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Editorials

Community acquired MRSA in Europe

BMJ 2007; 335 doi: https://doi.org/10.1136/bmj.39373.465903.BE (Published 08 November 2007) Cite this as: BMJ 2007;335:947
  1. Tristan Ferry, resident in infectious diseases,
  2. Jerome Etienne, professor of microbiology
  1. INSERM, U851, Université Lyon 1, Centre National de Référence des Staphylocoques, Faculté Laennec, Lyon F-69008, France
  1. jetienne{at}univ-lyon1.fr

    Is less common than in the US but spread must be actively controlled

    Infections caused by methicillin resistant Staphylococcus aureus (MRSA) were originally identified only in hospital settings. But new strains of MRSA have emerged and are now an important cause of community acquired infection worldwide,1 and they often affect patients with no risk factors for acquiring a strain of hospital origin. A study just published estimates that 94 360 invasive MRSA infections occurred in the United States in 2005, primarily but not entirely related to health care.2 In the study's surveillance sample, 58.4% of cases were defined as having community onset (cases with a healthcare risk factor but with a culture obtained ≤48 hours after hospital admission) and 13.7% were community associated (meaning that they started outside hospital and were not associated with health care).

    Many isolates of community acquired MRSA produce Panton-Valentine leucocidin (PVL), a toxin that is not detected in MRSA infections associated with health care. The toxin destroys leucocytes and causes extensive tissue necrosis. The prevalence of PVL positive community acquired MRSA varies greatly between continents. In the United States, 50% of patients with skin and soft tissue infections seen in emergency departments test positive for PVL positive MRSA.3 In Europe, the prevalence is generally lower, at around 1-3%,4 but a few countries, such as Greece, have reported a much higher prevalence.5 The risk of a wider spread through Europe is therefore a possibility. Moreover, PVL positive strains of community acquired MRSA are increasingly isolated in cases of hospital acquired infection in countries such as the US and Greece.5 6

    Most cases of community acquired MRSA are caused by a few specific clones, which are defined by molecular criteria that designate sequence type. The main European clone, with sequence type 80, has been detected in almost all European countries, including the most northern parts of Europe, where MRSA strains are rare in hospitals.7 One of the most prevalent clones in the US, designated USA300, belongs to sequence type 8, while the South West Pacific clone sequence type 30 is prevalent in Asia and Oceania.7 Some clones have spread all over the world to become pandemic. For instance, the USA300 clone has been introduced into Europe by travellers from the US and is now spreading sporadically.8

    Even young healthy people without risk factors can be infected with community acquired MRSA,2 usually directly through close contact with someone who has a skin infection. Behavioural risks for infection include use of injected drugs, poor personal hygiene, and the presence of open wounds or minor abrasions (for example, from shaving). Indirect contact with contaminated objects—such as towels, soap, bed linen, clothes, sports equipment, and wound dressings—seems to be another route of transmission. Epidemics of community acquired MRSA have occurred in members of “closed populations,” such as household members, competitive athletes, military recruits, jail inmates, men who have sex with men, and children in schools or childcare centres.

    Community acquired MRSA usually manifests itself as skin and soft tissue infections. It tends to produce larger abscesses that need to be drained more often than abscesses caused by PVL negative methicillin sensitive S aureus. Life threatening invasive infections such as necrotising pneumonia, necrotising fasciitis, and sepsis-like syndromes have been reported too.9 10 Necrotising pneumonia, which has a case fatality rate as high as 75%, often occurs after infection with a flu virus.9 The conjunction of both potential pandemics (flu virus and community acquired MRSA) could represent a health disaster.

    Uncomplicated community acquired MRSA infections of skin and soft tissue are managed primarily by incision and drainage of fluctuant lesions.11 Antibiotic treatment has only a moderate effect on clinical outcome and some authors have suggested limiting antibiotic treatment to patients with a suboptimal response to surgery.11 In countries with a high prevalence of community acquired MRSA, empirical treatment regimens consisting primarily of vancomycin, co-trimoxazole, or clindamycin are worth trying.7 Linezolid is an option for oral or intravenous treatment of infections caused by clindamycin resistant isolates.

    When PVL contributes to the severity of infection, misuse of oxacillin—the mode of action of which could lead to overproduction of this toxin—might exacerbate tissue necrosis.12 Drugs that shut down ribosomal translation of proteins in S aureus, such as clindamycin and linezolid, decrease production of PVL.12 The ability of community acquired MRSA strains to acquire resistance to other antimicrobials, however, will almost certainly pose a longer term challenge.

    Hygiene measures have proved to be successful in controlling community acquired outbreaks and should be taught more extensively in the community, as they are in hospital settings. Patients with community acquired MRSA infections of soft tissue should be counselled on the importance of hand hygiene, of not sharing personal items such as towels, and of appropriate wound care. Decolonisation of patients and contacts—for example, using topical mupirocin applied nasally—may prevent the spread of community acquired MRSA, especially within closed communities.13 Adequate prevention of spread is currently the only way to stop S aureus conquering the world with epidemics of virulent antibiotic resistant clones.

    Footnotes

    • This article was posted on bmj.com on 23 October 2007: http://bmj.com/cgi/doi/10.1136/bmj.39373.465903.BE

    • Competing interests: None declared.

    • Provenance and peer review: Commissioned, not externally peer reviewed

    References

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