AMED Research Program on Emerging and Re-emerging Infectious Disesses.
Study of antitoxins/antivenoms and their replacement by humanized monoclonal antibodies.[Ato Group]

Gas gangrene

In recent years, the frequency of the classic so-called gas gangrene with necrosis of muscles with gas in the extremities caused by Clostridium spp. has decreased. On the other hand, the frequency of gas gangrene caused by non-Clostridium species has increased in association with an aging population and comorbidities such as diabetes mellitus. Therefore, the frequency of use for the treatment of gas gangrene in traumatic wound infections produced primarily against Clostridiumperfringens (C. perfringens Type A, C. septicum, C. oedematiens) has decreased.

Clostridum perfringens sepsis: fever. Decreased blood pressure. Pus in the liver (liver abscess). Hematuria.

Unlike classical gas gangrene, sepsis, including liver abscesses caused by endogenous C. perfringens, is on the rise. Van Bunderen et al. reported a series of cases of C. perfringens septicemia resulting in intravascular hemolysis, severe anemia, DIC, and multiple organ damage leading to death within hours, with a mortality rate of The report states that the rate exceeds 80%. Although antimicrobials and drainage of infected lesions are the mainstay of treatment, the administration of gas gangrene antivenom against C. perfringens is beginning to be considered in addition to these treatments because of its pathogenesis. Currently, there is no established evidence.

About Gas gangrene

Clostridium spp. are Gram-positive, spore-forming anaerobic rods usually found in soil and in the gastrointestinal tracts of humans and animals. Endogenous sepsis caused by Welsh bacilli is not caused by trauma and differs from the typical gas gangrene associated with trauma.
Endogenous Welsh bacillus sepsis often develops as rapidly progressive intravascular hemolysis and metabolic acidosis, with high mortality rates exceeding 70% in standard intensive care. In such cases, alpha toxin, secreted by Welsh bacilli, is considered the primary toxin responsible for intravascular hemolysis, disseminated intravascular coagulation syndrome, and multiorgan failure. Theta toxins cause a cytokine cascade that leads to peripheral vasodilation similar to that seen in septic shock.
Antibiotics, such as high-dose penicillin, and surgical drainage as early as possible are the primary treatments for Welsh bacillus infection. However, given the current mortality rate of sepsis, the current standard of care for Welsh bacillus infection does not improve outcome. Monoclonal antibodies against theta toxin in combination with gas gangrene antivenom offer a promising treatment option.