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. 2003 Feb;41(2):586-91.
doi: 10.1128/JCM.41.2.586-591.2003.

Clonal diversity among streptogramin A-resistant Staphylococcus aureus isolates collected in French hospitals

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Clonal diversity among streptogramin A-resistant Staphylococcus aureus isolates collected in French hospitals

Julien Haroche et al. J Clin Microbiol. 2003 Feb.

Abstract

We analyzed 62 clinical isolates of streptogramin A-resistant (SGA(r)) Staphylococcus aureus collected between 1981 and 2001 in 14 hospitals located in seven French cities. These isolates, including five with decreased susceptibility to glycopeptides, were distributed into 45 antibiotypes and 38 SmaI genotypes. Each of these genotypes included between 1 and 11 isolates, the SmaI patterns of which differed by no more than three bands. Although numerous clones were identified, we observed the spread of monoclonal isolates either within the same hospital or within hospitals in distinct cities and at large time intervals. Hybridization with probes directed against 10 SGA(r) genes (vatA, vatB, vatC, vatD, vatE, vgaA, vgaB, vgaAv, vgbA, and vgbB) revealed six patterns: vgaAv (21 isolates), vatA-vgbA (24 isolates), vgaAv-vatB-vgaB (14 isolates), vgaAv-vatA-vgbA (1 isolate), vgaAv-vatA-vgbA-vatB-vgaB (1 isolate), and vgaA (1 isolate). We detected at least one SGA(r) determinant in all of the tested isolates. vgaAv, which is part of the recently characterized transposon Tn5406, was found in 59.7% of the tested isolates. Of the 16 streptogramin B-susceptible isolates, 14 carried vgaAv alone and were susceptible to the mixtures of streptogramins, whereas the 2 isolates carrying vgaAv-vatB-vgaB were resistant to these mixtures. vatA-vgbA was found on plasmids of the same apparent size in 26 (42%) of the tested clinical isolates from 18 unrelated SmaI genotypes. The possible dissemination of some of the multiple clones characterized in the present study with an expected increased selective pressure of streptogramins following the recent licensing of Synercid (quinupristin-dalfopristin) must be carefully monitored.

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Figures

FIG. 1.
FIG. 1.
Pulsed-field gel electrophoresis of SmaI-digested total DNA from SGAr S. aureus clinical isolates. Lanes A, G, M, and R, NCTC 8325 used as standard; lane B, genotype 17a strain; lane C, genotype 15a strain; lane D, genotype 17c strain; lane E, genotype 16b strain; lane F, genotype 17b strain; lane H, genotype 24h strain (Paris-A, 1997); lane I, genotype 24a strain; lane J, genotype 24a strain (Toulouse, 1998); lane K, genotype 24c strain (Paris-A, 1999); lane L, genotype 30a strain; lane N, genotype 30b strain; lane O, BM3318; lane P, BM3093; lane Q, BM10692.
FIG. 2.
FIG. 2.
Agarose gel electrophoresis patterns of plasmid DNA from SGAr S. aureus clinical isolates carrying vatA-vgbA (lanes C to J). (A) Plasmid migration patterns; (B) hybridization patterns with the vgbA probe (pIP1654). Lanes A, the Raoul marker (Appligene) used as a standard; lanes B, total DNA from BM3093; lanes C, plasmid DNA from genotype 22a strain (Paris-A, 1998); lanes D, plasmid DNA from genotype 36a strain; lanes E, plasmid DNA from genotype 8a strain; lanes F, plasmid DNA from genotype 32 strain; lanes G, plasmid DNA from genotype 3 strain; lanes H, plasmid DNA from genotype 19 strain; lanes I, plasmid DNA from genotype 20 strain; lanes J, plasmid DNA from genotype 16a strain.

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