Staphylococcus aureus

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cellular organisms - Bacteria - Firmicutes - Bacilli - Bacillales - Staphylococcaceae - Staphylococcus - Staphylococcus aureus

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General information

• Staphylococcus aureus, Gram-positive, potentially pathogenic bacteria found in nasal membranes, skin, hair follicles, and perineum of warm-blooded animals. They may cause a wide range of infections and intoxications.
• The word Staphylococcus is derived from Greek "grapes". Latin word aureus ("gold") refers to color of the Staphyloccocus colonies growing on agar.
• Staphylococcus aureus has remarkable ability to develop resistance to antibiotics: for example, within 5 years after Alexander Fleming's discovery of penicillin and its wide distribution as antimicrobial agent, 50% of all S. aureus strains were resistant to it.
• Methicillin-Resistant Staphylococcus aureus (MRSA) is strain of Staphylococcus aureus that is non-susceptible to the action of methicillin. The mechanism of resistance usually involves modification of normal or the presence of acquired penicillin binding proteins. MRSA strains emerged as a noticable adversary within a decade of the first introduction of the methicilin as an antibiotic in 1959-1960.
• Approximately 20% of populations have persistent asymptomatic nasal colonization by S. aureus and 30% aqcuire it intermittently.
• Number of MRSA infection-associated deaths in United States is about 19,000 annually which is similar to number of deaths due to AIDS, tuberculosis, and viral hepatitis combined.
• Staphylococcal bacterial chromosome easily incorporates various mobile genetic elements, such as bacteriophages, plasmids, and so-called "pathogenicity islands". The incorporated elements encoding virulence factors can transform commensal microorganism into a pathogenic one. Resistance to methicilin and other beta-lactam antibiotics is caused by the mecA gene, which is situated on a mobile genetic element, known as, the Staphylococcal Cassette Chromosome mec (SCCmec).
• Two basic groups of virulence factors play role in S. aureus infections: (1) proteins expressed on the surface of the bacterial cell (exponential growth phase) and (2) secreted proteins (stationary phase). The following common phases of the infection are usually described: attachement, colonization, invasion or penetration, and evasion of host immunity.

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Types of MRSA infections

• Hospital-aqcuired MRSA (HA-MRSA). There are five major clones of S aureus that are responsible for most cases of HA-MRSA internationally: the Iberian, Brazilian, Hungarian, New York/Japan, and Pediatric clones. Different nomenclatures exist.
  
• Community-acquired MRSA (CA-MRSA). MSRA infection considered CA-MRSA when it occured in individual who was not exposed to hospital settings for a while. Outbreaks of the CA-MRSA in communities with limited health care started recieving attention since 1989-1990. Majority of fatal cases involved skin and soft tissue infections and necrotizing pneumonia.
  CA-MRSA strains are usually produce Panton-Valentine leukocidin, which is usually absent in HA-MRSA strains.
  USA400 (or MW2) and USA300 are among most virulent and best studied strains of CA-MRSA.

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Virulence factors

• Presence of numerous microbial surface components recognizing adhesive matrix molecules (MSCRAMM proteins) that mediate adherence to host tissues.
• Ability to form biofilms (slime) on host tissues and surfaces of implants. Bacteria inside the biofilms are relatively protected from host defenses and antimicrobial agents by a hydrated matrix of polysaccharides and proteins. It is very difficult, if not impossible, to non-invasively eradicate the biofilm-formed pathogens from infected tissues and prosthetic surfaces.
• Production of leukocidins, pore forming proteins, that destroy leukocytes by lysis of the cytoplasmic granules.
• Ability to produce superantigens - microbial antigens that induce over-activation of T-cells, their anergy and death. The superantigens cause non-specific systemic immune response that weakens the host facilitating subversion of its defenses whereas normal immune response involves development of specific antibodies which inactivate the pathogen and protect the organism.
• Agr protein (accessory gene regulator), a quorum-sensing system, plays a critical role in the regulation of S. aureus virulence. It is resposible for orchestrating the pathogen's invasion strategies (adherence, subversion of host immune responses, formation of biofilm, intracellular invasion, etc) on different stages of infections. The quorum-sensing system is a unique mechanism of modulation of bacterial gene expression in response to increased cell density.
• In conclusion, the S. aureus uses so many powerful and complex strategies to invade the host that it is not possible to enumerate them all in short review. Moreover, most probably, some of them are still to be dicovered.

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Pathologies

• Furunculosis
• Abscess
• Staphylococcal Scalded Skin Syndrome (SSSS)

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Possible severe complications

• Necrotizing pneumonia
• Empyema - presence of pus in a hollow organ or body cavity
• Waterhouse-Friderichsen Syndrome - overwhelming bacterial infection, leading to hemorrhage and necrosis of the adrenal gland
• Necrotizing fasciitis - a serious fulminating infection causing extensive necrosis of superficial fascia (connective tissue)
• Pyomyositis - suppurative inflammation of muscle tissue
• Toxic Shock Syndrome (TSS). TSS is usually classified into two categories: (1) menstrual TSS (originally described as associated with tampon use) and (2) non-menstrual TSS (usually, hospital-acquired).
• Purpura Fulminans - large, rapidly spreading skin hemorrhages, fever, or shock
• Bacteremia - presence of viable bacteria circulating in the blood (mostly HA-MRSA)

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Risk groups and epidemiology of CA-MRSA

• Severe infections occur more frequently in the south (in United States as well in Europe).
• Prostheses and implants increase chances of HA-MRSA infections.
• Influenza or pneumonia positively correlate with cases of CA-MRSA pneumonia.
• Injuries in certain groups such as military personnel, prison inmates, athletes, farmers etc. (where immediate medical help can be delayed) are placing them at higher risk of acquiring the MRSA.
• Other groups with increased risk of infections are veterinarians, pet owners, children younger than 2 years, people older than 65 years, people with concurrent infection and people who are close to an infected individual.

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Treatment

• Antibiotics. There is a number of antibiotics that can be administered to out- and in-patients, such as doxycycline, trimethoprim-sulfamethoxazole, vancomycin, linezolid, and several other. All of them have severe side effects and are not universally effective. Each patient requres unique approach because of differences in age, body mass, pre-existing health conditions, and individual tolerance.
• Incision and drainage of subcutaneous infections, such as abscesses and furuncules, followed by application of antibiotics are very important.

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Prevention

• Diminishing the pathogen's capacity to adhere to the host's tissues. A low-pH cream and a gluco-oligosaccharide were reported to inhibit the attachment of S. aureus cells on the epithelial surfaces.
• Vaccination. Despite of many years of research in this direction, and development and testing of a number of patented or trademarked preparations, there are no commercially available vaccines for human infection and the single available vaccine for the prevention of bovine mastitis has inconsistent results.
• Screening of hospitalized patients for MRSA carriage.
• Limiting exposure to antibiotics to occasions where it is absolutely necessary. Prescribed antibiotics should be used to kill an on-going infection, not merely suppress it. It is important that patients use the prescribed doze fully without stopping or interuptions.
• Frequent hand washing.
• Constant decontamination of inanimate surfaces in department stores, public transprtation, public toilets, schools, gyms, and other highly populated areas.

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References

PubMed articles

• Gleeson TD. Prevention and control of methicillin-resistant Staphylococcus aureus. Dis Mon. 2008 Dec;54(12):801-6. PMID: 18996283
• Middleton JR. Staphylococcus aureus antigens and challenges in vaccine development. Expert Rev Vaccines. 2008 Aug;7(6):805-15. PMID: 18665778
• Powell JP, Wenzel RP. Antibiotic options for treating community-acquired MRSA. Expert Rev Anti Infect Ther. 2008 Jun;6(3):299-307. PMID: 18588495
• Powell JP, Wenzel RP. Antibiotic options for treating community-acquired MRSA. Expert Rev Anti Infect Ther. 2008 Jun;6(3):299-307. PMID: 18588495
• Gordon RJ, Lowy FD. Pathogenesis of methicillin-resistant Staphylococcus aureus infection. Clin Infect Dis. 2008 Jun 1;46 Suppl 5:S350-9. PMID: 18462090
• Boucher HW, Corey GR. Epidemiology of methicillin-resistant Staphylococcus aureus. Clin Infect Dis. 2008 Jun 1;46 Suppl 5:S344-9. PMID: 18462089
• Lambris JD, Ricklin D, Geisbrecht BV. Complement evasion by human pathogens. Expert Rev Anti Infect Ther. 2008 Jun;6(3):299-307. PMID: 18197169
• Deurenberg RH et al. The molecular evolution of methicillin-resistant Staphylococcus aureus. Clin Microbiol Infect. 2007 Mar;13(3):222-35. PMID: 17391376
• Iwatsuki K et al. Staphylococcal cutaneous infections: invasion, evasion and aggression. J Dermatol Sci. 2006 Jun;42(3):203-14. Epub 2006 May 6. PMID: 16679003

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