Host defense against opportunist microorganisms following trauma. I. Studies to determine the association between changes in humoral components of host defense and septicemia in burned patients.

Total hemolytic complement (CH(50)), conversion of C3 by inulin, and immunochemical levels of Clq, C4, C2, C3, C5, factor B, C3b inactivator (KAF), and properdin were measured in the sera of 15 patients with severe thermal injury during nine weeks postburn. Five of the 15 patients had multiple episodes of septicemia as documented by positive blood cultures and clinical findings. Decrease in CH(50), Clq, C4, C2, C3, and C5 occurred prior to and during septic episodes in these patients. Although conversion of C3 by inulin was often reduced during septic episodes, levels of factor B and KAF were generally normal or elevated. In only one patient did consumption of complement occurring during septicemia decrease the opsonic capacity of the patient's sera for the patient's infecting microorganism, an isolate of E. coli; sera from the same patient opsonized her infecting strain of S. aureus normally. The microorganisms isolated from the other septic patients, which were opsonized normally by the patients' sera despite complement consumption, were also with one exception strains of Staphylococci. In the nonseptic burned patients, decrease in properdin and C3 conversion by inulin, and increase in C3, factor B and KAF were demonstrated as we have previously reported. The results indicate that the classical complement pathway was activated during septicemia in burned patients and that activation of this pathway occurred preferentially due to inhibition of the alternative pathway. In addition, the data show that complement consumption may reduce the opsonic capacity of a patient's sera for certain microorganisms and not for others.