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Infection and Immunity, July 2009, p. 2650-2656, Vol. 77, No. 7
0019-9567/09/$08.00+0     doi:10.1128/IAI.00256-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

The Arginine Catabolic Mobile Element Is Not Associated with Enhanced Virulence in Experimental Invasive Disease Caused by the Community-Associated Methicillin-Resistant Staphylococcus aureus USA300 Genetic Background {triangledown}

Christopher P. Montgomery,1* Susan Boyle-Vavra,2 and Robert S. Daum2

Sections of Critical Care Medicine,1 Infectious Diseases, Department of Pediatrics, University of Chicago, Chicago, Illinois2

Received 5 March 2009/ Returned for modification 8 April 2009/ Accepted 12 April 2009

USA300 has become the predominant community-associated methicillin (meticillin)-resistant Staphylococcus aureus (CA-MRSA) genetic background in most U.S. communities. The reasons for the dominance of this genetic background are unclear, but the presence of the recently identified arginine catabolic mobile element (ACME) in the USA300 genome has been advocated as one possibility. CA-MRSA clinical isolates (USA300) differing in the presence or absence of ACME and a USA300 wild-type/ACME deletion mutant pair were analyzed for in vitro expression of global regulatory genes and production of virulence factors. The virulence of these isolates was compared in rodent models of necrotizing pneumonia and skin infection. There was no significant difference in the expression of selected genes mediating virulence (hla, lukSF-PV, agr, saeRS) among the isolates tested, regardless of the presence of ACME. There was a higher abundance of {alpha}-hemolysin in culture supernatants among ACME-positive isolates than among ACME-negative isolates, but there was no significant difference in the levels of protein A. The presence of ACME was not associated with increased virulence in a rat model of necrotizing pneumonia, as assessed by mortality, in vivo bacterial survival, and severity of lung pathology. Nor was the presence of ACME associated with increased dermonecrosis in a model of skin infection. We conclude that ACME is not necessary for virulence in rodent models of CA-MRSA USA300 pneumonia or skin infection.

* Corresponding author. Mailing address: Section of Critical Care Medicine, Department of Pediatrics, University of Chicago, 5841 S. Maryland Ave. MC 1145, Chicago, IL 60637. Phone: (773) 834-0897. Fax: (773) 702-4041. E-mail: cmontgomery{at}bsd.uchicago.edu

{triangledown} Published ahead of print on 20 April 2009.

Editor: A. Camilli

Infection and Immunity, July 2009, p. 2650-2656, Vol. 77, No. 7
0019-9567/09/$08.00+0     doi:10.1128/IAI.00256-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





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