Epidemiology

Blackleg mainly affects cattle between 6 months and 2 years of age that are in good nutritional condition. Occasionally, cases in animals outside this age range may occur. Although little information is available in this regard, it is thought that the spores of C. chauvoei can survive for many years in the soil. Similarly, it is assumed that both spores and vegetative forms of this microorganism can be found in the feces of healthy or sick animals, although, again, little information is available in the scientific literature to support this claim. Blackleg is most commonly observed in pastured animals, although cases may also occur in housed animals fed silage, hay, or other feed. The great majority of blackleg cases occur in the wet season and there is a positive correlation between annual rainfall and incidence of blackleg. Although the reason for this correlation is not fully understood, it has been postulated that the rain may assist in the dissemination of spores and that water saturation favors anaerobiosis of the soil, which is required for germination and multiplication of C. chauvoei spores. Cases of blackleg have frequently been reported in non-vaccinated cattle, approximately a week after they were moved to a fresh, lush pasture, suggesting the acquisition of infection from the environment.

Occasionally, cases of blackleg have been described in sheep, although, in many of those cases, the port of entry of the infection was reported to be a skin or mucosal wound. Because of that, those cases should be considered C. chauvoei-associated gas gangrene (Chapter 20) rather than true blackleg cases (see pathogenesis below). Infections by C. chauvoei have also been reported in humans, deer, goats, pigs, mink, horses, freshwater fish, whales, frogs, hens, and in an oryx, although the pathogenesis in these species has not been determined.

Pathogenesis

The pathogenesis of blackleg has not been fully elucidated. The classical model states that the pathogenesis of this disease starts with ingestion of spores of C. chauvoei, which sometimes may undergo one or more replication cycles in the intestine before being absorbed into the bloodstream. Once absorbed, the spores are distributed via blood circulation to multiple tissues, including skeletal and cardiac muscle. When they reach the muscle, the spores of C. chauvoei are phagocytized by local macrophages, in the cytoplasm of which they may remain latent for long periods of time without harmful effects to the host. When, and if, the redox potential decreases in areas of muscle where spores are present, the spores germinate and proliferate, producing the virulence factors that are responsible for the clinical signs and lesions of blackleg. Although blunt trauma has been traditionally blamed for reduction of the redox potential in muscle, this has never been proved, and the cause of this redox potential reduction remains undetermined. It has been suggested that, in addition to blunt trauma, hypoxia associated with excessive exercise or other factors may also predispose spore germination. One suggestion is that the peak of blackleg with lush summer conditions is also associated with “gadding” or running of cattle to try to escape biting flies. This sudden exertion by unfit fattening cattle may result in local ischemic muscle damage through lactic acidosis. The latter explanation of ischemia or hypoxia would help explain the few cases in which lesions have apparently been seen in the heart but not in skeletal muscles. Because of this pathogenesis, blackleg is regarded as an “endogenous” infection, as opposed to the “exogenous” mechanism of malignant edema (Chapter 20) in which the spores or vegetative forms of the clostridial species involved gain access to the tissues via skin or mucosal wounds.

This long-believed model of pathogenesis does not explain, however, outbreaks of disease that seem to happen year after year in some areas, or those cases that have occurred soon after animals have been moved to new pastures believed to be contaminated with C. chauvoei spores or fed feedstuff that is heavily contaminated with this microorganism. Although these cases do not necessarily rule out the classical model of blackleg pathogenesis (in which the spores remain latent in muscle until the ideal conditions for germination are met), they suggest that other pathogenic mechanisms may also exist. It is possible, for instance, that when animals are exposed to large loads of C. chauvoei, bacteremia or sporemia ensues directly from the intestine. Why there is an apparent preference for muscle for this microorganism to colonize and grow remains to be determined.

The pathogenesis of heart lesions in cases of blackleg is not completely understood either. In an outbreak of blackleg in sheep in which cardiac, but not skeletal, muscle lesions were seen, it was hypothesized that one or more of the following predisposing factors might have been involved: stress-induced increased cortisol and catecholamine levels, toxicants such as ionophores and gossypol, and selenium and vitamin E deficiency. In cases in which heart and musculoskeletal lesions occur together, it is possible that the latter develops first and the toxemia-associated hypoxia acts as predisposing factor for the cardiac lesions. The pericarditis observed usually associated with heart lesions is likely secondary to local extension of myocardial injury, although it might also be a consequence of septicemia.

It has been suggested that blackleg can also be caused by germination of spores from other clostridia endogenously present in muscle, for example Clostridium novyi, Clostridium septicum, and Clostridium sordellii, and this disease is often called “pseudoblackleg”, reserving the term blackleg for C. chauvoei infection.