Abstract
THE pathogenesis of endotoxin fever has been much elucidated since the observation of the appearance in the serum of a fever-producing substance (endogenous pyrogen) after endotoxin1. The transient profound leucopenia which follows the intravenous injection of endotoxin has been cited in support of the idea that leucocytes are a source of endogenous tissue pyrogen. These observations on rabbits were further extended by Petersdorf and Bennett2,3, who made their observations on dogs. However, these authors pointed out that under certain conditions the leucopenic response to endotoxin could not be correlated with the appearance of endogenous serum pyrogen and that the dissociation of the febrile response and levels of endogenous serum pyrogen was observed. This was noticed especially when endotoxin was given on successive days. Development of endogenous pyrogen markedly decreased on the second day, despite the full febrile and the leucopenic response.
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