Animal anatomy, histology, pathological anatomy

The causative agent of the disease.The causative agent is Clostridium [Cl.] chauvoei [Chavo's bacilli] a strict anaerobe. Caused by a spore-forming anaerobic bacillus capable of long-term preservation in the soil, most species are gram-positive and mobile. The incubation period lasts 1-3 days. The disease develops very rapidly, death occurs within 24 to 56 hours. Spores enter the body of animals when they ingest infected feed and water through microtraumas of the mucous membrane of the pharynx, abomasum, intestines, as well as wounds of the skin, birth canal, and muscles. In the body, the microbe produces hemolysin and aggressins. Characteristic of Cl. shauvoei is the presence of a lamellar layer. Division of clostridia occurs through the formation of a transverse septum.

3. Pathogenesis.The pathogenesis of emphysematous carbuncle is not yet well understood. Most researchers are of the opinion that infection is transmitted through the digestive tract. At the same time, the possibility of infection through the outer integument, especially if the latter is damaged, is not denied.
If we assume that the main method of infection is through the digestive tract, the question arises of how to explain the mechanism of muscle damage. Experimental studies have proven that intravenous infection does not yet produce a specific process in the muscles, despite the body’s reaction that occurs with an increase in temperature. If, when a febrile state appears, a skin injury is simultaneously inflicted, then changes typical for emkara appear in the corresponding place. The observations of practical workers regarding the appearance of muscle changes characteristic of emkar during vaccinations, if the latter were previously injured (for example, bruises), speak to the same thing.
Thus, for a specific muscle process to occur, one more penetration of the pathogen into the blood is not enough, since the intact vascular wall is impenetrable to it.
As for the nature of the damage to the vascular wall, it must be understood as damage in a broad sense, since not only the various origins of the injury, but also changes in the mesenchyme in general and, in particular, its reticulo-endothelial apparatus can affect the permeability of the vascular walls. In light of these facts, cases of multiple focal lesions of skeletal muscles in emkara become reversible. Young cattle are most sensitive to emphysematous carbuncle. Their gastrointestinal mucosa is known to allow microorganisms into the blood and lymph more easily than in adults. For the disease to occur, there must be damaged muscle fibers. This is often ensured by mechanical disruption of the integrity of the muscles when struck by horns, a whip or a stick. At the moment of impact, the walls of the blood vessels rupture and, along with the blood, pathogens enter the damaged muscle fibers. Typical emphysematous carbuncles usually appear at sites of muscle damage. Toxins released by Cl. chauvoei into muscle tissue, penetrate with the blood into the liver, causing its acute dystrophy. Pathogens from small pockets of specific muscle lesions accumulate here. The amount of toxic substances in the blood increases due to a sharp degeneration of liver cells and a decrease in its antiseptic and antitoxic functions. Against this background, damage to the brain, kidneys and, finally, acute myocardial dystrophy develop, causing the death of the animal from cardiac paralysis.