MadSci Network: Medicine |
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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