Responses of neutrophile AP were studied in volunteers during induced tularemia, Q fever, sandfly fever, and during artificial hyperthermia and endotoxin fever. Symptoms of typical early tularemia were accompanied by a slight increase in the neutrophile count and AP index. The latter continued to rise slowly and eventually became maximal 5 days after the height of clinical illness, long after fever and leukocytosis had disappeared. Similar but less obvious changes occurred after mild tularemia and after typical early Q fever. A transient rise of neutrophile AP occurred only at the onset of fever and neutropenia in sandfly fever. An early fall in neutrophile AP after endotoxin administration was confirmed; this was followed in turn by a prolonged rise not described heretofore. Despite the stress and leukocytosis of environmentally induced artificial hyperthermia, leukocyte AP did not increase.

Based upon these observations it seemed evident that increased leukocyte AP activity could not be correlated in all circumstances with fever per se, the appearance of band cells, or the magnitude or timing of "stress" as inferred from increased plasma and urinary steroids. Increased neutrophile AP activity in these infections did not seem to be related directly to glucocorticoid excess. Possible factors involved in the induction of neutrophile AP may include the genetic potential of various cell types, coenzyme requirements, hormonal responses, as well as other yet unknown factors associated with acute infection.

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