Definitions

clostridial myonecrosis

Myonecrosis

Myonecrosis is a condition of necrotic damage, specifically to muscle tissue. It is often seen in infections with Clostridium perfringens or any of myriad soil-borne anaerobic bacteria. Bacteria cause myonecrosis via specific exotoxins. These microorganisms are opportunistic and generally enter the body via significant skin breakage. In wartime particularly, the unhygienic conditions and frequent gross injuries meant that gangrenous infection of soil-borne bacteria was particularly prevalent. Indeed mankind has long suffered the ill-effects of gangrenous infections throughout history.

Other causes of myonecrosis include envenomation by snakes of the Bothrops genus (family Viperidae), ischemic necrosis, caused by vascular blockage (e.g. diabetes type II), tumours that block or hoard blood supply and disseminated intravascular coagulation (DIC) or other thromboses.

Pathophysiology

Myonecrosis differs slightly from other types of necrosis. While the underlying causes are almost identical, the type of affected tissue (namely muscle tissue) is significantly more important for the patient's general health. Superficial necrosis is unsightly, and can lead to unattractive scarring but otherwise does not affect the patient's likelihood of survival nor physical capability to the same extent. Conversely, massive myonecrosis will likely result in the loss of movement of the entire region. If the necrotic damage is allowed to continue throughout an affected limb then often that entire limb is lost permanently.

Soil-borne anaerobes are particularly well adapted to surviving harsh conditions. Often there is a scarcity of nutrition and the presence of numerous other species competing for resources. Changes in pH and temperature are often significant also. Competing bacteria often also possess the ability to create exotoxins that assist them in competing with other microbes in their natural environment. When such bacteria are able to enter a living host, they encounter a vast supply of nutrients, warm conditions and an abundance of water. This enables the microbes to rapidly proliferate, far in excess of the immune system's capability to defend, particularly as prokaryotic bacteria possess a far greater capacity for multiplication than the host's immune system. The combination of bacterial load and ability to multiply is the basis for the microbes' ability to cause massive infection. Alongside such rapid proliferation is a corresponding mass production of exotoxin that causes severe damage to local tissue in the host. One such exotoxin is produced by C. perfringens and is responsible for the disease manifestations. This exotoxin is known as alpha toxin.

Following a massive infection, gross injury and depletion of the host's immune capability results in system wide sepsis. This is partly due to the burden on the immune system, its corresponding release of inflammatory cytokines and the distribution of bacterial toxins. Massive infection is likely to result in death from a combination of system wide septic shock and the unintentionally damaging effects of the immune response. In animals, disability and distress caused by all of these factors markedly increases the chance of predation.

Treatment

Any significantly massive infection is a medical emergency. In cases of gangrene, the infection is so severe by the time that a diagnosis is made that countering the bacterial load is impossible even with the strongest available antibiotics, for example gentamicin and vancomycin. There are two major reasons for this; current antibiotics only prevent replication of bacteria and the production of toxins continues in pre-existing bacteria. Also, the extent of injury caused by the infection may leave the muscle tissues so damaged that the body will never be able to replace the lost structures (including vasculature). Often the only available cure is amputation, which physically removes the source of infection. Understandably this is not the favoured option unless circumstances are particularly dire.

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