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Three members of the genus Clostridium,
C. welchii (perfringens), C novyi (oedematiens), and C. septicum, may
produce gas gangrene; at least three other members of this genus may
contribute to such a process though incapable of producing it
themselves.
Infections associated with gas gangrene
are often mixed and include various anaerobic organisms as well as
toxicogenic clostridia.
Gas-forming clostridia are strictly
anaerobic, gram-positive, sporulating bacilli widely distributed in
nature.
Gas-forming clostridia may be
introduced into wounds as spores that, devoid of toxin, are incapable
of producing disease.
Predisposing factors:
Conditions that seem
to favour germination of spores and subsequent toxin production
include extensive necrosis (such as that produced by crushing
injuries) or the presence of foreign particulate matter (especially
that containing calcium salts or silicic acid).
Pig-bel: CLICK HERE
A curious and interesting
disease, known locally as pig-bel, occurs in the high lands of central
New Guinea. In that locality pig-bel is the most common cause of
acute abdominal emergencies. Anatomic lesions include enteritis with
deep, often perforating, peculiarly serpiginous ulcers. Epidemiologic
studies are ambiguous, but some emphasize the association of pig-bel
with ritual feasts on putrid pork carcasses. Gas-forming clostridia
have been cited as etiologically important.
In peacetime, sporadic cases of gas
gangrene are occasionally observed, particularly among agricultural
workers.
Treatment:
Appropriate surgical management, particularly debridement of all
devitalized tissue from wounds subject to gas gangrene, and prompt
initiation of antibiotic therapy have drastically reduced the
incidence and morbidity of this bacterial disease.
Pathological features:
Features of gas gangrene usually appear
with in hours to days after the relevant injury.
Tissues about the wound become swollen,
edematous, and painful as a result of increased tension.
Once established, the process often
advances with great rapidity.
The injured member becomes tense and
crepitant because of the accumulation of gas bubbles within the
tissues.
A scanty serosanguineous fluid exudes
from the wound. Rarely the fluid may be effervescent.
Soon the wounded tissue becomes grayish
black and extremely foul smelling.
This local process, called clostridial
cellulitis, may in itself occasionally threaten life.
The syndrome, gas gangrene, however,
includes the systemic toxic effects of several clostridial toxins and,
once it develops, has a significant mortality.
Changes in the muscle
: (Clostridial
myonecrosis)
The most conspicuous local effects involve muscle.
The muscle fibers undergo coagulative
necrosis and occasionally liquefy.
Large gram-positive bacilli are present
in great numbers.
In later cases a zone of intense
leukocytic reaction and hyperemia confines the area of infection.
In severe cases there is practically no
leukocytic response about the region of frank necrosis but a wide zone
of edema and congestion.
Capillary and venous thrombi are
common.
Toxins:
The various toxins produced by
gas-forming clostridia are locally toxic and perpetuate the local
process while being available for absorption and systemic effects as
well.
There are at least 12
immunologically distinct toxins produced by gas-forming clostridia.
The most important of these are the
potent lecithinase (alfa toxin) and another necrotizing toxin (sigma
toxin).
Potent hemolytic toxin may produce a
precipitous drop in the number of circulating erythrocytes.
Terminal stage:
Terminally, bacilli
invade the bloodstream and are distributed widely throughout the body.
Pulmonary edema and hyperemia are
usually pronounced.
If postmortem examination is
delayed even a few hours, the gas formation occurs in virtually any
organ of the body.
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