Review
Community-acquired methicillin-resistant Staphylococcus aureus infections

https://doi.org/10.1016/j.ijantimicag.2005.11.004Get rights and content

Abstract

Methicillin-resistant Staphylococcus aureus (MRSA) should no longer be regarded as a strictly nosocomial pathogen. During the past decade, community-acquired MRSA (CA-MRSA) infections among young persons without healthcare-associated (HCA) risk factors have emerged in several areas worldwide. These infections are caused by strains that almost exclusively carry the staphylococcal cassette chromosome mec type IV element and the Panton–Valentine leukocidin genes and, unlike HCA-MRSA strains, are not multiresistant. Although the majority of CA-MRSA infections are mild skin and soft tissue infections, severe life-threatening cases of necrotizing pneumonia, necrotizing fasciitis, myonecrosis and sepsis have been reported. Clindamycin is an effective agent for skin and soft tissue infections, however attention should be paid to the possibility of the emergence of resistance during treatment in strains with the macrolide, lincosamide and group B streptogramin (MLSB)-inducible resistance phenotype. For patients with invasive infections that may be caused be CA-MRSA, vancomycin, teicoplanin and linezolid represent appropriate empirical therapeutic options.

Introduction

It was only 1 year after the introduction of methicillin into clinical practice in the early 1960s that Staphylococcus aureus strains resistant to this agent emerged. Within the following two decades, methicillin-resistant S. aureus (MRSA) had been established as a major nosocomial pathogen worldwide with a significant economic impact on healthcare systems. Predisposing factors for acquisition of MRSA include recent hospitalisation, admission to an Intensive Care Unit (ICU), exposure to a patient who is colonised or infected with MRSA, household contact with individuals with hospital-acquired MRSA, prolonged antibacterial therapy and surgery. In the 1980s, the first cases of MRSA infection in the community were reported, which concerned intravenous drug users, residents in long-term care facilities, and patients with chronic conditions and frequent contact with healthcare services. These infections, although occurring in the community, are considered healthcare-associated (HCA) MRSA infections [1], [2], [3], [4]. During the past decade, however, MRSA infections occurring in the community among healthy persons without risk factors for MRSA acquisition are being reported with increasing frequency and from several areas of the world and are becoming the prevalent form. These are mostly isolated from cutaneous infections, especially among children, as reported from a Houston paediatric hospital where 74% of community-acquired S. aureus strains have been reported as MRSA since 2001 [5]. Such infections are referred to as community-acquired (CA) MRSA infections and are caused by strains that are distinct from HCA-MRSA strains in terms of genetic background, epidemiology, clinical spectrum and antibacterial resistance [5], [6], [7], [8], [9], [10], [11], [12], [13], [14], [15], [16], [17]. The emerging potential danger entailed in CA-MRSA invasive infections was illustrated between 1997 and 1999 by the deaths of four healthy children in Minnesota and North Dakota [7]. On the other hand, recent reports of nosocomial transmission of CA-MRSA strains represent a new challenge for healthcare professionals [17], [18], [19], [20]. The purpose of this article is to review the current state of knowledge regarding CA-MRSA infections, with an emphasis on its epidemiology and treatment.

Section snippets

Review methodology

A computerised search of the MEDLINE database from January 1966 to April 2005 was conducted by combining the words ‘S. aureus’, ‘methicillin-resistant’ and ‘community’. Articles reporting original data on CA-MRSA were selected for this review. Original articles were also identified from the bibliographies of articles selected through the first MEDLINE search round. Additional original articles and review articles were used based on their applicability to the topic reviewed.

Defining CA-MRSA infection

The term CA-MRSA infection refers to an MRSA infection that truly originates in the community. Currently there is controversy in the literature in defining CA-MRSA infection in terms of the time of MRSA identification (varying from 24 to 72 h after hospital admission in different studies), history and time of recent hospitalisation (varying from 1 to 24 months before MRSA identification), as well as exploration or not of additional risk factors for MRSA acquisition. Occasionally, the molecular

Molecular characteristics and virulence of CA-MRSA

Methicillin resistance in S. aureus is determined by the production of an altered low-affinity penicillin-binding protein (PBP) called PBP2a (or PBP2′). PBP2a is encoded by the mecA gene, which confers resistance to all β-lactam antibiotics. The mecA gene is comprised of mecA along with its regulator genes mecI and mecR and resides within a mobile genetic island, the so-called staphylococcal cassette chromosome mec (SCCmec). Some SCCmec types also contain other genetic elements, such as Tn554

Epidemiology

MRSA colonisation is extremely rare in the absence of exposure to healthcare services [30], [31], [32], [33], [34]. A recent meta-analysis reported a pooled MRSA colonisation prevalence rate of 1.3% in ten studies testing a total of 8350 persons in the community, whereas the respective prevalence rate was 0.2% in studies excluding persons exposed to healthcare services [2]. In this meta-analysis, it was also found that MRSA colonisation was more frequent among persons in the community from whom

Clinical manifestations and prognosis

CA-MRSA has been associated with a variety of clinical manifestations, ranging from mild skin infections to lethal pneumonia and sepsis. Like MSSA clinical isolates in the community, the majority of CA-MRSA clinical isolates are recovered from skin or soft tissue [16]. In community-based studies, CA-MRSA infections are almost exclusively located in skin or soft tissue [11], [16], [36], [41], [42], [43], [44]. Moreover, CA-MRSA and HCA-MRSA infections manifest a different clinical spectrum. In

The available antimicrobials

Unlike the multiresistant profile of HCA-MRSA strains, in general CA-MRSA strains are susceptible to most antibiotic classes except β-lactams. Most CA-MRSA isolates are susceptible to clindamycin, trimethoprim/sulphamethoxazole, doxycycline, minocycline, gentamicin, vancomycin, teicoplanin, chloramphenicol, fluoroquinolones, rifampicin and linezolid [3], [5], [6], [8], [10], [13], [15], [23]. The non-MDR profile of CA-MRSA strains is attributed to their evolution from MSSA strains following

Infection control

Surveillance to monitor the prevalence, epidemiology and antimicrobial resistance of CA-MRSA infections should be implemented in hospitals, outpatient clinics, emergency departments and microbiology laboratories. This knowledge will allow the establishment of recommendations for antimicrobial prescribing within local communities and for the implementation of rational antibiotic policies. Efforts should be made to obtain cultures from all patients with infections that may be caused by S. aureus,

References (102)

  • H.F. Chambers

    The changing epidemiology of Staphylococcus aureus?

    Emerg Infect Dis

    (2001)
  • C.D. Salgado et al.

    Community-acquired methicillin-resistant Staphylococcus aureus: a meta-analysis of prevalence and risk factors

    Clin Infect Dis

    (2003)
  • S. Deresinski

    Methicillin-resistant Staphylococcus aureus: an evolutionary, epidemiologic and therapeutic Odyssey

    Clin Infect Dis

    (2005)
  • F.D. Lowy

    Staphylococcus aureus infections

    N Engl J Med

    (1998)
  • T.S. Naimi et al.

    Epidemiology and clonality of community-acquired methicillin-resistant Staphylococcus aureus in Minnesota, 1996–1998

    Clin Infect Dis

    (2001)
  • S.C. Buckingham et al.

    Emergence of community-acquired methicillin-resistant Staphylococcus aureus at a Memphis, Tennessee children's hospital

    Pediatr Infect Dis J

    (2004)
  • 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)
  • S. Salmenlinna et al.

    Community-acquired methicillin-resistant Staphylococcus aureus, Finland

    Emerg Infect Dis

    (2002)
  • F. Vandenesch et al.

    Community-acquired methicillin-resistant Staphylococcus aureus carrying Panton–Valentine leukocidin genes: worldwide emergence

    Emerg Infect Dis

    (2003)
  • P. Dufour et al.

    Community-acquired methicillin-resistant Staphylococcus aureus infections in France: emergence of a single clone that produces Panton–Valentine leukocidin

    Clin Infect Dis

    (2002)
  • H.C. Baggett et al.

    Community-onset methicillin-resistant Staphylococcus aureus associated with antibiotic use and the cytotoxin Panton–Valentine leukocidin during a furunculosis outbreak in rural Alaska

    J Infect Dis

    (2004)
  • K. Mongkolrattanothai et al.

    Severe Staphylococcus aureus infections caused by clonally related community-acquired methicillin-susceptible and methicillin-resistant isolates

    Clin Infect Dis

    (2003)
  • D.W. Dietrich et al.

    Community-acquired methicillin-resistant Staphylococcus aureus in southern New England children

    Pediatrics

    (2004)
  • C.A. Morin et al.

    Population-based incidence and characteristics of community-onset Staphylococcus aureus infections with bacteremia in four Metropolitan Connecticut areas, 1998

    J Infect Dis

    (2001)
  • A.M. Avalos Mishaan et al.

    Emergence of a predominant clone of community-acquired Staphylococcus aureus among children in Houston, Texas

    Pediatr Infect Dis J

    (2005)
  • A.V. Groom et al.

    Community-acquired methicillin-resistant Staphylococcus aureus in a rural American Indian community

    JAMA

    (2001)
  • F.G. O’Brien et al.

    Community strain of methicillin-resistant Staphylococcus aureus involved in a hospital outbreak

    J Clin Microbiol

    (1999)
  • G. Regev-Yochay et al.

    Methicillin-resistant Staphylococcus aureus in neonatal intensive care unit

    Emerg Infect Dis

    (2005)
  • L. Saiman et al.

    Hospital transmission of community-acquired methicillin-resistant Staphylococcus aureus among postpartum women

    Clin Infect Dis

    (2003)
  • C. Eckhardt et al.

    Transmission of methicillin-resistant Staphylococcus aureus in the Neonatal Intensive Care Unit from a patient with community-acquired disease

    Infect Control Hosp Epidemiol

    (2003)
  • T. Baba et al.

    Genome and virulence determinants of high virulence community-acquired methicillin-resistant Staphylococcus aureus

    Lancet

    (2001)
  • E.A. Eady et al.

    Staphylococcal resistance revisited: community-acquired methicillin resistant Staphylococcus aureus—an emerging problem for the management of skin and soft tissue infections

    Curr Opin Infect Dis

    (2003)
  • K. Okuma et al.

    Dissemination of new methicillin-resistant Staphylococcus aureus clones in the community

    J Clin Microbiol

    (2002)
  • H. de Lencastre et al.

    Molecular aspects of methicillin resistance in Staphylococcus aureus

    J Antimicrob Chemother

    (1994)
  • B.A. Diep et al.

    Widespread skin and soft tissue infections due to two methicillin-resistant Staphylococcus aureus strains harboring the genes for Panton–Valentine leucocidin

    J Clin Microbiol

    (2004)
  • J.S. Francis et al.

    Severe community-onset pneumonia in healthy adults caused by methicillin-resistant Staphylococcus aureus carrying the Panton–Valentine leukocidin genes

    Clin Infect Dis

    (2005)
  • D.A. Robinson et al.

    Evolutionary models of the emergence of methicillin-resistant Staphylococcus aureus

    Antimicrob Agents Chemother

    (2003)
  • B. Shopsin et al.

    Prevalence of methicillin-resistant and methicillin-susceptible Staphylococcus aureus in the community

    J Infect Dis

    (2000)
  • J.A. Jernigan et al.

    Prevalence of and risk factors for colonization with methicillin-resistant Staphylococcus aureus at the time of hospital admission

    Infect Control Hosp Epidemiol

    (2003)
  • J.A. Jernigan et al.

    Prevalence of and risk factors for colonization with methicillin-resistant Staphylococcus aureus in an outpatient clinic population

    Infect Control Hosp Epidemiol

    (2003)
  • G. Zanelli et al.

    Staphylococcus aureus nasal carriage in the community: a survey from central Italy

    Epidemiol Infect

    (2002)
  • R. Sa-Leao et al.

    Low prevalence of methicillin-resistant strains among Staphylococcus aureus colonizing young and healthy members of the community in Portugal

    Microb Drug Resist

    (2001)
  • K.D. Schultz et al.

    The changing face of pleural empyemas in children: epidemiology and management

    Pediatrics

    (2005)
  • M.W. Ellis et al.

    Natural history of community-acquired methicillin-resistant Staphylococcus aureus colonization and infection in soldiers

    Clin Infect Dis

    (2004)
  • H. Faden et al.

    Community-acquired methicillin-resistant Staphylococcus aureus and intrafamily spread of pustular disease

    Pediatr Infect Dis J

    (2001)
  • R. Shahin et al.

    Methicillin-resistant Staphylococcus aureus carriage in a child-care center following a case of disease

    Arch Pediatr Adolesc Med

    (1999)
  • P.M. Adcock et al.

    Methicillin-resistant Staphylococcus aureus in two child care centers

    J Infect Dis

    (1998)
  • C.E. Zinderman et al.

    Community-acquired methicillin-resistant Staphylococcus aureus among military recruits

    Emerg Infect Dis

    (2004)
  • A. Borer et al.

    Community-acquired methicillin-resistant Staphylococcus aureus in institutionalized adults with developmental disabilities

    Emerg Infect Dis

    (2002)
  • D.M. Nguyen et al.

    Recurring methicillin-resistant Staphylococcus aureus infections in a football team

    Emerg Infect Dis

    (2005)
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