Staphylococcus aureus
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,
Toxic shock syndrome (TSS), 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.
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
etymological root of the bacteria's name:
aureus means "gold" in
Latin.
S. aureus is
catalase positive and thus able to convert
hydrogen peroxide (H
2O
2) 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.
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 1960, this had risen to 80%.
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.
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.
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.
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;
but the first case of
S. aureus truly resistant to glycopeptide antibiotics was only reported in 2002.
Three cases of VRSA infection have been reported in the United States.
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-lactamase-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 (PBP) that has a lower affinity for binding 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.
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, 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).
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.
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.
[Staphylococcus aureus. Electron Microscopy Unit, Beltsville Agricultural Research Center. U.S. Department of Agriculture. URL accessed 2006-07-22.M]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 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 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.
*
Staphylococcus - Todar's Online Textbook of Bacteriology
