Mild hemorrhagic shock does not enhance the risk of CD18 blockade to S. aureus skin inoculations.

Monoclonal antibody (MAb) 60.3 recognizes the leukocyte CD18 glycoprotein and ameliorates much of the injury after hemorrhagic shock in rabbits and nonhuman primates. This MAb blocks neutrophil emigration and has been shown to increase the risk of infection after high-dose inoculation of Staphylococcus aureus into skin. Hemorrhagic shock might also cause an increased sensitivity to bacterial injections. Therefore, we examined changes in host sensitivity to subcutaneous injections of 10(5)-10(8) colony-forming units (CFU) of S. aureus just before shock. Cardiac output was lowered to 40-45% of baseline by phlebotomy for 1 h. Intravenous saline or MAb 60.3 (2 mg/kg) treatment immediately preceded resuscitation with the shed blood. Cefazolin was given intravenously for 3 days, and the animals were killed after 7 days for analysis of infectious risk by measuring the incidence and surface area of skin abscess/necrosis. Bacteria injection resulted in no infections at 10(5) or 10(6) CFU and one abscess/necrotic region at 10(7) CFU (7% incidence) in the MAb-treated group. However, injection of 10(8) CFU resulted in more abscesses/necrotic regions in the MAb- vs. saline-treated group (86 vs. 25%; P < 0.05). The average size of these lesions was also larger in the MAb-treated group (4.6 +/- 7.1 vs. 0.5 +/- 0.6 cm2; P < 0.001). These results were similar to previously published results without shock (Sharar et al., Surgery St. Louis 110:213-220, 1991). We conclude that mild hemorrhagic shock does not enhance the infectious risk of MAb 60.3 after subcutaneous S. aureus injection.