Epidemiology

The incidence of gas gangrene seems to be higher in ruminants and horses than in other animal species. This, however, may be due to the environment in which these animals live and the way they are managed, rather than differences in species susceptibility. Cases of gas gangrene may occur in individuals of any age, including neonates; no breed or gender predisposition has been reported.

The clostridial agents of gas gangrene, including their spores, are ubiquitous, most of them being commonly isolated from the intestinal content of animals and the environment, mostly from soils rich in organic matter and high humidity. Soils that become flooded seasonally are more commonly contaminated by these microorganisms than are dry soils. The presence of wild or domestic animal feces and/or animal carcasses in the pastures can increase the level of soil contamination.

In several parts of the world, C. septicum is considered the most prevalent cause of gas gangrene. However, this microorganism is also a frequent post-mortem invader, and its presence should be cautiously interpreted in animals that have been dead for a while, since invasion of tissues by C. septicum present in the intestine may start very soon after death or even during the agonal period. Association between two or more of the histotoxic clostridia is not unusual as the cause of gas gangrene, and may further be complicated by the presence of aerobic bacteria such as E. coli.

Gas gangrene occurs sporadically, but outbreaks may also occur, mostly associated with injection of contaminated products or lack of hygiene during medical or surgical procedures. The disease is highly lethal.

Pathogenesis

Based on the limited current knowledge about gas gangrene of animals, it is thought that the pathogenesis of the disease is similar in all animal species. The disease starts with contamination of wounds with spores or vegetative forms of one or more of the clostridial species responsible for the disease, which are usually in the environment. Aerobic bacterial contamination can sometimes help render the local environment more anoxic and encourage the germination of spores. As is the case for tetanus, deep wounds or traumatic injuries help establish the anoxic environment required for the growth of clostridia.

The most frequent means of entry of these agents in animals include vaccination, parturition, shearing, branding, neutering, docking, and blood extraction. Gas gangrene can also occur in foals and sporadically in ruminants as a result of umbilical infections, while in rams, gas gangrene caused by C. novyi type A is commonly associated with fights (head butting), a condition sometimes known as “big head”. Cases of gangrenous mastitis have been described in cattle and sheep. In sheep, some of these cases were associated with excessive vacuum from the milking machine. The reduced redox potential caused by anoxia associated with traumatic or deep wounds, or by local irritants in the case of some injection wounds, and the presence of metabolites from decomposing protein commonly found in these initial tissue lesions contribute to germination of spores and proliferation of vegetative clostridia.

In addition to the main virulence factors mentioned earlier in this chapter for the agents of gas gangrene, most strains of the histotoxic clostridia produce numerous tissue-degrading enzymes such as collagenases, DNAses, hyaluronidases, and neuraminidases, and pore-forming toxins, which also contribute to tissue damage, nutrient acquisition, and evasion of host defenses, thus allowing the spread of infection. Most of the toxins produced by the histotoxic clostridia act first locally, producing tissue necrosis which, in turn, provides an ideal environment for further multiplication of these microorganisms and further production of toxins, which eventually gain access to the systemic circulation, producing toxemia, shock, and death. Bacteremia may also occur, and the agents of gas gangrene can be found in several distant organs. In some cases, intravascular hemolysis can also occur as a consequence of toxemia, mainly when C. perfringens type A is involved.

Although contaminated wounds are the most common port of entry for the agents of malignant edema in animals, some cases of gas gangrene in which no previous trauma has been identified have been described in humans and a non-human primate. The pathogenesis of this infection is not fully understood and it is believed that the agent, commonly C. perfringens, gains access to the bloodstream via a damaged mucosal barrier, thus reaching muscles and other organs. The pathogenesis of these infections may also be similar to that of blackleg, and involve germination of endogenous spores present in these tissues or previously healthy animals.

Clinical signs

Clinical signs are similar in most animal species. The disease is almost always acute, although occasionally sub-acute and chronic cases can occur. A few hours post infection, the area surrounding the port of entry shows swelling and erythema; this lesion is usually painful and hot. As time passes, and progress is usually rapid, there is increasing swelling associated with subcutaneous edema and emphysema; the latter becomes evident as crepitation on palpation. The skin is taut and diffusely red or black with bruises and suffusions. Depression, tachycardia, muscle tremors, and hyperthermia are almost always present. When a limb is affected, the animal shows reluctance to move and lameness, followed by recumbency. In later stages of the disease, the affected area becomes cold, the pain disappears due to the necrosis of local nerve endings, and sub-normal body temperatures are common. In most cases, death occurs by toxemia and systemic shock between a few hours to 2–4 days after the onset of clinical signs. Occasionally, animals are found dead without clinical signs having been observed. Rare cases of chronic disease with death occurring up to 30 days post infection have been reported. In these cases, treatment with penicillin G may have delayed the usual rapid progression of disease and localized the infection to necrotic tissue; the outcome is inevitably usually fatal, either because of the progression of disease or through euthanasia.

Despite the similarity of clinical signs in all species, a few specific forms of the disease have been described. In rams, fighting injuries can lead to a clinical condition called “big head”, a specific form of gas gangrene characterized by a non-gaseous, non-hemorrhagic, edematous swelling of the head, face, and neck of young individuals. This form is typically associated with C. novyi type A, but C. sordellii or C chauvoei

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