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'''Staphylococcus aureus''' , (literally "Golden Cluster Seed")is the most common cause of ''staph infections'', is a spherical bacterium, frequently living on the skin or in the nose of a person, that can cause a range of illnesses from minor skin infections, such as pimples, impetigo, boils, cellulitis and abscesses, to life-threatening diseases, such as pneumonia, meningitis, endocarditis, Toxic shock syndrome (TSS), and septicemia. Abbreviated to ''S. aureus'' or ''Staph aureus'' in medical literature, ''S. aureus'' should not be confused with the similarly named (and also medically relevant) species of the genus ''Streptococcus''.
''S. aureus'' was discovered in Aberdeen, Scotland in 1880 by the surgeon Sir Alexander Ogston in pus from surgical abscesses.[1] Each year some 500,000 patients in American hospitals contract a staphylococcal infection. Experimental Staph Vaccine Broadly Protective in Animal Studies John Bowersox
Microbiology
Gram stain of ''S. aureus''.
''S. aureus'' is a Gram-positive coccus, which appears as grape-like clusters when viewed through a microscope and has large, round, golden-yellow colonies, often with β-hemolysis, when grown on blood agar plates. Sherris Medical Microbiology, Ryan KJ; Ray CG (editors), , , McGraw Hill, 2004, ISBN 0-8385-8529-9 The golden appearance is the etymological root of the bacteria's name: ''aureus'' means "golden" in Latin.
''S. aureus'' is catalase positive and thus able to convert hydrogen peroxide (H2O2) to water and oxygen, which makes the catalase test useful to distinguish staphylococci from enterococci and streptococci. A large percentage of ''S. aureus'' can be differentiated from most other staphylococci by the coagulase test: ''S. aureus'' is primarily coagulase-positive, while most other ''Staphylococcus'' species are coagulase-negative. However, while the majority of ''S. aureus'' are coagulase-positive, some may be atypical in that they do not produce coagulase. Incorrect identification of an isolate can impact implementation of effective treatment and/or control measures.[2] It is medically important to identify ''S.aureus'' correctly as ''S.aureus'' is much more aggressive and likely to be antibiotic-resistant. ''Coagulase-negative S. aureus'' appears to be an increasing problem that clinical laboratories should be aware of. They are as virulent as those producing coagulase and can colonize, cause infections and spread among patients.[3]
''S. aureus'' has about 2,600 genes and 2.8 million bp of DNA in its chromosome. Plasmids can also comprise part of the species' genome.
The species has been subdivided into two subspecies: ''S. aureus aureus'' and ''S. aureus anaerobius''. The latter requires anaerobic conditions for growth, is an infrequent cause of infection, and is rarely encountered in the clinical laboratory.
Mechanisms of antibiotic resistance
Staphylococcal resistance to penicillin is mediated by penicillinase (a form of β-lactamase) production: an enzyme which breaks down the β-lactam ring of the penicillin molecule. Penicillinase-resistant penicillins such as methicillin, oxacillin, cloxacillin, dicloxacillin and flucloxacillin are able to resist degradation by staphylococcal penicillinase.
The mechanism of resistance to methicillin is by the acquisition of the mecA gene, which codes for an altered penicillin-binding protein (PBP) that has a lower affinity for binding β-lactams (penicillins, cephalosporins and carbapenems). This confers resistance to all β-lactam antibiotics and obviates their clinical use during MRSA infections.
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.
Staph infections lead to rapid weight loss and muscle depletion. Even after fully cured, it will still take months to recuperate fully.
Treatment and the development of antibiotic resistance
Antibiotic resistance in ''S. aureus'' was almost unknown when penicillin was first introduced in 1943; indeed, the original petri dish on which Alexander Fleming observed the antibacterial activity of the penicillium mould 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%.[4]
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, due to a penicillinase (a form of β-lactamase). 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 methicillin-resistant ''S. aureus'' ('MRSA') was reported in England.[5]If the bacteria produces the enzymes β-lactamase or penicillinase, these enzymes will break open the β-lactam ring of the antibiotic, rendering the antibiotic ineffective
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.[6]
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 lead 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, mainly centred around the need for intravenous administration (there is no oral preparation available), toxicity and the need to monitor drug levels regularly by means of blood tests. There are also concerns that 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'' as outcomes are inferior.[7]
Because of the high level of resistance to penicillins, and because of the potential for MRSA to develop resistance to vancomycin, the Centers for Disease Control and Prevention have 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. When the infection is confirmed to be due to a methicillin-susceptible strain of ''S. aureus'', then 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;[8]
but the first case of ''S. aureus'' truly resistant to glycopeptide antibiotics was only reported in 2002.[9]
Three cases of VRSA infection have been reported in the United States.[10] as of 2005.
Role in disease
''S. aureus'' may occur as a commensal on human skin (particularly the scalp, armpits and groins); it also occurs in the nose (in about 25% of the population) and throat and less commonly, may be found in the colon and in urine. The finding of ''Staph. aureus'' under these circumstances does not always indicate infection and therefore does not always require treatment (indeed, treatment may be ineffective and re-colonisation may occur). It can survive on domesticated animals such as dogs, cats and horses, and can cause bumblefoot in chickens. It can survive for some hours on dry environmental surfaces, but the importance of the environment in spread of ''S. aureus'' is currently debated. It can host phages, such as the Panton-Valentine leukocidin, that increase its virulence.
''S. aureus'' can infect other tissues when normal barriers have been breached (e.g. skin or mucosal lining). This leads to furuncles (boils) and carbuncles (a collection of furuncles). In infants ''S. aureus'' infection can cause a severe disease Staphylococcal scalded skin syndrome (SSSS).[11]
''S. aureus'' infections can be spread through contact with pus from an infected wound, skin-to-skin contact with an infected person, and contact with objects such as towels, sheets, clothing, or athletic equipment used by an infected person.
Deeply situated ''S. aureus'' infections can be very severe. Prosthetic joints put a person at particular risk for septic arthritis, and staphylococcal endocarditis (infection of the heart valves) and pneumonia, which may be rapidly fatal.
''Staphylococcus aureus'' and influenza
''S. aureus'' superinfection is an uncommon complication of influenza. However, in the last three influenza pandemics (1918, 1957–58, and 1968), added infection with ''S. aureus'' was a common complication.
Toxic Shock Syndrome
Certain strains of ''S. aureus'' are also the causative agent for Toxic Shock Syndrome.
Mastitis in cows
''S. aureus'' 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.[12]
Infection control
Spread of ''S. aureus'' (including MRSA) is through human-to-human contact, with environmental contamination thought to play a relatively unimportant part. Emphasis on basic hand washing techniques are therefore effective in preventing the transmission of ''S. aureus''. 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 article on infection control for further details.
An important and previously unrecognized means of community-associated methicillin-resistant S. aureus colonization and transmission is during sexual contact. [13]
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.
March 2007: The BBC has reported promising experiments in UK
where a vaporizer spraying some essential oils into the atmosphere reduced airborne bacterial counts by 90% and kept MRSA infections at bay. This may hold promise in MRSA infection control.
Virulence factors
Toxins
Depending on the strain, ''S. aureus'' is capable of secreting several toxins, which can be categorized into three groups. Many of these toxins are associated with specific diseases.
'Pyrogenic toxin superantigens' (PTSAgs) have superantigen activities that induce toxic shock syndrome (TSS). This group includes the toxin TSST-1, which causes TSS associated with tampon use. The staphylococcal enterotoxins, which cause a form of food poisoning, are included in this group.
'Exfoliative toxins' are implicated in the disease staphylococcal scalded-skin syndrome (SSSS), which occurs most commonly in infants and young children. The protease activity of the exfoliative toxins causes peeling of the skin observed with SSSS.
Staphylococccal 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. The genes encoding the components of PVL are encoded on a bacteriophage found in community-associated MRSA strains.
Role of pigment in virulence
The vivid yellow pigmentation of ''S. aureus'' may be a factor in its virulence. When comparing a normal strain of ''S. aureus'' with a strain modified to lack the yellow coloration, the pigmented strain was more likely to survive dousing with an oxidizing chemical such as hydrogen peroxide than the mutant strain was.
Colonies of the two strains were also exposed to human neutrophils. The mutant colonies quickly succumbed while many of the pigmented colonies survived. Wounds on mice were swiped with the two strains. The pigmented strains created lingering abscesses. Wounds with the unpigmented strains healed quickly.
These tests suggest that the yellow pigment may be key to the ability of ''S. aureus'' to survive immune system attacks. Drugs that inhibit the bacterium's production of the carotenoids responsible for the yellow coloration may weaken it and renew its susceptibility to antibiotics.[14]
Footnotes
1. “On Abscesses”. Classics in Infectious Diseases, Ogston A, , , Rev Infect Dis, 1984
2. Identification and Differentiation of Coagulase-Negative Staphylococcus aureus by Polymerase Chain Reaction, Matthews KR, Roberson J, Gillespie BE, Luther DA, Oliver SP, , , Journal of Food Protection, 1997
3. Isolation and Characterization of Coagulase-Negative Methicillin-Resistant Staphylococcus aureus from Patients in an Intensive Care Unit, Inaam A Al Obaida, EE Udob, LE Jacobb, M Johnya, , , Medical Principles and Practice, 1999
4. The changing epidemiology of Staphylococcus aureus?, Chambers HF, , , Emerg Infect Dis, 2001
5. Celbenin-resistant staphylococci, Jevons MP, , , BMJ, 1961
6. 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), Johnson AP, Aucken HM, Cavendish S, Ganner M, Wale MC, Warner M, Livermore DM, Cookson BD, , , J Antimicrob Chemother, 2001
7. Outcome and attributable mortality in critically Ill patients with bacteremia involving methicillin-susceptible and methicillin-resistant Staphylococcus aureus, Blot SI, Vandewoude KH, Hoste EA, Colardyn FA, , , Arch Intern Med, 2002
8. Methicillin-resistant Staphylococcus aureus clinical strain with reduced vancomycin susceptibility, Hiramatsu K, Hanaki H, Ino T, Yabuta K, Oguri T, Tenover FC, , , J Antimicrob Chemother, 1997
9. Infection with vancomycin-resistant Staphylococcus aureus containing the vanA resistance gene, Chang S, Sievert DM, Hageman JC, Boulton ML, Tenover FC, Downes FP, Shah S, Rudrik JT, Pupp GR, Brown WJ, Cardo D, Fridkin SK, , , N Engl J Med, 2003
10. Current and emerging serious Gram-positive infections, Menichetti F, , , Clin Microbiol Infect, 2005
11. Neonatal staphylococcal scalded skin syndrome: massive outbreak due to an unusual phage type, Curran JP, Al-Salihi FL, , , Pediatrics, 1980
12. ''Staphylococcus aureus''. Electron Microscopy Unit, Beltsville Agricultural Research Center. U.S. Department of Agriculture. URL accessed 2006-07-22.M
13. Heterosexual transmission of community-associated methicillin-resistant Staphylococcus aureus, Cook H, Furuya E, Larson E, Vasquez G, Lowy F, , , Clin Infect Dis, 2007
14. Staphylococcus aureus golden pigment impairs neutrophil killing and promotes virulence through its antioxidant activity, Liu GY, Essex A, Buchanan JT, Datta V, Hoffman HM, Bastian JF, Fierer J, Nizet V, , , J Exp Med, 2005
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