DermNet provides Google Translate, a free machine translation service. Note that this may not provide an exact translation in all languages
Author: Dr Amy Stanway MB ChB, Registrar, Department of Dermatology, Waikato Hospital, Hamilton, New Zealand, 2001. Updated by Dr Jannet Gomez, Postgraduate Student in Clinical Dermatology, Queen Mary University London, United Kingdom; Chief Editor: Dr Amanda Oakley, Dermatologist, Hamilton, New Zealand, December 2015.
MRSA is the term used for bacteria of the Staphylococcus aureus group that are resistant to the usual antibiotics used in the treatment of infections with such organisms. Traditionally MRSA stood for methicillin (meticillin) resistance but the term increasingly refers to a multi-drug resistant group. Such bacteria often have resistance to many antibiotics traditionally used against S. aureus.
MRSA now is usually categorised into two types.
Resistance to methicillin is due to the presence of the mec gene, situated on Staphylococcal Cassette Chromosome mec (SCCmec). This alters the site at which methicillin binds to kill the organism. Hence, methicillin is not able to effectively bind to the bacteria. CA-MRSA is similar phenotypically and genotypically to HA-MRSA. CA-MRSA harbours SCCmec type IV, V or VII. However, the distinction between the two types is becoming less over time.
Infections caused by MRSA are the same as other staphylococcal infections because the organism itself is not any more virulent (or infectious) than usual type S aureus.
Like other S aureus, MRSA can colonise the skin and body of an individual without causing sickness, and in this way it can be passed on to other individuals unknowingly. Problems arise in the treatment of overt infections with MRSA because antibiotic choice is very limited.
MRSA is found worldwide, predominantly in hospitals and institutions such as nursing homes, where it is referred by the name hospital-acquired MRSA (HA-MRSA). Less commonly, MRSA is found in the general community (CA-MRSA).
There are three main reservoirs (and hence sources of spread and infection) for MRSA in hospital and institutions: staff, patients and inanimate objects such as beds, linen and utensils. By far the most important reservoir is patients, who may be colonised with MRSA without evidence of infection.
The usual sites of colonisation with MRSA are:
Most health professionals that are colonised with MRSA do not develop infection and many spontaneously clear the organism without treatment. Once colonisation has been present for more than three months, it becomes much more difficult to clear.
Patients, however, have a 30–60% risk of infection following colonisation. This is probably due to factors related to the illness for which they are hospitalised, which impair their ability to clear or control colonisation with the organism.
Most MRSA infections occur in wounds (eg surgical wounds), skin (eg intravenous access sites), or in the bloodstream. Mortality from these infections is not significantly different from those seen with usual type S aureus infections.
Community acquired MRSA infections mostly occur:
Risk factors for severe skin infections with MRSA include:
Hospital acquired MRSA presents as:
CA-MRSA mainly presents with:
If untreated, MRSA can lead to sepsis with rash, headaches, muscle aches, chills, fever, chest pain and shortness of breath, and in some cases, the death of the patient. This is more common in HA-MRSA than CA-MRSA.
The standard method to diagnose MRSA is by culture and antibiotic sensitivity testing of Staphylococcus aureus bacteria from the infected site.
The following steps are used for treatment of carriers of MRSA:
Treatment of active infection involves drainage of pus from furuncles and abscesses, and antibiotics.
These antibiotics are no better than flucloxacillin in the treatment of usual type S aureus, but are much more effective in MRSA infections.
Other antibiotics are less effective and are used if there is resistance to vancomycin/clindamycin or in case of adverse reactions to these drugs.
In life-threatening infections such as infective endocarditis, multiple antibiotics are often prescribed simultaneously (eg vancomycin plus an aminoglycoside plus rifampicin).
In hospitals, patients who have been transferred from another hospital or institution should have swabs taken on admission to screen for MRSA colonisation or infection.
Common sites for swab collection are nostrils, armpits, groins, genital region and any areas of broken skin (eg surgical wounds, ulcers, sores).
New or transferring hospital staff are also screened. The results of swabs take a few days to be reported.
If an inpatient is found to have MRSA colonisation or infection:
The above precautions should be strictly enforced until repeat swabs from the patient are negative for MRSA. This may take some weeks. Staff found to be colonised with MRSA should be removed from patient contact.
The following basic hygiene practice can help lower the incidence of CA-MRSA:
There is growing concern about MRSA infections. They appear to be increasing in frequency and displaying resistance to a wider range of antibiotics.
Of particular concern are the VISA strains of MRSA (vancomycin intermediate susceptibility S aureus). These are beginning to develop resistance to vancomycin, which is currently the most effective antibiotic against MRSA. This new resistance has arisen because another species of bacteria, called enterococci, relatively commonly express vancomycin resistance. In the laboratory, enterococci are capable of transferring the gene for vancomycin resistance to S aureus.
Newer antibiotics such as linezolid and synercid look promising for treatment of infections not responding to vancomycin. Many newer drugs including glycopeptides (dalbavancin, oritavancin and telavancin), anti-MRSA beta lactams (ceftobiprole) and diaminopyrimidines (iclaprim) are being tested for use against MSRA.
Claeys KC, Zasowski EJ, Lagnf AM, Levine DP, Davis SL, Rybak MJ. Novel Application of Published Risk Factors for Methicillin-Resistant S. aureus in Acute Bacterial Skin and Skin Structure Infections. Int J Antimicrob Agents. 2017 Jun 28. pii: S0924-8579(17)30226-1. doi: 10.1016/j.ijantimicag.2017.05.015. [Epub ahead of print] PubMed PMID: 28668679.
© 2022 DermNet New Zealand Trust.
DermNet NZ does not provide an online consultation service. If you have any concerns with your skin or its treatment, see a dermatologist for advice.