Infection associated with burns.

Introduction Infection was recognized by some 19th and early 20th century workers to be an important and potentially lethal complication of severe burns (Lustgarten, 1891; Stockis, 1903). The bacterial flora of burns were studied by Pack (1926), Aldrich (1933), Cruickshank (1935), Colebrook, Duncan & Ross (1948) and others before and during the second World War, but their pathogenic importance was commonly disregarded at a time when the main interests of clinicians treating burns were directed towards shock caused by fluid loss and the more nebulous 'toxaemia' attributed to products of thermal injury. In the 1950s some of the illness loosely described as 'toxaemia' was seen to be due to bacterial infection; with the introduction of methods that were successful in the control of shock, sepsis became recognized as the main cause of death in severely burned patients (Jackson, Lowbury & Topley, 1951; Markley et al., 1957; Tumbusch et al., 1961). These fluctuations can be understood when we recall that severe burns cause a complex range of local and general pathological effects, including necrotic changes in the skin and underlying tissues which often make it hard to distinguish the added changes caused by microbial infection. At the same time it is well known that heavy colonization of most burns may occur without apparent sepsis; when sepsis does occur the patient is often very ill from other complications as well, and the infection is apt to be classed as 'opportunist'; this view is supported by the fact that some of the main pathogens (notably Pseudomonas aeruginosa) are organisms relatively harmless to healthy subjects and healthy tissues. It might be argued that extensively burned patients in this state are likely to die whether they become infected or not; but the mortality from severe burns has been reduced by successful control of such infections (Bull, 1971) showing that the presence of such infection can tip the scales against survival.