Temperature Regulation and the Pathogenesis of Fever

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Figure 47-6 Evolutionary tree of animals. A febrile response has been documented in the Vertebrata, Arthropoda, and Annelida. These observations suggest that the febrile response evolved more than 400,000,000 years ago at about the time evolutionary lines leading to arthropods and annelids diverged. Further evidence of fever’s beneficial effects can be found in numerous investigations demonstrating enhanced resistance of animals to infection with increases in body temperature within the physiologic range. [165] In classic studies involving experimental infection of the reptile Dipsosaurus dorsalis with Aeromonas hydrophila, Kluger and associates demonstrated a direct correlation between body temperature and survival. [166][167] They also showed in their model that suppression of the febrile response with sodium salicylate is associated with a substantial increase
in mortality. [167] Covert and Reynolds corroborated these findings in an experimental model involving goldfish. [168] In mammalian experimental models, increasing the body temperature by artificial means has been reported to enhance the resistance of mice to herpes simplex virus, [169] poliovirus, [170] Coxsackie B virus, [171] rabies virus, [172] and Cryptococcus neoformans [173] but to decrease resistance to Streptococcus pneumoniae. [174] Increased resistance of rabbits to S. pneumoniae [175] and C. neoformans, [176] dogs to herpesvirus, [177] piglets to gastroenteritis virus, [178] and ferrets to influenza virus [179] has also been observed after the induction of artificial fever. Unfortunately, because raising the body temperature by artificial means does not duplicate the physiologic alterations that occur during fever in homeotherms (and, indeed, entails a number of opposite physiologic responses [180] ), data obtained using mammalian experimental models must be interpreted with caution when used to understand the febrile response. Clinical data supporting an adaptive role for fever have accumulated slowly. Like animal data, clinical data include evidence of both beneficial effects of fever and adverse effects of antipyretics on the outcome of infections. In a retrospective analysis of 218 patients with gram-negative bacteremia, Bryant and associates reported a positive correlation between maximal temperature on the day bacteremia was diagnosed and survival. [181] A similar relationship has been observed in patients with polymicrobial sepsis and mild (but not severe) underlying diseases. [182] In an examination of factors influencing the prognosis of spontaneous bacterial peritonitis, Weinstein and co-workers identified a positive correlation between a temperature reading of greater than 38° C (100.4° F) and survival. [183] It has been reported that children with chickenpox who are treated with acetaminophen have a longer time to total crusting of lesions than placebo-treated controls. [184] Stanley and colleagues have reported that adults infected with rhinovirus exhibit more nasal viral shedding when they receive aspirin than when given placebo. [185] Furthermore, Graham and colleagues have reported a trend toward a longer duration of rhinovirus shedding in association with antipyretic therapy and have shown that the use of aspirin or acetaminophen is associated with suppression of the serum neutralizing antibody response and with increased nasal symptoms and signs. [186] A more recent, retrospective, observational analysis of studies of human volunteers infected with influenza A found a relationship between antipyretic therapy and prolonged illness. [187] These data, like those reviewed in the preceding paragraph, are subject to several interpretations and do not prove a causal relationship between fever and improved prognosis during infection. Nevertheless, they are consistent with such a relationship and when considered in concert with the phylogeny of the febrile response and the animal data summarized earlier, constitute strong circumstantial evidence that fever is an adaptive response in most situations. Whereas many of the foregoing investigations examined the relationship between the elevation of the core temperature and the outcome of infection, others have considered the endogenous mediators of the febrile response. In such studies, all of the principal pyrogenic cytokines have been shown to have immune-potentiating capabilities, which might theoretically enhance resistance to infection. [93][188] In vitro and in vivo investigations of these cytokines have provided
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Page 9 and 10: Figure 47-2 Mean oral temperatures
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Page 27 and 28: Although clinicians have long had a
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