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Staphylococcus epidermidis/epidermis
Scanning electron image of S. epidermidis.
Scientific classification
Kingdom: Bacteria
Phylum: Firmicutes
Class: Cocci
Order: Bacillales
Family: Staphylococcaceae
Genus: Staphylococcus
Species: S. epidermidis
Binomial name
Staphylococcus epidermidis
(Winslow & Winslow 1908)
Evans 1916

Staphylococcus epidermidis is one of thirty three known species belonging to the genus Staphylococcus. It is part of our human flora, and consequently part of skin flora. It can also be found in the mucous membranes and in animals. Due to contamination, it is probably the most common species found in laboratory tests.[1]

Although S. epidermidis is usually non-pathogenic, patients with a compromised immune system are often at risk for developing an infection. These infections can be both nosocomial or community acquired, but they are more of a threat to hospital patients. This is related to hospitals carrying more virulent strains of the organism, due to continuous use of antibiotics and disinfectants.

S. epidermidis is also a major concern for people with catheters or other surgical implants because it is known to cause biofilms that grow on these devices.[2]

Contents

[edit] Cellular morphology and biochemistry

S. epidermidis is a very hardy microorganism, consisting of non-motile Gram-positive cocci, arranged in grape-like clusters. It forms white raised colonies approximately 1–2 mm in diameter, after overnight incubation, and is non-hemolytic on blood agar.[2] It is a catalase-positive,[3] coagulase-negative, facultative anaerobe that can grow by aerobic respiration or by fermentation (although some strains may not ferment).[4]

Biochemical tests indicate this microorganism also carries out a weakly positive reaction to the Nitrate Reduction Test. It is positive for Urease production, is Oxidase negative, and can utilize Glucose, Sucrose, and Lactose to form acid products. In the presence of Lactose it will also produce gas. S. epidermidis possesses the Gelatinase enzyme, allowing it to hydrolyze gelatin. It is sensitive to Novobiocin

Similar to that of Staphylococcus aureus the cell walls of S. epidermidis have a transferrin binding protein that helps the organism obtain iron from transferrin. The tetramers of a surface exposed protein, GAPDH or glyceraldehyde-3-phosphate dehydrogenase, are believed to bind to transferrin and remove its iron. Subsequent steps include iron being transferred to surface lipoproteins, then to transport proteins which carry the iron into the cell. [2]

[edit] Virulence and antibiotic resistance

The ability to form biofilms on plastic devices is a major virulence factor for S. epidermidis. One probable cause is surface proteins that bind blood and extracellular matrix proteins. Its' capsule, known as polysaccharide intercellular adhesion (PIA), is made up of sulfated polysaccharide and allows other bacteria to bind to the already existing biofilm. Creating a multilayer biofilm. Such biofilms decrease the metabolic activity of bacteria within them. This in combination with impaired diffusion, of antibiotics, inhibits antibiotics from effectively clearing this type of infection.[2] Some other reasons this microorganism poses a threat are because even free living S. epidermidis are resistant to several antibiotics. A contributing factor may be that some antibiotics can be secreted in sweat, so the normal flora is routinely exposed to them.

Some of the antibiotics this organism is resistant to include penicillin, amoxicillin, and methicillin. Most commonly found in the intestines and may cause fatal concerns.

[edit] Disease

As mentioned above S. epidermidis causes biofilms to grow on plastic devices placed within the body. This occurs most commonly on intravenous catheters and on medical prostheses. [5] Infection can also occur in dialysis patients or anyone with a implanted plastic device that may have been contaminated. Another disease it causes is Endocarditis[2]. This occurs most often in patients with defective heart valves. In some other cases sepsis can occur in hospital patients.

Since antibiotics are ineffective in clearing biofilms the most common treatment for these infections is to remove or replace the plastic implant. In all cases prevention is ideal.

[edit] Identification

The normal practice of detecting S. epidermidis is by using the Baird-Parker Agar with egg yolk supplement. Colonies appear small and black. They can be confirmed using the coagulase test. Increasingly, techniques such as real-time PCR and quantitative PCR are being employed for the rapid detection and identification of Staphylococcus strains. [6][7] Normally sensitivity to desferrioxamine can also be used to distinguish it from most other staphylococci, except in the case of Staphylococcus hominis, which is also sensitive. In this case the production of acid from trehalose, by Staphylococcus hominis, can be used to tell the two species apart.

[edit] See also

[edit] References

  1. ^ Queck SY and Otto M (2008). "Staphylococcus epidermidis and other Coagulase-Negative Staphylococci". Staphylococcus: Molecular Genetics. Caister Academic Press. ISBN 978-1-904455-29-5. http://www.horizonpress.com/staph. 
  2. ^ a b c d Salyers, Abigail A. and Whitt, Dixie D. "Bacterial Pathogenesis: A Molecular Approach". Second ed. ASM Press (2002). Washington, D.C.
  3. ^ Todar, Kenneth. 2007. Todar's Online Textbook of Microbiology.[1]
  4. ^ Staphylococcus_epidermidis
  5. ^ Hedin, Goran. "Sthphylococcus epidermidis- Hospital Epidemiology and the Detection of Methicillin Resistance". Scandinavian Journal of Infectious Disease. (1993) Scandinavian University Press. Oslo Norway.
  6. ^ Francois P and Schrenzel J (2008). "Rapid Diagnosis and Typing of Staphylococcus aureus". Staphylococcus: Molecular Genetics. Caister Academic Press. ISBN 978-1-904455-29-5. http://www.horizonpress.com/staph. 
  7. ^ Mackay IM (editor). (2007). Real-Time PCR in Microbiology: From Diagnosis to Characterization. Caister Academic Press. ISBN 978-1-904455-18-9 . http://www.horizonpress.com/rtmic. 



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