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JAC Advance Access originally published online on April 25, 2007
Journal of Antimicrobial Chemotherapy 2007 59(6):1167-1170; doi:10.1093/jac/dkm106
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© The Author 2007. Published by Oxford University Press on behalf of the British Society for Antimicrobial Chemotherapy. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org

Presence of plasmid pA15 correlates with prevalence of constitutive MLSB resistance in group A streptococcal isolates at a university hospital in southern Taiwan

Yi-Fang Liu1, Chih-Hung Wang2, Rajendra Prasad Janapatla2, Hsiu-Mei Fu2, Hsiu-Mei Wu2 and Jiunn-Jong Wu1,2,*

1 Institute of Basic Medical Sciences, College of Medicine, National Cheng Kung University, Tainan, Taiwan 2 Department of Medical Laboratory Science and Biotechnology, College of Medicine, National Cheng Kung University, Tainan, Taiwan

Received 18 January 2007; returned 23 January 2007; revised 13 March 2007; accepted 19 March 2007

* Correspondence address. Department of Medical Laboratory Science and Biotechnology, College of Medicine, National Cheng Kung University, No. 1 University Road, Tainan 70101, Taiwan. Tel: +886-6-2353535 ext. 5775; Fax: +886-6-2363956; E-mail: jjwu{at}mail.ncku.edu.tw

Objectives: To investigate the role of a plasmid bearing the erm(B) gene on the prevalence of the macrolide, lincosamide and group B streptogramin (MLSB) phenotype of group A streptococci (GAS) and to characterize the plasmid and determine the clonal relation between the erythromycin-resistant isolates.

Methods: Two hundred and five erythromycin-resistant GAS isolates were collected from 1990 to 2006. Colony hybridization, PCR, plasmid curing and PFGE techniques were used to analyse the mechanisms behind the phenotypes.

Results: Among the 56 isolates with constitutive MLSB (cMLSB) resistance, 53 isolates harboured a plasmid, pA15, of 19 kb. erm(B) was on pA15 and it confered a cMLSB resistance phenotype. The prevalence rate of the pA15-containing isolates was 36.3% from 1993 to 1995, but the plasmid could not be detected from 2004 to 2006. To link the high-level resistance to pA15, clinical isolate A15 was selected and pA15 was cured by novobiocin. In the plasmid-cured strain SW503, the erythromycin MIC decreased from 256 to 0.032 mg/L. By electroporation, pA15 was re-introduced into the plasmid-cured erythromycin-susceptible strain, and the high-level erythromycin resistance was restored. Plasmid pA15 was also transferred to group B streptococci and group C streptococci by electroporation. In all the pA15-containing isolates, emm1 type was present and pulse type J was predominant (48 of 54 isolates).

Conclusions: The plasmid pA15 mediated cMLSB resistance in the mid-1990s, but pA15 was not detected in the clinical isolates from 2004 onwards, which correlates with the absence of cMLSB resistance in this region.

Keywords: erythromycin , clindamycin , plasmids , group A streptococci , PFGE


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