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MRSA Update

Posted May 1, 2009

Peter G. Pavlidakey, MD

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Staphylococcus aureus (S. aureus) is a gram positive bacterium that causes a variety of diseases. These include skin and soft tissue infections, endocarditis, blood stream infections, pneumonia, and deep-seated abscesses. Staphylococcus aureus also causes osteomyelitis, surgical wound infections, toxic shock syndrome, and food poisoning.1,2

It has become the most frequent cause of these infections seen in emergency room departments across the United States.3 Methicillin-resistant Staphylococcus aureus (MRSA) has emerged over the past 50 years as an important pathogen, particularly in the health care setting, and the prevalence of this disease-causing bacteria is increasing.

Methicillin is a penicillinase-resistant semi-synthetic penicillin that was introduced in 1959. By 1961 methicillin-resistant strains were first described in England. While initially a hospital-based pathogen, MRSA has evolved through numerous major lineage changes to now include a community-based component.4,5 The first community-acquired outbreak of MRSA (CAMRSA) occurred in 1982; documented in an intravenous drug user in Detroit, Michigan.6 Since then, CAMRSA has reached epidemic proportions.7-9 MRSA/CAMRSA is important to recognize early, as it is a virulent pathogen that often produces rapidly progressive disease and is often resistant to other commonly used antibiotics.

Epidemiology of CAMRSA infections has indicated that certain predisposing factors do exist. These include dialysis, immunosuppression, foley catheter or nasogastric tube placement, intravenous drug use, chronic disease, diabetes, and parental nutrition, all of which predispose to more severe cases of MRSA. The predisposing factors for less severe cases of CAMRSA include environmental exposure at day care centers, prisons, or long term care facilities; recent hospitalization; internal medical device usage; prolonged antibiotic therapy; and participation on sports teams. 10-14 Clinical manifestations of CAMRSA include, abscess formation, cellulitis, impetigo, folliculitis, ulcer, and paronychia. CAMRSA may be mistaken for a spider bite, which behooves the clinician to be very careful in making the distinction.15

The most practical approach for making a diagnosis is to perform a culture on a suspected lesion with susceptibility testing of the isolate. A local anabiogram (ie, a record of the susceptibility testing of local isolates) may help guide testing, until culture and susceptibility testing results become available. When severe infections such as sepsis, arthritis, or pneumonia are suspected to be due to CAMRSA, then fluids from abscesses, respiratory secretions, or bone or joint spaces may need to be evaluated, in conjunction with blood cultures.16

The two main standards for testing are 1) a broth microdilution minimum inhibitory concentration test and 2) an cefoxitin disk diffusion test. Oxacillin was long used as a gold standard, but it is no longer used since results with cefoxitin are easier to interpret yielding a higher sensitivity.16

Molecular testing is also becoming more prevalent. MRSA has a mecA gene, which susceptible strains do not possess. Polymerase Chain Reaction (PCR) has been used to detect isolates from clinical specimens within a few hours.17

Consultation and treatment by an experienced physician in infectious diseases are often warranted. Although there are numerous antibiotics available to the clinician, few drugs remain to treat patients with infections caused by MRSA/CAMRSA. There are multiple oral and intravenous (IV) drugs that are appropriate for treatment. As with all medication, each drug has advantages and disadvantages that must be considered prior to treatment. Initial coverage with oral agents, which are appropriate for non-complicated disease, may prove effective in eradicating the infection and prevent patients from dealing with the more severe side effects and the higher cost of IV drug treatments.

References

  1. Cunha, BA. Methicillin-resistant Staphylococcus aureus: clinical manifestations and antimicrobial therapy. Clinical Microbiol Infect. 2005;11(suppl. 4):33-42.
  2. Pavlidakey, K. Testing glycomimetic compounds for their ability to disrupt capsular polysaccharide production of type 5 Staphylococcus aureus. [master’s thesis.] Youngstown, Ohio: Youngstown State University, 2008.
  3. Moran GJ, Krishnadasan A, Gorwitz R.J., et al. Methicillin-Resistant S. aureus infections among patients in the emergency dept. N Engl J Med. 2006;355(7):666-674.
  4. Robinson DA, Enright MC. Evolutionary models of the emergence of methicillin-resistant Staphylococcus aureus. Antimicrob Agents Chemother. 2003;47(12):3926-3934.
  5. Lim TT, Chong FN, O’Brien FG, et al. Are all community methicillin-resistant Staphylococcus aureus related? A comparison of their mec regions. Pathology. 2003;35(4):336-343.
  6. Saravolatz LD, Markowitz N, Arking L, et al. Methicillin-resistant Staphylococcus aureus: epidemiologic observations during a community-acquired outbreak. Ann Intern Med. 1982;96(1):11-16.
  7. Young DM, Harris HW, Charlebois ED, et al. An epidemic of methicillin-resistant Staphylococcus aureus soft tissue infections among medically underserved patients. Arch Surg. 2004;139:947-953.
  8. Crawford SE, Daum RS. Epidemic community-associated methicillin-resistant Staphylococcus aureus. Modern times for an ancient pathogen. Pediatr Infec Dis J. 2005;24(5):459-460.
  9. Purcell K, Fergie J. Epidemic of community-acquired methicillin-resistant Staphylococcus aureus infections. a 14-year study at Driscoll Children’s Hospital. Arch Pediatr Adolesc Med. 2005;159(10):980-985.
  10. Naimi, TS, LeDell KH, Como-Sabetti K, et al. Comparison of community- and health care-associated methicillin-resistant Staphylococcus aureus infection. JAMA. 2003;290(22):2976-2984.
  11. Salgado, CD, Farr BM, Calfee DP. Community-acquired methicillin-resistant Staphylococcus aureus: a meta-analysis of prevalence and risk factors. Clin. Infect Dis. 2003;36(2):131-139.
  12. Centers for Disease Control and Prevention. Methicillin-resistant Staphylococcus aureus skin or soft tissue infections in a state prison–Mississippi, 2000. MMWR Morb Mortal Wkly Rep. 2001;50(42):919-922.
  13. Kirkland EB, Adams BB. Methicillin-resistant Staphylococcus aureus and athletes. J Am Acad Dermatol. 2008;59(3):494-502.
  14. Kowalski TJ, Berbari EF, Osmon DR. Epidemiology, treatment, and prevention of community-acquired methicillin-resistant Staphylococcus aureus infections. Mayo Clin Proc. 2005;80(9):1201-1208.
  15. Cohen PR, Kurzrock R. Community-acquired methicillin-resistant Staphylococcus aureus skin infection: an emerging clinical problem. J Am Acad Dermatol. 2004;50(2):277-280.
  16. Broekema N, Van T, Et al. Comparison of Cefoxitin and Oxacillin Disk Diffusion Methods for Detection of mecA- Mediated Resistance in Staphylococcus aureus in a Large-Scale Study. J Clin Micro. 2009;47(1):217-219.
  17. Babel BS, Decker CF. Microbiology and laboratory diagnosis of MRSA. Dis Mon. 2008;54(12):769-773.

NewsPath® Editor: C. Leilani Valdes, MD
This newsletter is produced in cooperation with the College of American Pathologists Public Affairs Committee and the NewsPath Editorial Board and may be reproduced in whole or in part as a service to the medical community. Copyright © 2009 by the College of American Pathologists.
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