Staphylococcus aureus

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Staphylococcus aureus

Scientific classification
Domain: Bacteria
Kingdom: Eubacteria
Phylum: Firmicutes
Class: Cocci
Order: Bacillales
Family: Staphylococcaceae
Genus: Staphylococcus
Species: S. aureus
Binomial name
Staphylococcus aureus
Rosenbach 1884

Staphylococcus aureus (pronounced /ˌstæfɨləˈkɒkəs ˈɔriəs/, literally the "golden cluster seed" or "the seed gold" and also known as golden staph) is the most common cause of staph infections. .It is a spherical bacterium, frequently found in the nose and skin of a person. About 20% of the population are long-term carriers of S. aureus.[1] S. aureus can cause a range of illnesses from minor skin infections, such as pimples, impetigo (may also be caused by Streptococcus pyogenes), boils, cellulitis folliculitis, furuncles, carbuncles, scalded skin syndrome and abscesses, to life-threatening diseases such as pneumonia, meningitis, osteomyelitis, endocarditis, Toxic shock syndrome (TSS), and septicemia. Its incidence is from skin, soft tissue, respiratory, bone, joint, endovascular to wound infections. It is still one of the four most common causes of nosocomial infections, often causing postsurgical wound infections. 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.[2] Each year some 500,000 patients in American hospitals contract a staphylococcal infection.[3]

Contents

[edit] Microbiology

Gram stain of S. aureus.

S. aureus is a facultatively anaerobic, Gram-positive coccus, which appears as grape-like clusters when viewed through a microscope and has large, round, golden-yellow colonies, often with hemolysis, when grown on blood agar plates.[4] The golden appearance is the etymological root of the bacteria's name: aureus means "golden" in Latin.

S. aureus is catalase positive (meaning that it can produce the enzyme "catalase") and able to convert hydrogen peroxide (H2O2) to water and oxygen, which makes the catalase test useful to distinguish staphylococci from enterococci and streptococci. A small percentage of S. aureus can be differentiated from most other staphylococci by the coagulase test: S. aureus is primarily coagulase-positive (meaning that it can produce "coagulase", a protein product, which is an enzyme) that causes clot formation while most other Staphylococcus species are coagulase-negative.[4] 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.[5]

[edit] Role in disease

Further information: Coagulase-positive staphylococcal infection

S. aureus may occur as a commensal on human skin; it also occurs in the nose frequently (in about a third of the population)[6] and throat less commonly. The occurrence of S. 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).[7]

S. aureus infections can be spread through contact with pus from an infected wound, skin-to-skin contact with an infected person by producing hyaluronidase that destroy tissues, and contact with objects such as towels, sheets, clothing, or athletic equipment used by an infected person. Deeply penetrating S. aureus infections can be 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 spread.

[edit] Atopic dermatitis

S. aureus is extremely prevalent in atopic dermatitis patients, who are less resistant to it than other people. It often causes complications. The disease is most likely found in fertile active places including, the armpits, hair and scalp. Large pimples in those areas, when popped will cause the worst of the infection. This can lead to Scalded Skin Syndrome. Severe form of this is Reiter's syndrome seen in neonates.

[edit] Toxic shock syndrome and S. aureus food poisoning

Some strains of S. aureus, which produce the exotoxin TSST-1, are the causative agents of toxic shock syndrome. Some strains of S. aureus also produce an enterotoxin that is the causative agent of S. aureus gastroenteritis. The gastroenteritis is self-limiting with the person getting better in 8-24 hours. Symptoms include nausea, vomiting, diarrhea, and abdominal pain.

[edit] 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.[8]

[edit] Protein A

Protein A is a protein that is anchored to staphylococcal peptidoglycan pentaglycine bridges by the transpeptidase Sortase A.[9] Protein A is an IgG-binding protein which binds to the Fc region of an antibody. In fact, studies involving mutation of genes coding for Protein A resulted in a lowered virulence of S. aureus as measured by survival in blood, and this has led to speculation that Protein A contributed virulence requires binding of antibody Fc regions.[10] Protein A in various recombinant forms has been used for decades to bind and purify a wide range of antibodies by immunoaffinity chromatography. Transpeptidases such as the sortases which are responsible for anchoring factors like Protein A to the staphylococcal peptidoglycan are being studied in hopes of developing new antibiotics to target MRSA infections.[11]

[edit] Virulence factors

[edit] 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
EF toxins are implicated in the disease staphylococcal scalded-skin syndrome (SSSS), which occurs most commonly in infants and young children. It also may occur as epidemics in hospital nurseries. The protease activity of the exfoliative toxins causes peeling of the skin observed with SSSS.
Other toxins
Staphylococcal 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.

[edit] Role of pigment in virulence

Some strains of S. aureus are capable of producing staphyloxanthin - a carotenoid pigment that acts as a virulence factor. Its has an antioxidant action that helps the microbe to evade killing with reactive oxygen used by the host immune system. It is thought that staphyloxantin is responsible for S. aureus' characteristic golden colour.[12] 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 designed to inhibit the bacterium's production of the staphyloxanthin may weaken it and renew its susceptibility to antibiotics.[13]

[edit] Diagnosis

Depending upon the type of infection present, an appropriate specimen is obtained accordingly and sent to the laboratory for definitive identification by using biochemical or enzyme-based tests. A Gram stain is first performed to guide the way, which should show typical gram-positive bacteria, cocci, in clusters. Secondly, culture the organism in mannitol salt agar, which is a selective medium with 7–9% NaCl that allows S. aureus to grow producing yellow-colored colonies as a result of mannitol fermentation and subsequent drop in the medium's pH. Furthermore, for differentiation on the species level, catalase (positive for all species), coagulase (fibrin clot formation), DNAse (zone of clearance on nutrient agar), lipase (a yellow color and rancid odor smell), and phosphatase (a pink color) tests are all done. For staphylococcal food poisoning, phage typing can be performed to determine if the staphylococci recovered from the food to determine the source of infection.

[edit] Rapid Diagnosis and Typing

Diagnostic microbiology laboratories and reference laboratories are key for identifying outbreaks and new strains of S. aureus. Recent genetic advances have enabled reliable and rapid techniques for the identification and characterization of clinical isolates of S. aureus in real-time. These tools support infection control strategies to limit bacterial spread and ensure the appropriate use of antibiotics. These techniques include Real-time PCR and Quantitative PCR and are increasingly being employed in clinical laboratories.[14][15]

[edit] Treatment and antibiotic resistance

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The article, Methicillin-resistant Staphylococcus aureus, contains related information on this topic

The treatment of choice for S. aureus infection is penicillin; but in most countries, penicillin-resistance is extremely common and first-line therapy is most commonly a penicillinase-resistant penicillin (for example, oxacillin or flucloxacillin). Combination therapy with gentamicin may be used to treat serious infections like endocarditis,[16][17] but its use is controversial because of the high risk of damage to the kidneys.[18][19] The duration of treatment depends on the site of infection and on severity.

Antibiotic resistance in S. aureus was almost unknown when penicillin was first introduced in 1943; indeed, the original petri dish on which Alexander Fleming of Imperial College London 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%.[20]

[edit] 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, nafcillin, oxacillin, cloxacillin, dicloxacillin and flucloxacillin are able to resist degradation by staphylococcal penicillinase.

The mechanism of resistance to methicillin is mediated via the mec operon, part of the staphylococcal cassette chromosome mec (SCCmec). Resistance is conferred by the mecA gene, which codes for an altered penicillin-binding protein (PBP2a or PBP2') that has a lower affinity for binding β-lactams (penicillins, cephalosporins and carbapenems). This allows for resistance to all β-lactam antibiotics and obviates their clinical use during MRSA infections. As such the glycopeptide, vancomycin, is often deployed against MRSA.

Aminoglycosides such as kanamycin, gentamicin, streptomycin, etc. were once effective against Staphylococcal infections until the organism evolved mechanisms to destroy the aminoglycosides action, which occurs via protonated amine and/or hydroxyl interactions with the ribosomal RNA of the bacterial 30S Ribosome[21] There are three main mechanisms of aminoglycoside resistance mechanisms which are currently and widely accepted: Aminoglycoside modifying enzymes, Ribosomal mutations, and active efflux of the drug out of the bacteria.

Aminoglycoside modifying enzymes are enzymes that inactivate the aminoglycoside by covalently attaching either a phosphate, nucleotide, or acetyl moiety to either the amine and/or alcohol functionality of the antibiotic; thus rendering the antibiotic through sterics or lack of charge, ineffective in ribosomal binding affinity. In Staphylococcus Aureus the best characterized aminoglycoside modifying enzyme is ANT(4')IA Aminoglycoside adenylyltransferase 4' IA. This enzyme has been solved by X-Ray Crystallography[22] The enzyme is able to attach an adenyl moiety to the 4' hydroxyl group of many aminoglycosides including kamamycin and gentamicin.

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.

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.[23]

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.[24]

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 led 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.[25]

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 guidelinesfor 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;[26] but the first case of S. aureus truly resistant to glycopeptide antibiotics was only reported in 2002.[27] Three cases of VRSA infection have been reported in the United States as of 2005.[28]

[edit] Infection control

Spread of S. aureus (including MRSA) is through human-to-human contact, although recently some vets have discovered that the infection can be spread through pets, 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.

Recently, there have been a myriad of reported cases of S. aureus in hospitals across America. The pathogen has had facilitated transportation in medical facilities mainly because of insufficient healthcare worker hygiene. S. aureus is an incredibly hardy bacterium, as was shown in a study where it survived on a piece of polyester for just under three months,[29] polyester being the main material used in hospital privacy curtains.

The bacterium is able to transport itself on the hands of healthcare workers who, for instance, get the bacteria from a seemingly healthy patient carrying a "benign" or commensal strain of the pathogen and then pass it on to the next patient being cared for. Introduction of the bacterium into the bloodstream can lead to various complications including, but not limited to, endocarditis, meningitis, and, if it is widespread, sepsis - toxins infecting the entire body.

Because of these infections in hospitals, as of February 14th, 2008, all California medical facilities must now report S. aureus infections that are checked into the hospitals, in the hope of starting a trend to aid disease trackers and pathologists in their search for a cure.[citation needed] 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.

An important and previously unrecognized means of community-associated methicillin-resistant S. aureus colonization and transmission is during sexual contact.[30]

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.

In March 2007, the BBC reported that a vaporizer spraying some essential oils (including tea tree oil[31]) into the atmosphere reduced airborne bacterial counts by 90% and kept MRSA infections at bay and may hold promise in MRSA infection control.[32]

[edit] References

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  31. ^ [1]
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