MadSci Network: Medicine
Query:

Re: how might a fever kill someone

Date: Thu Mar 23 13:41:12 2000
Posted By: Lyle Burgoon, Grad student, Pharmacology and Toxicology, College of Human Medicine, Michigan State University
Area of science: Medicine
ID: 953260515.Me
Message:

Thanks for the question.

Let’s start with a discussion of what is going on in a fever state.  When 
a person has a fever their thermostat in the hypothalamus is being 
manipulated such that the brain believes the core temperature should be 
higher than what it otherwise should be.  This causes a whole slough of 
physiologic changes, like piloerection (the hair on your body stands up 
helping to trap heated air near your skin), vasoconstriction in the 
periphery (the blood vessels in the peripheral parts of the body constrict 
to minimize heat loss due to blood flow), and secretion of epinephrine 
(mainly to initiate shivering, and increases in heart rate and blood flow 
to help circulate the heat being produced by the muscles as a result of 
shivering to other parts of the body).  All of these physiologic changes 
occur to warm the body up to the “new” temperature on the thermostat.

So we know that the fever involves physiologic changes, one of which is 
secretion of epinephrine.  We also know, from personal experience, that 
the body will eventually reach that elevated temperature.  The human body 
operates at peak efficiency at the “normal” core temperature (which varies 
from human to human).  This is the temperature at which the proteins in 
the body are the most stable, and can work at peak efficiency.  When the 
temperature of the environment a protein is in is increased you increase 
the risk of heat denaturing the protein.  Once the protein is denatured, 
it is non-functional.  Since proteins are absolutely necessary for proper 
cellular functioning, denaturation is a bad thing (unless you’re 
denaturing a bacterium’s proteins, then it could be a good thing!).  
Without proteins the cell cannot do ANYTHING!  This means there is no 
means to metabolize anything, no ATP synthesis or cleavage.  This means, 
essentially, the cell ends up dead.  Massive cell death leads to tissue 
death, and then to organism death.

Fever also induces apoptosis (programmed cell death).  It is hypothesized 
that the apoptosis pathways are activated in an attempt to slow down viral 
infections.  The thought is that by destroying the cell before it is able 
to lyse (open up) – once the cell lyses the virus is able to leave and 
infect other cells.  So if the cell self-destructs prior to that, before 
the virus particles are able to assemble, then the organism can stave off 
the infection.  But a great deal of apoptosis can also lead to tissue 
death.

If you remember from the top of the page I noted that there epinephrine is 
secreted, and that this secretion increases the pulse rate and cardiac 
output (blood flow).  This epinephrine secretion could, although it’s very 
unlikely, result in a heart attack of some sort.  A heart attack as a 
result of this endogenous epinephrine secretion is unlikely – not 
impossible, and not totally unprobable, but the chances of it happening in 
a normal, healthy adult is very acute.

Fever could also be a complicating factor, but not the actual cause of 
death in many pathologies.  Actually, complicating factor is not the best 
term to use.  It would be more appropriate to say that fever is the body’s 
response to a given stimulus, but that’s beside the point.  Various 
chemicals and entities elicit a fever response in humans.  These items, 
which are causing the fever, can also cause death.  So in these cases it’s 
not the fever that is lethal as much as it is the chemical/entity that 
causes the fever.  It’s important to note that when I say entity I mean 
any entity that has pyrogenic properties (pyrogenic means fever inducing), 
such as some bacteria, viruses, and the like.

Hope that answers your question.

Lyle D. Burgoon
Graduate Assistant
Department of Pharmacology and Toxicology
College of Human Medicine
National Food Safety and Toxicology Center
Michigan State University



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