082098 Staphylococcus aureus Infections - Goodsamim.com

MEDICAL PROGRESS
No. of Infections
3000
2000
1000
0
1987
No. of infections
Percent of infections resistant to methicillin
Percent of methicillin-resistant infections
sensitive only to vancomycin
1988
1989
1990
1991
1992
Year
1993
1994
1995
1996
1997
Figure 3. S. aureus Infections in Intensive Care Units in the
National Nosocomial Infections Surveillance System, 1987
through 1997.
Data include total infections, infections with methicillin-resistant
strains, and infections with methicillin-resistant strains sensitive
only to vancomycin. Isolates were tested for sensitivity to
the following antimicrobial agents: gentamicin, tobramycin,
amikacin, ciprofloxacin, clindamycin, erythromycin, chloramphenicol,
trimethoprim–sulfamethoxazole, and vancomycin.
Some hospitals did not test for susceptibility to all these antibiotics.
Data were kindly provided by Dr. Robert Gaynes, Hospital
Infection Program, National Center for Infectious Diseases.
in 1987 to 56.2 percent in 1997 (Fig. 3). These isolates
constitute the subgroup of strains from which
the S. aureus strains with intermediate sensitivity to
vancomycin (glycopeptide-intermediate S. aureus)
have recently emerged. 39 New molecular typing techniques
have clearly documented the ability of epidemic,
disease-producing clones of methicillin-resistant
S. aureus to populate hospitals and spread to
diverse geographic regions rapidly. 40,41 The rapid
spread and pathogenicity of these clones suggest
that they possess unique, as yet undefined, determinants
of virulence.
PATHOGENESIS OF STAPHYLOCOCCAL
DISEASE
S. aureus has a diverse arsenal of components and
products that contribute to the pathogenesis of infection.
These components and products have overlapping
roles and can act either in concert or alone.
A great deal is known about the contribution of
these bacterial factors to the development of infection.
14,31,42,43 Considerably less is known about their
80
70
60
50
40
30
20
10
0
Percent of Infections
interaction with each other and with host factors
and their relative importance in infection.
The virulence of S. aureus infection is remarkable,
given that the organism is a commensal that colonizes
the nares, axillae, vagina, pharynx, or damaged skin
surfaces. 21,22 Infections are initiated when a breach of
the skin or mucosal barrier allows staphylococci access
to adjoining tissues or the bloodstream. Whether an
infection is contained or spreads depends on a complex
interplay between S. aureus virulence determinants
and host defense mechanisms.
The biology of colonization of the nares, the primary
reservoir for staphylococci, is incompletely
understood. Mucin appears to be the critical host
surface that is colonized in a process involving interactions
between staphylococcal protein and mucin
carbohydrate. 44,45 The role of other commensals,
secretory IgA, or specific staphylococcal adhesins is
unknown.
The risk of infection is increased by the presence
of foreign material. Elek and Conen 46 first demonstrated
the ability of sutures to reduce the threshold
for infection. Several factors contribute to the increased
susceptibility to infection. Phagocytic function
in the presence of foreign material is seriously
impaired. 47 Devices such as intravenous catheters are
rapidly coated with serum constituents, such as
fibrinogen or fibronectin, which enable staphylococci
to adhere through MSCRAMM-mediated mechanisms
and to elaborate glycocalices that further facilitate
colonization. 48,49 Intravenous catheters are
frequently implicated in the pathogenesis of nosocomial
endocarditis. The introduction of long-term
indwelling catheters has led to cases of nosocomial
endocarditis that resemble the animal model of endocarditis.
The catheter traumatizes the valvular surface,
creating a nonbacterial thrombus on the cardiac
valve that facilitates subsequent bacterial adherence. 50
Invasive Infections
Staphylococcal bacteremia may be complicated by
endocarditis, metastatic infection, or the sepsis syndrome.
The endothelial cell is central to these pathogenic
processes. Not only is it a potential target for
injury, but also its activation contributes to the progression
of endovascular disease. Staphylococci avidly
adhere to endothelial cells and bind through adhesin–receptor
interactions. 51-53 In vitro studies demonstrate
that after adherence, staphylococci are phagocytized
by endothelial cells (Fig. 4). 52,55
The intracellular environment protects staphylococci
from host defense mechanisms as well as the
bactericidal effects of antibiotics. Vesga et al. 56 demonstrated
that the intraendothelial-cell milieu fosters
the formation of small-colony variants. These factors
may enhance bacterial survival and contribute to the
development of persistent or recurrent infections. 57
Staphylococcal strains that cause endocarditis are
Volume 339 Number 8 · 523
Downloaded from www.nejm.org at ARIZONA HEALTH INFORMATION NETWORK on December 7, 2009 .
Copyright © 1998 Massachusetts Medical Society. All rights reserved.