MRSA: When to suspect it, how to treat it

April 18, 2008

Patients are presenting with drug-resistant staph infections in doctors' offices nationwide. Here's how to detect and treat them.

Healthcare-associated infections caused by methicillin-resistant Staphylococcus aureus (HA-MRSA) were first reported in the US in the early 1960s,1 and invasive infections including bacteremia, endocarditis, osteomyelitis, and pneumonia continue to be common among hospitalized patients whose conditions or circumstances put them at risk.2, 3 Starting in the 1990s, though, otherwise healthy individuals with no recent hospitalization and no known risk factors for resistant bacteria began presenting with MRSA infections.4 In the years since, community associated-or CA-MRSA, as it's now known, has been detected in office-based practices with increasing frequency.

Unlike the vast spectrum of infections associated with HA-MRSA, CA-MRSA has a predilection for the skin and skin structures. It most commonly presents in the form of an abscess, a furuncle or carbuncle or, occasionally, as cellulitis4-6 -and is often mistaken for a spider bite. Indeed, CA-MRSA is rapidly becoming a predominant pathogen in skin and skin structure infections (SSTIs), although cases of invasive infections, including bacteremia, endocarditis, and necrotizing pneumonia have recently been detected.3, 7, 8

While there's significant variation in the incidence of CA-MRSA from one part of the country to another, there is mounting evidence of its rapid spread. This underscores the need for office-based physicians to consult local experts and state boards of health to determine whether CA-MRSA has been detected in the communities in which they practice, to maintain a high degree of suspicion, and to know what antibiotics are effective in treating this drug-resistant pathogen.

CA-MRSA is defined as a positive culture for MRSA, either in an outpatient setting or within 48 hours of hospitalization in a patient with no recognized risk factors for HA-MRSA. (The risks for HA-MRSA include recent hospitalization or surgery, undergoing dialysis, presence of a permanent indwelling catheter or other invasive device, infection or colonization with MRSA, and residence in a long-term care facility within the last year.)3

CA-MRSA is not just a factor of the setting in which it is detected, however. Other distinguishing factors between CA-MRSA and HA-MRSA are genetic composition, virulence, and drug resistance: While both are resistant to all beta-lactam antimicrobials, CA-MRSA is usually more susceptible to non-beta-lactam antibiotics.

Researchers reported an increase in the number of MRSA infections in patients in the Baltimore area without previous history of colonization or infection, from 0.2 per 1,000 visits to an outpatient clinic in 2001 to 5.9 per 1,000 visits in 2005. They further found that 66 percent of those with a positive culture for CA-MRSA had had no contact with the healthcare system in the previous year, and that approximately 85 percent of the infections were SSTIs.6 Another study reported an increase in the incidence of CA-MRSA skin and skin structure infections from 24 per 100,000 in 2000 to 164 cases per 100,000 in 2005 in a healthcare/hospital system in Chicago serving the urban poor.9 In a multicenter study conducted in emergency departments in 11 US cities, MRSA was isolated in 59 percent of patients with purulent SSTIs.10

Risk factors for CA-MRSA are not yet well defined, but several studies have identified the following:

Perhaps the biggest factor associated with the identification of CA-MRSA, however, is a report of a lesion attributed to a spider bite,4, 9, 10 even in areas of the country where spiders capable of causing necrotic skin lesions are not common.11

In addition, community-acquired pneumonia (especially after influenza or flu-like illness), surgical site infections, bacteremia and endocarditis have also been reported in association with CA-MRSA.3, 7, 8 More serious life-threatening illnesses associated with CA-MRSA have presented with unusual skin manifestations such as necrotizing fasciitis, purpura fulminans, and Waterhouse-Friderichsen syndrome (generally associated with fulminant meningococcemia, the syndrome is characterized by petechial rash, coagulopathy, cardiovascular collapse, and bilateral adrenal hemorrhage).12, 13