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M Chauvel

Publications and source records attributed to M Chauvel.

3 recordsLinked to original sources
PubMed2006

[Prevalence of community-acquired methicillin-résistant Staphylococcus aureus].

OBJECTIVE: The authors had for aim to assess the prevalence of community-acquired methicillin-resistant Staphylococcus aureus in France. METHOD: Two hundred fifty-four strains identified in 1,079 nasal samples from voluntary individuals were analyzed in 2002. An antibiogram (especially measuring the inhibition diameter of cefoxitine) and screening by oxacillin (6 mug/ml) allowed the identification of strains resistant to betalactams. The resistant phenotype was confirmed by amplification of the mecA gene by PCR. The distribution of strains was compared to the resistance to various antibiotics and especially to cotrimoxazole, macrolides, aminosides, and the mechanisms of resistance were determined. RESULTS: Eleven methicillin-resistant strains were detected in 254 carriers (4.33%), or 1% of the total population studied. CONCLUSION: Complementary tests (detection of the Panton-Valentine toxin, pulsed field electrophoresis) will be necessary to finish strain characterization. It can already be stated that compared to previous studies, community-acquired MRSA carriage is weak in France.

Adult↗
PubMed1999

Vancomycin-dependent Enterococcus faecalis clinical isolates and revertant mutants.

Three vancomycin-dependent clinical isolates of Enterococcus faecalis of the VanB type were studied by determining (i) the sequence of the ddl gene encoding the host D-Ala:D-Ala ligase and the vanSB-vanRB genes specifying the two-component regulatory system that activates transcription of the vanB operon, (ii) the level of expression of resistance genes by using DD-dipeptidase activity as a reporter, and (iii) the proportions of the peptidoglycan precursors synthesized. Each strain had a mutation in ddl leading to an amino acid substitution (D295 to V; T316 to I) or deletion (DAK251-253 to E) at invariant positions in D-Ala:D-Ala, D-Ala:D-Lac, and D-Ala:D-Ser ligases. These mutations resulted in impaired host D-Ala:D-Ala ligases since only precursors terminating in D-Ala-D-Lac were synthesized under vancomycin-inducing conditions. Two types of vancomycin-independent revertants of one isolate were obtained in vitro after growth in the absence of vancomycin: (i) vancomycin-resistant, teicoplanin-susceptible mutants had a 6-bp insertion in the host ddl gene, causing the E251-to-EYK change that restored D-Ala:D-Ala ligase activity, (ii) constitutive vancomycin-resistant, teicoplanin-resistant mutants had substitutions (S232 to F or E247 to K) in the vicinity of the autophosphorylation site of the VanSB sensor and produced exclusively precursors ending in D-Ala-D-Lac. Vancomycin- and teicoplanin-dependent mutants obtained by growth in the presence of teicoplanin had an 18-bp deletion in VanSB, affecting residues 402 to 407 and overlapping the G2 ATP binding domain. The rapid emergence of vancomycin-independent revertants in vitro suggests that interruption of vancomycin therapy may not be sufficient to cure patients infected with vancomycin-dependent enterococci.

Anti-Bacterial Agents↗