Open AccessMRSA virulence and spread
Author(s) -
Otto Michael
Publication year - 2012
Publication title -
cellular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.542
H-Index - 138
eISSN - 1462-5822
pISSN - 1462-5814
DOI - 10.1111/j.1462-5822.2012.01832.x
Subject(s) - virulence , biology , leukocidin , staphylococcus aureus , microbiology and biotechnology , penicillin , antibiotics , mobile genetic elements , methicillin resistant staphylococcus aureus , vancomycin , staphylococcal infections , gene , antibiotic resistance , panton–valentine leukocidin , host adaptation , virology , genome , genetics , bacteria
Summary Methicillin‐resistant S taphylococcus aureus ( MRSA ) is one of the most frequent causes of hospital‐ and community‐associated infections. Resistance to the entire class of β‐lactam antibiotics, such as methicillin and penicillin, makes MRSA infections difficult to treat. Hospital‐associated MRSA strains are often multi‐drug‐resistant, leaving only lower efficiency drugs such as vancomycin as treatments options. Like many other S . aureus strains, MRSA strains produce a series of virulence factors, such as toxins and adhesion proteins. Recent findings have shed some new light on the molecular events that underlie MRSA epidemic waves. Newly emerging MRSA clones appear to have acquired phenotypic traits that render them more virulent or able to colonize better, either via mobile genetic elements or via adaptation of gene expression. Acquisition of P anton‐ V alentine leukocidin genes and increased expression of core genome‐encoded toxins are being discussed as potentially contributing to the success of the recently emerged community‐associated MRSA strains. However, the molecular factors underlying the spread of hospital‐ and community‐associated MRSA strains are still far from being completely understood, a situation calling for enhanced research efforts in that area.