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Journal of Clinical Microbiology, May 2009, p. 1528-1535, Vol. 47, No. 5
0095-1137/09/$08.00+0     doi:10.1128/JCM.01497-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Changes in the agr Locus Affect Enteritis Caused by Methicillin-Resistant Staphylococcus aureus{triangledown}

Yoichi Sugiyama,1* Kazuya Okii,1 Yoshiaki Murakami,1 Takashi Yokoyama,1 Yoshio Takesue,2 Hiroki Ohge,1 Taijiro Sueda,1 and Eiso Hiyama3,4

Department of Surgery, Division of Clinical Medical Science, Graduate School of Biomedical Sciences, Hiroshima University, Hiroshima, Japan,1 Division of Infection Control and Prevention, Hyogo College of Medicine, Nishinomiya, Japan,2 Department of Biomedicine, Division of Clinical Medical Science, Graduate School of Biomedical Science, Hiroshima, Japan,3 Natural Science Center for Basic Research and Development, Hiroshima University, Hiroshima, Japan4

Received 4 August 2008/ Returned for modification 7 October 2008/ Accepted 2 March 2009

We studied the characteristics of methicillin (meticillin)-resistant Staphylococcus aureus (MRSA) strains that caused enteritis. In a previous report, we demonstrated that both phenotypic and genotypic changes were associated with MRSA enteritis; and we hypothesized that the accessory gene regulator (agr), which is a global regulator of staphylococcal virulence and upregulates several exoproteins, is the key factor associated with the development of MRSA enteritis. In this study, we examined 12 MRSA isolates associated with enteritis from stool samples and 17 MRSA isolates not associated with enteritis that had the following characteristics: the strains associated with enteritis had the same genotype (genotype A), as detected by pulsed-field gel electrophoresis, or the strains were isolated from stools. The differences between strains that caused enteritis and those that did not cause enteritis strains were examined by quantitative reverse transcription-PCR to assess RNAII, agrA, RNAIII, and tst expression and by sequencing of the agr locus. The levels of expression of agrA, RNAIII, and tst were higher by the MRSA isolates associated with enteritis than by the MRSA isolates not associated with enteritis, whether or not they were of the same genotype. The levels of expression of RNAII by almost all the clinical isolates were similar. Sequencing of the agr locus showed that all MRSA isolates that caused enteritis have agr mutations, whereas the MRSA isolates that did not cause enteritis, with three exceptions, did not. Many of the isolates associated with enteritis had the same mutation, especially at the C-terminal end of agrA. These results suggest a trend in which mutations in the agr locus modify the expression of agrA and RNAIII and the production of toxin, all of which may increase the virulence and influence the occurrence of MRSA enteritis.

* Corresponding author. Mailing address: Department of Surgery, Division of Clinical Medical Science, Graduate School of Biomedical Sciences, Hiroshima University, 1-2-3 Kasumi, Minami-ku, Hiroshima 734-8551, Japan. Phone: 81-82-257-5216. Fax: 81-82-257-5219. E-mail: yoichi-sugiyama{at}hiroshima-u.ac.jp

{triangledown} Published ahead of print on 18 March 2009.

Journal of Clinical Microbiology, May 2009, p. 1528-1535, Vol. 47, No. 5
0095-1137/09/$08.00+0     doi:10.1128/JCM.01497-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





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