Abstract

THE mechanism whereby bacterial infections induce fever has been elucidated in some detail1,2. Bacteria and bacterial pyrogens (exogenous pyrogen) interact with polymorphonuclear granulocytes of the host, resulting in release into the circulation of a soluble product of the granulocyte (endogenous pyrogen) which is the proximate cause of the fever through its action on the temperature control centre of the host. Exogenous pyrogen arid endogenous pyrogen may be distinguished in several ways, but the most striking difference between their actions is that tolerance to the first develops rapidly, whereas endogenous pyrogen continues to cause fever after a long sequence of daily injections.

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