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''Staphylococcus aureus'' became methicillin resistant by acquiring a ''[[mecA]]'' [[gene]], usually carried on a larger piece of DNA called a staphylococcal cassette chromosome ''[[SCCmec]]''. Expression of mecA yields PBP2a, a [[penicillin binding protein]] with reduced affinity for β-lactam antibiotic binding.<ref>{{cite journal | author=Guignard B, Entenza JM, Moreillon P | title=Beta-lactams against methicillin-resistant ''Staphylococcus aureus'' | journal=Curr Opin Pharmacol | year=2005 | pages=479-89 | volume=5 | issue=5 | pmid = 16095969}}</ref> Penicillin binding proteins are necessary for correct synthesis of the bacterial cell wall, and when they are blocked by penicillin, the cell wall is incorrectly formed, and the cell is liable to lyse. PBP2a allows the bacterium to synthesise cell wall normally in the presence of methicillin.
''Staphylococcus aureus'' became methicillin resistant by acquiring a ''[[mecA]]'' [[gene]], usually carried on a larger piece of DNA called a staphylococcal cassette chromosome ''[[SCCmec]]''. Expression of mecA yields PBP2a, a [[penicillin binding protein]] with reduced affinity for β-lactam antibiotic binding.<ref>{{cite journal | author=Guignard B, Entenza JM, Moreillon P | title=Beta-lactams against methicillin-resistant ''Staphylococcus aureus'' | journal=Curr Opin Pharmacol | year=2005 | pages=479-89 | volume=5 | issue=5 | pmid = 16095969}}</ref> Penicillin binding proteins are necessary for correct synthesis of the bacterial cell wall, and when they are blocked by penicillin, the cell wall is incorrectly formed, and the cell is liable to lyse. PBP2a allows the bacterium to synthesise cell wall normally in the presence of methicillin.


Some strains of ''S. aureus'' over-express [[Beta lactamase|β-lactamase]] and thus can appear to be resistant to [[oxacillin]] and, rarely, methicillin despite being ''mecA''-negative. Beta-lactamase is an enzyme that cleaves the penicillin molecule at its cyclic ring, and second generation penicillins like methicillin were specifically designed to resist beta-lactamase activity.
Some strains of ''S. aureus'' over-express [[Beta lactamase|β-lactamase]] and are resistant to [[oxacillin]] and, rarely, methicillin despite being ''mecA''-negative. Beta-lactamase is an enzyme that cleaves the penicillin molecule at its cyclic ring, and second generation penicillins like methicillin were specifically designed to resist beta-lactamase activity.


Recent outbreaks of CA-MRSA appear to be caused by isolates that also carry genes for [[Panton-Valentine leukocidin]] (PVL),<ref name=Miller_2005>{{cite journal |author=Miller L, Perdreau-Remington F, Rieg G, Mehdi S, Perlroth J, Bayer A, Tang A, Phung T, Spellberg B |title=Necrotizing fasciitis caused by community-associated methicillin-resistant ''Staphylococcus aureus'' in Los Angeles |journal=N Engl J Med |volume=352 |issue=14 |pages=1445-53 |year=2005 | url=http://content.nejm.org/cgi/content/abstract/352/14/1445 | pmid = 15814880}}</ref> a toxin that is known to cause lysis of white blood cells. It has been shown that PVL contributes to severe haemolytic and necrotic pneumonia in children,<ref>{{cite journal |author=Labandeira-Rey M, Couzon F, Boisset S, Brown EL, Bes M, Benito Y, Barbu EM, Vazquez V, Hook M, Etienne J, Vandenesch F, Bowden MG. |title=''Staphylococcus aureus'' Panton-Valentine leukocidin causes necrotizing pneumonia.|journal=Science |volume=315 |issue=5815 |pages=1130-3 |year=2007 | url=http://www.sciencemag.org/cgi/content/full/315/5815/1130}}</ref> but its role in severe skin and soft tissue infection is currently debated. <ref> {{cite journal | author=Voyich JM, Otto M, Mathema B, Braughton KR, Whitney AR, Welty D, Long RD, Dorward DW, Gardner DJ, Lina G, Kreiswirth BN, DeLeo FR |title=Is Panton-Valentine leukocidin the major virulence determinant in community-associated methicillin-resistant ''Staphylococcus aureus'' disease? |journal=J Infect Dis |volume=194 |issue=12 |pages=1761-70 |year=2006 | url=http://www.journals.uchicago.edu/JID/journal/issues/v194n12/36574/36574.html}}</ref>
Recent outbreaks of CA-MRSA appear to be caused by isolates that also carry genes for [[Panton-Valentine leukocidin]] (PVL),<ref name=Miller_2005>{{cite journal |author=Miller L, Perdreau-Remington F, Rieg G, Mehdi S, Perlroth J, Bayer A, Tang A, Phung T, Spellberg B |title=Necrotizing fasciitis caused by community-associated methicillin-resistant ''Staphylococcus aureus'' in Los Angeles |journal=N Engl J Med |volume=352 |issue=14 |pages=1445-53 |year=2005 | url=http://content.nejm.org/cgi/content/abstract/352/14/1445 | pmid = 15814880}}</ref> a toxin that is known to cause lysis of white blood cells. It has been shown that PVL contributes to severe haemolytic and necrotic pneumonia in children,<ref>{{cite journal |author=Labandeira-Rey M, Couzon F, Boisset S, Brown EL, Bes M, Benito Y, Barbu EM, Vazquez V, Hook M, Etienne J, Vandenesch F, Bowden MG. |title=''Staphylococcus aureus'' Panton-Valentine leukocidin causes necrotizing pneumonia.|journal=Science |volume=315 |issue=5815 |pages=1130-3 |year=2007 | url=http://www.sciencemag.org/cgi/content/full/315/5815/1130}}</ref> but its role in severe skin and soft tissue infection is currently debated. <ref> {{cite journal | author=Voyich JM, Otto M, Mathema B, Braughton KR, Whitney AR, Welty D, Long RD, Dorward DW, Gardner DJ, Lina G, Kreiswirth BN, DeLeo FR |title=Is Panton-Valentine leukocidin the major virulence determinant in community-associated methicillin-resistant ''Staphylococcus aureus'' disease? |journal=J Infect Dis |volume=194 |issue=12 |pages=1761-70 |year=2006 | url=http://www.journals.uchicago.edu/JID/journal/issues/v194n12/36574/36574.html}}</ref>

Revision as of 00:18, 26 September 2007

Methicillin-resistant Staphylococcus aureus
Electron micrograph of MRSA
Scientific classification
Domain:
Bacteria
Kingdom:
Bacteria
Phylum:
Firmicutes
Class:
Bacilli
Order:
Bacillales
Family:
Staphylococcaceae
Genus:
Staphylococcus
Species:
S. aureus
Binomial name
Staphylococcus aureus
Rosenbach 1884

Methicillin-resistant Staphylococcus aureus (MRSA) is an isolate of the bacterium Staphylococcus aureus characterized by antibiotic resistance to all penicillins, including methicillin and other narrow-spectrum β-lactamase-resistant penicillin antibiotics.[1] MRSA was discovered for the first time in 1961 in the UK, but it is now widespread in the hospital setting. MRSA is commonly termed a superbug.

MRSA may also be known as oxacillin-resistant Staphylococcus aureus (ORSA) and multiple-resistant Staphylococcus aureus. Strains of S. aureus that are non-resistant to methicillin are sometimes called methicillin-susceptible Staphylococcus aureus (MSSA) if an explicit distinction must be made.

Although MRSA has traditionally been seen as a hospital-associated infection, community-acquired MRSA strains have appeared in recent years, notably in the U.S. and Australia.[2] The abbreviations CA-MRSA (community-associated MRSA) and HA-MRSA (hospital-associated MRSA) are now commonly seen in medical literature.

Microbiology

Staphylococcus aureus became methicillin resistant by acquiring a mecA gene, usually carried on a larger piece of DNA called a staphylococcal cassette chromosome SCCmec. Expression of mecA yields PBP2a, a penicillin binding protein with reduced affinity for β-lactam antibiotic binding.[3] Penicillin binding proteins are necessary for correct synthesis of the bacterial cell wall, and when they are blocked by penicillin, the cell wall is incorrectly formed, and the cell is liable to lyse. PBP2a allows the bacterium to synthesise cell wall normally in the presence of methicillin.

Some strains of S. aureus over-express β-lactamase and are resistant to oxacillin and, rarely, methicillin despite being mecA-negative. Beta-lactamase is an enzyme that cleaves the penicillin molecule at its cyclic ring, and second generation penicillins like methicillin were specifically designed to resist beta-lactamase activity.

Recent outbreaks of CA-MRSA appear to be caused by isolates that also carry genes for Panton-Valentine leukocidin (PVL),[4] a toxin that is known to cause lysis of white blood cells. It has been shown that PVL contributes to severe haemolytic and necrotic pneumonia in children,[5] but its role in severe skin and soft tissue infection is currently debated. [6]

Morbidity and mortality

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.[7] Cosgrove et al,[8] 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; P[9] 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%.[10]

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 because of their underlying illness. However, several studies including one by Blot and colleagues that have adjusted for underlying disease still found MRSA bacteraemia to have a higher attributable mortality than MSSA bacteraemia.[11]

Clinical presentation and concerns

S. aureus most commonly colonises 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. Patients with compromised immune systems are at significantly greater risk of a symptomatic secondary infection.

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.[12]

Many people who are symptomatic present with pus-filled boils, and occasionally with rashes.

In the United States the Centers for Disease Control and Prevention, in guidelines issued 19 October 2006, citing the need for additional research, declined to recommend such screening.[13][14]

Treatment

Community-acquired MRSA often results in abscess formation that requires incision and drainage to treat. Prior to ca-MRSA, abscesses were not considered contagious (it was assumed that violation of skin integrity with introduction of staph from normal skin colonization was required). However, newly emerging ca-MRSA is transmissible (similar, but with very important differences) from hospital-acquired MRSA. ca-MRSA is less likely to cause cellulitis than other forms of MRSA.

Both ca-MRSA and ha-MRSA are resistant to traditional anti-staph beta lactam antibiotics, eg cephalexin. ca-MRSA has a greater sensitivity spectrum that includes sulfa drugs, tetracyclines, and clindamycin. ha-MRSA is resistant to even those antibiotics and often only sensitive to vancomycin. Newer drugs such as linezolid (newer oxazolidinones class) may be effective against both ca-MRSA and ha-MRSA.

Vancomycin and teicoplanin are glycopeptide antibiotics used to treat MRSA infections.[15] Teicoplanin is a structural congener of vancomycin that has a similar activity spectrum, but a longer half-life (t½).[16] The oral absorption of vancomycin and teicoplanin is very low and must be administered intravenously in order to control systematic infections.[17] One of the problems with vancomycin is not just that its route of administration is inconvenient, but also that it is inferior in terms of its efficacy compared to antistaphylococcal penicillins.[18][19]

Several new strains of MRSA have been found showing antibiotic resistance even to vancomycin and teicoplanin; those new evolutions of the MRSA bacteria are dubbed vancomycin intermediate-resistant Staphylococcus aureus (VISA).[20][21] Linezolid, quinupristin/dalfopristin, daptomycin, tigecycline are used to treat more severe infections that do not respond to the glycopeptides such as vancomycin.[22] MRSA infections can be treated with oral agents such as linezolid, rifampicin+fusidic acid, rifampicin+fluoroquinolone, pristinamycin, co-trimoxazole (trimethoprim-sulfamethoxazole), doxycycline or minocycline, and clindamycin.[23]

On 18 May 2006, a team of researchers from Merck Pharmaceuticals published in Nature that they had discovered an entirely new type of antibiotic, called platensimycin, and they have demonstrated that it can be used successfully to fight MRSA.[24][25]

An entirely different and promising approach is phage therapy (e.g., at the Tbilisi Institute in Georgia), which reports efficacy against up to 95% of tested Staphylococcus isolates.[26]

Raw honey dressings are also being successfully used for prevention and treatment of MRSA.[27][28]

It has been reported that use of maggots to treat an MRSA infection has been successful. Studies have been done on diabetic patients and the treatment time has been significantly less than that of other standard treatments. [29] [30]

Prevention and infection control strategies

Alcohol has proven to be an effective topical sanitizer against MRSA. Quaternary ammonium can be used in conjunction with alcohol to increase the duration of the sanitizing action. The prevention of nosocomial infections involve routine and terminal cleaning. Nonflammable alcohol vapor in CO2 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.

As MRSA has the capability to survive on surfaces and fabrics including privacy curtains or garments worn by care providers, the need for complete surface sanitation is necessary to eliminate MRSA in areas where patients are recovering from invasive procedures. Vaporized sanitizers reach areas missed by traditional cleaning methods, particularly in ICU and ER units. Ambulances, police vehicles, artificial turf surfaces, and sports equipment are also areas where MRSA can be found.

At the end of August 2004, after a successful pilot scheme to tackle MRSA, the UK National Health Service announced its Clean Your Hands campaign. Wards will be required to ensure that alcohol-based hand rubs are placed near to all beds so that staff can hand wash more regularly. It is thought that if this cuts infection by just 1% the plan will pay for itself many times over. Health care workers are reportedly largely neglecting the simple, yet effective, practice of hand-washing,[citation needed] despite the Centers for Disease Control and Prevention (CDC)'s report that hand-washing alone would save the lives of roughly 30,000 patients per year in the US, not from MRSA alone, but from all nosocomial infections.

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.[31] 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.[32] However, the number of MRSA infected people in the Netherlands is currently rising, because of numerous infections in pig farms. The MRSA strain is carried from pig to human. Very recently, the Dutch food association has discovered strains of the MRSA bacterium on pork meat. These strains were able to infect humans. For countries that have been overwhelmed by MRSA (such as the U.S. and UK), the Dutch model suggests that a co-ordinated re-instatement of search and destroy measures can still bring MRSA under control,[32] but given the enormous investment in facilities that would be required others have suggested that for all practical purposes the point of no return has already been passed.[33]

Epidemiology

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.[34] In the United States, 95 million carry S. aureus in their noses; of these 2.5 million (2.6% of carriers) carry MRSA.[35] 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.[36]

Because cystic fibrosis patients are often treated with multiple antibiotics in hospital settings, they are often colonised with MRSA, potentially increasing the rate of life-threatening MRSA pneumonia in this group. The risk of cross-colonisation 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 colonised with MRSA,[37] this is probably because many circulating strains of MRSA are fluoroquinolone-resistant, which means that MRSA is able to colonise 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 colonisation and infection through skin contact in locker rooms and gymnasiums, even among healthy populations. MRSA also is becoming a problem in paediatrics, [38] including hospital nurseries.[39] A 2007 study found that 4.6% of patients in US healthcare facilities were infected or colonized with MRSA. [40]

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.[41]

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.[42] 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.

During the summer of 2005, researchers in The Netherlands discovered that three pig farmers or their families were infected by MRSA bacteria that were also found on their pigs.[43] Researchers from Radboud University Nijmegen are now investigating how widespread the MRSA bacteria is in pigs, and whether it will become characterised among the zoonoses.

Recently, it has been observed that MRSA can replicate inside of Acanthamoeba, increasing MRSA numbers 1000-fold. [44] Since Acanthamoeba can form cysts easily picked up by air currents, these organisms can spread MRSA via airborne routes. Whether control of Acanthamoeba in the clinical environment will also help to control MRSA, remains an area for research.

Strains

In the UK, the most common strains are EMRSA15 and EMRSA16.[45] EMRSA16 is the best described epidemiologically: it originated in Kettering, England, and the full genomic sequence of this strain has been published.[46] This has been recognised 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.[47] 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, whereas 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,[48] 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.[47] Other community-associated strains of MRSA are ST8:USA500 and ST59:USA1000.

See also

References

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  26. ^ Matsuzaki S, Yasuda M, Nishikawa H, Kuroda M, Ujihara T, Shuin T, Shen Y, Jin Z, Fujimoto S, Nasimuzzaman MD, Wakiguchi H, Sugihara S, Sugiura T, Koda S, Muraoka A, Imai S (2003). "Experimental protection of mice against lethal Staphylococcus aureus infection by novel bacteriophage phi MR11". J. Infect. Dis. 187 (4): 613–24. PMID 12599078.{{cite journal}}: CS1 maint: multiple names: authors list (link)
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  36. ^ Jernigan JA, Arnold K, Heilpern K, Kainer M, Woods C, Hughes JM (2006-05-12). "Methicillin-resistant Staphylococcus aureus as community pathogen". Symposium on Community-acquired Methicillin-resistant Staphylococcus aureus (Atlanta, Georgia, USA). Cited in Emerg Infect Dis. Centers for Disease Control and Prevention. Retrieved 2007-01-27. {{cite conference}}: Unknown parameter |booktitle= ignored (|book-title= suggested) (help)CS1 maint: multiple names: authors list (link)
  37. ^ Charbonneau P, Parienti J, Thibon P, Ramakers M, Daubin C, du Cheyron D, Lebouvier G, Le Coutour X, Leclercq R (2006). "Fluoroquinolone use and methicillin-resistant Staphylococcus aureus isolation rates in hospitalized patients: a quasi experimental study". Clin Infect Dis. 42 (6): 778–84. PMID 16477553.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  38. ^ MRSA: the problem reaches paediatrics - Archives of Disease in Childhood
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  40. ^ Association for Professionals in Infection Control & Epidemiology (2007-06-25). "National Prevalence Study of Methicillin-Resistant Staphylococcus aureus (MRSA) in U.S. Healthcare Facilities". Retrieved 2007-07-14. {{cite web}}: External link in |author= (help)
  41. ^ Community-acquired meticillin-resistant Staphylococcusaureus: an emerging threat - The Lancet
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  44. ^ Single Cell Amoeba Increases MRSA Numbers One Thousand Fold
  45. ^ Johnson AP, Aucken HM, Cavendish S; et al. (2001). "Dominance of EMRSA-15 and -16 among MRSA causing nosocomial bacteraemia in the UK: analysis of isolates from the European Antimicrobial Resistance Surveillance System (EARSS)". J Antimicrob Chemother. 48 (1): 143–4. PMID 11418528. {{cite journal}}: Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
  46. ^ Holden MTG, Feil EJ, Lindsay JA; et al. (2004). "Complete genomes of two clinical Staphylococcus aureus strains: Evidence for the rapid evolution of virulence and drug resistance". Proc Natl Acad Sci U S A. 101: 9786–91. doi:10.1073/pnas.0402521101. PMID 15213324. {{cite journal}}: Explicit use of et al. in: |author= (help); Unknown parameter |issues= ignored (help)CS1 maint: multiple names: authors list (link)
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Further reading

  • Carson CF, Cookson BD, Farrelly HD, Riley TV (1995). "Susceptibility of methicillin-resistant Staphylococcus aureus to the essential oil of Melaleuca alternifolia". J. Antimicrob. Chemother. 35 (3): 421–4. PMID 7782258.{{cite journal}}: CS1 maint: multiple names: authors list (link)
  • Edwards-Jones V, Buck R, Shawcross SG, Dawson MM, Dunn K (2004). "The effect of essential oils on methicillin-resistant Staphylococcus aureus using a dressing model". Burns : journal of the International Society for Burn Injuries. 30 (8): 772–7. doi:10.1016/j.burns.2004.06.006. PMID 15555788.{{cite journal}}: CS1 maint: multiple names: authors list (link)
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