Methicillin-resistant Staphylococcus aureus

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Methicillin-resistant Staphylococcus aureus
Human neutrophil ingesting MRSA.jpg
Scanning electron micrograph of a human neutrophil ingesting MRSA
Scientific classification
Domain: Bacteria
Kingdom: Eubacteria
Phylum: Firmicutes
Class: Bacilli
Order: Bacillales
Family: Staphylococcaceae
Genus: Staphylococcus
Species: S. aureus
Binomial name
Staphylococcus aureus

Methicillin-resistant Staphylococcus aureus (MRSA) (/ɛmɑːrɛs/ or /ˈmɜːrsə/) is a gram-positive bacterium responsible for several difficult-to-treat infections in humans. MRSA is any strain of Staphylococcus aureus that has developed, through horizontal gene transfer and natural selection, multiple drug resistance to beta-lactam antibiotics. β-lactam antibiotics are a broad spectrum group which includes some penamspenicillin derivatives such as methicillin and oxacillin, and cephems such as the cephalosporins. MRSA evolved from horizontal gene transfer of the mecA gene to at least five distinct S. aureus lineages.[1] Strains unable to resist these antibiotics are classified as methicillin-susceptible Staphylococcus aureus, or MSSA. The evolution of such resistance does not cause the organism to be more intrinsically virulent than strains of S. aureus that have no antibiotic resistance, but resistance does make MRSA infection more difficult to treat with standard types of antibiotics and thus more dangerous.

MRSA is prevalent in hospitals, prisons, and nursing homes, where people with open wounds, invasive devices such as catheters, and weakened immune systems are at greater risk of nosocomial infection (hospital-acquired infection). MRSA began as a hospital-acquired infection, but has developed limited endemic status and is now community-acquired as well as livestock-acquired. The terms HA-MRSA (healthcare-associated MRSA), CA-MRSA (community-associated MRSA) and LA-MRSA (livestock-associated) reflect this distinction.

Signs and symptoms[edit]

S. aureus most commonly colonizes under the nostrils.[2] The rest of the respiratory tract, open wounds, intravenous catheters, and the urinary tract are also potential sites for infection.[3] Healthy individuals may carry MRSA asymptomatically for periods ranging from a few weeks to many years. People with compromised immune systems are at a significantly greater risk of symptomatic secondary infection.[citation needed]

MRSA can usually be detected by swabbing the nostrils and isolating the bacteria found inside the nostrils. Combined with extra sanitary measures for those in contact with infected people, swab screening people admitted to hospitals has been found to be effective in minimizing the spread of MRSA in hospitals in the United States, Denmark, Finland, and the Netherlands.[4]

MRSA may progress substantially within 24–48 hours of initial topical symptoms.[3] After 72 hours, MRSA can take hold in human tissues and eventually become resistant to treatment. The initial presentation of MRSA is small red bumps that resemble pimples, spider bites, or boils; they may be accompanied by fever and, occasionally, rashes. Within a few days, the bumps become larger and more painful; they eventually open into deep, pus-filled boils.[5] About 75 percent of community-associated (CA-) MRSA infections are localized to skin and soft tissue and usually can be treated effectively.[6] Some CA-MRSA strains display enhanced virulence, spreading more rapidly and causing illness much more severe than traditional HA-MRSA infections, and they can affect vital organs and lead to widespread infection (sepsis), toxic shock syndrome, and necrotizing pneumonia. This is thought to be due to toxins carried by CA-MRSA strains, such as PVL and PSM, though PVL was recently found not to be a factor in a study by the National Institute of Allergy and Infectious Diseases at the National Institutes of Health. It is not known why some healthy people develop CA-MRSA skin infections that are treatable while others infected with the same strain develop severe infections or die.[7]

People are occasionally colonized with CA-MRSA and are completely asymptomatic. The most common manifestations of CA-MRSA are simple skin infections, such as impetigo, boils, abscesses, folliculitis, and cellulitis. Rarer, but more serious, manifestations can occur, such as necrotizing fasciitis and pyomyositis (most commonly found in the tropics), necrotizing pneumonia, and infective endocarditis (which affects the valves of the heart), and bone (osteomyelitis) and joint infections.[8] CA-MRSA often results in abscess formation that requires incision and drainage. Before the spread of MRSA into the community, abscesses were not considered contagious, because infection was assumed to require violation of skin integrity and the introduction of staphylococci from normal skin colonization. However, newly emerging CA-MRSA is transmissible (similar, but with very important differences) from HA-MRSA. CA-MRSA is less likely than other forms of MRSA to cause cellulitis.

Risk factors[edit]

Some of the populations at risk:

Hospitalized people[edit]

Many MRSA infections occur in hospitals and healthcare facilities. Such infections are called nosocomial or healthcare acquired MRSA (HA-MRSA). People who are in hospital often are immunocompomised, which increases their susceptibility to all infections, including MRSA. Surgical wounds also increase the risk of infection generally.[21] SSIs can occur on the surface of the skin similar to other infections, but can sometimes infect internal organs as well as cause blood sepsis.[21] Healthcare provider-to-patient transfer is common, especially when healthcare providers move from patient to patient without performing necessary hand-washing techniques between patients.[13][22]

People in nursing homes are at at risk for all the reasons above, further complicated by the generally weaker immune systems of the elderly or other residents in need of such care.[14]

Prison inmates, military recruits[edit]

Prisons, and military barracks,[19] can be crowded and confined, and poor hygiene practices may proliferate, thus putting inhabitants at increased risk of contracting MRSA.[18] Cases of MRSA in such populations were first reported in the United States, and then in Canada. The earliest reports were made by the Center for Disease Control (CDC) in US state prisons. In the news media, hundreds of reports of MRSA outbreaks in prisons appeared between 2000 and 2008. For example, in February 2008, the Tulsa County jail in Oklahoma started treating an average of 12 S. aureus cases per month.[23] A report on skin and soft tissue infections in the Cook County jail in Chicago in 2004–05 demonstrated MRSA was the most common cause of these infections among cultured lesions, and few risk factors were more strongly associated with MRSA infections than infections caused by methicillin-susceptible S. aureus. In response to these and many other reports on MRSA infections among incarcerated and recently incarcerated persons, the Federal Bureau of Prisons has released guidelines for the management and control of the infections, although few studies provide an evidence base for these guidelines. During a recent study in Fort Benning Georgia, a variety of military recruits both healthy and those suffering from soft tissue infections were tested for MRSA as well as other pathogens.[24] The researchers determined that a significant portion of trainees were either asymptomatic carriers of MRSA or that MRSA was the cause of their infection.[24]


Antibiotic use in livestock increases the risk that MRSA will develop among the livestock; strains MRSA ST 398 and CC398 are transmissable to humans.[25][19]

Domestic pets are susceptible to MRSA infection from their owners; MRSA infected pets can also transmit MRSA to humans.[26]


Locker rooms, gyms, and related athletic facilities offer potential sites for MRSA contamination and infection.[27] Athletes have been identified as a high risk group.[19] A study linked MRSA to the abrasions caused by artificial turf.[28] Three studies by the Texas State Department of Health found the infection rate among football players was 16 times the national average. In October 2006, a high-school football player was temporarily paralyzed from MRSA-infected turf burns. His infection returned in January 2007 and required three surgeries to remove infected tissue, as well as three weeks of hospital stay.[29] In 2013, Lawrence Tynes, Carl Nicks, and Johnthan Banks of the Tampa Bay Buccaneers were diagnosed with MRSA. Tynes and Nicks apparently did not contract the infection from each other, but it is unknown if Banks contracted it from either individual.[30] In 2015, Los Angeles Dodgers' infielder Justin Turner was infected while the team visited the New York Mets.[31] In October 2015, New York Giants tight end Daniel Fells was hospitalized with a serious MRSA infection.[32]


MRSA is becoming a critical problem in pediatric settings;[33] recent studies found 4.6% of patients in U.S. health-care facilities, (presumably) including hospital nurseries,[34] were infected or colonized with MRSA.[35] Children (and adults, as well) who come in contact with day-care centers,[19] playgrounds, locker rooms, camps, dormitories, classrooms and other school settings, and gyms and workout facilities are at higher risk of getting MRSA. Parents should be especially cautious of children who participate in activities where sports equipment is shared, such as football helmets and uniforms.[36]


A selective and differential chromogenic medium for the qualitative direct detection of MRSA.
The MRSA resistance to oxacillin being tested, the top s. aureus isolate is control and sensitive to oxacillin, the other three isolates are MRSA positive
Mueller Hinton agar showing MRSA resistant to oxacillin disk

Diagnostic microbiology laboratories and reference laboratories are key for identifying outbreaks of MRSA. Faster techniques for identifying and characterizing MRSA have recently been developed.[37] Normally, the bacterium must be cultured from blood, urine, sputum, or other body-fluid samples, and in sufficient quantities to perform confirmatory tests early-on. Still, because no quick and easy method exists to diagnose MRSA, initial treatment of the infection is often based upon 'strong suspicion' and techniques by the treating physician; these include quantitative PCR procedures, which are employed in clinical laboratories for quickly detecting and identifying MRSA strains.[38][39]

Another common laboratory test is a rapid latex agglutination test that detects the PBP2a protein. PBP2a is a variant penicillin-binding protein that imparts the ability of S. aureus to be resistant to oxacillin.[40]


Antimicrobial resistance is genetically based; resistance is mediated by the acquisition of extrachromosomal genetic elements containing resistance genes. Examples include plasmids, transposable genetic elements, and genomic islands, which are transferred between bacteria through horizontal gene transfer.[41] A defining characteristic of MRSA is its ability to thrive in the presence of penicillin-like antibiotics, which normally prevent bacterial growth by inhibiting synthesis of cell wall material. This is due to a resistance gene, mecA, which stops β-lactam antibiotics from inactivating the enzymes (transpeptidases) critical for cell wall synthesis.[citation needed]


Staphylococcal cassette chromosome mec (SCCmec) is a genomic island of unknown origin containing the antibiotic resistance gene mecA.[42][43] SCCmec contains additional genes beyond mecA, including the cytolysin gene psm-mec, which may suppress virulence in HA-acquired MRSA strains.[44] In addition this locus encodes strain dependent gene regulatory RNA called psm-mecRNA.[45] SCCmec also contains ccrA and ccrB; both genes encode recombinases that mediate the site-specific integration and excision of the SCCmec element from the S. aureus chromosome.[42][43] Currently, six unique SCCmec types ranging in size from 21–67 kb have been identified;[42] they are designated types I-VI and are distinguished by variation in mec and ccr gene complexes.[41] Owing to the size of the SCCmec element and the constraints of horizontal gene transfer, a minimum of five clones are thought to be responsible for the spread of MRSA infections, with clonal complex (CC) 8 most prevalent.[42][46] SCCmec is thought to have originated in the closely related Staphylococcus sciuri species and transferred horizontally to S. aureus. [47]

Different SCCmec genotypes confer different microbiological characteristics, such as different antimicrobial resistance rates.[48] Different genotypes are also associated with different types of infections. Types I-III SCCmec are large elements that typically contain additional resistance genes and are characteristically isolated from HA-MRSA strains.[43][48] Conversely, CA-MRSA is associated with types IV and V, which are smaller and lack resistance genes other than mecA.[43][48]

These distinctions were thoroughly investigated by Collins et al. in 2001 and can be explained by the fitness differences associated with carriage of a large or small SCCmec plasmid. Carriage of large plasmids, such as SCCmecI-III, is costly to the bacteria, resulting in compensatory decrease in virulence expression.[49] MRSA is able to thrive in hospital settings with increased antibiotic resistance but decreased virulence- HA-MRSA targets immunocompromised, hospitalized hosts, thus a decrease in virulence is not maladaptive.[49] In contrast, CA-MRSA tends to carry lower fitness cost SCCmec elements to offset the increased virulence and toxicity expression required to infect healthy hosts.[49]


mecA is a biomarker gene responsible for resistance to methicillin and other β-lactam antibiotics.[3] After acquisition of mecA, the gene must be integrated and localized in the S. aureus chromosome.[42] mecA encodes penicillin-binding protein 2a (PBP2a), which differs from other penicillin-binding proteins as its active site does not bind methicillin or other β-lactam antibiotics.[42] As such, PBP2a can continue to catalyze the transpeptidation reaction required for peptidoglycan cross-linking, enabling cell wall synthesis in the presence of antibiotics. As a consequence of the inability of PBP2a to interact with β-lactam moieties, acquisition of mecA confers resistance to all β-lactam antibiotics in addition to methicillin.[42][50]

mecA is under the control of two regulatory genes, mecI and mecR1. MecI is usually bound to the mecA promoter and functions as a repressor.[41][43] In the presence of a β-lactam antibiotic, MecR1 initiates a signal transduction cascade that leads to transcriptional activation of mecA.[41][43] This is achieved by MecR1-mediated cleavage of MecI, which alleviates MecI repression.[41] mecA is further controlled by two co-repressors, BlaI and BlaR1. blaI and blaR1 are homologous to mecI and mecR1, respectively, and normally function as regulators of blaZ, which is responsible for penicillin resistance.[42][51] The DNA sequences bound by MecI and BlaI are identical;[42] therefore, BlaI can also bind the mecA operator to repress transcription of mecA.[51]

Arginine catabolic mobile element[edit]

The arginine catabolic mobile element (ACME) is a virulence factor present in many MRSA strains but not prevalent in MSSA.[52] SpeG-positive ACME compensates for the polyamine hypersensitivity of S. aureus and facilitates stable skin colonization, wound infection, and person-to-person transmission.


Diagram depicting antibiotic resistance through alteration of the antibiotic's target site, modeled after MRSA's resistance to penicillin. Beta-lactam antibiotics permanently inactivate PBP enzymes, which are essential for bacterial life, by permanently binding to their active sites. Some forms of MRSA, however, express a PBP that will not allow the antibiotic into their active site.

Acquisition of SCCmec in methicillin-sensitive staphylococcus aureus (MSSA) gives rise to a number of genetically different MRSA lineages. These genetic variations within different MRSA strains possibly explain the variability in virulence and associated MRSA infections.[53] The first MRSA strain, ST250 MRSA-1 originated from SCCmec and ST250-MSSA integration.[53] Historically, major MRSA clones: ST2470-MRSA-I, ST239-MRSA-III, ST5-MRSA-II, and ST5-MRSA-IV were responsible for causing hospital-acquired MRSA (HA-MRSA) infections.[53] ST239-MRSA-III, known as the Brazilian clone, was highly transmissible compared to others and distributed in Argentina, Czech Republic, and Portugal.[53]

In the UK, the most common strains of MRSA are EMRSA15 and EMRSA16.[54] EMRSA16 is the best described epidemiologically: it originated in Kettering, England, and the full genomic sequence of this strain has been published.[55] EMRSA16 has been found to be identical to the ST36:USA200 strain, which circulates in the United States, and to carry the SCCmec type II, enterotoxin A and toxic shock syndrome toxin 1 genes.[56] Under the new international typing system, this strain is now called MRSA252. EMRSA 15 is also found to be one of the common MRSA strains in Asia. Other common strains include ST5:USA100 and EMRSA 1.[57] These strains are genetic characteristics of HA-MRSA.[58]

Community-acquired MRSA (CA-MRSA) strains emerged in late 1990 to 2000, infecting healthy people who had not been in contact with health care facilities.[58] A later study that analyzed data from more than 300 microbiology labs associated with hospitals all over the United States have found a seven-fold increase, jumping from 3.6% of all MRSA infections to 28.2%, in the proportion of community-associated strains of MRSA between 1999 and 2006.[59] Researchers suggest that CA-MRSA did not evolve from the HA-MRSA.[58] This is further proven by molecular typing of CA-MRSA strains[60] and genome comparison between CA-MRSA and HA-MRSA, which indicate that novel MRSA strains integrated SCCmec into MSSA separately on its own.[58] By mid 2000, CA-MRSA was introduced into the health care systems and distinguishing CA-MRSA from HA-MRSA became a difficult process.[58] Community-acquired MRSA (CA-MRSA) is more easily treated and more virulent than hospital-acquired MRSA (HA-MRSA).[58] The genetic mechanism for the enhanced virulence in CA-MRSA remains an active area of research. Especially the Panton–Valentine leukocidin (PVL) genes are of interest because they are a unique feature of CA-MRSA.[53]

In the United States, most cases of CA-MRSA are caused by a CC8 strain designated ST8:USA300, which carries SCCmec type IV, Panton–Valentine leukocidin, PSM-alpha and enterotoxins Q and K,[56] and ST1:USA400.[61] The ST8:USA300 strain results in skin infections, necrotizing fasciitis and toxic shock syndrome, whereas the ST1:USA400 strain results in necrotizing pneumonia and pulmonary sepsis.[53] Other community-acquired strains of MRSA are ST8:USA500 and ST59:USA1000. In many nations of the world, MRSA strains with different predominant genetic background types have come to predominate among CA-MRSA strains; USA300 easily tops the list in the U.S. and is becoming more common in Canada after its first appearance there in 2004. For example, in Australia ST93 strains are common, while in continental Europe ST80 strains, which carry SCCmec type IV, predominate.[62][63] In Taiwan, ST59 strains, some of which are resistant to many non-beta-lactam antibiotics, have arisen as common causes of skin and soft tissue infections in the community. In a remote region of Alaska, unlike most of the continental U.S., USA300 was found rarely in a study of MRSA strains from outbreaks in 1996 and 2000 as well as in surveillance from 2004–06.[64] In 2015, CA-MRSA has been reported in the urban and rural school settings of Kurdistan, Iraq.[3]

A MRSA strain, CC398, is found in intensively reared production animals (primarily pigs, but also cattle and poultry), where it can be transmitted to humans as LA-MRSA (livestock-associated MRSA).[57][65][66]



In health care settings, isolating those with MRSA from those without the infection, is one method to prevent transmission. Rapid culture and sensitivity testing and molecular testing identifies carriers and reduces infection rates.[67]

Surface sanitizing[edit]

Complete surface sanitation is necessary to eliminate MRSA in areas where people are recovering from invasive procedures. Testing people for MRSA upon admission, isolating MRSA-positive people, decolonization of MRSA-positive people, and terminal cleaning of rooms and all other clinical areas occupied by MRSA-positive people is the current best practice protocol for nosocomial MRSA.[citation needed]

Studies published from 2004-2007 reported hydrogen peroxide vapor could be used to decontaminate hospital rooms, despite taking significantly longer than traditional cleaning. One study noted rapid recontamination by MRSA following the hydrogen peroxide application.[68][69][70][71][72]

Metal alloys[edit]

In 2004, the University of Southampton research team was the first to clearly demonstrate that copper inhibits MRSA.[73] On copper alloys — C19700 (99% copper), C24000 (80% copper), and C77000 (55% copper) — significant reductions in viability were achieved at room temperatures after 1.5 hours, 3.0 hours and 4.5 hours, respectively. Faster antimicrobial efficacies were associated with higher copper alloy content. Stainless steel did not exhibit any bactericidal benefits.

Hand washing[edit]

NAV-CO2 sanitizing in Pennsylvania hospital exam room

The CDC offers suggestions for preventing the contraction and spread MRSA infection which are applicable to those in community settings, including incarcerated populations, childcare center employees, and athletes. To prevent the spread of MRSA the recommendations are to wash hands using soap and water or an alcohol-based sanitizer. Additional recommendations are to keep wounds clean and covered, avoid contact with other people's wounds, avoid sharing personal items such as razors or towels, shower after exercising at athletic facilities, and shower before using swimming pools or whirlpools.[74]

In September 2004, the UK National Health Service announced its Clean Your Hands campaign. It was recommended that alcohol-based hand rubs be placed near beds to encourage staff to use the sanitizer more regularly. It was thought that even if this cuts infection by no more than 1%, the plan will pay for itself many times over.[75]


Excluding medical facilities, current US guidance does not require workers with MRSA infections to be routinely excluded from the general workplace.[76] Therefore, unless directed by a health care provider, exclusion from work should be reserved for those with wound drainage that cannot be covered and contained with a clean, dry bandage and for those who cannot maintain good hygiene practices.[76] Workers with active infections should be excluded from activities where skin-to-skin contact is likely to occur until their infections are healed. Health care workers should follow the Centers for Disease Control and Prevention's Guidelines for Infection Control in Health Care Personnel.[77]

To prevent the spread of staph or MRSA in the workplace, employers should ensure the availability of adequate facilities and supplies that encourage workers to practice good hygiene; that surface sanitizing in the workplace is followed; and that contaminated equipment are sanitized with Environmental Protection Agency (EPA)-registered disinfectants.[76]

Restricting antibiotic use[edit]

Glycopeptides, cephalosporins, and, in particular, quinolones are associated with an increased risk of colonisation of MRSA. Reducing use of antibiotic classes that promote MRSA colonisation, especially fluoroquinolones, is recommended in current guidelines.[13][22]

Public health considerations[edit]

The burden of MRSA is significant. In 2009, there were an estimated 463,017 (95% confidence interval: 441,595, 484,439) MRSA-related hospitalizations, or a rate of 11.74 (95% confidence interval: 11.20, 12.28) per 1,000 hospitalizations.[78] Many of these infections are less serious, but the Centers for Disease Control and Prevention (CDC) estimates that there are 80,461 invasive MRSA infections and 11,285 deaths due to MRSA annually.[79]

Mathematical models describe one way in which a loss of infection control can occur after measures for screening and isolation seem to be effective for years, as happened in the UK. In the "search and destroy" strategy that was employed by all UK hospitals until the mid-1990s, all hospitalized people with MRSA were immediately isolated, and all staff were screened for MRSA and were prevented from working until they had completed a course of eradication therapy that was proven to work. Loss of control occurs because colonised people are discharged back into the community and then readmitted; when the number of colonised people in the community reaches a certain threshold, the "search and destroy" strategy is overwhelmed.[80] One of the few countries not to have been overwhelmed by MRSA is the Netherlands: An important part of the success of the Dutch strategy may have been to attempt eradication of carriage upon discharge from hospital.[81]

The Centers for Disease Control and Prevention (CDC) estimated that about 1.7 million nosocomial infections occurred in the United States in 2002, with 99,000 associated deaths.[82] The estimated incidence is 4.5 nosocomial infections per 100 admissions, with direct costs (at 2004 prices) ranging from $10,500 (£5300, €8000 at 2006 rates) per case (for bloodstream, urinary tract, or respiratory infections in immunocompetent people) to $111,000 (£57,000, €85,000) per case for antibiotic-resistant infections in the bloodstream in people with transplants. With these numbers, conservative estimates of the total direct costs of nosocomial infections are above $17 billion. The reduction of such infections forms an important component of efforts to improve healthcare safety. (BMJ 2007)[citation needed] MRSA alone was associated with 8% of nosocomial infections reported to the CDC National Healthcare Safety Network from January 2006 to October 2007.[83]

This problem is not unique to one country; the British National Audit Office estimated that the incidence of nosocomial infections in Europe ranges from 4% to 10% of all hospital admissions. As of early 2005, the number of deaths in the United Kingdom attributed to MRSA has been estimated by various sources to lie in the area of 3,000 per year.[84] Staphylococcus bacteria account for almost half of all UK hospital infections. The issue of MRSA infections in hospitals has recently been a major political issue in the UK, playing a significant role in the debates over health policy in the United Kingdom general election held in 2005.

On January 6, 2008, half of 64 non-Chinese cases of MRSA infections in Hong Kong in 2007 were Filipino domestic helpers. Ho Pak-leung, professor of microbiology at the University of Hong Kong, traced the cause to high use of antibiotics. In 2007, there were 166 community cases in Hong Kong compared with 8,000 hospital-acquired MRSA cases (155 recorded cases—91 involved Chinese locals, 33 Filipinos, 5 each for Americans and Indians, and 2 each from Nepal, Australia, Denmark and England).[85]

Worldwide, an estimated 2 billion people carry some form of S. aureus; of these, up to 53 million (2.7% of carriers) are thought to carry MRSA.[86] In the United States, 95 million carry S. aureus in their noses; of these, 2.5 million (2.6% of carriers) carry MRSA.[87] A population review conducted in three U.S. communities showed the annual incidence of CA-MRSA during 2001–2002 to be 18–25.7/100,000; most CA-MRSA isolates were associated with clinically relevant infections, and 23% of people required hospitalization.[88]

One possible contribution to the increased spread of MRSA infections comes from the use of antibiotics in intensive pig farming. A 2008 study in Canada found MRSA in 10% of tested pork chops and ground pork; a U.S. study in the same year found MRSA in the noses of 70% of the tested farm pigs and in 45% of the tested pig farm workers.[89] There have also been anecdotal reports of increased MRSA infection rates in rural communities with pig farms.[90]


Care should be taken when trying to drain boils, as disruption of surrounding tissue can lead to larger infections, or even infection of the blood stream (often with fatal consequences).[91] Any drainage should be disposed of very carefully. After the drainage of boils or other treatment for MRSA, people can shower at home using chlorhexidine (Hibiclens) or hexachlorophene (Phisohex) antiseptic soap (available over-the-counter at many pharmacies) from head to toe.[citation needed] Alternatively, a dilute bleach bath can be taken at a concentration of 2.5 μL/mL dilution of bleach (about 1/2 cup bleach per 1/4-full bathtub of water).[92] Care should be taken to use a clean towel, and to ensure that nasal discharge doesn't infect the towel (see below).

All infectious lesions should be kept covered with a dressing.[91] Mupirocin (Bactroban) 2% ointment can be effective at reducing the size of lesions. A secondary covering of clothing is preferred.[93] As shown in an animal study with diabetic mice, the topical application of a mixture of sugar (70%) and 3% povidone-iodine paste is an effective agent for the treatment of diabetic ulcers with MRSA infection.[94]

The nose is a common refuge for MRSA, and a test swab can be taken of the nose to indicate whether MRSA is present.[95] If MRSA is detected via nasal culture, Mupirocin (Bactroban) 2% ointment can be applied inside each nostril twice daily for 7 days, using a cotton-tipped swab. However, care should be taken so that the swab doesn't penetrate into the sinus. Household members are recommended to follow the same decolonization protocol. After treatment, the nose should be swabbed again to ensure that the treatment was effective. If not, the process should be repeated.

In the hospital setting toilet seats are a common vector for infection, and wiping seats clean before and/or after use can help to prevent the spread of MRSA. Door handles, faucets, light switches, etc. can be disinfected regularly with disinfectant wipes.[93] Spray disinfectants can be used on upholstery. Carpets can be washed with disinfectant, and hardwood floors can be scrubbed with diluted tea tree oil (e.g. Melaleuca). Laundry soap containing tea tree oil may be effective at decontaminating clothing and bedding, especially if hot water and heavy soil cycles are used, however tea tree oil may cause a rash which MRSA can re-colonize. Alcohol-based sanitizers can be placed near bedsides, near sitting areas, in vehicles etc. to encourage their use.

Doctors may also prescribe antibiotics such as clindamycin, doxycycline, or trimethoprim/sulfamethoxazole.

Community settings[edit]

It may be difficult for people to maintain the necessary cleanliness if they do not have access to facilities such as public toilets with handwashing facilities. In the United Kingdom, the Workplace (Health, Safety and Welfare) Regulations 1992 requires businesses to provide toilets for their employees, along with washing facilities including soap or other suitable means of cleaning. Guidance on how many toilets to provide and what sort of washing facilities should be provided alongside them is given in the Workplace (Health, Safety and Welfare) Approved Code of Practice and Guidance L24, available from Health and Safety Executive Books. But there is no legal obligation on local authorities in the United Kingdom to provide public toilets, and although in 2008 the House of Commons Communities and Local Government Committee called for a duty on local authorities to develop a public toilet strategy[96] this was rejected by the Government.[97]


Some advocate regulations on the use of antibiotics in animal food to prevent the emergence of drug resistant strains of MRSA.[25] MRSA is established in animals.[19]


Livestock associated MRSA has been observed in Korea, Brazil, Switzerland, Malaysia, India, Great Britain, Denmark, and China.[19]

In a US cohort of 1300 healthy children, 2.4% carried MRSA in their nose.[98]


Treatment is urgent because delays in administering antibiotics results in the likelihood of an infection resulting in death.[99] Both CA-MRSA and HA-MRSA are resistant to traditional anti-staphylococcal beta-lactam antibiotics, such as cephalexin. CA-MRSA has a greater spectrum of antimicrobial susceptibility to sulfa drugs (like co-trimoxazole (trimethoprim/sulfamethoxazole)), tetracyclines (like doxycycline and minocycline) and clindamycin (for osteomyelitis) The drug of choice for treating CA-MRSA is now believed to be vancomycin. HA-MRSA is resistant even to these antibiotics and often is susceptible only to vancomycin. Newer drugs, such as linezolid (belonging to the newer oxazolidinones class) and daptomycin, are effective against both CA-MRSA and HA-MRSA. The Infectious Disease Society of America recommends vancomycin, linezolid, or clindamycin (if susceptible) for treating people with MRSA pneumonia.[100] Ceftaroline, a fifth-generation cephalosporin, is the first beta-lactam antibiotic approved in the US to treat MRSA infections (skin and soft tissue or community acquired pneumonia only).[101]

Vancomycin and teicoplanin are glycopeptide antibiotics used to treat MRSA infections.[102] Teicoplanin is a structural congener of vancomycin that has a similar activity spectrum but a longer half-life.[103] Because the oral absorption of vancomycin and teicoplanin is very low, these agents must be administered intravenously to control systemic infections.[104] Treatment of MRSA infection with vancomycin can be complicated, due to its inconvenient route of administration. Moreover, many clinicians believe that the efficacy of vancomycin against MRSA is inferior to that of anti-staphylococcal beta-lactam antibiotics against methicillin-susceptible Staphylococcus aureus (MSSA).[105][106]

Several newly discovered strains of MRSA show antibiotic resistance even to vancomycin and teicoplanin. These new evolutions of the MRSA bacterium have been dubbed vancomycin intermediate-resistant Staphylococcus aureus (VISA).[107] [108] Linezolid, quinupristin/dalfopristin, daptomycin, ceftaroline, and tigecycline are used to treat more severe infections that do not respond to glycopeptides such as vancomycin.[109] Current guidelines recommend daptomycin for VISA bloodstream infections and endocarditis.[110]


United States and United Kingdom[edit]

Incidence of MRSA in human blood samples in countries which took part in the study in 2008

A 1,000-year-old eye salve recipe found in the medieval Bald's Leechbook at the British Library, one of the earliest known medical textbooks, was found to have activity against MRSA in vitro and in skin wounds in mice.[111]

In 1959 methicillin was licensed in England to treat penicillin-resistant S. aureus infections. Just as bacterial evolution had allowed microbes to develop resistance to penicillin, strains of S. aureus evolved to become resistant to methicillin. In 1961 the first known MRSA isolates were reported in a British study, and from 1961 to 1967 there were infrequent hospital outbreaks in Western Europe and Australia.[112] The first United States hospital outbreak of MRSA occurred at the Boston City Hospital in 1968. From 1968 to the mid-1990s the percent of S. aureus infections that were caused by MRSA increased steadily, and MRSA became recognized as an endemic pathogen. In 1974 2% of hospital-acquired S. aureus infections could be attributed to MRSA.[113] The rate had increased to 22% by 1995, and by 1997 the percent of hospital S. aureus infections attributable to MRSA had reached 50%.

The first report of community-associated MRSA (CA-MRSA) occurred in 1981, and in 1982 there was a large outbreak of CA-MRSA among intravenous drug users in Detroit, Michigan.[112] Additional outbreaks of CA-MRSA were reported through the 1980s and 1990s, including outbreaks among Australian Aboriginal populations that had never been exposed to hospitals. In the mid-1990s there were scattered reports of CA-MRSA outbreaks among US children. While HA-MRSA rates stabilized between 1998 and 2008, CA-MRSA rates continued to rise. A report released by the University of Chicago Children's Hospital comparing two time periods (1993–1995 and 1995–1997) found a 25-fold increase in the rate of hospitalizations due to MRSA among children in the United States.[114] In 1999 the University of Chicago reported the first deaths from invasive MRSA among otherwise healthy children in the United States.[112] By 2004 MRSA accounted for 64% of hospital-acquired S. aureus infections in the United States.

The Office for National Statistics reported 1,629 MRSA-related deaths in England and Wales during 2005, indicating a MRSA-related mortality rate half the rate of that in the United States for 2005, even though the figures from the British source were explained to be high because of "improved levels of reporting, possibly brought about by the continued high public profile of the disease"[115] during the time of the 2005 United Kingdom General Election. MRSA is thought to have caused 1,652 deaths in 2006 in UK up from 51 in 1993.[116]

It has been argued that the observed increased mortality among MRSA-infected people may be the result of the increased underlying morbidity of these people. Several studies, however, including one by Blot and colleagues, that have adjusted for underlying disease still found MRSA bacteremia to have a higher attributable mortality than methicillin-susceptible S. aureus (MSSA) bacteremia.[117]

A population-based study of the incidence of MRSA infections in San Francisco during 2004–05 demonstrated that nearly 1 in 300 residents suffered from such an infection in the course of a year and that greater than 85% of these infections occurred outside of the healthcare setting.[118] A 2004 study showed that people in the United States with S. aureus infection had, on average, three times the length of hospital stay (14.3 vs. 4.5 days), incurred three times the total cost ($48,824 vs. $14,141), and experienced five times the risk of in-hospital death (11.2% vs 2.3%) than people without this infection.[119] In a meta-analysis of 31 studies, Cosgrove et al.,[120] concluded that MRSA bacteremia is associated with increased mortality as compared with MSSA bacteremia (odds ratio= 1.93; 95% CI = 1.93 ± 0.39).[121] In addition, Wyllie et al. report a death rate of 34% within 30 days among people infected with MRSA, a rate similar to the death rate of 27% seen among MSSA-infected people.[122]

In the US, the Centers for Disease Control and Prevention issued guidelines on October 19, 2006, citing the need for additional research, but declined to recommend such screening.[123]

According to the CDC, the most recent estimates of the incidence of healthcare-associated infections that are attributable to MRSA in the United States indicate a decline in such infection rates. Incidence of MRSA central line-associated blood stream infections as reported by hundreds of intensive care units decreased 50–70% from 2001–2007.[113] A separate system tracking all hospital MRSA bloodstream infections found an overall 34% decrease between 2005–2008.[113]

MRSA is sometimes sub-categorised as community-acquired MRSA (CA-MRSA) or healthcare-associated MRSA (HA-MRSA), although the distinction is complex. Some researchers have defined CA-MRSA by the characteristics of people whom it infects, while others define it by the genetic characteristics of the bacteria. By 2005, identified CA-MRSA risk factors included athletes, military recruits, incarcerated people, people in emergency rooms, urban children, HIV-positive individuals, men who have sex with men, and indigenous populations.[112]

By 2015 the proportion of resistant infections in the UK had dropped from 40% down to about 15% a result of intense efforts in hospital hygiene.[124]


The first reported cases of CA-MRSA began to appear in the mid-1990s in Australia, New Zealand, the United States, the United Kingdom, France, Finland, Canada and Samoa, and were notable because they involved people who had not been exposed to a healthcare setting.[8]

Because measurement and reporting varies, it is difficult to compare rates of MRSA in different countries. An international comparison of 2004 MRSA-attributable S. aureus rates in middle and high income countries released by the Center For Disease Dynamics, Economics, and Policy in showed that Iceland had the lowest rate of infection, and Romania had the highest at over 70%.[125]

Across Europe, based mostly on data from 2013 seven countries (Iceland, Norway, Sweden, Netherlands, Denmark, Finland, and Estonia, from lowest to higher) had low levels of hospital-acquired MRSA infections compared to the others,[126]:92–93 and among countries with higher levels significant improvements had been made only in Bulgaria, Poland and the British Isles.[126]:40


  • The herbs daphne genkwa and Olresin both have shown to have constitiuents in them that when combined with traditional antibiotics elicit a strong response against MRSA infections.[127]

Additional images[edit]

See also[edit]


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  • Ficalora, Robert (2013). Mayo Clinic internal medicine board review. Oxford: Oxford University Press. ISBN 9780199948949. 
  • Karch, Amy (2017). Focus on nursing pharmacology. Philadelphia: Wolters Kluwer. ISBN 9781496318213. 
  • Vallerand, April (2017). Davis's drug guide for nurses. Philadelphia: F.A. Davis Company. ISBN 9780803657052. 

Further reading[edit]