Oxygen uptake by Clostridium welchii type A: its possible role in experimental infections in passively immunised animals.

When small numbers of virulent Clostridium welchii type A are mixed with sterile soil and injected intraperitoneally into passively immunised guinea-pigs, death follows in 18-24 hr. with symptoms of profound shock attributable to hypovolaemia (Bullen and Cushnie, 1963). The development of gross hypovolaemia coincides with the peak of bacterial growth. Exactly the same syndrome can be produced in 5-12 hr by intraperitoneal injection of large numbers of washed organisms without soil. The actual reason for the development of hypovolaemia is puzzling. There is no evidence that any of the well-recognised exotoxins produced by Cl. welchii are responsible. Not only is shock produced in animals possessing large amounts of circulating antitoxin, but the peritoneal exudates are non-toxic (Bullen and Cushnie, 1963). Passive sensitisation or anaphylaxis are unlikely to be involved since neither dead organisms nor oc-toxin cause shock in passively immunised animals. The close relationship between the total number of bacteria and the production of fatal shock led us to believe that the loss of circulating fluid and subsequent haemoconcentration, which is a prime feature of the shock, must be associated with some metabolic activity of Cl. welchii. Under suitable conditions these organisms can remove large amounts of oxygen from their environment. We have evidence to suggest that this in itself may be responsible for the chain of events leading to death.