Treatment of Community-Associated MRSA

John G. Bartlett, MD


June 08, 2011

In This Article

Guidelines for Community-Associated MRSA

In January of 2011, the Infectious Diseases Society of America (IDSA) released its first set of guidelines[1] for the treatment of methicillin-resistant Staphylococcus aureus (MRSA) infections. This article is based on the IDSA guidelines for management[1,2,3] and a recent authoritative review.[4]

History of Community-Associated MRSA

MRSA was first described in 1961 and was largely a nosocomial pathogen. The epidemic community-associated MRSA (CA-MRSA) strain, first found in Australia in the early 1990s,[5] spread globally and was first reported in the United States as a sometimes lethal infection in children in 1997-1999.[6] This severity was unusual, because the pathogen was community-acquired and the hosts were healthy. Initially, the implicated strains were pulsed-field USA 400, but that strain was largely replaced by the USA 300 strains that represented 1 of 4 global pandemic MRSA clones designated ST5, ST8, ST36, and ST45. The USA 300 clone is a ST8 strain that quickly became the dominant cause of CA-MRSA infection in the United States, distinct from the ST80 strain found in Europe.[4]

In the early 2000s, large outbreaks of skin and soft tissue infections occurred in people with close interpersonal contact: correctional facilities, military, gay men, athletes, and children in daycare centers.[7] Other industrialized countries had outbreaks of CA-MRSA infections that represented different clones with variable penetration. All of these MRSA clones have the chromosomal cassette designated SSCmec IV, which confers resistance to methicillin and the Panton Valentine Leukocidin (PVL), a leukotoxin that initially was thought to represent an important virulence factor. Although the USA 300 strain usually caused skin and soft tissue infections, it was also responsible for some severe infections and generally caused disease in previously young healthy people.[4,6,7,8]

Initially, concern was raised that this strain would enter hospitals and cause healthcare-associated infections, a frightening prospect considering the strain's devastating consequences in some previously healthy young people. However, recent data suggest that the USA 300 strain now accounts for about 18% of nosocomial invasive (mainly bacteremic) MRSA infections and has no unique pathologic features.[9]

Clinical features. In approximately 7000 patients with CA-MRSA infections involving the USA 300, 90% had skin and soft tissue infections. Bone/joint, pulmonary, bacteremia, urinary and "other" infections each comprised 2%-4% of the remainder.[4,10,11,12] Although skin and soft tissue infections predominate, this strain has sometimes been associated with severe infections that are life-threatening or fatal in previously healthy hosts. These include cases of purpura fulminans, pyomyositis, necrotizing pneumonia, necrotizing fasciitis, suppurative phlebitis, and osteomyelitis.[3,13,14,15,16]

Where is the USA 300 strain found? Approximately 30% of healthy people on earth have nasal colonization with methicillin-sensitive S aureus (MSSA), not MRSA.[4] Screening for MRSA shows that nasal colonization is positive in approximately 1%-5%, and perhaps up to 9% in some populations.[18,19] Favored colonization sites for MRSA are inguinal, axillary, and perineal areas.[17,18,19,20,21] Infection is usually the result of cutaneous/nasal carriage or skin contact.[21,22,23,24]

The Centers for Disease Control and Prevention (CDC) emphasize the "4 Cs" as risks for transmission:

  • Crowding;

  • Contact: skin-to-skin;

  • Contaminated items such as towels, surfaces; and

  • (lack of) Cleanliness.

Virulence. In 2002, Gillet and coworkers reported 13 young patients (median age, 15 years) with influenza complicated by necrotizing pneumonia involving a strain of MRSA with PVL.[8] The mortality rate in this series was 37% at 48 hours and the assumption was that PVL was a distinctive virulence factor. PVL is a known leukotoxin that attracts neutrophils and then lyses them in vitro ("fatal attraction"). Early studies involving pulmonary challenges in mice suggested that PVL was a virulence factor.[25] Subsequent studies using deletion of the genes responsible for PVL production showed that the USA strain was equally virulent with or without PVL.[26,27] The current assumptions are[4]:

  • PVL is not important as a virulence factor but characterizes most of the strains considered to be CA-MRSA found in large resource countries[4] including the ST8 (United States and Canada), the ST80 (Europe), and ST30 (South America) and

  • Studies of gene expression show that the ST8 clonal complex (which includes USA 300 strains) produces exceptional amounts of alpha toxin.[29] The implication is that the distinctive factor is gene expression rather than a unique virulence factor.[4]


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