Infectious Disease Online
Pathology of Gas Gangrene (Clostridial Myonecrosis)
Three members of the genus Clostridium, Clostridium welchii (perfringens), Clostridium novyi (oedematiens), and Clostridium 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 : 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.
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.
Copyright © 2017 histopathology-india.net