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Molecular nature of methicillin‐resistant Staphylococcus aureus derived from explosive nosocomial outbreaks of the 1980s in Japan
Author(s) -
Taneike Ikue,
Otsuka Taketo,
Dohmae Soshi,
Saito Kohei,
Ozaki Kyoko,
Takano Misao,
Higuchi Wataru,
Takano Tomomi,
Yamamoto Tatsuo
Publication year - 2006
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2006.03.049
Subject(s) - staphylococcus aureus , microbiology and biotechnology , methicillin resistant staphylococcus aureus , outbreak , leukocidin , multilocus sequence typing , panton–valentine leukocidin , staphylococcal skin infections , typing , virology , biology , medicine , gene , bacteria , genotype , genetics
Community‐acquired methicillin‐resistant Staphylococcus aureus (CA‐MRSA) with Panton‐Valentine leukocidin (PVL) genes is increasing worldwide. Nosocomial outbreak‐derived (hospital‐acquired) MRSA (HA‐MRSA) in Japan in the 1980s was also largely PVL + . PVL + HA‐MRSA and CA‐MRSA shared the same multi‐locus sequence type (ST30) and methicillin resistance cassette (SCC mec IV), but were divergent in oxacillin resistance, spa typing, PFGE analysis or clfA gene analysis. PVL + HA‐MRSA, which probably originated in PVL + S. aureus ST30, was highly adhesive (carrying cna and bbp genes), highly‐toxic (carrying luk PV and sea genes) and highly drug‐resistant. PVL + HA‐MRSA was once replaced by other PVL − HA‐MRSA (e.g., ST5), and is re‐emerging as CA‐MRSA.