Expert opinion: community-acquired MRSA

An assessment by Dr Anton Alexandroff, Dr Nelun Perera, Dr Philip Gothard and Dr Ekaterina Burova

Community-acquired (CA) MRSA began to emerge in the 1990s and by 2003, according to a meta-analysis of mainly US studies, the prevalence of its colonisation had reached 1 per cent in adults and 2.5 per cent in children.

The major concern is that, as for penicillin in the 1950s, methicillin resistance will become the norm. Methicillin was developed as a broad spectrum antibiotic, but there is early evidence of widespread resistance to it.

Based on its susceptibility to methicillin, Staphylococcus aureus is categorised as methicillin-sensitive (MSSA) or resistant (MRSA). MRSA is divided into hospital-acquired (HA) and CA strains. Initially thought to be a hospital-only infection, there has been a recent emergence in the community, particularly in the US; however, the carriage rate remains low.

CA-MRSA carries the mecA gene type IV, which often expresses the Panton-Valentine leukocidin gene. An important difference is that it tends to be susceptible to non-beta-lactam antibiotics.1 Infection with CA-MRSA is suspected if it is acquired in the community or within 72 hours of admission to hospital and the patient has not been hospitalised within the previous 12 months.

Clinical presentation and treatment
Typically, patients with CA-MRSA present with skin and soft tissue infections – impetigo, folliculitis, furunculosis, solitary abscess and/or cellulitis.1 Rarely, CA-MRSA may cause serious infections, including bacteraemia, necrotising fasciitis, endocarditis, staphylococcal scalded skin syndrome and pulmonary syndrome.1,2

CA-MRSA pulmonary syndrome is a distinct and rare syndrome that may affect previously well adolescents. It is characterised by coexisting osteomyelitis, septic arthritis and pneumonia or septic pulmonary emboli and may be fatal. Co-infection with influenza may aggravate its course.

The vast majority of S aureus skin infections are still due to MSSA and should be treated empirically with flucloxacillin in the absence of clear risk factors. CA-MRSA should be suspected in those who fail to respond to flucloxacillin or have evidence of carriage of CA-MRSA.

Skin and nasal swabs should be taken and empiric therapy switched to a drug such as vancomycin, pending sensitivities. CA-MRSA is usually susceptible to chloramphenicol, co-trimoxazole, tetracyclines, fluoroquinolones, rifampicin and clindamycin (but not macrolides), in addition to more modern treatments; therefore, in mild-to-moderate disease, outpatient management is possible.

Uncomplicated CA-MRSA abscesses and furunculosis often respond to incision and drainage alone.1 Mild folliculitis and cellulitis can be treated with one of the oral agents listed above.

Doxycycline and clindamycin are valuable antistaphylococcal agents with excellent penetration of skin and, in animal studies, good antitoxin properties. Clindamycin is licensed as a second-line agent for MRSA skin and soft tissue infections in the UK and can be used at a dosage of 300–600mg three or four times daily.

There have been reports of inducible resistance to clindamycin and while this should not preclude its use, we recommend repeat susceptibility testing and possibly switching to another agent in patients who are slow to respond. Rifampicin or sodium fusidate are effective but should not be used on their own because resistance develops rapidly. However, when combined with other anti-MRSA agents, they are useful in treating complicated and deep-seated infections.

Co-trimoxazole (trimethoprim/sulfamethoxazole), although a low-cost, effective alternative, is less used because, rarely, it may cause bone marrow suppression and severe drug reactions, such as Stevens-Johnson syndrome and toxic epidermal necrolysis.1,3 Patients with signs of severe sepsis, a history of a recent hospital admission, any other risk factors for MRSA or potential necrotising fasciitis should be referred urgently to hospital and treated empirically with drugs such as vancomycin, teicoplanin, tigecycline, daptomycin or linezolid, pending further sensitivities. Therapy should not be delayed pending microbiology reports.

Prevention and eradication of CA-MRSA
MRSA colonisation is the main risk factor for subsequent MRSA infection. Moreover, patients who are colonised with MRSA are more likely to develop clinical infection than those who are colonised with MSSA.4

Prevention of CA-MRSA is difficult: the low prevalence of colonisation means screening is not cost-effective, other than in situations of possible epidemic spread. The key is keeping the hands thoroughly clean with soap and water or an alcohol-based sanitiser, cleaning and covering cuts and scrapes until they heal, avoiding touching other people’s wounds or bandages, and not sharing personal items, such as towels and razors.

- Dr Anton Alexandroff is a specialist registrar, department of dermatology, Leicester Royal Infirmary; Dr Nelun Perera is consultant microbiologist, department of clinical microbiology, Leicester Royal Infirmary; Dr Philip Gothard is consultant in infectious diseases, Hospital for Tropical Diseases, University College London Hospitals NHS Foundation Trust; Dr Ekaterina Burova is consultant dermatologist, Bedford Hospital NHS Trust

References
1. Elston DM. Community-acquired methicillin-resistant Staphylococcus aureus. J Am Acad Dermatol 2007; 56: 1-16.
2. Lee YT, Lin JC, Wang NC et al. Necrotizing fasciitis in a medical center in northern Taiwan: emergence of methicillin-resistant Staphylococcus aureus in the community. J Microbiol Immunol Infect 2007; 40: 335-41.
3. See S, Mumford JM. Trimethoprim/sulfamethoxazole-induced toxic epidermal necrolysis. Ann Pharmacother 2001; 35: 694-7.
4. Ellis MW, Hospenthal DR, Dooley DP et al. Natural history of community-acquired methicillin-resistant Staphylococcus aureus colonization and infection in soldiers. Clin Infect Dis 2004; 39: 971-9.

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