Ann B. Bjornson

Changes in humoral components of host defense following burn trauma.

Serum opsonic activity for E. coli 075, conversion of C3 by inulin, total hemolytic complement (CH(50)), levels of native C3, factor B, C3b inactivator (KAF), properdin (P), and immunoglobulins (Ig) were determined in 14 patients with burns involving 13% to 91% body surface during 6 to 8 weeks postburn. In the 12 uninfected patients, levels of IgG and IgA were reduced during the first 10 days postburn, and decreased concentrations of P and IgM were demonstrated from three to 6 weeks postburn. C3 conversion was reduced from 10 days to 6 weeks postburn. Levels of C3, factor B, and KAF were normal or elevated for the entire study period. No difference in the occurrence of humoral abnormalities was noted in patients with burns caused by flame, immersion scald, or acid contact. Reduction in C3 conversion and P concentration were the only abnormalities which correlated with increasing burn size. Bacteremia and/or fungemia was documented in the other two patients. In one of these patients, reduction in CH(50) occurred during septicemia due to S. aureus, and in the other, reduction in all measurements of complement was associated with candidemia and Pseudomonas septicemia and occurred prior to the development of shock. Serum opsonic activity was only reduced significantly during sepsis, suggesting that this abnormality occurred as a result rather than a cause of infection. These results indicate that consumption of components of the classical and/or alternative pathways of complement activation may be an important mechanism by which infection is perpetuated in the burn patient. They also emphasize the importance of the clinical management of the burn patient in preventing the development of septic complications.

Serum-mediated inhibition of polymorphonuclear leukocyte function following burn injury.

Serial scrum samples from 12 bacteremic burned patients were tested at a physiologic concentration for their ability to facilitate phagocytosis and intracellular killing of the homologous infecting Staphylococcus aureus strains by normal human polymorphonuclear leukocytes in comparison to pooled normal human serum. Serum-mediated inhibition of leukocyte bactericidal activity was demonstrated in three of the patients during 13 to 56 days after burn. Decreased bactericidal activity was related to an inhibitory effect of the burn sera on the phagocytic process, which reduced the number of internalized bacteria available for intracellular killing. The serum-mediated inhibition of phagocytosis was not found to be dependent on bacterial surface properties unique to S. aureus. The inhibitory effect was shown to involve a direct interaction of the burn sera with the leukocytes, which was not associated with cell death and was not reversed by washing of the leukocytes

Theoretical Interrelationships Among Immunologic and Hematologic Sequelae of Thermal Injury

A hypothesis of possible interrelationships among immunologic and hematologic sequelae of thermal injury is presented. It is postulated that there are definable pathways involving series of abnormalities with multiple interconnections among these pathways. The initiating step of each pathway should be amenable to blockade. Such blockade would theoretically circumvent the occurrence of the abnormalities or lessen their severity and thereby preserve host resistance.