Journal Article

A new phenotype of resistance to lincosamide and streptogramin A-type antibiotics in <i>Streptococcus agalactiae</i> in New Zealand

Brigitte Malbruny, Anja M. Werno, Trevor P. Anderson, David R. Murdoch and Roland Leclercq

in Journal of Antimicrobial Chemotherapy

Published on behalf of British Society for Antimicrobial Chemotherapy

Volume 54, issue 6, pages 1040-1044
Published in print December 2004 | ISSN: 0305-7453
Published online December 2004 | e-ISSN: 1460-2091 | DOI: http://dx.doi.org/10.1093/jac/dkh493
A new phenotype of resistance to lincosamide and streptogramin A-type antibiotics in Streptococcus agalactiae in New Zealand

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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

Journal Article.  3114 words.  Illustrated.

Subjects: Medical Oncology ; Critical Care

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