Abstract
ALTHOUGH fever is often a prominent sign in diseases associated with agranulocytosis1 its pathogenesis has remained obscure. Most experimental studies of the mechanism of fever have been carried out in rabbits that have been either injected intravenously or infected with various microbes or their products.2 From this work it now seems clear that such agents produce fever indirectly by liberating a circulating endogenous pyrogen from the tissues of the host. This material, in turn, appears to act directly on the hypothalamic thermoregulatory center to produce fever. Since granulocytes derived from sterile acute exudates liberate large quantities of pyrogen,3 it has . . .
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