Staphylococcus aureus
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{{Taxobox
| color = lightgrey | name = Staphylococcus aureus | image = Staphylococcus aureus Gram.jpg | image_width = 200px | regnum = Bacteria | phylum = Firmicutes | classis = Bacilli | ordo = Bacillales | familia = Staphylococcaceae | genus = Staphylococcus | species = S. aureus | binomial = Staphylococcus aureus | binomial_authority = Rosenbach 1884 }}
Staphylococcus aureus (which is occasionally given the nickname golden staph) is a bacterium, frequently living on the skin or in the nose of a healthy person, that can cause illnesses ranging from minor skin infections (such as pimples, boils, and cellulitis) and abscesses, to life-threatening diseases such as pneumonia, meningitis, endocarditis and septicemia. Each year some 500,000 patients in American hospitals contract a staphylococcal infection. It is a spherical bacterium. It is abbreviated to S. aureus or sometimes referred to as Staph aureus in medical literature, and should not be confused with the somewhat similar named streptococci which are also medically important.
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Microbiology
S. aureus is a Gram-positive coccus, which appears as grape-like clusters when viewed through a microscope and as large, round, golden-yellow colonies, often with β-hemolysis, when grown on blood agar plates. The golden appearance is the eytmological root of the bacteria's name: aureus means "gold" 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. S. aureus can be differentiated from most other staphylococci by the coagulase test: S. aureus is coagulase-positive, while most other Staphylococcus species are coagulase-negative.
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.
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 reisistant; and by 1950, this had risen to 80%.<ref name="EmergInfectDis2001-Chambers">Template:Cite journal</ref>
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 methicillin-resistant S. aureus (MRSA) was reported in England.<ref name="BMJ1961-Jevons">Template:Cite journal</ref> Despite this, MRSA generally remained an uncommon finding even in hospital settings until the 1990's when there was an explosion in MRSA prevalence in hospitals where it is now endemic.<ref name="JAntimicrobChemother2001-Johnson">Template:Cite journal</ref>
First line treatment for 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. <ref name="ArchInternMed2002-Blot">Template:Cite journal</ref>
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;<ref name="JAntimicrobChemother1997-Hiramatsu">Template:Cite journal</ref> but the first case of S. aureus truly resistant to glycopeptide antibiotics was only reported in 2002.<ref name="NEJM-Chang">Template:Cite journal</ref> Three cases of VRSA infection have been reported in the United States.<ref name="ClinMicroInf2005-Menichetti">Template:Cite journal</ref>
Mechanisms of antibiotic resistance
Staphylococcal resistance to penicillin and cephalosporins is mediated by β-lactamase production: enzymes which break down the β-lactam ring of the penicillin molecule. β-lacatamase-resistant penicillins such as methicillin, oxacillin, cloxacillin and flucloxacillin are able to resist degradation by staphylococcal β-lacatamase.
The mechanism of resistance to methicillin is by the acquisition of the mecA gene, which codes for an altered penicillin-binding protein (ABP) that fails to bind β-lactams (penicillins, cephalosporins and carbapenems).
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 that vancomycin will not bind to.
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 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, but has never been found on food animals such as poultry or swine. It can survive for some hours on dry environmental surfaces, but the importance of the environment in spread of Staph. aureus is currently debated.
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).<ref name="Pediatrics1980-Curran">Template:Cite journal</ref>
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 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 an important cause of increased morbidity and mortality from this disease.
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 Staph. 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 chapter on infection control for further details.
Staff or patients who are found to carry resistant strains of S. aureus may be required to undergo "eradication therapy" usually 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.
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 Staph. 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 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.<ref name="JExpMed2005-Liu">Template:Cite journal</ref>
References and footnotes
- Template:Cite book
- Staphylococcus - Todar's Online Textbook of Bacteriology
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