) sequence (P < 0.001). Thus, the ST9 clone of S. pneumoniae is a significant cause of invasive pneumococcal disease in northeast Scotland and is the single most important contributor to M phenotype erythromycin resistance.

* Corresponding author. Mailing address: Department of Medical Microbiology, University of Aberdeen, Medical School Buildings, Foresterhill, Aberdeen AB25 2ZD, Scotland, United Kingdom. Phone: 1224 552446. Fax: 1224 685604. E-mail: mmb041{at}abdn.ac.uk.

{dagger} Present address: Institute of Environmental Science and Research Ltd., Kenepuru Science Centre, Porirua, New Zealand.

Journal of Clinical Microbiology, September 2002, p. 3313-3318, Vol. 40, No. 9
0095-1137/02/$04.00+0     DOI: 10.1128/JCM.40.9.3313-3318.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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