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The Influence of Hemolysis on Susceptibility to Salmonella Infection: Additional Observations¹

From the Department of Medicine, The New York Hospital-Cornell Medical Center, New York, New York

Abstract

Parenteral administration of antiserum against mouse erythrocytes or injection of phenylhydrazine hydrochloride results in an increase in susceptibility of mice to infection with Salmonella typhimurium.

The initial clearance rates of S. typhimurium injected intravenously are the same in mice pretreated with anti-mouse-erythrocyte serum or phenylhydrazine as they are in controls. Within 1 hr after injection, the majority of detectable bacteria can be demonstrated in liver and spleen, and either no organisms or relatively small numbers of organisms can be recovered from blood, kidney, lungs and mesenteric lymph nodes. Subsequently, multiplication of Salmonella in liver and spleen can be detected earlier and in a higher proportion of mice pretreated with anti-erythrocyte serum or phenylhydrazine hydrochloride than in controls. Multiplication of Salmonella in liver and spleen is usually followed by increasing bacteremia and eventual death.

The present studies show clearly that the bactericidal mechanisms which operate to eradicate microorganisms from livers and spleens of normal mice are severely impaired in animals with hemolysis. No evidence was obtained that the enhanced susceptibility of animals with hemolysis was mediated by an effect of antierythrocyte serum or phenylhydrazine hydrochloride on the bactericidal activity of mouse serum or mouse blood, the total number of polymorphonuclear leukocytes, or the rate of phagocytosis by reticuloendothelial cells as measured by rate of removal of viable Salmonella from the circulation. The most reasonable explantion of the altered susceptibility observed in these experiments is that reticuloendothelial cells in the livers and spleens of mice pretreated with anti-erythrocyte serum or phenylhydrazine are less effective in killing engulfed bacteria than are the reticuloendothelial cells of normal mice.

Footnotes

¹ This work was supported by the Health Research Council of The City of New York under Contract U-1107 and by Grants H-3479 and E-3285 from the United States Public Health Service.

² This investigation was carried out during the tenure of a Postdoctoral Fellowship from the National Cancer Institute, United States Public Health Service.

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