Methicillin-resistant Staphylococcus aureus: an established pathogen with emerging infections.

Despite the general improvement in public health, the use of potent antimicrobial agents, and the strict application of hospital infection-control measures, the prevalence of methicillin-resistant Staphylococcus aureus (MRSA) continues to increase with multidrug resistance as a common phenotype. Analysis of data obtained from The Surveillance Network-USA (TSN), an electronic surveillance network that collects microbiology data from 300 clinical microbiology laboratories across the United States, showed that as of March 2005, MRSA rates were 59.2%, 55%, and 47.9% for strains from non-ICU inpatients, ICU, and outpatients, respectively. Mainous et al reported an estimated population carriage of MRSA of 0.84%, or 2.2 million persons, of the noninstitutionalized US population, including children and adults. In a recent multivariate analysis, risk factors for colonization with MRSA in patients admitted to an urban hospital included antibiotic use within 3 months before admission, hospitalization during the past 12 months, diagnosis of skin or soft-tissue infection at admission, and HIV infection. The widespread use and misuse of fluoroquinolones have also been blamed for the selection and increase in the prevalence of MRSA. Healthcare–associated MRSA is defined as an isolate that results in (1) an MRSA infection identified after 48 hours of admission to a hospital; (2) an MRSA infection associated with a history of hospitalization, surgery, dialysis, or residence in a long-term care facility within 1 year of the MRSA culture date; (3) an MRSA infection related to a permanent indwelling catheter or percutaneous medical device present at the time of culture; or (4) an MRSA infection with a known prior positive culture for MRSA. Community-associated MRSA causes infections with none of these aforementioned features. Community-associated MRSA isolates are likely to be susceptible to more antibiotics, particularly, fluoroquinolones and clindamycin compared with healthcare–associated MRSA. Staphylococcal chromosome cassette mec type IV (SCCmecIV) that encodes for methicillin resistance and certain genes that encode for multiple virulence factors, such as the Panton-Valentine leucocidin and enterotoxins a, c, and k, are mainly encountered with community-associated MRSA. Furthermore, community-associated MRSA may well be differentiated from healthcare–associated MRSA by their distinct band patterns on pulse-field gel electrophoresis. Isolation of Staphylococcus aureus from urine samples always raised concerns about underlying staphylococcal bacteremia and endocarditis. However, MRSA is increasingly recognized as a urinary pathogen particularly in the setting of prior MRSA colonization, urinary tract instrumentation and/or the presence of an indwelling urinary catheters. Muder et al recently reported symptomatic urinary tract infections in 33% of 102 patients colonized with Staphylococcus aureus with 86% prevalence of methicillin resistance. The same authors documented late-onset staphylococcal urinary tract infections that occurred several months after initial detection of colonization. The reported case of concomitant perinephric and prostatic abscesses remind us of the ability of Staphylococcus aureus to result in metastatic infections and illustrates an emerging role of this pathogen to cause urinary tract infection. Prior urinary tract instrumentation, urinary catheterization, and anatomic structural abnormalities leading to incontinence or retention are important risk factors for healthcare–associated MRSA urinary tract infections. The frequent digital examination would be difficult to blame as a risk factor for prostatic abscess as the prostate has protective fascial layers, and its ducts drain into the urethra where the infection usually starts. From the Division of Infectious Diseases, Department of Internal Medicine, James H. Quillen College of Medicine, East Tennessee State University, Johnson City, TN. Reprint requests to Wael E. Shams, MD, Assistant Professor of Medicine, Department of Internal Medicine, Division of Infectious Diseases, James H. Quillen College of Medicine, East Tennessee State University, Box 70622, Johnson City, TN 37614. Email: shams@etsu.edu Accepted December 14, 2006. Copyright © 2007 by The Southern Medical Association 0038-4348/