Colonization, Fomites, and Virulence: Rethinking the Pathogenesis of Community-Associated Methicillin-Resistant Staphylococcus aureus Infection
Author(s) -
Loren G. Miller,
Binh An Diep
Publication year - 2008
Publication title -
clinical infectious diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.44
H-Index - 336
eISSN - 1537-6591
pISSN - 1058-4838
DOI - 10.1086/526773
Subject(s) - staphylococcus aureus , medicine , pathogenesis , methicillin resistant staphylococcus aureus , staphylococcal infections , outbreak , staphylococcal skin infections , transmission (telecommunications) , skin infection , antibiotics , virulence , infection control , colonization , immunology , microbiology and biotechnology , intensive care medicine , virology , biology , bacteria , biochemistry , genetics , engineering , gene , electrical engineering
Community-associated methicillin-resistant Staphylococcus aureus (MRSA) infection is increasingly common worldwide and causes considerable morbidity and mortality. Of concern, community-associated MRSA infections are often recurrent and are highly transmissible to close contacts. The traditional tenet of pathogenesis is that MRSA colonization precedes infection. This has prompted persons involved in efforts to prevent community-associated MRSA infection to incorporate the use of intranasal topical antibiotics for nasal decolonization. However, data from outbreaks of community-associated MRSA infection suggest that skin-skin and skin-fomite contact represent important and common alternative routes of acquisition of the infecting strain. Furthermore, strain characteristics of the most successful community-associated MRSA strain, USA300, may contribute to a distinct pathogenesis. As we develop strategies to prevent community-associated MRSA infection, we must reconsider the pathogenesis of S. aureus. Reliance on models of health care-associated MRSA transmission for prevention of community-associated MRSA infection may result in the development of flawed strategies that attenuate our ability to prevent this serious and potentially deadly infection.
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