Hello jen247,
Staphylococcus aureus is definitely the winner with respect to
virulence factors. It produces large amounts of a large number of
virulence factors, which affect every stage of the infecton process,
thus making it highly pathogenic even in healthy people.
Staphylococcus epidermidis does not produce many virulence factors and
produces them only in small amounts. For this reason, it only tends
to be pathogenic in individuals that are already compromised in some
way.
The main factor which determines the virulence of different strains of
S. epidermidis is slime, which results in formation of a biofilm. This
is thought to be the most important mechanisms which causes the
bacteria to adhere to and colonize catheters and prosthetic devices.
Slime also helps to protect the bacteria from phagocytosis. It is
mainly formed by secretion of teichoic acid, normally from the cell
wall. Biofilm is not usually cited as a virulence factor for S.
aureus, but an article by Cramton et al (see refs below) makes the
point that an intercellular adhesin, which is also required for
biofilm formation, is also an important virulence factor in both
species with respect to their ability to infect catheters and
prostheses: “Products of the intercellular adhesion (ica) operon in
Staphylococcus aureus and Staphylococcus epidermidis synthesize a
linear β-1,6-linked glucosaminylglycan. This extracellular
polysaccharide mediates bacterial cell-cell adhesion and is required
for biofilm formation, which is thought to increase the virulence of
both pathogens in association with prosthetic biomedical implants...
Here we demonstrate that anaerobic in vitro growth conditions lead to
increased polysaccharide expression in both S. aureus and S.
epidermidis, although the regulation is less stringent in S.
epidermidis”
Another virulence factor of some importance in S. epidermidis is the
polysaccharide capsule, which again protects the bacteria from
phagocytosis. The capsule of most clinical isolates of S. aureus,
unlike those of S. epidermidis can only be seen under the electron
microscope, and thus it is usually called a microcapsule. The role of
the capsule in S. aureus virulence has been a more controversial
topic, but Luong and Lee (see reference citation below) emphasize its
significance: “Type 8 capsular polysaccharide (CP8) is the most
prevalent capsule type in clinical isolates of Staphylococcus aureus.
However, its role in virulence has not been clearly defined. CP8
strains such as strain Becker produce a small amount of capsule on
their surface in vitro. In contrast, CP1 strains such as strain M
produce a large amount of capsule, which has been shown to be an
important antiphagocytic virulence factor… we replaced the weak
native promoter of the cap8 operon in strain Becker with the strong
constitutive promoter of the cap1 operon of strain M. The resultant
strain, CYL770… produced about 80-fold more CP8…. persisted longer in
the bloodstream, the liver, and the spleen in mice… was more
resistant to ospsonophagocytosis in vitro… These results indicate
that CP8 is an antiphagocytic virulence factor of S. aureus.”
Both S. aureus and S. epidermidis produce catalase, which degrades
H202, thus helping to protect against the host’s oxygen-dependent
bacteriocidal system.
The remaining virulence factors listed are found in S. aureus, but not
in S. epidermidis:
Coagulase – this enzyme causes the formation of a layer of
host-derived fibrin around the bacterial cells, which possibly
protects them against phagocytosis and also “hides” them from the
host’s immune system as a whole. However, not all authors agree that
this is a virulence factor.
Another way in which S. aureus is protected from phagocytosis is
through the action of one of its toxins, leukocidin, which attacks
polymorphonuclear leukocytes. Leukocidin is only found in 2% of S.
aureus isolates as a whole, but it is found in about 90% of isolates
obtained from severe dermonecrotic lesions, and it therefore likely
also to play an important role in causing the skin necrosis that can
occur in S. aureus infection.
Protein A is a surface protein, which binds to the Fc region of IgG
antibodies. This prevents the antibodies from coating the bacterial
cells (the process of opsonization) and therefore helps further to
protect the bacteria against phagocytosis.
S. aureus has a number of other proteins on its surface which aid the
attachment of bacteria to the extracellular matrix of host epithelial
and endothelial tissues. Most strains also have a surface protein that
binds to blood clots and wounded tissues. Strains which cause
osteomyelitis and septic arthritis also have an adhesin that binds to
collagen. Mutant strains which are defective in these various proteins
have been found to be less virulent.
S. aureus is able to damage host tissues in a number of ways. The
substances responsible are considered to be virulence factors because
they aid the bacteria in invading and spreading through the body.
These include various enzymes such as kinases, hyaluronidase and
lipase. Staphylokinase lyses fibrin clots. Its role as a virulence
factor is in clearing the way for the bacteria to spread more easily
through the tissues.
Tissue damage is also caused by a number of toxins produced by S.
aureus. Toxins causing membrane damage to host cells include the
leukocidin mentioned above, and also:
a-toxin which binds with a receptor on susceptible cells, especially
platelets and monocytes, and causes the formation of pores that make
the membrane leaky. The binding of this toxin also triggers the
production of inflammatory mediators that are responsible for the
septic shock that can occur in S. aureus infections.
beta-toxin damages cell membranes that contain a lot of sphingomyelin,
however this toxin is not found in most strains of S. aureus isolated
from humans.
g-toxin is also called leukotoxin, and it has hemolytic activity
A fatty acid modifying enzyme (FAME) could be important in abscesses,
where it could help bacteria to survive by modifying anti-bacterial
lipids.
Superantigens activate a large proportion of T-cells, by bypassing the
normal mechanisms of antigen presentation through their ability to
bind directly to class II major histocompatibility complexes. They
affect many more cells than would be stimulated by a normal immune
mechanism and cause a massive release of interferon and IL-2, giving
rise to symptoms similar to those of endotoxic shock. The six
enterotoxins (SE-A, B, C, D, E and G) and toxic shock syndrome toxin
(TSST-1) produced by S. aureus are superantigens. As well as causing
toxic shock, the enterotoxins are responsible for S. aureus food
poisoning, causing diarrhea and vomiting when ingested.
Exfoliatin toxins are responsible for scalded skin syndrome, which
causes separation of the dermal and epidermal layers of the skin
There are two forms, A and B. They have specific esterase activity and
it is thought that they also have protease activity, which could mean
that they target a specific protein that is necessary to maintain the
integrity of the epidermis.
Resistance to antibiotics is an important virulence factor.
Practically all S. aureus strains have a beta lactamase which makes
them resistant to penicillin G and multiple-resistance S. aureus
(MSRA), which is resistance to most antibiotics is becoming an
increasing problem.
Information obtained and synthesized from the following sources:
Infect Immun. 2001 June; 69 (6): 4079–4085
Anaerobic Conditions Induce Expression of Polysaccharide Intercellular
Adhesin in Staphylococcus aureus and Staphylococcus epidermidis
Sarah E. Cramton, Martina Ulrich, Friedrich Götz, and Gerd Döring
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=98472
Infect Immun. 2002 July; 70 (7): 3389–3395
Overproduction of Type 8 Capsular Polysaccharide Augments
Staphylococcus aureus Virulence
Thanh T. Luong and Chia Y. Lee
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=128096
Todar’s Online Textbook of Bacteriology, Chapter on Staphylococci
http://textbookofbacteriology.net/staph.html
“Virulence Factors” Information from the database of "BUGS" Index –
Organisms” by Donna Duckworth Ph.D., Richard Crandall Ph.D. and
Richard Rathe M.D, University of Florida, College of Medicine
http://www.medinfo.ufl.edu/year2/mmid/bms5300/bugs/virufact.html
Bacteriology at UW-Madison
Staphylococcus
by Kenneth Todar University of Wisconsin-Madison Department of
Bacteriology
http://www.bact.wisc.edu/Bact330/lecturestaph
Pathogenesis of Staphylococcal Infections by Gordon D. Christensen,
M.D.
http://www.muhealth.org/~md2004/update8/03-18staph.doc
Search strategy: virulence aureus epidermidis |
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