JAC Advance Access originally published online on November 10, 2004
Journal of Antimicrobial Chemotherapy 2004 54(6):1040-1044; doi:10.1093/jac/dkh493
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JAC vol.54 no.6 © The British Society for Antimicrobial Chemotherapy 2004; all rights reserved
A new phenotype of resistance to lincosamide and streptogramin A-type antibiotics in Streptococcus agalactiae in New Zealand
1 Service de Microbiologie, CHU Côte de Nacre, 14033 Caen, France; 2 Microbiology Unit, Canterbury Health Laboratories, Christchurch; 3 Department of Pathology, Christchurch School of Medicine and Health Sciences, Christchurch, New Zealand
* Corresponding author. Tel: +33-2-31-06-45-72; Fax: +33-2-31-06-45-73; Email: leclercq-r{at}chu-caen.fr
Objectives: To characterize a new type of resistance to clindamycin in Streptococcus agalactiae.
Methods: Nineteen erythromycin-susceptible, clindamycin-resistant S. agalactiae isolates from New Zealand were studied. MICs of macrolide, lincosamide and streptogramin antibiotics were determined. Clindamycin and streptogramin resistance genes were searched for by PCR. Isolates were compared by serotyping and by DNA macrorestriction patterns determined by PFGE. Conjugative transfer of resistance traits to recipient strains of S. agalactiae and Enterococcus faecium was assayed.
Results: The 19 S. agalactiae isolates were intermediate or resistant to clindamycin (MIC range: 0.5–2 mg/L) and lincomycin (MIC range: 1–8 mg/L) and had high MICs of dalfopristin (4–32 mg/L), a streptogramin A-type antibiotic, compared with controls. By contrast, the strains were susceptible to macrolides and quinupristin, a streptogramin B-type antibiotic. This new phenotype was called LSA (lincosamide–streptogramin A). Clindamycin resistance could not be transferred to recipient strains. Thirteen isolates belonged to serotype III and to a single PFGE genotype A, and five isolates belonged to serotype I and to genotype B. One isolate was non-typeable and belonged to a distinct genotype C.
Conclusions: We have characterized a new LSA phenotype in S. agalactiae. Analysis of restriction patterns of S. agalactiae chromosomal DNA showed that the resistance was spread in a minimum of three bacterial clones. The genetic and biochemical basis for the resistance remains unknown.
Keywords: streptococci , resistance mechanism , inhibition of protein synthesis , drug resistance , group B streptococcus
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