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Antimicrobial Susceptibility Pattern and Biochemical Characteristics of Staphylococcus aureus: Impact of Biofield Treatment


Study background: Staphylococci are widespread in nature, mainly found on the skin and mucous membranes. Staphylococcus aureus (S. aureus) is the key organism for food poisoning due to massive production of heat stable exotoxins. The current study was attempted to investigate the effect of biofield treatment on antimicrobial susceptibility pattern and biochemical characteristics of S. aureus (ATCC 25923).

Methods: S. aureus cells were procured from MicroBioLogics in sealed packs bearing the American Type Culture Collection (ATCC 25923) number and stored according to the recommended storage protocols until needed for experiments. Revived and lyophilized state of ATCC strains of S. aureus were selected for the study. Both revived (Group; Gr. II) and lyophilized (Gr. III) strain of S. aureus were subjected to Mr. Trivedi’s biofield treatment. Revived treated cells were assessed on day 5 and day 10 while lyophilized treated cells on day 10 only. After biofield treatment both treated cells were analysed for its antimicrobial sensitivity, minimum inhibitory concentration value, biochemical reactions and biotype number with respect to control (Gr. I).

Results: The antimicrobial susceptibility and minimum inhibitory concentration of S. aureus showed significant (86.67%) alteration in lyophilized cells while no alteration was found in revived treated cells as compared to control. It was observed that overall 37.93% (eleven out of twenty nine) biochemical reactions were altered in the treated groups with respect to control. Moreover, biotype numbers were substantially changed in revived treated cells, Gr. II (303137, Staphylococcus capitis subsp. ureolyticus) on day 5 and in lyophilized treated cells, Gr. III (767177, S. cohnii subsp. urealyticum) on day 10 as compared to control (307016, S. aureus).

Conclusion: The result suggested that biofield treatment has significant impact on S. aureus in lyophilized treated cells with respect to antimicrobial susceptibility, MIC values and biochemical reactions pattern. Apart from these, biotype numbers with new species were observed in revived treated group on day 5 as Staphylococcus capitis subsp. ureolyticus and in lyophilized cells as Staphylococcus cohnii subsp. urealyticum with respect to control, i.e., S. aureus.

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Antibiogram, Biochemical Reactions and Genotyping Characterization of Biofield Treated Staphylococcus aureus


Staphylococcus aureus (S. aureus) is the key organism for food poisoning due to massive production of heat stable exotoxins. The current study was attempted to investigate the effect of Mr. Trivedi’s biofield treatment on S. aureus. S. aureus (ATCC 25923) was divided into two parts, Group (Gr.) I: control and Gr. II: treatment. After biofield treatment, Gr. II was further subdivided into two parts, Gr. IIA and Gr. IIB. Gr. IIA was analyzed on day 10, while Gr. IIB was stored and analyzed on day 159 after revival (Study I). The revived sample (Gr. IIB) were retreated on day 159 (Study II), and divided into three separate tubes. Tube 1 was analyzed on day 5, likewise, tube 2 and 3 were analyzed on day 10 and 15, respectively. All the experimental parameters were studied using automated MicroScan Walk-Away® system. The 16S rDNA sequencing was carried out in Gr. IIA sample to correlate the phylogenetic relationship of S. aureus with other bacterial species. The antimicrobial susceptibility and minimum inhibitory concentration showed significant alteration i.e. 92.86% and 90.00% respectively in treated cells of S. aureus as compared to control. The biochemical reactions also showed the significant (35.71%) alteration in treated sample with respect to control. The biotype number and microbial species were substantially changed in Gr. IIA (767177; Staphylococcus cohnii subsp. urealyticum) on day 10, while only the biotype numbers were changed in rest of the treated samples as compared to control (307016; S. aureus). The 16S rDNA analysis showed that the identified strain in this experiment was S. aureus (GenBank Accession No.: L37597) after biofield treatment. However, the nearest homolog genus-species was found as Staphylococcus simiae (GenBank Accession No.: DQ127902). These results suggested that biofield treatment has a significant impact on S. aureus in lyophilized as well as revived state.

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Under a microscope, staph bacteria look like bunches of grapes. Yet what looks pretty can turn ugly fast. Harmless Staphylococcus aureus lives in many people’s noses and on their skin. But it sometimes causes pus-filled boils and other skin infections. When eaten in tainted food, it can cause food poisoning. Staphylococcus aureus shows looks really can be deceiving.

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Methicillin-resistant Staphylococcus aureus

"MRSA" redirects here. For other uses, see MRSA (disambiguation).

Methicillin-resistant Staphylococcus aureus (MRSA) (/ˈmɜrsə/ or /ɛmɑrɛs/) is a bacterium responsible for several difficult-to-treat infections in humans. It is also called oxacillin-resistant Staphylococcus aureus (ORSA).[1] MRSA is any strain of Staphylococcus aureus that has developed, through the process of natural selection, resistance to beta-lactam antibiotics, which include the penicillins (methicillin, dicloxacillin, nafcillin, oxacillin, etc.) and the cephalosporins. Strains unable to resist these antibiotics are classified as methicillin-sensitive 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 especially troublesome in hospitals, prisons, and nursing homes, where patients with open wounds, invasive devices, and weakened immune systems are at greater risk of nosocomial infection than the general public. MRSA began as a hospital-acquired infection, but has developed limited endemic status and is now sometimes community-acquired. The terms HA-MRSA (healthcare-associated MRSA) and CA-MRSA (community-associated MRSA) reflect this distinction.

Signs and symptoms[edit]

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

In most patients, MRSA can 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 patients, swab screening patients admitted to hospitals has been found to be effective in minimizing the spread of MRSA in hospitals in the United States,[3] Denmark, Finland, and the Netherlands.[4]

MRSA may progress substantially within 24–48 hours of initial topical symptoms. 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 ("flesh-eating") 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 very commonly 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, infective endocarditis (which affects the valves of the heart), and bone 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:

Hospital patients[edit]

Many MRSA infections occur in hospitals and healthcare facilities. Infections occurring in this manner are known as healthcare acquired MRSA (HA-MRSA). The rates of MRSA infection are also increased in hospitalized patients who are treated with quinolones. 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][19] Online tools predicting probability of nasal carriage in hospital admissions are available.[20]

Prison inmates, military recruits, and the homeless[edit]

Prisons, military barracks, and homeless shelters 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. Subsequent reports of a massive rise in skin and soft tissue infections were reported by the CDC in the Los Angeles County Jail system in 2001, and this has continued. Pan et al. reported on the changing epidemiology of MRSA skin infection in the San Francisco County Jail, noting MRSA accounted for more than 70% of S. aureus infection in the jail by 2002. Lowy and colleagues reported on frequent MRSA skin infections in New York state prisons. Two reports on inmates in Maryland have demonstrated frequent colonization with MRSA.

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.[21] 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.


Cases of MRSA have increased in livestock animals. CC398, a new variant of MRSA, has emerged in animals and is found in intensively reared production animals (primarily pigs, but also cattle and poultry), where it can be transmitted to humans. Though dangerous to humans, CC398 is often asymptomatic in food-producing animals.[22] In a single study conducted in Denmark, MRSA was shown to originate in livestock and spread to humans,[23] though the MRSA strain may have originated in humans and was transmitted to livestock.[24]

A 2011 study reported 47% of the meat and poultry sold in surveyed U.S. grocery stores was contaminated with S. aureus, and of those, 52% — or 24.4% of the total — were resistant to at least three classes of antibiotics. "Now we need to determine what this means in terms of risk to the consumer," said Dr. Keim, a co-author of the paper.[25] Some samples of commercially sold meat products in Japan were also found to harbor MRSA strains.[26]


Locker rooms, gyms, and related athletic facilities offer potential sites for MRSA contamination and infection.[27] 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]


MRSA is becoming a critical problem in pediatric settings;[31] recent studies found 4.6% of patients in U.S. health-care facilities, (presumably) including hospital nurseries,[32] were infected or colonized with MRSA.[33] Children (and adults, as well) who come in contact with day-care centers, 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.[34]


A selective and differential chromogenic medium for the qualitative direct detection of MRSA.
The MRSA resistance to oxcacillin 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.[35] 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.[36][37]

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.[38]


Antimicrobial resistance is genetically based; resistance is mediated by the acquisition of extrachromosomal genetic elements containing resistance genes. Exemplary are plasmids, transposable genetic elements, and genomic islands, which are transferred between bacteria by horizontal gene transfer.[39] 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.


Staphylococcal cassette chromosome mec (SCCmec) is a genomic island of unknown origin containing the antibiotic resistance gene mecA.[40][41] SCCmec contains additional genes beyond mecA, including the cytolysin gene psm-mec, which may suppress virulence in HA-acquired MRSA strains.[42] 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.[40][41] Currently, six unique SCCmec types ranging in size from 21–67 kb have been identified;[40] they are designated types I-VI and are distinguished by variation in mec and ccr gene complexes.[39] Owing to the size of the SCCmec element and the constraints of horizontal gene transfer, a limited number of clones is thought to be responsible for the spread of MRSA infections.[40]

Different SCCmec genotypes confer different microbiological characteristics, such as different antimicrobial resistance rates.[43] 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.[41][43] Conversely, CA-MRSA is associated with types IV and V, which are smaller and lack resistance genes other than mecA.[41][43]


mecA is responsible for resistance to methicillin and other β-lactam antibiotics. After acquisition of mecA, the gene must be integrated and localized in the S. aureus chromosome.[40] 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.[40] 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.[40][44]

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.[39][41] In the presence of a β-lactam antibiotic, MecR1 initiates a signal transduction cascade that leads to transcriptional activation of mecA.[39][41] This is achieved by MecR1-mediated cleavage of MecI, which alleviates MecI repression.[39] 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.[40][45] The DNA sequences bound by MecI and BlaI are identical;[40] therefore, BlaI can also bind the mecA operator to repress transcription of mecA.[45]

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.[46] 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.[47] The first MRSA strain, ST250 MRSA-1 originated from SCCmec and ST250-MSSA integration.[47] 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.[47] ST239-MRSA-III, known as the Brazilian clone, was highly transmissible compared to others and distributed in Argentina, Czech Republic, and Portugal.[47]

In the UK, the most common strains of MRSA are EMRSA15 and EMRSA16.[48] EMRSA16 is the best described epidemiologically: it originated in Kettering, England, and the full genomic sequence of this strain has been published.[49] 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.[50] 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.[51] These strains are genetic characteristics of HA-MRSA.[52]

It is not entirely certain why some strains are highly transmissible and persistent in healthcare facilities.[47] One explanation is the characteristic pattern of antibiotic susceptibility. Both the EMRSA15 and EMRSA16 strains are resistant to erythromycin and ciprofloxacin. It is known that Staphylococcus aureus can survive intracellularly,[53] for example in the nasal mucosa [54] and in the tonsil tissue.[55] Erythromycin and ciprofloxacin are precisely the antibiotics that best penetrate intracellularly; it may be that these strains of S. aureus are therefore able to exploit an intracellular niche.

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.[52] 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.[56] Researchers suggest that CA-MRSA did not evolve from the HA-MRSA.[52] This is further proven by molecular typing of CA-MRSA strains[57] and genome comparison between CA-MRSA and HA-MRSA, which indicate that novel MRSA strains integrated SCCmec into MSSA separately on its own.[52] By mid 2000, CA-MRSA was introduced into the health care systems and distinguishing CA-MRSA from HA-MRSA became a difficult process.[52] Community-acquired MRSA (CA-MRSA) is more easily treated and more virulent than hospital-acquired MRSA (HA-MRSA).[52] 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.[47]

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,[50] and ST1:USA400.[58] 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.[47] 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.[59][60] 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.[61]

In June 2011, the discovery of a new strain of MRSA was announced by two separate teams of researchers in the UK. Its genetic makeup was reportedly more similar to strains found in animals, and testing kits designed to detect MRSA were unable to identify it.[62] This MRSA strain, Clonal Complex 398 (CC398), is responsible for Livestock-associated MRSA (LA-MRSA) infections.[51] Although it is known to be more persistent in colonizing pigs and calves, there have been cases of LA-MRSA carriers with pneumonia, endocarditis, and necrotising fasciitis.[63]


Screening programs[edit]

Patient screening upon hospital admission, with nasal cultures, prevents the cohabitation of MRSA carriers with non-carriers, and exposure to infected surfaces. The test used (whether a rapid molecular method or traditional culture) is not as important as the implementation of active screening.[64] In the United States and Canada, 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.[65][66]

In some UK hospitals screening for MRSA is performed in every patient[67] and all NHS surgical patients, except for minor surgeries, are previously checked for MRSA.[68] There is no community screening in the UK; however, screening of individuals is offered by some private companies.[69]

In a US cohort of 1300 healthy children, 2.4% carried MRSA in their nose.[70]

Surface sanitizing[edit]

NAV-CO2 sanitizing in Pennsylvania hospital exam room

Alcohol has been proven to be an effective surface sanitizer against MRSA. Quaternary ammonium can be used in conjunction with alcohol to extend the longevity of the sanitizing action.[citation needed] The prevention of nosocomial infections involves routine and terminal cleaning. Non-flammable Alcohol Vapor in Carbon Dioxide systems (NAV-CO2) do not corrode metals or plastics used in medical environments and do not contribute to antibacterial resistance.

In healthcare environments, MRSA can survive on surfaces and fabrics, including privacy curtains or garments worn by care providers. Complete surface sanitation is necessary to eliminate MRSA in areas where patients are recovering from invasive procedures. Testing patients for MRSA upon admission, isolating MRSA-positive patients, decolonization of MRSA-positive patients, and terminal cleaning of patients' rooms and all other clinical areas they occupy is the current best practice protocol for nosocomial MRSA.

Studies published from 2004-2007 reported hydrogen peroxide vapor could be used to decontaminate busy hospital rooms, despite taking significantly longer than traditional cleaning. One study noted rapid recontamination by MRSA following the hydrogen peroxide application.[71][72][73][74][75]

Also tested, in 2006, was a new type of surface cleaner, incorporating accelerated hydrogen peroxide, which was pronounced "a potential candidate" for use against the targeted microorganisms.[76]

Research on copper alloys[edit]

In 2008, after evaluating a wide body of research mandated specifically by the United States Environmental Protection Agency (EPA), registration approvals were granted by EPA in 2008 granting that copper alloys kill more than 99.9% of MRSA within two hours.

Subsequent research conducted at the University of Southampton (UK) compared the antimicrobial efficacies of copper and several non-copper proprietary coating products to kill MRSA.[77][78] At 20 °C, the drop-off in MRSA organisms on copper alloy C11000 is dramatic and almost complete (over 99.9% kill rate) within 75 minutes. However, neither a triclosan-based product nor two silver-containing based antimicrobial treatments (Ag-A and Ag-B) exhibited any meaningful efficacy against MRSA. Stainless steel S30400 did not exhibit any antimicrobial efficacy.

In 2004, the University of Southampton research team was the first to clearly demonstrate that copper inhibits MRSA.[79] 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]

In September 2004,[80] after a successful pilot scheme to tackle MRSA, the UK National Health Service announced its Clean Your Hands campaign. Wards were required to ensure that alcohol-based hand rubs are placed near all beds so that staff can hand wash more regularly. It is thought that even if this cuts infection by no more than 1%, the plan will pay for itself many times over.[citation needed]

As with some other bacteria, MRSA is acquiring more resistance to some disinfectants and antiseptics. Although alcohol-based rubs remain somewhat effective, a more effective strategy is to wash hands with running water and an anti-microbial cleanser with persistent killing action, such as Chlorhexidine.[81] In another study chlorhexidine (Hibiclens), p-chloro-m-xylenol (Acute-Kare), hexachlorophene (Phisohex), and povidone-iodine (Betadine) were evaluated for their effectiveness. Of the four most commonly used antiseptics, povidone-iodine, when diluted 1:100, was the most rapidly bactericidal against both MRSA and methicillin-susceptible S. aureus.[82]

A June 2008 report, centered on a survey by the Association for Professionals in Infection Control and Epidemiology, concluded that poor hygiene habits remain the principal barrier to significant reductions in the spread of MRSA.

Proper disposal of hospital gowns[edit]

Used paper hospital gowns are associated with MRSA hospital infections, which could be avoided by proper disposal.[83]


Excluding medical facilities, current US guidance does not require workers with MRSA infections to be routinely excluded from the general workplace.[84] 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.[84] 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.[85]

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.[84]

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][19]

Public health considerations[edit]

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 patients 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 patients are discharged back into the community and then readmitted; when the number of colonised patients in the community reaches a certain threshold, the "search and destroy" strategy is overwhelmed.[86] 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.[87]

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.[88] 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 patients) to $111,000 (£57,000, €85,000) per case for antibiotic-resistant infections in the bloodstream in patients 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.[89]

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.[90] 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).[91]

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.[92] In the United States, 95 million carry S. aureus in their noses; of these, 2.5 million (2.6% of carriers) carry MRSA.[93] 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 patients required hospitalization.[94]

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.[95] There have also been anecdotal reports of increased MRSA infection rates in rural communities with pig farms.[96]

Healthcare facilities with high bed occupancy rates, high levels of temporary nursing staff, or low cleanliness scores no longer have significantly higher MRSA rates. Simple tabular evidence helps provide a clear picture of these changes, showing, for instance, that hospitals with occupancy over 90% had, in 2006–2007, MRSA rates little above those in hospitals with occupancy below 85%, in contrast to the period 2001–2004. In one sense, the disappearance of these relationships is puzzling. Reporters now blame IV cannula and catheters for spreading MRSA in hospitals. (Hospital organisation and speciality mix, 2008)[citation needed]


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).[97] Any drainage should be disposed of very carefully. After the drainage of boils or other treatment for MRSA, patients can shower at home using chlorhexidine (Hibiclens) or hexachlorophene (Phisohex) antiseptic soap (available over-the-counter at many pharmacies) from head to toe. 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).[98] 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.[97] Mupirocin (Bactroban) 2% ointment can be effective at reducing the size of lesions. A secondary covering of clothing is preferred.[99] 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.[100]

The nose is a common refuge for MRSA, and a test swab can be taken of the nose to indicate whether MRSA is present.[101] 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 (with care!), etc. can be disinfected regularly with disinfectant wipes.[99] 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]

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 MRSA infection, individuals should regularly wash hands using soap and water or an alcohol-based sanitizer, 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 (including gyms, weight rooms, and school facilities), shower before using swimming pools or whirlpools, and maintain a clean environment.[102]

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 [103] this was rejected by the Government.[104]


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, including to sulfa drugs (like co-trimoxazole/trimethoprim-sulfamethoxazole), tetracyclines (like doxycycline and minocycline) and clindamycin (for osteomyelitis), but the drug of choice for treating CA-MRSA is now believed to be vancomycin, according to a Henry Ford Hospital Study. 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 patients with MRSA pneumonia.[105] 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).[106]

Vancomycin and teicoplanin are glycopeptide antibiotics used to treat MRSA infections.[107] Teicoplanin is a structural congener of vancomycin that has a similar activity spectrum but a longer half-life.[108] Because the oral absorption of vancomycin and teicoplanin is very low, these agents must be administered intravenously to control systemic infections.[109] 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).[110][111]

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).[112] [113] Linezolid, quinupristin/dalfopristin, daptomycin, ceftaroline, and tigecycline are used to treat more severe infections that do not respond to glycopeptides such as vancomycin.[114] Current guidelines recommend daptomycin for VISA bloodstream infections and endocarditis.[115]

Studies suggest that allicin, a compound found in garlic, may prove to be effective in the treatment of MRSA.[116]

In 2015, a medieval treatment for eye infections [117] was found to almost completely wipe out MRSA, according to a BBC report on a recent experiment from the University of Nottingham.


US and UK[edit]

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

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 between 1961-1967 there were infrequent hospital outbreaks in Western Europe and Australia.[118] The first United States hospital outbreak of MRSA occurred at the Boston City Hospital in 1968. Between 1968-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.[119] 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 CA-MRSA occurred in 1981, and in 1982 there was a large outbreak of CA-MRSA among intravenous drug users in Detroit, Michigan.[118] 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 1998–2008, 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.[120] In 1999 the University of Chicago reported the first deaths from invasive MRSA among otherwise healthy children in the United States.[118] 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"[121] 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.[122]

It has been argued that the observed increased mortality among MRSA-infected patients may be the result of the increased underlying morbidity of these patients. 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.[123]

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.[124] A 2004 study showed that patients 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 patients without this infection.[125] In a meta-analysis of 31 studies, Cosgrove et al.,[126] concluded that MRSA bacteremia is associated with increased mortality as compared with MSSA bacteremia (odds ratio = 1.93; 95% CI = 1.93 ± 0.39).[127] In addition, Wyllie et al. report a death rate of 34% within 30 days among patients infected with MRSA, a rate similar to the death rate of 27% seen among MSSA-infected patients.[128]

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.[119] A separate system tracking all hospital MRSA bloodstream infections found an overall 34% decrease between 2005–2008.[119]

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 patients whom it infects, while others define it by the genetic characteristics of the bacteria themselves. By 2005, identified CA-MRSA risk factors included athletes, military recruits, incarcerated people, emergency room patients, urban children, HIV-positive individuals,and indigenous populations.[118]


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%.[129]



Many antibiotics against MRSA are in phase II and phase III clinical trials. e.g.:

Development of Aurograb, a treatment intended to complement antibiotics used to treat MRSA, was discontinued after showing a lack of efficacy in Phase II trials.[131]

It has been reported that maggot therapy to clean out necrotic tissue of MRSA infection has been successful. Studies in diabetic patients reported significantly shorter treatment times than those achieved with standard treatments.[132][133][134]


Phage therapy[edit]

An entirely different approach is phage therapy (e.g., at the Eliava Institute in Georgia[135]). Experimental phage therapy tested in mice had a reported efficacy against up to 95% of tested Staphylococcus isolates.[136]


  • On May 18, 2006, a report in Nature identified a new antibiotic, called platensimycin, that had demonstrated successful use against MRSA.[137][138]
  • A new class of non-β-lactam antibiotics, oxadiazoles, was reported to be effective against MRSA infection in mouse models. The mechanisms of oxadiazoles’ antibacterial effect are the inhibition of the penicillin binding protein, PBP2a and biosynthesis of the bacterial cell wall. It was found to have bactericidal activity against vancomycin- and linezolid-resistant MRSA and other Gram-positive bacterial strains.[139][140]

Natural products[edit]

  • Some in vitro studies with honey have identified components in honey that kill MRSA.[141][142]
  • Ocean-dwelling living sponges produce compounds that may make MRSA more susceptible to antibiotics.[143]
  • Some semi-toxic fungi/mushrooms excrete broad spectrum antibiotics, not all of which have been fully identified; some been shown to inhibit the growth of Staphylococcus aureus.[144]
  • In vitro studies have shown that oakin, an oak extract, can kill MRSA.[148]

Additional images[edit]

See also[edit]


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Further reading[edit]

There are several web-based resources available for further research and treatment options.

  • The Center for Disease Control maintains MRSA pages that provide information surrounding the bacteria, including prevention, statistics, at risk groups, causes, educational resources, and environmental factors.
  • The Mayo Clinic maintains an online site, updated by Mayo Clinic staff, that covers the basic definition, symptoms, and patient education for MRSA.
  • The online medical resource site, WebMD, maintains on MRSA that provide basic information about the bacteria, as well as some multimedia resources for patient education.
  • MRSA MD is an online medical site devoted solely to MRSA education, treatment, and prevention. Maintained by Dr. Kirk Bortel, MRSA MD provides treatment information and prevention education.
  • Maryn McKenna (2011). Superbug: The Fatal Menace of MRSA. Free Press. ISBN 978-1416557289. 
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Staphylococcus aureus

Staphylococcus aureus is a gram-positive coccal bacterium that is a member of the Firmicutes, and is frequently found in the human respiratory tract and on the skin. It is positive for catalase and nitrate reduction. Although S. aureus is not always pathogenic, it is a common cause of skin infections (e.g. boils), respiratory disease (e.g. sinusitis), and food poisoning. Disease-associated strains often promote infections by producing potent protein toxins, and expressing cell-surface proteins that bind and inactivate antibodies. The emergence of antibiotic-resistant forms of pathogenic S. aureus (e.g. MRSA) is a worldwide problem in clinical medicine.

Staphylococcus was first identified in 1880 in Aberdeen, Scotland, by the surgeon Sir Alexander Ogston in pus from a surgical abscess in a knee joint.[1] This name was later appended to Staphylococcus aureus by Friedrich Julius Rosenbach who was credited by the official system of nomenclature at the time. It is estimated that 20% of the human population are long-term carriers of S. aureus[2] which can be found as part of the normal skin flora and in anterior nares of the nasal passages.[2][3] S. aureus is the most common species of staphylococcus to cause Staph infections and is a successful pathogen due to a combination of nasal carriage and bacterial immuno-evasive strategies.[2][3] S. aureus can cause a range of illnesses, from minor skin infections, such as pimples,[medical citation needed] impetigo, boils (furuncles), cellulitis folliculitis, carbuncles, scalded skin syndrome, and abscesses, to life-threatening diseases such as pneumonia, meningitis, osteomyelitis, endocarditis, toxic shock syndrome (TSS), bacteremia, and sepsis. Its incidence ranges from skin, soft tissue, respiratory, bone, joint, endovascular to wound infections. It is still one of the five most common causes of nosocomial infections and is often the cause of postsurgical wound infections. Each year, some 500,000 patients in United States' hospitals contract a staphylococcal infection.[4]

Staphylococcus aureus
Classification and external resources


Gram stain of S. Saprophyticus cells which typically occur in clusters. The cell wall readily absorbs the crystal violet stain.
Yellow colonies of S. aureus on a blood agar plate, note regions of clearing around colonies caused by lysis of red cells in the agar (beta hemolysis).

S. aureus (/ˌstæfɨlɵˈkɒkəs ˈɔriəs/, Greek σταφυλόκοκκος, "grape-cluster berry", Latin aureus, "golden") is a facultative anaerobic gram-positive coccal bacterium also known as "golden staph" and Oro staphira. In medical literature the bacteria is often referred to as S. aureus or Staph aureus. Staphylococcus should not be confused with the similarly named and medically relevant genus Streptococcus. S. aureus appears as grape-like clusters when viewed through a microscope, and has large, round, golden-yellow colonies, often with hemolysis, when grown on blood agar plates.[5] S. aureus reproduces asexually by binary fission. The two daughter cells do not fully separate and remain attached to one another. This is why the cells are observed in clusters.[6]

S. aureus is catalase-positive (meaning it can produce the enzyme catalase). Catalase converts hydrogen peroxide (H
) to water and oxygen. Catalase-activity tests are sometimes used to distinguish staphylococci from enterococci and streptococci. Previously, S. aureus was differentiated from other staphylococci by the coagulase test. However it is now known that not all S. aureus are coagulase-positive[5][7] and that incorrect species identification can impact effective treatment and control measures.[8]

Role in disease[edit]

SEM of methicillin-resistant Staphylococcus aureus.

S. aureus is responsible for many infections but it may also occur as a commensal. The presence of S. aureus does not always indicate infection. S. aureus can survive from hours to weeks, or even months, on dry environmental surfaces, depending on strain.[9]

S. aureus can infect tissues when the skin or mucosal barriers have been breached. This can lead to many different types of infections including furuncles and carbuncles (a collection of furuncles).

S. aureus infections can spread through contact with pus from an infected wound, skin-to-skin contact with an infected person by producing hyaluronidase that destroys tissues, and contact with objects such as towels, sheets, clothing, or athletic equipment used by an infected person. Deeply penetrating S. aureus infections can be severe. Prosthetic joints put a person at particular risk of septic arthritis, and staphylococcal endocarditis (infection of the heart valves) and pneumonia. Strains of S. aureus can host phages, such as Φ-PVL (produces Panton-Valentine leukocidin), that increase virulence.

Atopic dermatitis[edit]

S. aureus is extremely prevalent in persons with atopic dermatitis. It is mostly found in fertile, active places, including the armpits, hair, and scalp. Large pimples that appear in those areas may exacerbate the infection if lacerated. This can lead to staphylococcal scalded skin syndrome (SSSS). A severe form of this, Ritter's disease, can be observed in neonates.[10]

The presence of S. aureus in persons with atopic dermatitis is not an indication to treat with oral antibiotics, as evidence has not shown this to give benefit to the patient.[11] The relationship between S. aureus and atopic dermatitis is unclear.[11] Evidence shows that attempting to control S. aureus with oral antibiotics is not efficacious.[11]

Animal infections[edit]

S. aureus can survive on dogs,[12] cats,[13] and horses,[14] and can cause bumblefoot in chickens.[15] Some believe health-care workers' dogs should be considered a significant source of antibiotic-resistant S. aureus, especially in times of outbreak.[12] S. aureus is one of the causal agents of mastitis in dairy cows. Its large polysaccharide capsule protects the organism from recognition by the cow's immune defenses.[16]

Virulence factors[edit]


Staphylococcus aureus produces various enzymes such as coagulase (bound and free coagulases) which clots plasma and coats the bacterial cell to probably prevent phagocytosis. Hyaluronidase (also known as spreading factor) breaks down hyaluronic acid and helps in spreading of Staphylococcus aureus. S.aureus also produces DNAse (deoxyribonuclease) which breaks down the DNA, lipase to digest lipids, staphylokinase to dissolve fibrin and aid in spread, and beta-lactamase for drug resistance.[17]


Depending on the strain, S. aureus is capable of secreting several exotoxins, which can be categorized into three groups. Many of these toxins are associated with specific diseases.[18]

(PTSAgs) have superantigen activities that induce toxic shock syndrome (TSS). This group includes the toxin TSST-1, enterotoxin type B, which causes TSS associated with tampon use. This is characterized by fever, erythematous rash, hypotension, shock, multiple organ failure, and skin desquamation. Lack of antibody to TSST-1 plays a part in the pathogenesis of toxic shock syndrome. Other strains of S. aureus can produce an enterotoxin that is the causative agent of S. aureus gastroenteritis. This gastroenteritis is self-limiting, characterized by vomiting and diarrhea one to six hours after ingestion of the toxin with recovery in eight to 24 hours. Symptoms include nausea, vomiting, diarrhea, and major abdominal pain.[19][20]

Exfoliative toxins
See also: Exfoliatin
EF toxins are implicated in the disease staphylococcal scalded-skin syndrome (SSSS), which occurs most commonly in infants and young children. It also may occur as epidemics in hospital nurseries. The protease activity of the exfoliative toxins causes peeling of the skin observed with SSSS.[20]
Other toxins
Staphylococcal toxins that act on cell membranes include alpha toxin, beta toxin, delta toxin, and several bicomponent toxins. The bicomponent toxin Panton-Valentine leukocidin (PVL) is associated with severe necrotizing pneumonia in children.[21][22] The genes encoding the components of PVL are encoded on a bacteriophage found in community-associated methicillin-resistant S. aureus (MRSA) strains.

Other immunoevasive strategies[edit]

Protein A

Protein A is anchored to staphylococcal peptidoglycan pentaglycine bridges (chains of five glycine residues) by the transpeptidase sortase A.[23] Protein A, an IgG-binding protein, binds to the Fc region of an antibody. In fact, studies involving mutation of genes coding for protein A resulted in a lowered virulence of S. aureus as measured by survival in blood, which has led to speculation that protein A-contributed virulence requires binding of antibody Fc regions.[24]

Protein A in various recombinant forms has been used for decades to bind and purify a wide range of antibodies by immunoaffinity chromatography. Transpeptidases, such as the sortases responsible for anchoring factors like Protein A to the staphylococcal peptidoglycan, are being studied in hopes of developing new antibiotics to target MRSA infections.[25]

Staphylococcus aureus on Tryptic Soy Agar. The strain is producing a yellow pigment staphyloxanthin.
Staphylococcal pigments

Some strains of S. aureus are capable of producing staphyloxanthin — a golden coloured carotenoid pigment. This pigment acts as a virulence factor, primarily by being a bacterial antioxidant which helps the microbe evade the reactive oxygen species which the host immune system uses to kill pathogens.[26][27]

Mutant strains of S. aureus modified to lack staphyloxanthin are less likely to survive incubation with an oxidizing chemical, such as hydrogen peroxide than pigmented strains. Mutant colonies are quickly killed when exposed to human neutrophils, while many of the pigmented colonies survive.[26] In mice, the pigmented strains cause lingering abscesses when inoculated into wounds, whereas wounds infected with the unpigmented strains quickly heal.

These tests suggest the Staphylococcus strains use staphyloxanthin as a defence against the normal human immune system. Drugs designed to inhibit the production of staphyloxanthin may weaken the bacterium and renew its susceptibility to antibiotics.[27] In fact, because of similarities in the pathways for biosynthesis of staphyloxanthin and human cholesterol, a drug developed in the context of cholesterol-lowering therapy was shown to block S. aureus pigmentation and disease progression in a mouse infection model.[28]

Classical diagnosis[edit]

Typical gram-positive cocci, in clusters, from a sputum sample, Gram stain

Depending upon the type of infection present, an appropriate specimen is obtained accordingly and sent to the laboratory for definitive identification by using biochemical or enzyme-based tests. A Gram stain is first performed to guide the way, which should show typical gram-positive bacteria, cocci, in clusters. Second, the isolate is cultured on mannitol salt agar, which is a selective medium with 7–9% NaCl that allows S. aureus to grow, producing yellow-colored colonies as a result of mannitol fermentation and subsequent drop in the medium's pH.

Furthermore, for differentiation on the species level, catalase (positive for all Staphylococcus species), coagulase (fibrin clot formation, positive for S. aureus), DNAse (zone of clearance on DNase agar), lipase (a yellow color and rancid odor smell), and phosphatase (a pink color) tests are all done. For staphylococcal food poisoning, phage typing can be performed to determine whether the staphylococci recovered from the food were the source of infection.

Rapid diagnosis and typing[edit]

Diagnostic microbiology laboratories and reference laboratories are key for identifying outbreaks and new strains of S. aureus. Recent genetic advances have enabled reliable and rapid techniques for the identification and characterization of clinical isolates of S. aureus in real time. These tools support infection control strategies to limit bacterial spread and ensure the appropriate use of antibiotics. Quantitative PCR is being increasingly employed in clinical laboratories as a technique to identifying outbreaks.[29][30]

When observing the evolvement of S. aureus and its ability to adapt to each modified antibiotic, in general, there are two basic methods known as “band-based” or “sequence-based”.[31] Keeping these two methods in mind, other methods like multilocus sequence typing (MLST), pulsed-field gel electrophoresis (PFGE), bacteriophage typing, spa locus typing, and SCCmec typing are often conducted more than others.[32] With these methods,not only are we able to determine where strains of MRSA originated from, but where they currently reside.[33]

With MLST, this technique of typing utilizes fragments of several housekeeping genes known as aroE, glpF, gmk, pta, tip, and yqiL. These sequences are then assigned a number which give to a strong of several numbers that serve as the allelic profile. Although this is a common method, a limitation about this method is the maintenance of the micro-array which detects newly allelic profiles, making it a costly and time consuming experiment.[31]

With PFGE, a method which is still very much utilized dating back to its first success in 1980s remains capable of helping differentiate Methicillin-resistant S. aureus isolates.[33] To accomplish this, the technique uses multiple gel electrophoresis, along with a voltage gradient to display clear resolutions of molecules. The S. aureus fragments then transition down the gel producing specific band patters that are later compare with other isolates in hopes of identifying related strains. Limitations of the method include, practical difficulties with uniform band patterns and PFGE sensitivity as a whole.

Spa locus typing is also considered a popular technique that uses a single locus zone in a polymorphic region of S. aureus to distinguish any form of mutations.[33] Although this technique is often inexpensive and less time consuming, the chance of losing discriminatory power makes it hard to differentiate between MLST CC’s exemplifies a crucial limitation.

Treatment and antibiotic resistance[edit]

The treatment of choice for S. aureus infection is penicillin. Penicillin, an antibiotic derived from Penicillum fungus, inhibits the formation of peptidoglycan cross-linkages that provide the rigidity and strength in a bacterial cell wall. The four-membered β-lactam ring of penicillin is bound to enzyme DD-transpeptidase, an enzyme that when functional, cross-links chains of peptidoglycan that form bacterial cell walls. The binding of β-lactam to DD-transpeptidase inhibits the enzyme’s functionality and it can no longer catalyze the formation of the cross-links. As a result, cell wall formation and degradation is imbalanced, thus resulting in cell death. In most countries, however, penicillin resistance is extremely common, and first-line therapy is most commonly a penicillinase-resistant β-lactam antibiotic (for example, oxacillin or flucloxacillin, both of which have the same mechanism of action as penicillin). Combination therapy with gentamicin may be used to treat serious infections, such as endocarditis,[34][35] but its use is controversial because of the high risk of damage to the kidneys.[36] The duration of treatment depends on the site of infection and on severity.

Antibiotic resistance in S. aureus was uncommon when penicillin was first introduced in 1943. Indeed, the original petri dish on which Alexander Fleming of Imperial College London observed the antibacterial activity of the Penicillium fungus was growing a culture of S. aureus. By 1950, 40% of hospital S. aureus isolates were penicillin-resistant; and, by 1960, this had risen to 80%.[37]

Methicillin-resistant S. aureus, abbreviated MRSA and often pronounced /ˈmɜrsə/ or /ɛm ɑː ɛs /, is one of a number of greatly feared strains of S. aureus which have become resistant to most β-lactam antibiotics. For this reason, vancomycin, a glycopeptide antibiotic, is commonly used to combat MRSA. Vancomycin inhibits the synthesis of peptidoglycan, but unlike β-lactam antibiotics, glycopeptide antibiotics target and bind to amino acids in the cell wall, preventing peptidoglycan cross-linkages from forming. MRSA strains are most often found associated with institutions such as hospitals, but are becoming increasingly prevalent in community-acquired infections. A recent study by the Translational Genomics Research Institute showed that nearly half (47%) of the meat and poultry in U.S. grocery stores were contaminated with S. aureus, with more than half (52%) of those bacteria resistant to antibiotics.[38] This resistance is commonly caused by the widespread use of antibiotics in the husbandry of livestock, including prevention or treatment of an infection as well as promoting growth.

Researchers from Italy have identified a bacteriophage active against S. aureus, including methicillin-resistant strains (MRSA), in mice and possibly humans.[39]

Mechanisms of antibiotic resistance[edit]

Bacterial cells of Staphylococcus aureus, which is one of the causal agents of mastitis in dairy cows. Its large capsule protects the organism from attack by the cow's immunological defenses.

Staphylococcal resistance to penicillin is mediated by penicillinase (a form of β-lactamase) production: an enzyme that cleaves the β-lactam ring of the penicillin molecule, rendering the antibiotic ineffective. Penicillinase-resistant β-lactam antibiotics, such as methicillin, nafcillin, oxacillin, cloxacillin, dicloxacillin, and flucloxacillin, are able to resist degradation by staphylococcal penicillinase.

Resistance to methicillin is mediated via the mec operon, part of the staphylococcal cassette chromosome mec (SCCmec). Resistance is conferred by the mecA gene, which codes for an altered penicillin-binding protein (PBP2a or PBP2') that has a lower affinity for binding β-lactams (penicillins, cephalosporins, and carbapenems). This allows for resistance to all β-lactam antibiotics, and obviates their clinical use during MRSA infections. As such, the glycopeptide vancomycin is often deployed against MRSA.

Aminoglycoside antibiotics, such as kanamycin, gentamicin, streptomycin, etc., were once effective against staphylococcal infections until strains evolved mechanisms to inhibit the aminoglycosides' action, which occurs via protonated amine and/or hydroxyl interactions with the ribosomal RNA of the bacterial 30S ribosomal subunit.[40] There are three main mechanisms of aminoglycoside resistance mechanisms which are currently and widely accepted: aminoglycoside modifying enzymes, ribosomal mutations, and active efflux of the drug out of the bacteria.

Aminoglycoside-modifying enzymes inactivate the aminoglycoside by covalently attaching either a phosphate, nucleotide, or acetyl moiety to either the amine or the alcohol key functional group (or both groups) of the antibiotic. This changes the charge or sterically hinders the antibiotic, decreasing its ribosomal binding affinity. In S. aureus, the best-characterized aminoglycoside-modifying enzyme is aminoglycoside adenylyltransferase 4' IA (ANT(4')IA). This enzyme has been solved by x-ray crystallography.[41] The enzyme is able to attach an adenyl moiety to the 4' hydroxyl group of many aminoglycosides, including kamamycin and gentamicin.

Glycopeptide resistance is mediated by acquisition of the vanA gene. The vanA gene originates from the enterococci and codes for an enzyme that produces an alternative peptidoglycan to which vancomycin will not bind.

Today, S. aureus has become resistant to many commonly used antibiotics. In the UK, only 2% of all S. aureus isolates are sensitive to penicillin, with a similar picture in the rest of the world. The β-lactamase-resistant penicillins (methicillin, oxacillin, cloxacillin, and flucloxacillin) were developed to treat penicillin-resistant S. aureus, and are still used as first-line treatment. Methicillin was the first antibiotic in this class to be used (it was introduced in 1959), but, only two years later, the first case of MRSA was reported in England.[42]

Despite this, MRSA generally remained an uncommon finding, even in hospital settings, until the 1990s, when there was an explosion in MRSA prevalence in hospitals, where it is now endemic.[43]

MRSA infections in both the hospital and community setting are commonly treated with non-β-lactam antibiotics, such as clindamycin (a lincosamine) and co-trimoxazole (also commonly known as trimethoprim/sulfamethoxazole). Resistance to these antibiotics has also led to the use of new, broad-spectrum anti-gram-positive antibiotics, such as linezolid, because of its availability as an oral drug. First-line treatment for serious invasive infections due to MRSA is currently glycopeptide antibiotics (vancomycin and teicoplanin). There are number of problems with these antibiotics, such as the need for intravenous administration (there is no oral preparation available), toxicity, and the need to monitor drug levels regularly by blood tests. There are also concerns glycopeptide antibiotics do not penetrate very well into infected tissues (this is a particular concern with infections of the brain and meninges and in endocarditis). Glycopeptides must not be used to treat methicillin-sensitive S. aureus (MSSA), as outcomes are inferior.[44]

Because of the high level of resistance to penicillins and because of the potential for MRSA to develop resistance to vancomycin, the U.S. Centers for Disease Control and Prevention has published guidelines for the appropriate use of vancomycin. In situations where the incidence of MRSA infections is known to be high, the attending physician may choose to use a glycopeptide antibiotic until the identity of the infecting organism is known. After the infection is confirmed to be due to a methicillin-susceptible strain of S. aureus, treatment can be changed to flucloxacillin or even penicillin, as appropriate.

Vancomycin-resistant S. aureus (VRSA) is a strain of S. aureus that has become resistant to the glycopeptides. The first case of vancomycin-intermediate S. aureus (VISA) was reported in Japan in 1996;[45] but the first case of S. aureus truly resistant to glycopeptide antibiotics was only reported in 2002.[46] Three cases of VRSA infection had been reported in the United States as of 2005.[47]

Carriage of Staphylococcus aureus[edit]

The carriage of Staphylococcus aureus is an important source of nosocomial infection and community-acquired methicillin-resistant S. aureus (MRSA). Although S. aureus can be present on the skin of the host, a large proportion of its carriage is through the anterior nares of the nasal passages.[2] The ability of the nasal passages to harbour S. aureus results from a combination of a weakened or defective host immunity and the bacteria's ability to evade host innate immunity.[48]

Infection control[edit]

Spread of S. aureus (including MRSA) generally is through human-to-human contact, although recently some veterinarians have discovered the infection can be spread through pets,[49] with environmental contamination thought to play a relatively unimportant part. Emphasis on basic hand washing techniques are, therefore, effective in preventing its transmission. The use of disposable aprons and gloves by staff reduces skin-to-skin contact and, therefore, further reduces the risk of transmission. Please refer to the main article on infection control for further details.

Recently, there have been myriad reported cases of S. aureus in hospitals across America. Transmission of the pathogen is facilitated in medical settings where healthcare worker hygiene is insufficient. S. aureus is an incredibly hardy bacterium, as was shown in a study where it survived on polyester for just under three months;[50] polyester is the main material used in hospital privacy curtains.

The bacteria are transported on the hands of healthcare workers, who may pick them up from a seemingly healthy patient carrying a benign or commensal strain of S. aureus, and then pass it on to the next patient being treated. Introduction of the bacteria into the bloodstream can lead to various complications, including, but not limited to, endocarditis, meningitis, and, if it is widespread, sepsis.

Ethanol has proven to be an effective topical sanitizer against MRSA. Quaternary ammonium can be used in conjunction with ethanol to increase the duration of the sanitizing action. The prevention of nosocomial infections involves routine and terminal cleaning. Nonflammable alcohol vapor in CO
NAV-CO2 systems have an advantage, as they do not attack metals or plastics used in medical environments, and do not contribute to antibacterial resistance.

An important and previously unrecognized means of community-associated MRSA colonization and transmission is during sexual contact.[51]

Staff or patients who are found to carry resistant strains of S. aureus may be required to undergo "eradication therapy", which may include antiseptic washes and shampoos (such as chlorhexidine) and application of topical antibiotic ointments (such as mupirocin or neomycin) to the anterior nares of the nose.

S. aureus is killed in 1 minute at 78 °C and 10 minutes at 64 °C.[52]

The nonprotein amino acid L-homoarginine is a growth inhibitor of S. aureus as well as Candida albicans. It is assumed to be an antimetabolite of arginine.

Biological control might be a new possible way to control Staphylococcus aureus in body surfaces. Colonization of body surfaces (especially in the nose) by Staphylococcus epidermidis(inhibitory strain JK16) impairs the establishment of S. aureus.

A 2011 study[53] points to this new possible way to control S. aureus. This study was performed from observations of the nasal microbial flora of a diverse group of people. It was discovered that there are two different strains of S. epidermidis, one that inhibits biofilm formation by S. aureus, S. epidermidis strain JK16 (inhibitory type), and one that does not (non-inhibitory type) S. epidermidis strain JK11. In this study they observed that there were some patients that were not affected by Staphylococcus aureus; this was because these patients had S. aureus together with S. epidermis (inhibitory type), in their nasal microbial flora. This is due to an amensalistic relationship between these microorganisms, the inhibitory strain of S. epidermidis and Staphylococcus aureus.

These findings open the way to a biological control therapy to help in the treatment of S. aureus infections which are becoming a growing threat due to the rise of resistance to conventional antibiotic treatments.

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Further reading[edit]

Loskill, Peter; Pereira, Pedro M.; Jung, Philipp; Bischoff, Markus; Herrmann, Mathias; Pinho, Mariana G.; Jacobs, Karin (2 September 2014). "Reduction of the Peptidoglycan Crosslinking Causes a Decrease in Stiffness of the Staphylococcus aureus Cell Envelope". Biophysical Journal 107 (5): 1082–1089. doi:10.1016/j.bpj.2014.07.029. PMID 25185544. Retrieved 14 November 2014. 

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ST8:USA300 is a strain of community-associated MRSA that has emerged as a particularly antibiotic resistant epidemic that is responsible for rapidly progressive, fatal diseases including necrotizing pneumonia, severe sepsis and necrotizing fasciitis.[1] The epidemiology of infections caused by MRSA is rapidly changing: in the past 10 years, infections caused by this organism have emerged in the community. The 2 MRSA clones in the United States most closely associated with community outbreaks, USA400 (MW2 strain, ST1 lineage) and USA300, often contain Panton-Valentine leukocidin (PVL) genes and, more frequently, have been associated with skin and soft tissue infections. Outbreaks of community-associated (CA)-MRSA infections have been reported in correctional facilities, among athletic teams, among military recruits, in newborn nurseries, and among sexually active homosexual men. CA-MRSA infections now appear to be endemic in many urban regions and cause most MRSA infections.[2] [3]


  1. ^ Boyle-Vavra S, Daum RS (2007). "Community-acquired methicillin-resistant Staphylococcus aureus: the role of Panton-Valentine leukocidin". Lab. Invest. 87 (1): 3–9. doi:10.1038/labinvest.3700501. PMID 17146447. 
  2. ^ Maree CL, Daum RS, Boyle-Vavra S, Matayoshi K, Miller LG (2007). "Community-associated methicillin-resistant Staphylococcus aureus isolates causing healthcare-associated infections". Emerging Infect. Dis. 13 (2): 236–42. doi:10.3201/eid1302.060781. PMC 2725868. PMID 17479885. 
  3. ^ Diep BA, Chambers HF, Graber CJ, et al. (February 2008). "Emergence of multidrug-resistant, community-associated, methicillin-resistant Staphylococcus aureus clone USA300 in men who have sex with men". Ann. Intern. Med. 148 (4): 249–57. doi:10.7326/0003-4819-148-4-200802190-00204. PMID 18283202. 
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