Changes in the agr Locus Affect Enteritis Caused by Methicillin-Resistant Staphylococcus aureus
- 1 May 2009
- journal article
- research article
- Published by American Society for Microbiology in Journal of Clinical Microbiology
- Vol. 47 (5) , 1528-1535
- https://doi.org/10.1128/jcm.01497-08
Abstract
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.Keywords
This publication has 37 references indexed in Scilit:
- A slipped‐mispairing mutation in AgrA of laboratory strains and clinical isolates results in delayed activation of agr and failure to translate δ‐ and α‐haemolysinsMolecular Microbiology, 2006
- Molecular epidemiology of enteritis-causing methicillin-resistant Staphylococcus aureusJournal of Hospital Infection, 2006
- Evolutionary Genetics of the Accessory Gene Regulator ( agr ) Locus in Staphylococcus aureusJournal of Bacteriology, 2005
- Comparison of two standardisation methods in real-time quantitative RT-PCR to follow Staphylococcus aureus genes expression during in vitro growthJournal of Microbiological Methods, 2004
- Staphylococcus aureusagrandsarAFunctions Are Required for Invasive Infection but Not Inflammatory Responses in the LungInfection and Immunity, 2002
- Exfoliatin-Producing Strains Define a Fourth agr Specificity Group in Staphylococcus aureusJournal of Bacteriology, 2000
- Molecular Analysis of the Accessory Gene Regulator(agr)Locus and Balance of Virulence Factor Expression in Epidemic Methicillin‐ResistantStaphylococcus aureusThe Journal of Infectious Diseases, 2000
- IL-15 IS ELEVATED IN THE PATIENTS OF POSTOPERATIVE ENTEROCOLITISCytokine, 1999
- Detection of the response regulator AgrA in the cytosolic fraction of Staphylococcus aureus by monoclonal antibodiesFEMS Microbiology Letters, 1996
- Regulation of exoprotein gene expression in Staphylococcus aureus by agrMolecular Genetics and Genomics, 1986