Host Defense Against Opportunist Microorganisms Following Trauma

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Abstract
Total hemolytic complement (CH50), conversion of C3 [3rd component of complement] by inulin and immunochemical levels of C1q, C4, C2 C3, C5, factor B, C3b inactivator (KAF) and properdin were measured in the sera of 15 patients with severe thermal injury during 9 wk postburn. Five of the 15 patients had multiple episodes of septicemia as documented by positive blood cultures and clinical findings. Decrease in CH50, C1q, 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 1 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 Escherichia coli; sera from the same patient opsonized from infecting strain of Staphylococcus aureus normally. The microorganisms isolated from the other septic patients, which were opsonized normally by the patients'' sera despite complement consumption, were also with 1 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. The classical complement pathway was activated during septicemia in burned patients and activation of this pathway occurred preferentially due to inhibition of the alternative pathway. Complement consumption may reduce the opsonic capacity of a patient''s sera for certain microorganisms and not for others.