Beta-lactam resistance mechanisms of methicillin-resistant Staphylococcus aureus.

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1991

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info:eu-repo/semantics/altIdentifier/doi/10.1093/infdis/163.3.514

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info:eu-repo/semantics/altIdentifier/pmid/1995724

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info:eu-repo/semantics/altIdentifier/pissn/0022-1899

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info:eu-repo/semantics/altIdentifier/urn/urn:nbn:ch:serval-BIB_D80288903E3E2

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M. Franciolli et al., « Beta-lactam resistance mechanisms of methicillin-resistant Staphylococcus aureus. », Serveur académique Lausannois, ID : 10.1093/infdis/163.3.514


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In vitro and in vivo activity of amoxicillin and penicillin G alone or combined with a penicillinase inhibitor (clavulanate) were tested against five isogenic pairs of methicillin-resistant Staphylococcus aureus (MRSA) producing or not producing penicillinase. Loss of the penicillinase plasmid caused an eight times or greater reduction in the MICs of amoxicillin and penicillin G (from greater than or equal to 64 to 8 micrograms/ml), but not of the penicillinase-resistant drugs methicillin and cloxacillin (greater than or equal to 64 micrograms/ml). This difference in antibacterial effectiveness correlated with a more than 10 times greater penicillin-binding protein 2a affinity of amoxicillin and penicillin G than of methicillin and a greater than or equal to 90% successful amoxicillin treatment of experimental endocarditis due to penicillinase-negative MRSA compared with cloxacillin, which was totally ineffective (P less than .001). Amoxicillin was also effective against penicillinase-producing parent MRSA, provided it was combined with clavulanate. Penicillinase-sensitive beta-lactam antibiotics plus penicillinase inhibitors might offer a rational alternative treatment for MRSA infections.

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