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Student presentation on
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Introduction
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)
Disease
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.
Virulence
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.
Treatment
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)
Epidemiological Data
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:
Movie: http://www-micro.msb.le.ac.uk/video/Staphylococcus.html
References:
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
2. http://home.nycap.rr.com/piab/
3. http://www.heartpoint.com/endocarditis.html
4. http://www.molbio.princeton.edu/courses/mb427/2001/projects/02/staph.htm
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
Web Page By:
Mohammad Bukhari
September 27, 2004
