Malignant Edema

MALIGNANT EDEMA, Oedema malignum, an acute infectious disease of domestic animals, usually associated with damage to the skin or mucous membranes and characterized by the appearance of edematous infiltrates at the site of infection, which subsequently crepitate. The causative agent of this affliction is primarily Vibrion septique Pasteur (Bacillus oedematis maligni Koch, Clostridium oedematis maligni Bergey, Pararauschbrandbacillus) and, less frequently, other microbes from the group of anaerobes, the causative agents of anaerobic wound infections (Clostr. Welchii, oedematiens, Chauveaui, etc.). V. septique was discovered by Pasteur in 1877. For a long time, there were very contradictory ideas about it, which was explained by the fact that authors were dealing with impure strains of this microbe. At present, its individuality is firmly established.

The microbe is distinguished by a sharply pronounced polymorphism, depending on the conditions under which it is cultivated and in smears from material from sick animals. It is encountered in the form of individual rods of various sizes, in pairs, and even in long threads and chains. Also characteristic is the presence in smears of flask-shaped, swollen, intensely staining forms. It does not form capsules. It stains with all aniline dyes and by Gram's method. In young cultures and in material from sick animals, it is motile. Motility depends on the peritrichous arrangement of flagella. It forms spores. The spores are oval in shape and are usually located eccentrically, but centrally located ones are also encountered. During sporulation, it swells, as a result of which boat-shaped or lemon-shaped forms characteristic of the microbe are produced.

This can be observed most often in media rich in proteins or in material from sick animals. When cultivated on solid media, the microbe usually grows in a continuous layer, and dried agar should be used to study individual colonies. The colonies are transparent, slightly opalescent, with smooth or serrated edges. It is a strict anaerobe. The microbe possesses great activity and develops vigorously on suitable nutrient media with the formation of a large amount of gas. It belongs to the saccharolytic group of anaerobes—causative agents of wound infections. It ferments glucose, levulose, galactose, maltose, lactose, and salicin with the formation of gas; it does not ferment glycerin, sucrose, mannitol, or dulcitol. It liquefies gelatin and does not change coagulated serum. In milk, it forms acid and coagulates it, but coagulation occurs no earlier than the 3rd–6th day. Cultures emit a sharp odor resembling the smell of butyric acid. The temperature optimum is 35–37°, but it also grows at 20–23°. It forms a toxin. The maximum toxin formation is 24–48 hours. The toxin is unstable. Serologically (by the agglutination reaction), 3 groups are distinguished, but the toxin in all of them is identical. In nature, V. septique is very widely distributed; it is a permanent inhabitant of the intestine of all animals, from where it enters the soil and water. It is pathogenic for all laboratory animals. In natural infection, the disease is most often observed in horses, then in sheep. Cattle fall ill incomparably less often. Pigs and dogs are especially resistant. Infection occurs during injury to the skin or mucous membranes, sometimes during birth and during such operations as castration. Infection occurs especially easily when the injury is accompanied by bruising or crushing of the underlying tissues. Along with V. septique, other causative agents of wound infection can be found in the discharge from the wound. The disease develops 12–72 hours after infection. At the site of the wound, an edematous swelling appears, initially very tense, hot, and very painful to the touch. Then the tension passes, the swelling becomes flaccid, doughy, and less sensitive in the center. Upon palpation, crepitation is felt. Most often, crepitation appears in places with developed subcutaneous tissue. The edema spreads rapidly and in a short time can seize, for example, an entire half of the body, hindering the animal's movement. When incised, bloody serous fluid flows out with a greater or lesser amount of gas. The fluid emits a disgusting, ichorous odor. The disease proceeds in the form of a general infection, with high temperature, difficulty in breathing, and weakening of cardiac activity. All symptoms develop extremely rapidly, and death occurs in 12–72 hours. Recovery is rare.

This entire symptom complex can be explained by the sharply pronounced biological activity of the microbe. Having penetrated into the crushed tissue, V. septique rapidly ferments the carbohydrates present there with abundant formation of acids and gas. The gas, spreading along the intercellular pathways, causes compression of the blood vessels, which disrupts the proper nutrition of the surrounding tissues, which, in the presence of toxic substances, leads to their rapid necrosis. The acid melts the dead tissues, preparing the ground for the further spread of the microbe. The absorbed toxins cause general poisoning and quickly lead to a fatal end. Since the wound is usually open, other microbes penetrating there accelerate the process. Phenomena develop especially rapidly when such proteolytic microbes as Clostridium sporogenes and histolyticum join the main process. The synergism of proteolytic microbes with V. septique causes especially violent processes. The disease has a similarity to symptomatic anthrax (blackleg), differing from it in general only by the degree of tissue damage. The presence of crepitation is a sufficient sign to distinguish malignant edema from the edema in anthrax. Treatment is surgical. Since the World War, specific therapy with antitoxic serum has been successfully developed. Active immunization was carried out successfully with edematous fluid, previously heated for several hours at 90°, and also with killed cultures. Recently, immunization with anatoxin—broth cultures treated with 4–5‰ formalin—has been proposed; seroprophylaxis has also been used. In humans, V. septique, together with Cl. Welchii, oedematiens, histolyticum, and others, is a causative agent of gas gangrene.