Abstract
Four clinical U.S. glycopeptide intermediate resistant Staphylococcus aureus (GISA) isolates were resistant to Triton X-100-induced autolysis. Similar resistance was demonstrated in an isolate obtained after a single passage of a susceptible clinical isolate in low-level vancomycin. Strains with the vancomycin-induced Triton X-100 resistance phenotype produced active murein hydrolases but were resistant to lysis by murein hydrolases.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Amino Acid Sequence
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Anti-Bacterial Agents / pharmacology*
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Base Sequence
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Humans
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Molecular Sequence Data
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N-Acetylmuramoyl-L-alanine Amidase / metabolism
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Octoxynol / metabolism
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Sequence Alignment
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Staphylococcal Infections / microbiology*
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Staphylococcus aureus / drug effects*
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Staphylococcus aureus / genetics
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Staphylococcus aureus / growth & development
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Staphylococcus aureus / isolation & purification
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Vancomycin / pharmacology*
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Vancomycin Resistance
Substances
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Anti-Bacterial Agents
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Vancomycin
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Octoxynol
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N-Acetylmuramoyl-L-alanine Amidase