Abstract

Bacterial sepsis is one of the major challenges facing clinicians who treat critically ill and injured patients. This is especially true in those cases in which the immune response is impaired, such as following trauma or major surgery [1], and approximately 75% of late deaths following trauma are attributable to systemic sepsis [2]. The progression from sepsis to multiple organ failure and death is complex and depends on a number of factors. Among these factors are a variety of specific and nonspecific host defense mechanisms, including phagocytosis, complement activation, and specific antibody production. In recent years, it has also become clear that specific cell-mediated responses also play important roles in the control of bacterial infection, and it is therefore possible that such responses influence the outcome of sepsis. Pseudomonas aeruginosa is an important cause of morbidity and mortality in severely compromised patients, and it is therefore under intense study. Animal models of infection with this organism have required extensive pretreatment with cyclophosphamide [3], very large numbers of bacteria [4, 5], or full-thickness burn [6, 7] in order to produce susceptibility to sepsis.

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