Preventing Nosocomial Spread of MRSA is in Your Hands

Teri Capriotti

Disclosures

Dermatology Nursing. 2003;15(6) 

In This Article

Introduction

Antibiotic-resistant bacteria have become the scourge of the practices of medicine and nursing, particularly in the hospital setting. Pharmacologic innovations can barely keep pace with the development of drug resistance among strains of bacteria. One of the most troublesome bacterial strains is methicillin-resistant Staphylococcus aureus (MRSA). MRSA infections can lead to death, predominantly in hospitalized, debilitated patients. Health care providers may be confused about the contagion and transmission of this pathogen. Particularly in hospital settings, nurses must be knowledgeable about the epidemiology of MRSA to prevent its spread. The hardy S. aureus bacterium has developed resistance to every antibiotic in its path, beginning with penicillin 60 years ago.

The Natural History of MRSA

The discovery of penicillin in 1940 dramatically reduced the incidence of bacterial infections around the world. This single antibiotic was effective against a broad spectrum of bacteria for years, until S. aureus developed the ability to produce beta-lactamase, an enzyme that destroys penicillin. S. aureus develops resistance to antibiotics through plasmid-mediated genetic mutations (Chambers, 2001). These mutations confer S. aureus with a remarkable ability to adapt to changing antibiotic environments. The resiliency of S. aureus motivated pharmacologists to create a class of semi-synthetic penicillins that could withstand beta-lactamase. These antibiotics became known as beta-lactam penicillins, with methicillin as the prototype. For years, infections with S. aureus were reliably eradicated with methicillin and its analogs, nafcillin and cloxacillin. However, the resourceful bacterium soon became able to resist these beta-lactam antibiotics, and the first strain of MRSA was identified in 1961. Since the mid-1980s, antibiotic resistance among nosocomial S. aureus isolates has been increasing appreciably.

In addition to methicillin, strains of S. aureus have developed resistance to other antibiotics. MRSA is resistant to cephalosporins, erythromycin, clindamycin (Cleocin®), gentamycin, trimethoprim-sulfamethoxazole (Bactrim®), and ciprofloxacin (Cipro®). Vancomycin, a glycopeptide antibiotic, was relied upon until recently to eradicate MRSA infection. As expected, strains of vancomycin-resistant S. aureus (VRSA) have been isolated and are fast becoming a new treatment challenge (Hiramatsu, 2001).

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