Staphylococcus (page 2)
© Kenneth Todar, PhD
Pathogenesis of S. aureus infections
Staphylococcus aureus causes a variety of suppurative
(pus-forming) infections and toxinoses in humans. It causes superficial skin lesions
such as boils, styes and furuncules; more serious
infections such as pneumonia, mastitis, phlebitis, meningitis,
and urinary tract infections; and deep-seated infections, such as
osteomyelitis and endocarditis. S. aureus is a major cause of hospital
acquired (nosocomial) infection of surgical wounds and infections associated with indwelling
medical devices. S. aureus causes food poisoning by releasing enterotoxins into food,
and toxic shock syndrome by release of superantigens into the blood stream.
Although methicillin-resistant Staph aureus (MRSA) have been entrenched in hospital settings for several decades, MRSA strains have recently emerged outside the hospital becoming known as community associated- MRSA( (CA-MRSA) or superbug strains of the organism, which now account for the majority of staphylococcal infections seen in the ER or clinic.
S. aureus expresses many potential virulence factors:
(1) surface proteins that promote colonization of host tissues;
(2) invasins that promote bacterial spread in tissues (leukocidin,
kinases, hyaluronidase);
(3) surface factors that inhibit phagocytic engulfment (capsule,
Protein A);
(4) biochemical properties that enhance their survival in
phagocytes (carotenoids, catalase production);
(5) immunological disguises
(Protein A,
coagulase);
(6) membrane-damaging toxins that lyse eucaryotic cell membranes (hemolysins,
leukotoxin, leukocidin;
(7) exotoxins that damage host tissues or otherwise provoke symptoms of
disease (SEA-G, TSST, ET); and
(8) inherent and acquired resistance to antimicrobial agents.
For the majority of diseases caused by S. aureus,
pathogenesis
is multifactorial, so it is difficult to determine precisely the role
of
any given factor. However, there are correlations between strains
isolated
from particular diseases and expression of particular virulence
determinants,
which suggests their role in a particular diseases. The application of
molecular biology has led to advances in unraveling the pathogenesis of
staphylococcal diseases. Genes encoding potential virulence factors
have
been cloned and sequenced, and many protein toxins have been purified.
With some staphylococcal toxins, symptoms of human disease can be
reproduced
in animals with the purified protein toxins, lending an understanding
of
their mechanism of action.
Human staphylococcal infections are frequent, but usually remain
localized
at the portal of entry by the normal host defenses. The portal may be a
hair follicle, but usually it is a break in the skin which may be a
minute
needle-stick or a surgical wound. Foreign bodies, including sutures,
are
readily colonized by staphylococci, which may make infections
difficult
to control. Another portal of entry is the respiratory tract.
Staphylococcal
pneumonia is a frequent complication of influenza. The localized host
response
to staphylococcal infection is inflammation, characterized by an
elevated
temperature at the site, swelling, the accumulation of pus, and
necrosis
of tissue. Around the inflamed area, a fibrin clot may form, walling
off
the bacteria and leukocytes as a characteristic pus-filled boil or
abscess.
More serious infections of the skin may occur, such as furuncles or
impetigo.
Localized infection of the bone is called osteomyelitis. Serious
consequences
of staphylococcal infections occur when the bacteria invade the blood
stream.
A resulting septicemia may be rapidly fatal; a bacteremia may result in
seeding other internal abscesses, other skin lesions, or infections in
the lung, kidney, heart, skeletal muscle or meninges.
chapter continued
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