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Staphylococcus epidermidis is a gram-positive, coagulase-negative cocci that is a part of our normal flora. Consequently, it is a true opportunistic pathogen, as it requires a major breach in the host’s innate defenses. It is one of the leading pathogens of nosocomial infections, particularly associated with foreign body infections. Those most susceptible to infection are intravenous drug users, newborns, elderly, and those using catheters or other artificial appliances. The organism produces a glycocalyx "slime" that acts as a glue adhering it to plastic and cells, and also causes resistance to phagocytosis and some antibiotics.The S. epidermidis family contributes to approximately 65-90% of all staphylococci recovered from human aerobic flora. Healthy individuals can posses up to 24 strains of the species, some of which can survive on a dry surface for long periods. (Nilsson, et al. 1998). It is approximately 0.5 to 1.5 micrometers in diameter. While S. epidermidis is a facultative anaerobe, it grows best in aerobic conditions. The hosts for the organism are humans and other warm-blooded animals. (Nilsson, et al. 1998)
Infections are associated with intravascular devices (prosthetic heart valves, shunts, etc.) but also commonly occur in prosthetic joints, catheters, and large wounds. Catheter infections along with catheter-induced UTIs lead to serious inflammation and pus secretion. In these instances, urination is extremely painful. Septicemia and endocarditis are also diseases associated with S. epidermidis. Their symptoms run the gamut from fever, headache, and fatigue to anorexia and dyspnea. Septicemia is especially prevalent resulting from neonatal infections, particularly in very low birth weights. Endocarditis is an infection of the heart valves and parts of the inside lining of the heart muscle. S. epidermidis is very likely to contaminate patient-care equipment and environmental surfaces, possibly explaining the high incidence of S. epidermidis in the hospital setting.
The organism produces slime layers, which forms a hydrophobic biofilm. This film is adhesive to hydrophobic biopolymers of prosthetics, creating diseases such as endocarditis. The gene icaADBC has been found to code for both the polysaccharide capsule and the polysaccharide intracellular adhesin used in biofilm formation. The biofilm of S. epidermidis consists of clusters of cells that are embedded in extracellular slime substance that is up to 160 micrometers thick, exceeding 50 cells. Biofilms as such act as a diffusion barrier to antibiotics and host defense. (Nilsson, et al. 1998)
Another potential virulence factor that’s currently being researched is the fibrinogen binding of S. epidermidis. The complete gene, termed fbe, was found to consist of an open reading frame of 3,276 nucleotides encoding a protein, called Fbe, with a deduced molecular mass of ~119 kDa. (Nilsson, et al. 1998) Implant biomaterials are instantly covered by circulating plasma components, like Fibrinogen, promoting adhesion of host cells. One complication that may arise is when contaminating bacteria adhere to the same components on the biomaterial surfaces, leading to infection. (Nilsson, et al. 1998)
While there is much research regarding S. epidermidis’ virulence factor, little has been done to understand its mode of action.
As S. epidermidis is part of the human normal flora, it has developed resistance to many common antibiotics such as methicillin, novobiocin, clindamycin, and benzyl penicillin. As a result, vancomycin or rifampin is used to treat an infection. (#4 WWW)
A significant study of neonatal infections was conducted in Naples between January 1996 and December 1998. Results found indicated that of a total 184 infections, 56 were directly attributed to S. epidermidis (30.4%). Of these, S. epidermidis was the primary causative pathogen leading to bloodstream infections (39.8%), surface infections (29.8%), and meningitis (58.3%). Percentages provided indicate number of infections caused by S. epidermidis out of total infections of that type. (Villari, et al. 2000)
To View a movie of S. epidermidis:
1. Nilsson, Lars, Flock, Pei, Lindberg, Guss. “A Fibrinogen-Binding Protein of Staphylococcus epidermidis.” Infection and Immunity. Vol. 66, No. 6 (June 1998); p. 2666-2673
5. Villari, Sarnataro, Iacuzio. “Molecular Epidemiology of Staphylococcus epidermidis in a Neonatal Intensive Care Unit over a Three-Year Period.” Journal of Clinical Microbiology. Vol. 38, No. 5 (May 2000); p. 1740-1746
6. Picture: http://www.buddycom.com/bacteria/gpc/staphepi4.jpg
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September 27, 2004