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Journal of Bacteriology, September 2003, p. 5465-5472, Vol. 185, No. 18
0021-9193/03/$08.00+0     DOI: 10.1128/JB.185.18.5465-5472.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.

Jumping the Barrier to ß-Lactam Resistance in Staphylococcus aureus

Yuki Katayama, Hong-Zhong Zhang, Dong Hong, and Henry F. Chambers*

Division of Infectious Diseases, San Francisco General Hospital, University of California, San Francisco, California

Received 10 April 2003/ Accepted 23 June 2003

Although the staphylococcal methicillin resistance determinant, mecA, resides on a mobile genetic element, staphylococcus cassette chromosome mec (SCCmec), its distribution in nature is limited to as few as five clusters of related methicillin-resistant Staphylococcus aureus (MRSA) clones. To investigate the potential role of the host chromosome in clonal restriction of the methicillin resistance determinant, we constructed plasmid pYK20, carrying intact mecA, and introduced it into several methicillin-susceptible Staphylococcus aureus strains, five of which were naive hosts (i.e., mecA not previously resident on the host chromosome) and five of which were experienced hosts (i.e., methicillin-susceptible variants of MRSA strains from which SCCmec was excised). We next assessed the effect of the recipient background on the methicillin resistance phenotype by population analysis, by assaying the mecA expression of PBP2a by Western blot analysis, and by screening for mutations affecting mecA. Each experienced host transformed with pYK20 had a resistance phenotype and expressed PBP2a similar to that of the parent with chromosomal SCCmec, but naive hosts transformed with pYK20 selected against its expression, indicative of a host barrier. Either inducible ß-lactamase regulatory genes blaR1-blaI or homologous regulatory genes mecR1-mecI, which control mecA expression, acted as compensatory elements, permitting the maintenance and expression of plasmid-carried mecA.

* Corresponding author. Mailing address: Infectious Diseases Laboratory/SFGH, Box 0811, 3rd and Parnassus Ave., San Francisco, CA 94143-0811. Phone: (415) 206-5437. Fax: (415) 648-8425. E-mail: chipc{at}itsa.ucsf.edu.

Journal of Bacteriology, September 2003, p. 5465-5472, Vol. 185, No. 18
0021-9193/03/$08.00+0     DOI: 10.1128/JB.185.18.5465-5472.2003
Copyright © 2003, American Society for Microbiology. All Rights Reserved.



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