The main point of this post is to help me to understand the mechanism and logic behind fever production in response to bacterial infection. If anyone else happens to gain valuable insight from this, then that will be an added benefit.
The body has a preferred core body temperature that is maintained via homeostatic mechanisms. As I’m sure most of you know, this body temperature is, on average, 98.6 degrees Fahrenheit, although it does vary minimally from person to person. Temperature sensors in your skin and in the hypothalamus monitor this core temperature and relay any deviations to the anterior hypothalamus. The anterior hypothalamus then compares this measured temperature to the preferred set-point core temperature. If the measured temperature is below the preferred set-point core temperature, the anterior hypothalamus communicates this to the posterior hypothalamus. The posterior hypothalamus is in charge of communicating to the rest of the body that heat needs to be produced, so it sends out signals to ensure that this happens. For example, the posterior hypothalamus sends a message to skeletal muscle, via alpha motor neurons, telling them to rapidly contract. This resultant “shivering” generates heat, just as a car engine generates heat when work is being performed. Another mechanism of heat production is prompted by the activation of the sympathetic nervous system (SNS) by cold temperatures; cold temperatures tell the SNS to activate beta receptors in brown fat, which increases the metabolic rate and heat production in these tissues. This is one reason, besides having extra insulation, that overweight people in general can stay warmer than thinner people.
So, now that we’ve talked about ways the body generates heat in response to cold, we need to consider ways the body can get rid of excess heat. For example, if you’ve been out in the heat for an extended period, your core body temperature would also increase to the point of causing tissue damage if not for homeostatic mechanisms to counteract this. See, heat causes proteins to denature (what we call what happens when heat causes proteins to unravel from their most functional form). Just think about what happens when you cook hamburger meet. If not for certain of these homeostatic mechanisms, your heart muscle, for example, would become overheated and denature into a less functional form, which could lead to decreased contractility and death. The anterior hypothalamus orchestrates the response to excess heat. One way it does this is by decreasing sympathetic tone to cutaneous blood vessels, which causes them to dilate, allowing more blood to flow through them. This allows more blood, which is carrying heat, to flow to the skin, enabling the release of excess heat at the body surface. Furthermore, sweat glands are under sympathetic muscarinic control, so sympathetic stimulation also leads to more evaporation of heat from the body surface.
Now we’ll talk about how bacterial infections cause fever. Certain bacteria cause an increase in the production of interleukin-1 (IL-1) in macrophages. IL-1 in turn acts on the anterior hypothalamus, leading to an increase in the production of prostaglandins. Prostaglandins, in turn, lead to an increase in the set-point core temperature. This will cause the anterior hypothalamus to perceive the core temperature as being too low (since the prostaglandins caused the resetting of the core temperature), prompting it to correct the temperature by implementing heat generating mechanisms, such as shivering.
You see, fever is the body’s natural response to fight off infection. Bacteria are made of proteins, and excess heat causes those bacterial structural proteins to denature the same way our own proteins would denature. At the same time, certain bacterial enzymes–which are made of protein– that the bacteria require to proliferate are denatured. So, as you can see, fever is a good thing in moderation and it isn’t necessarily in our best interest to short-circuit it prematurely. If, for instance, you give aspirin prematurely to reduce a fever, you aren’t giving your body time to kill off the bacteria. In essence, the bacteria are happy when you take aspirin to reduce the fever because that means that they can proliferate and wreak havoc. Just for your information, aspirin works by inhibiting an enzyme, called cyclooxygenase. Cyclooxygenase normally functions in the formation of prostaglandins, which, as you may recall, are required to increase the set point temperature. So, if you inhibit cyclooxygenase, there are no prostaglandins being produced to increase the set-point temperature. Therefore, aspirin works by lowering the set-point temperature back to its original pre-infection temperature. This causes the hypothalamus to read the increased body temperature (caused by the fever) as being higher than the set-point temperature, so the body responds by activating heat loss mechanisms. So, you may be able to see how giving aspirin to break a fever isn’t always in your best interest. I personally would rather let my body fight off the infection naturally and would only recommend giving aspirin if the fever stays above a certain temperature for a certain period of time. I don’t, however, feel comfortable explicitly defining that temperature and time frame, as each situation is different and requires medical expertise to evaluate the specific situation. That’s why you have doctors!