S. epidermidis biofilms – clinical relevance

Staphylococci are recognized as the most frequent causes of biofilm-associated infections. Approximately, 75% of  infections caused by CoNS are due to S. epidermidis, ranking the first among the most important bacterial pathogen involved in nosocomial biofilm-associated infections worldwide [1].

Despite its generally innocuous nature, S. epidermidis has emerged as a frequent cause of nosocomial infections particularly in patients with indwelling medical devices [2] such as catheter systems, pacemaker electrodes [3], intrauterine device, artificial hip prosthesis and a range of other polymer and metal implants [4].

Although S. epidermidis infections only rarely develop into life-threatening diseases, their frequency and the fact that they are extremely difficult to treat represents a very serious burden for the public health system [5] . This has been related to its ability to adhere to the surface of the indwelling medical devices and form biofilms [1]. A biofilm is defined as a complex and structured community of bacteria attached to a surface and surrounded by a matrix of extrapolymeric substances such as proteins, lipids, DNA and polysaccharides [6]. S. epidermidis biofilm-based infections are a clinically significant problem since biofilm bacterial cells are more resistant to antibiotics [7]  and also more resilient to phagocyotosis than their planktonic counterparts [8].

The importance of biofilms in the pathogenesis of the S. epidermidis infections is obvious and more studies are nedeed to provide details on the complexity of the interactions existing between the host and the biofilm cells in order to mount a effective strategy or either  to treat the medical devices or to act direcly on the biofilm.

 

References

[1] Otto, M (2008)  Curr Top in Microbiol and Immunol, 322:207-228;   [2] O’Gara J and Humphrey H. (2001) J Med Microbiol, 50: 582-587;   [3] Ziebuhr W, Hennig S, Eckart M, Kranzler H, Batzilla C, Kozitskaya S. (2006)  Int J of Antimicrob Agents, 28 Suppl 1:S14-S20;   [4] Donlan R (2002)  Emerging Infect Dis, 8: 881–890;   [5] Otto, M (2009) Nature, 7:555-567;   [6] Donlan R and Costerton JW (2002) Clin Microbio Rev, 15: 167-193;   [7] Cerca N, Pier GB, Vilanova M, Oliveira R, Azeredo J (2005) Res in Microbiol, 156:506-514;   [8] Cerca N, Jefferson K, Oliveira R, Pier GB, Azeredo, J (2006)  Infect Immun, 74:4849-4855.

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