Methicillin resistant staphylococcus aureus infections

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

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Methicillin-resistant Staphylococcus Aureus is a type of staphylococcus that is resistant to certain antibiotics. These antibiotics include methicillin and other more common antibiotics such as oxacillin, penicillin and amoxicillin. Staph infections, including MRSA, occur most frequently among persons in hospitals and healthcare facilities (such as nursing homes and dialysis centers) who have weakened immune systems (see healthcare-associated MRSA).

MRSA infections that are acquired by patients who have not been recently (within the past year) hospitalized or had a medical procedure (such as dialysis, surgery, catheters) are known as CA-MRSA infections. Staph or MRSA infections in the community are usually manifested as skin infections, such as pimples and boils, and occur in otherwise healthy people.

Worldwide, an estimated 2 billion people carry some form of S. aureus. Of these 2 billion, up to 53 million (2.7% of carriers) are thought to carry MRSA. In the United States, 95 million carry S. aureus in their noses; of these 2.5 million (2.6% of carriers) carry MRSA. A population review conducted in 3 communities in the US 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.

S. aureus most commonly colonizes the anterior nares (the nostrils) although the respiratory tract, open wounds, intravenous catheters and urinary tract are also potential sites for infection. MRSA infections are usually asymptomatic in healthy individuals and may last from a few weeks to many years.

The surgery for MRSA infections may be as simple and minimally invasive as a biopsy, but they can be more extreme when infected areas are surgically removed.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Staphylococcus aureus remains an important cause of nosocomial infection, especially nosocomial pneumonia, surgical wound infection, and bloodstream infection. Methicillin-resistant S aureus (MRSA) first emerged as an important clinical problem in the United Kingdom in the early 1960s, shortly after methicillin came into clinical use. Although MRSA was first recognized in the United States in 1961, it was not until the late 1960s that reports of outbreak investigations began to appear in the U.S. medical literature.

Most of the sources of data on the prevalence and distribution of MRSA in the United States are reports of outbreak investigations and surveys of hospitals and laboratories, including pediatric and Veterans Affairs hospitals. MRSA outbreaks have been reported from all U.S. geographic regions, although a wide variation in the geographic distribution of MRSA isolates appear to exist.

Several reports also have suggested an increasing prevalence of MRSA in U.S. hospitals. However, some of these reports provide no information on current trends. The most recent report by Boyce was based on a questionnaire survey of U.S. hospital epidemiologists during 1987-1989. In addition, all these reports covered relatively limited time periods.

The National Nosocomial Infections Surveillance (NNIS) System, which began in 1970, is the only source of national information on nosocomial infections in the United States. One of the objectives of the NNIS System is to identify changes in nosocomial pathogens and antimicrobial resistance. To determine whether the proportion of S aureus resistant to methicillin has increased over a 17-year period, 1975 through 1991, we analyzed NNIS data in which S aureus was associated with a nosocomial infection.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Two types of MRSA exist based on the type of patients they infect. They are:

• Healthcare associated MRSA (HA-MRSA) – MRSA among persons in hospitals and healthcare facilities (such as nursing homes and dialysis centers) who have weakened immune systems. These healthcare-associated staph infections include:

• Surgical wound infections
• Urinary tract infections
• Bloodstream infections (including central-line associated bloodstream infections)
• Pneumonia

• Community-associated MRSA (CA-MRSA) – MRSA infections that are acquired by persons who have not been recently (within the past year) hospitalized or had a medical procedure (such as dialysis, surgery, catheters) (MRSA causing illness in persons outside of hospitals and healthcare facilities).

Persons with MRSA infections that meet all of the following criteria likely have CA-MRSA infections:

• Diagnosis of MRSA was made in the outpatient setting or by a culture positive for MRSA within 48 hours after admission to the hospital.
• No medical history of MRSA infection or colonization.
• No medical history in the past year of:

• Hospitalization
• Admission to a nursing home, skilled nursing facility, or hospice
• Dialysis
• Surgery

• No permanent indwelling catheters or medical devices that pass through the skin into the body.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

The main mode of transmission of Methicillin resistant Staphylococcus aureus to other patients is through human hands, especially healthcare workers’ hands. Hands may become contaminated with MRSA bacteria by contact with infected or colonized patients. If appropriate hand hygiene, such as washing with soap and water or using an alcohol-based hand sanitizer, is not performed, the bacteria can be spread when the healthcare worker touches other patients.

Staphylococcus aureus became methicillin resistant by acquiring a mecA gene, usually carried on a larger piece of DNA called a staphylococcal cassette chromosome SCCmec.

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 via horizontal gene transfer.^[1] 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) that are critical for cell wall synthesis.

Staphylococcal cassette chromosome mec (SCCmec) is a genomic island of unknown origin containing the antibiotic resistance gene mecA.^[2][3] SCCmec contains additional genes beyond mecA, including the cytolysin gene psm-mec, which may suppress virulence in hospital-acquired MRSA strains.^[4] 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.^[2][3] Currently, six unique SCCmec types ranging in size from 21–67 kb have been identified;^[2] they are designated types I-VI and are distinguished by variation in mec and ccr gene complexes.^[5] 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.^[2]

Different SCCmec genotypes confer different microbiological characteristics, such as different antimicrobial resistance rates.^[6] 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.^[3][6] Conversely, CA-MRSA is associated with types IV and V, which are smaller and lack resistance genes other than mecA.^[3][6]

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.^[2] 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.^[2] 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.^[2]

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.^[3][5] In the presence of a β-lactam antibiotic, MecR1 initiates a signal transduction cascade that leads to transcriptional activation of mecA.^[3][5] This is achieved by MecR1-mediated cleavage of MecI, which alleviates MecI repression.^[5] 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.^[2][7] The DNA sequences bound by MecI and BlaI are identical;^[2] therefore, BlaI can also bind the mecA operator to repress transcription of mecA.^[7]

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 explains the variability in virulence and associated MRSA infections.^[8] The first MRSA strain, ST250 MRSA-1 originated from SCCmec and ST250-MSSA integration.^[8] 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.^[8] ST239-MRSA-III, known as the Brazilian clone, was highly transmissible compared to others and distributed in Argentina, Czech Republic, and Portugal.^[8]

In the UK, where MRSA is commonly called “Golden Staph”, the most common strains of MRSA are EMRSA15 and EMRSA16.^[9] EMRSA16 is best described by epidemiology: it originated in Kettering, England, and the full genomic sequence of this strain has been published.^[10] EMRSA16 has been found to be identical to the ST36:USA200 strain, which circulates in the United States, and carries the SCCmec type II, enterotoxin A and toxic shock syndrome toxin 1 genes.^[11] 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.^[12] These strains are genetic characteristics of HA-MRSA.^[13]

It is not entirely certain why some strains are highly transmissible and persistent in healthcare facilities.^[8] 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,^[14] such as in the nasal mucosa ^[15] and in the tonsil tissue.^[16] 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 have not been in contact with health care facilities.^[13] Researchers suggests that CA-MRSA did not evolve from the HA-MRSA.^[13] This is further proven by molecular typing of CA-MRSA strains^[17] and genome comparison between CA-MRSA and HA-MRSA, which indicate that novel MRSA strains integrated SCCmec into MSSA separately on its own.^[13] By mid 2000, CA-MRSA was introduced into the health care systems and distinguishing between CA-MRSA from HA-MRSA was a difficult process.^[13] Community-acquired MRSA (CA-MRSA) is more easily treated and more virulent than hospital-acquired MRSA (HA-MRSA).^[13] The genetic mechanism for the enhanced virulence in CA-MRSA remains as an active area of research. The Panton-Valentine leukocidin (PVL) genes are of special interest because they are a unique feature of CA-MRSA.^[8]

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, enterotoxins Q and K,^[11] and ST1:USA400.^[18] ST8:USA300 strain results in skin infections, necrotizing fasciitis, and toxic shock syndrome. On the other hand, the ST1:USA400 strain results in necrotizing pneumonia and pulmonary sepsis.^[8] 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 predominate (Tristan et al., Emerging Infectious Diseases, 2006), which carries SCCmec type IV.^[19] 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 (David et al., Emerg Infect Dis 2008).

In June 2011, the discovery of a new strain of MRSA was announced by two separate teams of researchers in the UK. Its genetic make-up was reportedly more similar to strains found in animals, and testing kits designed to detect MRSA were unable to identify it.^[20] This MRSA strain, Clonal Complex 398 (CC398), is responsible for Livestock-associated MRSA (LA-MRSA) infections.^[12] 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.^[21]

MRSA is associated with the following infections:

• Skin and soft tissue infections:

• Furuncles
• Carbuncles
• Abscesses

• Stye / Hordeolum
• Osteomyelitis
• Septic arthritis
• Sepsis

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Worldwide, an estimated 2 billion people carry some form of S. aureus. Of these 2 billion, up to 53 million (2.7% of carriers) are thought to carry MRSA. In the United States, 95 million carry S. aureus in their noses; of these 2.5 million (2.6% of carriers) carry MRSA. A population review conducted in 3 communities in the US 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.

It has been difficult to quantify the degree of morbidity and mortality attributable to MRSA. Patients with S. aureus infection had, on average, 3 times the length of hospital stay (14.3 vs 4.5 days), 3 times the total charges ($48,824 vs $14,141), and 5 times the risk of in-hospital death (11.2% vs 2.3%) than inpatients without this infection. Cosgrove et al, in a meta-analysis of 31 studies, conclude that bacteremia as a result of MRSA is associated with an increased mortality compared with MSSA bacteraemia with an odds ratio of 1.93 (95% CI, 1.54±2.42; In addition, Wyllie et al. report a death rate of 34% within 30 days among patients infected with MRSA, while among MSSA patients the death rate was similar at 27%.

Because cystic fibrosis patients are often treated with multiple antibiotics in hospital settings, they are often colonized with MRSA, potentially increasing the rate of life-threatening MRSA pneumonia in this group. The risk of cross-colonization has led to increased use of isolation protocols among these patients. In a hospital setting, patients who have received fluoroquinolones are more likely to become colonized with MRSA. This is probably because many circulating strains of MRSA are fluoroquinolone-resistant, which means that MRSA is able to colonize patients whose normal skin flora have been cleared of non-resistant S. aureus by fluoroquinolones.

In the USA, reports have been increasing of outbreaks of MRSA colonization and infection through skin contact in locker rooms and gymnasiums, even among healthy populations. MRSA also is becoming a problem in pediatrics, including hospital nurseries. A 2007 study found that 4.6% of patients in US healthcare facilities were infected or colonized with MRSA.

MRSA causes as many as 20% of Staphylococcus aureus infections in populations that use intravenous drugs. These out-of-hospital strains of MRSA, now designated as community-acquired, methicillin-resistant Staphylococcus aureus, or CA-MRSA, are more easily treated than hospital-acquired MRSA (although more virulent than MSSA). CA-MRSA apparently did not evolve de novo in the community, but represents a hybrid between MRSA which escaped from the hospital environment and the once easily treatable community organisms. Most of the hybrid strains also acquired a virulence factor which makes their infections invade more aggressively, resulting in deep tissue infections following minor scrapes and cuts, and many cases of fatal pneumonia as well.

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 3000 per year. Staphylococcus bacteria accounts 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.

During the summer of 2005, researchers in The Netherlands discovered that three pig farmers or their families were infected by MRSA bacteria that was also found on their pigs. Researchers from Radboud University Nijmegen are now investigating how widespread the MRSA bacteria is in pigs, and whether it will become characterized among the zoonoses.

Recently, it has been observed that MRSA can replicate inside of Acanthamoeba, increasing MRSA numbers 1000-fold. Since Acanthamoeba can form cysts easily picked up by air currents, these organisms can spread MRSA via airborne routes. Whether or not control of Acanthamoeba in the clinical environment will help to contain MRSA remains an area for research.

Strains

In the UK, the most common strains are EMRSA15 and EMRSA16. EMRSA16 is the best described by epidemiology: it originated in Kettering, England, and the full genomic sequence of this strain has been published. This has been recognized as being identical to the ST36:USA200 strain which circulates in the USA, and carries the SCCmec type II, enterotoxin A and toxic shock syndrome toxin 1 genes. Under the new international typing system, this strain is now called MRSA252, and the entire genome sequence of this strain has been published. It is not entirely certain why this strain has become so successful, where previous strains have failed to persist: one explanation is the characteristic pattern of antibiotic sensitivities. Both the EMRSA-15 and -16 strains are resistant to erythromycin and ciprofloxacin. It is known that Staphylococcus aureus can survive intracellularly, and these 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.

In the USA, the epidemic of community-associated MRSA is due to a CC8 strain designated ST8:USA300, which carries mec type IV, Panton-Valentine leukocidin, and enterotoxins Q and K. Other community-associated strains of MRSA are ST8:USA500 and ST59:USA1000.

MRSA: a Growing Problem in the Healthcare Setting, But One with a Cure

MRSA is becoming more prevalent in healthcare settings. According to CDC data, the proportion of infections that are antimicrobial resistant has been growing. In 1974, MRSA infections accounted for two percent of the total number of staph infections; in 1995 it was 22%; in 2004 it was some 63%.

The good news is that MRSA is preventable. The first step to prevent MRSA, is to prevent healthcare infections in general. Infection control guidelines produced by CDC and the Healthcare Infection Control and Prevention Advisory Committee (HICPAC) are central to the prevention and control of healthcare infections and ultimately, MRSA in healthcare settings. To learn more about infection control guidelines to prevent infections and MRSA go to http://www.cdc.gov/ncidod/dhqp. CDC welcomes the increased attention and dialogue on the important problem of MRSA in healthcare. CDC, state and local health departments and partners nationwide are collaborating to prevent MRSA infections in healthcare settings. For example, CDC

• Monitors trends in infections and MRSA through surveillance systems such as the National Healthcare Safety Network, formerly the National Nosocomial Infection Surveillance System and the Dialysis Surveillance Network to identify which patients are at highest risk and where prevention efforts should be targeted.
• Works with multiple prevention partners including state health departments, academic medical centers, and regional and national collaboratives to identify and promote effective strategies to prevent MRSA transmission.
• Developed an overarching strategy to help guide healthcare facilities to control antibiotic resistance called The Campaign to Prevent Antimicrobial Resistance in Healthcare Settings. This campaign includes specific strategies for various healthcare populations, including hospitalized adults and children, dialysis patients, surgical patients, and long-term care patients.

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MRSA occurs most frequently among

• Patients who undergo invasive medical procedures such as:
  • Nasogastric tube
  • Gastrostomy tube
  • Foley catheter
  • Total parenteral nutrition or enteral feeding
  • Mechanical ventilation with endotracheal tube or tracheostomy tube
  • Invasive indwelling devices
  • Hemodialysis or peritoneal dialysis
• Patients who are being treated in hospitals and healthcare facilities such as nursing homes and dialysis centers.
• People with weak immune systems – immunosuppression (people living with HIV/AIDS, people living with lupus, cancer patients, transplant recipients, severe asthmatics, etc.)
• Diabetics^[1]
• Chronic illness
• Intravenous drug users ^[2]
• Users of quinolone antibiotics^[3]
• Young children, especially those in day care centers
• The elderly
• College students living in dormitories^[2]
• People staying or working in a health care facility for an extended period of time^[2]
• People who spend time in coastal waters where MRSA is present, such as some beaches in Florida and the west coast of the United States^[4][5]
• People who spend time in confined spaces with other people, including occupants of homeless shelters and warming centers, prison inmates, military recruits in basic training,^[6] and individuals who spend considerable time in changerooms or gyms.
• Men who have sex with men
• Urban under-served^[7]
• Indigenous populations, including Native Americans, Native Alaskans, and Australian Aboriginals^[7]
• Veterinarians, Livestock handlers, and Pet owners^[7]

Many MRSA infections occur in hospitals and healthcare facilities, with a higher incidence rate in nursing homes or long-term care facilities. When infections occur in this manner it is known as healthcare acquired MRSA or HA-MRSA. These 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.^[3]

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.^[7] Cases of MRSA in such populations were first reported in the United States, and then in Canada. The earliest reports were made by the CDC in state prisons. Subsequently, 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 the 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 the U.S. State of Oklahoma started treating an average of twelve Staphylococcus cases per month.^[8] A report on skin and soft tissue infections in the Cook County Jail in Chicago in 2004–05 demonstrated that MRSA was the most common cause of these infections among cultured lesions. Furthermore, 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 is a new clone of MRSA that 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.^[9]

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.^[10] Some samples of commercially sold meat products in Japan were also found to harbor MRSA strains.^[11]

In the United States, there have been increasing numbers of reports of outbreaks of MRSA colonization and infection through skin contact in locker rooms and gyms, even among healthy populations. A study published in the New England Journal of Medicine linked MRSA to the abrasions caused by artificial turf.^[12] Three studies by the Texas State Department of Health found that 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.^[13]

MRSA is also becoming a problem in pediatric settings,^[14] including hospital nurseries.^[15]

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The National Committee for Clinical Laboratory Standards (NCCLS), now called the Clinical and Laboratory Standards Institute (CLSI), recommends the cefoxitin disk screen test, the latex agglutination test for PBP2a, or a plate containing 6 μg/ml of oxacillin in Mueller-Hinton agar supplemented with NaCl (4% w/v; 0.68 mol/L) as alternative methods of testing for MRSA. For methods of inoculation, see CLSI Approved Standard M100-S15. According to Betsy McCaughey, founder of the Committee to Reduce Infection Deaths, MRSA can be detected in asymptomatic patients by a blood test. Combined with extra sanitary measures for those in contact with infected patients, screening patients admitted to hospitals has been found effective in minimizing spread of MRSA in hospitals in Denmark, Finland and the Netherlands.

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

• People in good health with a healthy immune system recover well from MRSA infections.
• Immunodeficiency patients suffer from severe forms of the disease, resulting in complications.

Complications of MRSA infection depends on the site of involvement. Some of the complications include:

• Septicemia
• Endocarditis
• Osteomyelitis
• Septic arthritis
• Pneumonia
• Necrotizing fasciitis
• Toxic shock syndrome
• CA-MRSA is associated with thrombosis
• Death

The major issue is that there are a number of factors that can lead to someone’s death, and it is believed that patients with MRSA bacteraemia are sicker and will consequently have a higher mortality rate because of their underlying illness. However, several studies, including one by Blot and colleagues, have adjusted for underlying disease, and they still found MRSA bacteraemia to have a higher attributable mortality than MSSA bacteraemia.

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