Gas gangrene pathophysiology
|
Gas gangrene Microchapters |
|
Diagnosis |
|---|
|
Treatment |
|
Case Studies |
|
Gas gangrene pathophysiology On the Web |
|
American Roentgen Ray Society Images of Gas gangrene pathophysiology |
|
Risk calculators and risk factors for Gas gangrene pathophysiology |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Gas gangrene is caused by exotoxin-producing Clostridial species (most often Clostridium perfringens), which is mostly found in soil but also found as normal gut flora, and other anaerobes (e.g. Bacteroides and anaerobic streptococci). Staphylococcus aureus and Vibrio vulnificus can cause similar infections.
Pathophysiology
Clostridium is found most everywhere. The exotoxin is commonly found in C. perfringens type A strain and is known as alpha toxin. These environmental bacteria may enter the muscle through a wound and go on to proliferate in necrotic tissue and secrete powerful toxins. These toxins destroy nearby tissue, generating gas at the same time.
A gas composition of 5.9% hydrogen, 3.4% carbon dioxide, 74.5% nitrogen and 16.1% oxygen was reported in one clinical case.[1]
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.[2]
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.
References
- ↑ ^ Chi CH, Chen KW, Huang JJ, Chuang YC, Wu MH (1995). "Gas composition in Clostridium septicum gas gangrene". J Formos Med Assoc. 94 (12): 757–9. PMID 8541740.
- ↑ Awad, M.M., Bryant, A.E., Stevens, D.L. & Rood, J.I. Virulence studies on chromosomal alpha-toxin and alpha-toxin mutants constructed by allelic exchange provide genetic evidence for the essential role of alpha-toxin in Clostridium perfringens-mediated gas gangrene. Mol. Microbiol. 15:191−202 (1995).