ReviewCommunity-acquired methicillin-resistant Staphylococcus aureus infections
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,
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