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Staphylococcus aureus



Staphylococcus aureus

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

Staphylococcus aureus /ˌstæf.ə.ləˈkɒ.kəs ˈoɹˌiː.əs/, literally "Golden Cluster Seed" and also known as golden staph, is the most common cause of staph infections. It is a spherical bacterium, frequently living on the skin or in the nose of a person. Approximately 20–30% of the general population are "staph carriers" Staphylococcus aureus can cause a range of illnesses from minor skin infections, such as pimples, impetigo (may also be caused by Staphylococcus 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.[1] Each year some 500,000 patients in American hospitals contract a staphylococcal infection.[2]

Additional recommended knowledge

Contents

Microbiology

  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.[3] The golden appearance is the etymological root of the bacteria's name: aureus means "golden" in Latin.

S. aureus is a facultative anaerobe and opportunistic pathogen.

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 large 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 the enzyme "coagulase" that causes clot formation) while most other Staphylococcus species are coagulase-negative.[3] 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.[4] It is medically important to identify S.aureus correctly as S.aureus is much more aggressive and likely to be antibiotic-resistant.

Role in disease

S. aureus may occur as a commensal on human skin (particularly the scalp, armpits, penis and vagina); 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 occurence 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).[5]

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 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 spread.

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.

Toxic shock syndrome

Some strains of S. aureus produce toxic shock syndrome toxin, which are the causative agent for toxic shock syndrome. Some strains that produce an enterotoxin are the cause of staphylococcal food poisoning.

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.[6]

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. It also may occur as epidemics in hospital nuseries. he 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.[7]

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 salt utilization and subsequet 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.

Treatment and antibiotic resistance

For more details on this topic, see Methicillin-resistant Staphylococcus aureus (MRSA).

Staph infection that is not anibiotic resistant can be treated in about a month (depending on severity) using antibiotics.

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%.[8]

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 MSRA 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.

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.[9]

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.[10]

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.[11]

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;[12] but the first case of S. aureus truly resistant to glycopeptide antibiotics was only reported in 2002.[13] Three cases of VRSA infection have been reported in the United States.[14] as of 2005.

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.

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. [15]

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.

  1. ^ Ogston A (1984). "“On Abscesses”. Classics in Infectious Diseases". Rev Infect Dis 6 (1): 122–28. PMID 6369479.
  2. ^ Bowersox, John. "Experimental Staph Vaccine Broadly Protective in Animal Studies", NIH, 1999-05-27. Retrieved on 2007-07-28. 
  3. ^ a b Ryan KJ; Ray CG (editors) (2004). Sherris Medical Microbiology, 4th ed., McGraw Hill. ISBN 0-8385-8529-9. 
  4. ^ Matthews KR, Roberson J, Gillespie BE, Luther DA, Oliver SP (1997). "Identification and Differentiation of Coagulase-Negative Staphylococcus aureus by Polymerase Chain Reaction". Journal of Food Protection 60 (6): 686-8.
  5. ^ Curran JP, Al-Salihi FL (1980). "Neonatal staphylococcal scalded skin syndrome: massive outbreak due to an unusual phage type". Pediatrics 66 (2): 285–90. PMID 6447271.
  6. ^ Staphylococcus aureus. Electron Microscopy Unit, Beltsville Agricultural Research Center. U.S. Department of Agriculture. URL accessed 2006-07-22.M
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  10. ^ Johnson AP, Aucken HM, Cavendish S, Ganner M, Wale MC, Warner M, Livermore DM, Cookson BD (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.
  11. ^ Blot SI, Vandewoude KH, Hoste EA, Colardyn FA (2002). "Outcome and attributable mortality in critically Ill patients with bacteremia involving methicillin-susceptible and methicillin-resistant Staphylococcus aureus". Arch Intern Med 162 (19): 2229–35. PMID 12390067.
  12. ^ Hiramatsu K, Hanaki H, Ino T, Yabuta K, Oguri T, Tenover FC (1997). "PDF Methicillin-resistant Staphylococcus aureus clinical strain with reduced vancomycin susceptibility". J Antimicrob Chemother 40 (1): 135–6. PMID 9249217.
  13. ^ Chang S, Sievert DM, Hageman JC, Boulton ML, Tenover FC, Downes FP, Shah S, Rudrik JT, Pupp GR, Brown WJ, Cardo D, Fridkin SK (2003). "Infection with vancomycin-resistant Staphylococcus aureus containing the vanA resistance gene". N Engl J Med 348 (14): 1342–7. PMID 12672861.
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  15. ^ Cook H, Furuya E, Larson E, Vasquez G, Lowy F (2007). "Heterosexual transmission of community-associated methicillin-resistant Staphylococcus aureus". Clin Infect Dis 44 (3): 410–3. PMID 17205449.

Editing resource: Burton, Gwendolyn R.W. "Microbiology for the Health Sciences"

 
This article is licensed under the GNU Free Documentation License. It uses material from the Wikipedia article "Staphylococcus_aureus". A list of authors is available in Wikipedia.
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