I. et al., 2015). Pyrogens are fever-inducing

I. Overview

The chills, multiple layers
of clothing, feeling lethargic—does this sound familiar? Medically termed
pyrexia but commonly referred to as a fever, it is a temporary elevation in the
body temperature from the normal range of 37C (“Fever”, 2017). Fevers may become
concerning if they reach too high of a temperature: 39.4C or greater (“Fever”,
2017). There are multiple causes of a fever—infections, tumors, inflammatory
conditions, etc. (“Fever”, 2017). Knowing these causes of pyrexia, it is important
to note that a fever is not a disease but is a symptom often indicative of an
underlying disease process. Because there are various fever associated
conditions, this essay will mainly focus on the more frequent cause of fevers— bacterial
and viral infections.

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Fevers are commonly
viewed as maladaptive due to it being metabolically expensive and its
association with lethargy, muscle aches, etc. (Mackowiak, 1994; “Fever”, 2017). Sometimes,
cellular damage, systemic damage, and death may result from exceptionally high
fevers (Walter et al., 2016). While fevers may be maladaptive, embedded in the
vulnerability to develop fevers is the adaptive value of mounting an effective
immune response against invading infectious pathogens, enhancing an
individual’s resistance to an infection.


II. Mechanism

The physiological mechanism
of fever is dependent upon the interaction between the innate immune system and
the nervous system (Evans et al., 2015). Pyrogens are fever-inducing substances
within the immune system and can be divided into two groups: exogenous and
endogenous (Anochie, 2013). When exogenous pyrogens such as bacterial toxins invade
the body, the bacterium binds to pathogen recognition receptors (Evans et al.,
2015). This binding induces the release of endogenous pyrogens, known as
cytokines; cytokines increase the set body temperature in the hypothalamus, a
region of the brain that maintains the body’s homeostasis (Anochie, 2013). This
leads to a release of PGE2, a mediator of inflammatory response that maintains the
febrile response through the stimulation of the sympathetic nervous system—
shivering and vasoconstriction within the skin (Anochie, 2013). This response decreases
the body heat loss while generating body heat, effectively elevating body
temperature (Anochie, 2013).


III. Development

Not surprisingly so,
fevers occur the most often among children and infants (McIntyre, 2011). The
immune system among newborns and infants are underdeveloped, so they are
especially susceptible to infections (Hollander & McMichael, 2015). Data
indicates that an increased susceptibility to infections correlates with a high
mortality rate in infants and young children (Hollander & McMichael, 2015).
As an individual matures, the immune system develops and is better able to
fight against invading pathogens, leading to a decrease in fever incidence
among adults (Hollander & McMichael, 2015). However, immunity gradually
declines later in life and is seen among the elderly (Hollander &
McMichael, 2015).  Unlike the increased
fever incidence in the young, there is an absence or diminished temperature
response to infections among the elderly (Norman, 2000). In 20-30% of serious
infections among the elderly, a febrile response is not seen; data suggests
that this lack of fever is not beneficial to the individual (Norman, 2000).



IV. Phylogeny

across the animal kingdom, pyrexia is particularly common among mammalian
endotherms. These mammals range from cattles, pigs, horses, etc. They display
pyrexia once infected, either naturally or experimentally, with a particular
pathogen. It is interesting to see that elevated temperatures are also seen
among ectothermic fish and lizards. It seems that ectotherms do not necessarily
exhibit pyrexia, where a fever is developed both physiologically and
behaviorally, but a fever that is developed behaviorally (Rakus et al., 2017).
Ectotherms develop a behavioral fever in response to exogenous pyrogens, but it
is uncertain whether or not enodgenous pyrogens are involved (Rakus et al.,
2017). Looking at the phylogenic tree, It is seen that pyrexia is well
conserved within and throughout the evolution of the animal kingdom; its
expansiveness suggests and supports that there must an adaptive value behind


V. Adaptive Value

It emerges
that the pyrogenic cytokines involved in the mechanism of fever are also
involved in engendering a larger immune response to pathogen infected tissues (Evans et al., 2015). Specifically, fever-inducing cytokines increase
lymphocyte trafficking through endothelial adhesion (Evans et al., 2015). Lymphocytes
are crucial in recognizing toxins and producing antibodies to attack and kill
infected cells, and endothelial adhesion functions to aid the transport of lymphocytes
to the infected tissue (Larosa & Orange, 2008; Smith, 1993). Therefore,
producing pyrogenic cytokines allow for the downstream effect of a more effective
and rampant immune response. Studies have also shown that increasing elevating
temperature affect leukocytes, white blood cells in the immune system that eliminate
foreign substances (“The Adaptive Value of Fever,” 2015). Leukocytes are more
mobile, able to ingest more bacteria, and better able to kill bacteria in
elevated temperatures, thus supporting the adaptive hypothesis of fever (“The
Adaptive Value of Fever,” 2015). A fever may also be adaptive in that it has a
direct effect on the pathogenic microorganisms’ growth (“The Adaptive Value of
Fever,” 2015). Experimental data have suggested that increasing body
temperature results in an inhibition in growth of various microorganisms while
still maintaining an ideal temperature range for the host (“The Adaptive Value
of Fever,” 2015). Although some microorganisms are able to better grow in
warmer environments, majority does not (“The Adaptive Value of Fever,” 2015).
Because there is a greater net benefit, pyrexia is conserved. Overall, pyrexia has both an indirect and direct
effect on an individual’s resistance to infection. It orchestrates a greater
and more effective immune response while also limiting the growth of pathogens.


VI. Experiment

would be able to test this adaptive hypothesis by utilizing rats, an infectious
pathogen, and an antipyretic. Knowing that rats can develop pyrexia, one would
first divide the rats into a control group where only the pathogen is injected
and an experimental group where both the antipyretic and pathogen is injected.
The survival rate of each group or time until a healthy state is achieved may
be indicative of whether or not an elevated temperature increases the
resistance to infection.


VII. Summary

at pyrexia through a Tinbergen lens allows one to understand its adaptive
value.  While having a fever is
maladaptive, embedded within the vulnerability to develop fevers is the
adaptive value to better fight off infections through its downstream effects of
engendering a greater immune response and inhibiting the growth of bacterial
pathogens. Applying this knowledge to the clinical field, it may be beneficial
to allow a fever to run its course in the case that it is not extremely high
rather than taking an anti-pyrogenic.

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