Abstract

Summary Male white rats of the Sprague-Dawley strain were maintained on a well-defined diet deficient in thiamine, and a) various physiologic factors of importance to infection, b) phagocytosis and c) susceptibility to infection were studied. Adequate numbers of inanition and ad libitum control animals were included. The following physiologic factors were studied: a) the cellular composition of the peripheral blood, b) complement activity, c) cellular migration in inflammation, d) the cellular composition of the exudate in inflammation and e) “leukotaxine” activity. The following observations were made from these studies: No change was noted in the total leucocyte count in the peripheral blood. An increase in erythrocytes and hemoglobin concentration was evident in the thiamine deficient and inanition controls. Differential cell counts of the blood leucocytes of the vitamin deficient and inanition controls showed an absolute and relative increase in polymorphonuclear cells and a reduction in the percentage of lymphocytes.Complement activity of the sera of the thiamine deficient rats was less than either the inanition or ad libitum control rats.There was a marked decrease (50%) in the total number of leucocytes in the peritoneal exudates of the thiamine deficient animals when inflammation was established.A relative granulocytosis with an absolute decrease was observed in the exudates removed from the inflamed areas of the deficient animals as compared with the controls.No alteration in capillary permeability, as measured by the Menkin dye accumulation technique, was noted in any group.Thiamine deficiency had no apparent effect on the capacity of the leucocyte to phagocytize Diplococcus pneumoniae. Phagocytosis was approximately the same in all groups of animals.Thiamine deficient animals were highly susceptible to D. pneumoniae. However, after receiving 40 μg of thiamine daily for seven days, they were able to resist the invasion and infection.The reduced complement activity and cellular migration to the site of inflammation suggest that these significant factors play a role in the inability of a thiamine deficient animal to resist bacterial infection.

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