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With advances in technology, critically ill patients have improved survival rates. With this increased life span there is increased occurrence of infectious complications that are only indirectly related to the patient's primary disease. There is little information regarding the effect on the immune system of these short exposures to infection, and the system's response to later bacterial exposure. Two problems frequently encountered by surgeons are development of bacterial infection from contamination within the abdomen, and development of intra-abdominal infection in patients with nonabdominal disease. The infections usually respond well to treatment but the effects of these antigen exposures on the immune system are not well understood. A previous study on mice has shown that intra-abdominal contamination with a sublethal dose of bacteria results in increased intra-abdominal abscesses (pus-filled cavities). The current study was undertaken to determine the relative contributions of systemic and local immune mechanisms to the development of these late abscesses. Mice were injected with live bacteria, either systemically or at a specific distant site. Compared with controls, the two experimental groups developed a significantly higher number of intraperitoneal abscesses one week later when bacteria were injected into the peritoneal cavity. These results seem to indicate that short-lived or focal non-fatal infections can significantly change the immune system's response to later bacterial exposure, particularly the development of intraperitoneal abscesses. (Consumer Summary produced by Reliance Medical Information, Inc.)

• The systemic tumor necrosis factor (TNF) response has been extensively studied during infection. In addition, antibiotics that cause cell-wall lysis have been associated with endotoxinemia and, therefore, could trigger TNF release. We studied the effects of pretreatment with cefoxitin and/or anti-TNF antibody on mortality and early (90 minutes) and delayed (6 hours) serum TNF levels in a murine model of mixed Escherichia coli/Bacteroides fragilis peritonitis. At low and intermediate inocula levels, cefoxitin, but not anti-TNF antibody, prevented death, and low serum TNF levels were noted in all groups. At the highest inoculum level, mortality was uniform in control, cefoxitin, and anti-TNF antibody groups, and a significant elevation in serum TNF levels was seen only at the 6-hour point in animals receiving cefoxitin. The addition of anti-TNF antibody to cefoxitin at this inoculum level abrogated the 6-hour rise in serum TNF levels and reduced mortality to 40%. These results emphasize that the cytokine response in disease is dependent on both the nature of the insult and other forms of therapeutic interventions.(Arch Surg. 1993;128:73-78)