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Volume 12, Number 11–November 2006

Conference Summary

Methicillin-Resistant Staphylococcus aureus as Community Pathogen

John A. Jernigan,*†Comments to Author Kathryn Arnold,‡ Katherine Heilpern,† Marion Kainer,§ Christopher Woods,¶ James M. Hughes†
*Centers for Disease Control and Prevention, Atlanta, Georgia, USA; †Emory University School of Medicine, Atlanta, Georgia, USA; ‡Georgia Department of Human Resources, Atlanta, Georgia, USA; §Tennessee Department of Health, Nashville, Tennessee, USA; and ¶Duke University Medical Center, Durham, North Carolina, USA

Suggested citation for this article

Symposium on Community-acquired Methicillin-resistant Staphylococcus aureus
Atlanta, Georgia, USA
May 12, 2006-09-26

On May 12, 2006, members of the Southeastern Center for Emerging Biologic Threats, a consortium of public health officials and academicians from 8 states (Alabama, Florida, Georgia, Kentucky, Mississippi, North Carolina, South Carolina, and Tennessee) met in Atlanta, Georgia, USA, to address the challenges of methicillin-resistant Staphylococcus aureus (MRSA) as a community pathogen (1). Objectives were to share pertinent scientific information, identify knowledge gaps, discuss current public health approaches to control, and determine research priorities. The complete conference report is available at http://www.secebt.org.

Community-associated MRSA (CA-MRSA) infection refers to MRSA infection in a person lacking established MRSA risk factors such as recent hospitalization, surgery, residence in a long-term care facility, receipt of dialysis, or presence of invasive medical devices. After publication of a report of 4 children who died of fulminant CA-MRSA in Minnesota and North Dakota during 1997–1999 (2), clusters of CA-MRSA have been identified in groups with close person-to-person contact, including daycare center attendees, jail and prison residents, athletic teams, and military personnel. A population review conducted in 3 communities showed the annual incidence of CA-MRSA during 2001–2002 to be 18–25.7/100,000 (3); most CA-MRSA isolates were associated with clinically relevant infections, and 23% of patients required hospitalization. Most infections (77%) involved skin and soft tissues, but 6% were considered invasive. Subsequent studies suggested an increase in the incidence of invasive CA-MRSA infections.

Molecular evidence indicates that strains associated with CA-MRSA evolved spontaneously rather than migrating from hospitals to communities. In most CA-MRSA strains in the United States, methicillin resistance is encoded in a novel genetic element, staphylococcal cassette chromosome mec type IV, which until recent years has not been characteristic of healthcare-associated strains. Furthermore, unlike healthcare-associated strains, CA-MRSA strains retain susceptibility to many non–β-lactam antimicrobial drugs. CA-MRSA also produces several toxins not commonly found in nosocomial strains, notably Panton-Valentine leukocidin, which causes leukocyte destruction and tissue necrosis. During the early phase of the CA-MRSA epidemic, genotypes of CA-MRSA differed from those of healthcare-associated strains; in the United States, the predominant types that cause CA-MRSA infections are USA 300 and USA 400; USA 300 is rapidly establishing predominance (4,5). In a recent multistate study, 59% of purulent skin and soft tissue infections were caused by MRSA, and 97% of those were caused by USA 300 (6). As the epidemic emerges, the distinctions between community-associated and healthcare-associated strains of MRSA may be blurring; USA 300 has emerged as an important cause of healthcare-associated infections in some hospitals and has caused infections among healthy infants in nurseries (7–9).

Approaches to clinical management of CA-MRSA infections have been summarized and are available at http://www.cdc.gov/ncidod/dhqp/pdf/ar/CAMRSA_ExpMtgStrategies.pdf. Improved physician recognition of CA-MRSA as the major cause of staphylococcal skin and soft tissue infections is the key to ensuring initiation of appropriate therapy; awareness and knowledge of the local epidemiology of MRSA can help guide appropriate treatment. Several attempts to develop an S. aureus vaccine are under way, but availability of an effective active vaccine remains at least several years away.

As MRSA becomes more common in the community, the problem is also emerging in animals. Clinical cases or outbreaks of MRSA infection among household pets have been described, and interspecies transmission between animals and humans has been documented (10). In horses, MRSA appears to be endemic to certain populations worldwide and readily moves between animals and humans. More research is needed to understand the relationship between animal and human MRSA infection and colonization.

The emergence of CA-MRSA has forced public health practitioners to face challenging issues in surveillance, education, and community prevention. Surveillance challenges related to CA-MRSA center on the changing epidemiology and need for constant monitoring, on nonstandard case definitions, and on inadequate funding. One approach is to make invasive MRSA a reportable condition, as was done in Tennessee in 2004. Surveillance has shown that invasive MRSA is a major public health problem in Tennessee (overall incidence 33.4/100,000) and is now the third most common reportable condition in that state, following only chlamydia and gonorrhea. In Los Angeles County, surveillance for pediatric MRSA, also reportable, provides evidence of a considerable public health effect. For example, the rate of hospitalization for children <18 years of age (10.3/100,000) is substantially higher for CA-MRSA than for the most common reportable diseases. Some public health agencies have assumed leadership roles and provide educational material—improved diagnosis and treatment, recognition of risk factors, and improved prevention—for healthcare personnel. Public education has focused on early recognition of infection and basic hygiene measures that are critical for preventing transmission. Control of outbreaks among tightly linked epidemiologic groups such as athletic teams, military personnel, daycare centers, and correctional facilities has centered on active surveillance for skin lesions, standardized diagnosis and treatment, hygiene education, and environmental cleaning.

Symposium participants were reminded of the association between epidemic S. aureus infections and secondary respiratory infections associated with the concurrent Asian influenza pandemic in the 1950s and were cautioned about the potentially catastrophic implications of widespread MRSA infections in the community concurrent with a pandemic of influenza (e.g., H5N1). During a discussion of research needs, participants emphasized the need for more research on the epidemiology of CA-MRSA, specifically the trajectory of the epidemic, the role of host factors, the epidemiology of MRSA colonization in the community, and the association between colonization and infection. A key unknown factor is how and why USA 300 has become dominant in the community. A better understanding of the pathogenesis of severe infections is needed, including further elucidation of the role of Panton-Valentine leukocidin and other potential virulence factors. Although participants stressed the importance of new approaches to prevention, little is known about the best strategies. Efforts to study the effectiveness of individual interventions are complicated by the bundling of infection control measures often used in outbreak settings. In terms of therapy, data from clinical trials are needed to identify the optimal antimicrobial agents for treatment of CA-MRSA infections and to determine whether antimicrobial therapy of less serious skin infections prevents invasive complications.

Acknowledgment

We thank Kathryn Arnold, Elizabeth Bancroft, Henry Blumberg, Susan Boyle-Vavra, Roberta Carey, Theodore Eickhoff, Monica Farley, Marion Kainer, R. Monina Klevens, Jean Lee, André Nahmias, Susan Ray, and Scott Weese for knowledgeable presentations and discussions. We also thank Tonya Dixon and Allison Greenspan for their contributions to and support of this project.

References

  1. Southeastern Center for Emerging Biologic Threats (SECEBT) (cited 2006 September 11). Available at http://www.secebt.org/
  2. Centers for Disease Control and Prevention. Four pediatric deaths from community-acquired methicillin-resistant Staphylococcus aureus—Minnesota and North Dakota, 1997–1999. MMWR Morb Mortal Wkly Rep. 1999;48:707–10.
  3. Fridkin SK, Hageman JC, Morrison M, Sanza LT, Como-Sabetti K, Jernigan JA, et al. Methicillin-resistant Staphylococcus aureus disease in three communities. N Engl J Med. 2005;352:1436–44.
  4. McDougal LK, Steward CD, Killgore GE, Chaitram JM, McAllister SK, Tenover FC. Pulsed-field gel electrophoresis typing of oxacillin-resistant Staphylococcus aureus isolates from the United States: establishing a national database. J Clin Microbiol. 2003;41:5113–20.
  5. King MD, Humphrey BJ, Wang YF, Kourbatova EV, Ray SM, Blumberg HM. Emergence of community-acquired methicillin-resistant Staphylococcus aureus USA 300 clone as the predominant cause of skin and soft-tissue infections. Ann Intern Med. 2006;144:309–17.
  6. Moran GJ, Krishnadasan A, Gorwitz RJ, Fosheim GE, McDougal LK, Carey RB, et al. Methicillin-resistant S. aureus infections among patients in the emergency department. N Engl J Med. 2006;355:666–74.
  7. Klevens RM, Edwards JR, Tenover FC, McDonald LC, Horan T, Gaynes R. Changes in the epidemiology of methicillin-resistant Staphylococcus aureus in intensive care units in U.S. hospitals, 1992–2003. Clin Infect Dis. 2006;42:389–91.
  8. Seybold U, Kourbatova EV, Johnson JG, Halvosa SJ, Wang YF, King MD, et al. Emergence of community-associated methicillin-resistant Staphylococcus aureus USA 300 genotype as a major cause of health care-associated blood stream infections. Clin Infect Dis. 2006;42:647–56.
  9. Centers for Disease Control and Prevention. Community-associated methicillin-resistant Staphylococcus aureus infection among healthy newborns—Chicago and Los Angeles County, 2004. MMWR Morb Mortal Wkly Rep. 2006;55:329–32.
  10. Weese JS, Dick H, Willey BM, McGeer A, Kreiswirth BN, Innis B, et al. Suspected transmission of methicillin-resistant Staphylococcus aureus between domestic pets and humans in veterinary clinics and in the household. Vet Microbiol. 2006;115:148–55.

Suggested Citation for this Article

Jernigan JA, Arnold K, Heilpern K, Kainer M, Woods C, Hughes JM. Methicillin-resistant Staphylococcus aureus as community pathogen [conference summary]. Emerg Infect Dis [serial on the Internet]. 2006 Nov [date cited]. Available from http://www.cdc.gov/ncidod/EID/vol12no11/06-0911.htm

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This page posted October 19, 2006
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