TY - JOUR
T1 - Mutations in agr do not persist in natural populations of methicillin-resistant Staphylococcus aureus
AU - Shopsin, Bo
AU - Eaton, Christian
AU - Wasserman, Gregory A.
AU - Mathema, Barun
AU - Adhikari, Rajan P.
AU - Agolory, Simon
AU - Altman, Deena R.
AU - Holzman, Robert S.
AU - Kreiswirth, Barry N.
AU - Novick, Richard P.
N1 - Funding Information:
Received 29 April 2010; accepted 11 June 2010; electronically published 13 October 2010. Potential conflicts of interest: B.S. has served as an advisor to and has received research support from Pfizer. All other authors report no potential conflicts. Presented in part: Gordon Conference on Staphylococcal Diseases, September 2009, Waterville Valley, New Hampshire. Financial support: American Heart Association Fellow-to-Faculty Transition Award (to B.S.); National Institutes of Health (grant R01-AI30138 to R.P.N.); Cystic Fibrosis Foundation (grant to B.S.). Reprints or correspondence: Dr Bo Shopsin, Skirball Institute of Biomolecular Medicine, 540 First Ave, Second Floor, Lab 1, New York, NY 10016 ([email protected]).
PY - 2010/11/15
Y1 - 2010/11/15
N2 - Staphylococcus aureus organisms vary in the function of the staphylococcal virulence regulator gene agr. To test for a relationship between agr and transmission in S. aureus, we determined the prevalence and genetic basis of agr dysfunction among nosocomial methicillin-resistant S. aureus (MRSA) in an area of MRSA endemicity. Identical inactivating agr mutations were not detected in epidemiologically unlinked clones within or between hospitals. Additionally, most agr mutants had single mutations, indicating that they were short lived. Collectively, the results suggest that agr dysfunction is adaptive for survival in the infected host but that it may be counter-adaptive outside infected host tissues.
AB - Staphylococcus aureus organisms vary in the function of the staphylococcal virulence regulator gene agr. To test for a relationship between agr and transmission in S. aureus, we determined the prevalence and genetic basis of agr dysfunction among nosocomial methicillin-resistant S. aureus (MRSA) in an area of MRSA endemicity. Identical inactivating agr mutations were not detected in epidemiologically unlinked clones within or between hospitals. Additionally, most agr mutants had single mutations, indicating that they were short lived. Collectively, the results suggest that agr dysfunction is adaptive for survival in the infected host but that it may be counter-adaptive outside infected host tissues.
UR - http://www.scopus.com/inward/record.url?scp=78349265764&partnerID=8YFLogxK
U2 - 10.1086/656915
DO - 10.1086/656915
M3 - Article
C2 - 20942648
AN - SCOPUS:78349265764
SN - 0022-1899
VL - 202
SP - 1593
EP - 1599
JO - Journal of Infectious Diseases
JF - Journal of Infectious Diseases
IS - 10
ER -