Abstract Peritoneal neutrophil mobilization in mice following the intraperitoneal injection of S. typhimurium was markedly suppressed by anesthetizing the mice with halothane. Under the conditions of these experiments halothane anesthesia produced moderate hypothermia in the mice, but this was shown not to be responsible for the suppression of neutrophil response to endotoxin. Halothane concentrations of 30 mg. percent in culture medium supporting in vitro growth of S. typhimurium caused a diminution in bacterial growth rate, suggesting bacteriostasis. A series of tenfold dilutions of S. typhimurium were given to groups of mice, half of whom were anesthetized, the other half not anesthetized. Mortality rates of mice given halothane anesthesia developed more rapidly, although after discontinuing anesthesia the mortality rates of unanesthetized and anesthetized animals eventually became equal. The cause of the rapidity of death in anesthetized mice was shown not to be due to the endotoxin content of the bacteria. A combination of decreased extravasation of neutrophils into the peritoneal cavity plus a depression of their function of phagocytosis allowed a relatively greater bacterial growth rate in the anesthetized mice given viable S. typhimurium, despite the bacteriostatic effect on the Salmonella itself. It is possible that prolonged general anesthesia may contribute to the incidence of infection through depression of the host's natural defenses.