COMMENTARY

Community-Acquired Methicillin-Resistant Staphylococcus aureus Infections: Changes in Practice Required?

Lena M. Napolitano, MD, FACS, FCCP, FCCM

Disclosures

December 20, 2007

In This Article

Case Presentation

A teacher presents to the emergency department with a swollen, painful, red upper extremity for evaluation. Physical examination confirms a cellulitis extending from the hand to the elbow with a 2-cm skin lesion in the midforearm that is raised and violaceous in color with some small necrotic areas. She has never had a skin infection before. She has no chronic medical problems.

Her husband is a healthcare worker and has never had a skin infection. Her son is in high school and has had a number of skin infections, initially acquired through participation in football. He has received a number of antibiotic courses of oral clindamycin in the past year, and he still has draining skin lesions present.

Ultrasound examination of the arm reveals a fluid collection under the central skin lesion. Incision and drainage was performed with drainage of purulent fluid and necrotic debris; a culture was sent; and the wound was packed open with clorpactin-moistened gauze. Appropriate empiric antibiotics were initiated, and she was admitted to the hospital for systemic antibiotics, wound care, and arm elevation with careful monitoring of the progression of the cellulitis. Three days later the abscess culture confirmed methicillin-resistant Staphylococcus aureus (MRSA).

This is now a common presentation to emergency departments across the United States. Your patient has a community-acquired (CA)-MRSA skin and soft-tissue infection.

MRSA remains a major human pathogen. Traditionally, MRSA infections occurred exclusively in hospitals and were limited to immunocompromised patients or individuals with predisposing risk factors. In 2003, MRSA accounted for 64.4% of all S aureus infections in US intensive care units. A recent report from the Active Bacterial Core surveillance MRSA investigators examined the incidence of invasive MRSA disease from July 2004 through December 2005, with 8987 observed MRSA cases and 1598 in-hospital deaths reported. Most infections were healthcare-associated (HA)-MRSA, but 5250 (58.4%) were community-onset infections and 2389 (26.6%) were hospital-onset infections. Community-associated MRSA infections occurred in 1234 (13.7%) of the cohort. On the basis of these surveillance data, it was estimated that 94,360 invasive MRSA infections occurred in the United States in 2005, and these infections were associated with death in 18,650 cases.

However, recently there has been an alarming epidemic of CA-MRSA strains that can cause a spectrum of disease ranging from uncomplicated skin infections to severe infections that can result in necrotizing soft-tissue infections and necrotizing pneumonia and death in otherwise healthy humans outside of the healthcare setting. The emerging potential danger associated with CA-MRSA invasive infections was demonstrated by the deaths of 4 healthy children in Minnesota and North Dakota between 1997 and 1999.

The US Centers for Disease Control and Prevention (CDC) has defined CA-MRSA as having no healthcare risk factors. Persons with MRSA infections that meet all of the following criteria likely have CA-MRSA infections:

  • Diagnosis of MRSA was made in the outpatient setting or by a culture positive for MRSA within 48 hours after admission to the hospital

  • No medical history of MRSA infection or colonization

  • No medical history in the past year of

    • Hospitalization, dialysis, or surgery

    • Admission to a nursing home, skilled nursing facility, or hospice

  • No permanent indwelling catheters or medical devices that pass through the skin into the body.

This is in contrast to HA-MRSA infections, defined as those cases with at least 1 healthcare risk factor. More recently, HA-MRSA infections were further classified as either "community-onset" (cases with a healthcare risk factor but with a positive culture obtained ≤ 48 hours after hospital admission) or "hospital-onset" (cases with positive culture obtained more than 48 hours after admission, regardless of whether they also had other healthcare risk factors) ( Table ).

CA-MRSA differs from HA-MRSA in several important ways. These include the lack of traditional risk factors associated with MRSA among patients, a bacterial susceptibility pattern with resistance to fewer classes of antimicrobial drugs, and the inclusion of specific virulence factors. CA-MRSA strains typically carry the Panton-Valentine leukocidin (PVL) genes, which produce cytotoxins that can cause tissue necrosis and leukocyte destruction and are associated with community-associated staphylococcal skin infections and necrotizing pneumonia. CA-MRSA strains currently circulating can also be distinguished, to a certain extent, by molecular typing methods, such as pulsed-field gel electrophoresis (PFGE) and multilocus sequence typing. It appears that a few strains of S aureus (mostly USA300) are responsible for much of the CA-MRSA disease that is seen in the United States.

CA-MRSA strains can be highly virulent, and have been documented to cause life-threatening necrotizing infections. Many strains of CA-MRSA encode for the PVL toxin, a pore-forming cytotoxin associated with necrotic lesions or abscess formation. More rarely, CA-MRSA infection can lead to cases of serious, life-threatening diseases, such as necrotizing pneumonia, necrotizing soft-tissue infections, and purpura fulminans -- which may prove fatal.

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