ABSTRACT
Fever most likely evolved hundreds of millions of years ago as a mechanism to enhance the ability of the host to resist infection (see also Chapter 6). The elevation in body temperature during fever represents a large metabolic cost that would seem to be counterproductive to survival. However, the febrile response to infection has been shown to be beneficial to the host organism, allowing it to recover more quickly and survive the infection. Briefly, it has been shown that febrile temperatures increase mobility and function of white blood cells, stimulate cytokine production and activation of T lymphocytes, and impair the growth of bacteria in a hypoferremic environment. That is, plasma iron concentrations decrease during fever, and the growth of some bacteria in a low iron media is markedly hampered with a febrile rise in temperature (for review, see Kluger, 1986). Fever is thus adaptive and has been conserved in the evolution of vertebrates. Likewise, the hypothermic response to toxicants may also represent an adaptive response. However, unlike fever, the hypothermic response to xenobiotics is not omnipresent across species but is likely restricted to those with a relatively small mass. To this end, the following sections elaborate on the critical nature of body mass and the behavioral and autonomic regulation of a hypothermic response to xenobiotic agents and other insults.
