Abstract
Infectious gaseous gangrene can no longer be conceived of as being necessarily a monomicrobic disease. On the contrary it is frequently the result of an association of bacteria, not all of which are by themselves pathogenic or even under the most favorable condition of animal inoculation capable of causing a pathological lesion. The causative agents of infectious gaseous gangrene are found in a certain group of anaërobes, all of which are capable of elaborating a powerful toxin which has not only a local but also a systemic action. Death in gaseous gangrene is not the direct result of the local lesion but of the absorption of toxin into the general circulation with a consequent general toxemia.
The spread of the local lesion is dependent upon local tissue necrosis. The tissue necrosis in turn is dependent upon the elaboration of bacterial toxins, which are distributed along the line of the muscle sheaths and facia, and through the lymph spaces. There is no evidence that the toxin producing the local tissue necrosis differs from the toxin which is the cause of the general toxemia. If for any reason toxins are not elaborated within the wound or are not absorbed from the wound a gaseous gangrene does not develop despite the fact that there may be within the wound a large number of potentially pathogenic anaërobes.
All the aerobes can be dismissed as a cause of infectious gaseous gangrene. Any effects which they produce are in the nature of a complication. At the most their r61e in this disease process is confined to the absorption of oxygen, the turning upon themselves of the processes which tend to produce an immunity and in causing the death of tissue thus preparing a favorable media for the multiplication of the anagrobes.
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