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Romanovsky, Andrej A. Do fever and anapyrexia exist? Analysis of set point-based definitions. Am J Physiol Regul Integr Comp Physiol 287: R992-R995, 2004. First published June 24, 2004; 10.1152/ ajpregu.00068.2004.—Fever and anapyrexia are the most studied thermoregulatory responses. They are defined as a body temperature (Tb) increase and decrease, respectively, occurring because of a shift in the set point (SP) and characterized by active defense of the new Tb. Although models of Tb control with a single SP (whether obvious or hidden) have been criticized, the SP-based definitions have remained unchallenged. In this article, the SP-based definitions of fever and anapyrexia were subjected to two tests. In test 1, they were compared with experimental data on changes in thresholds for activation of different thermoeffectors. Changes in thresholds were found compatible with an SP increase in some (but not all) cases of fever. In all cases of what is called anapyrexia, its mechanism (dissociation of thresholds of different effectors) was found incompatible with a decrease in a single SP. In test 2, experimental data on the dependence of Tb on ambient temperature (Ta) were analyzed. It was found that the febrile level of Tb is defended in some (but not all) cases. However, strong dependence on Ta was found in all cases of anapyrexia, which agrees with threshold dissociation but not with a decrease of the SP. It is concluded that fever (as defined) has only limited experimental support, whereas anapyrexia (as defined) does not exist. Two solutions are offered. A palliative is to accept that SP-based terms (anapyrexia, cryexia, regulated hypothermia, and such) are inadequate and should be abandoned. A radical solution is to transform all definitions based on comparing Tb with the SP into definitions based on balancing active and passive processes of Tb control. [ABSTRACT FROM AUTHOR]

Mphahlele, Noko R., Andrea Fuller, Joachim Roth, and Peter R. Kamerman. Body temperature, behavior, and plasma cortisol changes induced by chronic infusion of Staphylococcus aureus in goats. Am J Physiol Regul Integr Comp Physio1 287: R863-R869, 2004. First published June 24, 2004; 10.1152/ajpregu.00064.2004.—Most ex- perimentally induced fevers are acute, usually lasting ∼6–12 h, and thus do not mimic chronic natural fevers, which can extend over several days or more. To produce a model of chronic natural fever, we infused eight goats (Capra hircus) intravenously with 2 ml of 2 × 1011 cell walls of Staphylococcus aureus (S. aureus) for 6 days using osmotic infusion pumps (10 μ1/h) while measuring changes in body temperature, behavior, and plasma cortisol concentration. Seven control animals were infused with sterile saline. Abdominal temperature- sensitive data loggers and osmotic infusion pumps were implanted under halothane anesthesia. To compare our new model with existing models of experimental fever, we also administered 2-ml bolus intravenous injections of 2 × 1011 S. aureus cell walls, 0.1 μg/kg lipopolysaccharide (Escherichia coli, serotype 011l:B4), and sterile saline in random order to six other goats. Bolus injection of lipopoly- saccharide and S. aureus induced typical acute phase responses, characterized by fevers lasting ∼6 h, sickness behavior, and increased plasma cortisol concentration. Infusion of S. aureus evoked prolonged fevers, which lasted for ∼3 days, starting on day 4 of infusion (ANOVA, P < 0.05), and did not disrupt the normal circadian rhythm of body temperature. However, pyrogen infusion did not cause plasma cortisol concentration to rise (ANOVA, P > 0.05) or the expression of sickness behavior. In conclusion, infusion of S. aureus produced a fever response resembling that of sustained natural fevers but did not elicit the cortisol and behavioral responses that often are described clinically and during short-term experimental fevers. [ABSTRACT FROM AUTHOR]