Prophylactic antibiotics for surgery.

This article discusses the determination of surgical patients to be given antibiotic prophylaxis. In addition, current concepts regarding selection of antibiotic prophylaxis necessary for a variety of surgical procedures are reviewed.

Acute pancreatitis associated with pentamidine therapy.

Two patients receiving pentamidine isethionate for the treatment of Pneumocystis carinii experienced acute pancreatitis temporally related to pentamidine therapy. In one patient, pancreatitis recurred when a second course of pentamidine therapy was given. We discuss pentamidine toxicity.

The role of antibody and complement in phagocytosis by rabbit alveolar macrophages.

The relative importance of antibody and complement in the phagocytosis of Staphylococcus aureus and Pseudomonas aeruginosa, two common bacterial pathogens, by alveolar macrophages from rabbits was studied. Normal rabbit serum was a satisfactory opsonin for the phagocytosis of S. aureus but not for P. aeruginosa. Normal rabbit serum opsonized S. aureus by both the classic and the alternative complement pathways; loss of both pathways destroyed opsonic activity. The presence of complement was not required for maximal phagocytosis when 10% staphylococcal immune serum was used. However, an intact alternative complement pathway enhanced phagocytosis when the concentration of staphlyococcal immune serum was lowered to 0.3%. Similarly, 10% pseudomonas immune serum opsonized P. aeruginosa without complement. When the concentration of pseudomonas immune serum was lowered to 1%, either the classic or the alternative complement pathway could significantly enhance phagocytosis of P. aeruginosa. Similar results were obtained with alveolar macrophages activated with bacille Calmette-Guérin. These studies demonstrate the importance of complement in enhancing phagocytosis by alveolar macrophages of bacterial pathogens when antibody concentration is the limiting factor.

Effects of oxygen exposure on it vitro function of pulmonary alveolar macrophages.

Bacterial infection may complicate pulmonary oxygen (O2) toxicity, and animals exposed to high O2 concentrations show depressed in vivo pulmonary bacterial inactivation. Therefore, in vitro studies were undertaken to define the mechanism by which O2 alters pulmonary antibacterial activity. Normal and BCG pretreated rabbits were exposed to 100% O2 for 24, 48, and 72-h periods. Pulmonary alveolar macrophages (PAM) were obtained from the experimental animals and from nonoxygen exposed controls by bronchopulmonary lavage. O2 exposure did not alter cell yield or morphology. PAMs were suspended in 10% serum-buffer, and phagocytosis of (14C)Staphylococcus aureus 502A and (14C)Pseudomonas aeruginosa was measured. Comparison of the precent uptake of the 14C-labeled S. aureus after a 60-min incubation period demonstrated that normal PAMs exposed to O2 for 48 h showed a statistically significant increase in phagocytosis when compared to their controls (43.5 vs. 29.2%). A similar, but smaller increase was seen after 24-h O2 exposures. 48 and 72-h O2 exposures produced no significant changes in phagocytosis in PAMs from BCG-stimulated rabbits. Normal PAMs also showed an increased phagocytosis of Ps. aeruginosa after 48-h oxygen exposure. No impairment of in vitro bactericidal activity against either S. aureus 502A or Ps. aeruginosa could be demonstrated in PAMs from normal rabbits exposed to O2 for 48 h. These results indicate that the in vitrophagocytic and bactericidal capacity of the rabbit PAM is relatively resistant to the toxic effects of oxygen, and that imparied in vivo activity may possibly be mediated by effects other than irreversible metabolic damage to these cells. The mechanism for the observed stimulation of phagocytosis remains to be determined.