Disease Information

Methicillin-Resistant Staphylococcus aureus (MRSA)

By Stephanie Wise, RN, BSN

STAPHYLOCOCCUS AUREUS & RESISTANCE

• Staphylococcus aureus is an aerobic or facultative anaerobic, coagulase-positive organism. It appears as gram positive clusters on gram stain.(1,4)
• S. aureus colonizes the skin of humans, which leads to localized, superficial, self-limiting abscesses when the skin is disrupted.
• S. aureus was the most common cause of nosocomial infections reported in 1990-1996 (1).
• Methicillin-resistant S. aureus (MRSA) is resistant to methicillin and other beta (ß) lactamase-resistant penicillins and cephalosporins (2).
• Methicillin resistance is gained by the production of a unique, low-affinity penicillin binding protein (PBP 2a) encoded by a chromosomal gene mec-A.
• Neither the protein nor the mec-A gene is present in methicillin-sensitive S. aureus (MSSA) (2).

EPIDEMIOLOGY

• First report of a penicillin-resistant strain of S. aureus was published in 1945, revealing its association with penicillinase enzyme produced by the bacteria (3).
• The development of methicillin antibiotics, synthetic penicillinase resistant penicillin, followed within 2 years. S. aureus developed resistance to methicillin shortly thereafter.
• MRSA was first reported in the UK and Europe in the 1960’s, and in the US in 1968 (4,5).
• MRSA was recognized as an important nosocomial infection in the U.S. in the late 1960s, and became endemic in some health care settings.
• The National Nosocomial Infections Surveillance system (NNIS) reports an increasing trend of MRSA. A 40% increase in resistance in 1999 was noted compared to 1994-1998 data (6).
• MRSA accounts for 52.3% of S. aureus nosocomial infections (6).
• MRSA is now endemic in many hospitals, and is one of the leading causes of nosocomial pneumonia and surgical site infection and the second leading cause of nosocomial blood stream infections (7).
• In 1999, MRSA treatment costs were estimated to be 6-10% more than treating an MSSA infection (resulting from the increased cost of vancomycin use and costly isolation procedures), and that the attributable death rate of MRSA was 21% as compared to 8% in MSSA (8). COST DATA SLIDE

NOSOCOMIAL TRANSMISSION OF MRSA

• Common factors associated with acquiring MRSA in any acute care setting include prolonged hospital stay, use of broad spectrum antibiotics, greater number and longer duration of antibiotic use, stay in an ICU or burn unit, surgical wounds, decubitus ulcers, poor functional status and proximity to another patient with MRSA (7).
• MRSA can colonize the anterior nares, skin, wounds, and in rare instances the rectum of infected or colonized persons.
• Healthcare workers’ hands, the environment, and airborne transmission (in the case of staphylococcol pneumonia) are the most common means of spreading MRSA.
• MRSA may invade the blood and cause potentially serious complications such as bacteremia, septic shock, and serious metastatic infections (endocarditis, pneumonia, osteomyelitis, and arthritis) (9).
• In most epidemics of MRSA, a relatively low level of nasal carriage (3%) has been found in hospital personnel (7). However, it is very common to find a high rate of MRSA nasal carriage in health care workers where MRSA is endemic (7). 
    Reservoirs of Infection, Prevention, and Treatment of S. aureus
• The sharp increase in the prevalence of MRSA in many communities has led to the consideration of outpatients as an infected or as a potential source of infection outbreak in an institution (10).
• Populations that are more susceptible to MRSA colonization, given other risk factors, include intravenous drug users, persons with dermatologic diseases, or diabetes, and persons on renal dialysis (7).

DIAGNOSIS OF MRSA

The National Committee for Clinical Laboratory Standards (NCCLS)-recommends the “Screening Test for Oxacillin-resistant S. aureus” which uses an agar plate containing 6mg/ml of oxacillin and Mueller-Hinton agar supplemented with NaCL (4% w/v; 0.68 mol/L) (11). For methods of inoculation, the CDC recommends the NCCLS Approved Standard M100-S9 (11). Note: Oxacillin-resistant S. aureus (ORSA) and MRSA are used interchangeably.

TREATMENT OF MRSA

• Vancomycin is the drug of choice for MRSA.
  Reasons to Control MRSA
• Alternative antibiotics include linezolid and quinupristin/dalfopristin. Rifampin and trimethroprim-sulfamethoxazole (TMP-SMX) are used in combination with other antibiotics (12).
• Mupirocin ointment has also shown promising results in decreasing nasal carriage. Wide spread use is only indicated in certain settings to avoid mupirocin resistance. Nasal Decolonization

CONTROL AND PREVENTIVE MEAUSRES

• Hand Hygiene: By far, the most important strategy in preventing MRSA transmission. Educate healthcare workers and patients on the importance of hand hygiene. Hand Hygiene
• Private Room: Place patient in a private room or in a room with another MRSA infected patient.
• Contact Precautions: Wear gloves and a gown (if expected contact with patient or environment), transport only in essential circumstances, clean equipment daily, and dedicate equipment and items. Jernigan found a 16-fold reduction in transmission when contact precautions were implemented (13). Some experts advocate masks also.
• Droplet Precautions: Place on droplet precautions only if patient is diagnosed with MRSA pneumonia.
• Active Surveillance: in high-risk populations, routine surveillance cultures done on admission and weekly thereafter assist infection control professionals in tracking MRSA cases. Also the use of a hospital wide “flagging system” which identifies patients with MRSA on any readmission, assists an infection control professional in expediting isolation practices. Several authors have found this strategy to be cost effective. Computerized Flagging System

Special Thanks to Dr. Trish M. Perl and Dr. Tobi Karchmer for providing their slide presentations from the 2001 Fellows Course to be linked to this article.

References:

1. Centers for Disease Control and Prevention. National Nosocomial Infections Surveillance system report: data from 1986-1996. Atlanta (GA); 1996.


2. Chambers HF. Methicillin resistance in Staphylococci: genetics and mechanisms of resistance. Clinical Microbiology Rev. 1997; 10: 781-91.


3. Spink WW, Ferris V. Quantitative action of penicillin inhibitor from penicillin-resistant strain of Staphylococcus. Science 1945; 102:102-221.


4. Stewart GP, Holt RJ. Evolution of natural resistance of the new penicillin. Br Med J 1962; 1: 309-11.


5. Barrett FF. et al. Methicillin-resistant S. aureus at Boston City Hospital. Bacteriologic and epidemiologic observation. New England Journal of Medicine. 1968; 279:441-8.


6. National Nosocomial Infections Surveillance (NNIS) System Report, Data Summary from January 1992-Aprill 2000. AJIC Am J Infect Control 2000; 28: 429-48.


7. Boyce JM. et al. MRSA: a briefing for acute care hospitals and nursing facilities. Infection Control Hospital Epidemiology. 1994; 15:105-15.


8. Rubin RJ. et al. The economic impact of Staphylococcus infection in New York Hospitals. Emerging Infectious Diseases. 1999; 5: 9-17.


9. Locksley RM. Staphylococcal infections. In: Wilson JD et al., editors. Harrison’s Principles of Internal Medicine 12th edition, USA: MacGraw-Hill Inc.; 1995. P557-62.


10. Herold BC. et al. Community-acquired MRSA in children with no identified predisposing risk. JAMA 1998; 279:593-8.


11. Centers for Disease Control and Prevention. Laboratory detection of oxacillin/methicillin resistant staphylococcus aureus (MRSA). 1999; 1-3;
         http://www.cdc.gov/ncidod/hip/Lab/FactSheet/mrsa.htm


12. Murray P, Baron E, Pfaller M, Tenover F, & Yolken, R. (1995) Manual of Clinical Microbiology, (6th edition). Washington, DC: ASM Press. 282-293.


13. Jernigan. American Journal of Epidemiology. 1996; 143:496.

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