Why body temperature increases when there is bacterial infection ?

Why body temperature increases when there is bacterial infection ?

Whenever we are falling sick due to bacterial infection, most of the time there is increase in body temperature.

Can anybody explain why this happens?

P.J.LAKHAPATE
plakhapate@rediffmail.com

 

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Inflammation is the first response of the immune system to infection or irritation and may be referred to as the innate cascade. Inflammation is characterised by the following quintet: redness (rubor), heat (calor), swelling (tumor), pain (dolor) and dysfunction of the organs involved (functio laesa). The first four characteristics have been known since ancient times and are attributed to Celsus; functio laesa was added to the definition of inflammation by Rudolf Virchow in 1858.

Inflammation has two main components - cellular and exudative.

The exudative component involves the movement of fluid, usually containing many important proteins such as fibrin and immunoglobulins (antibodies). Blood vessels are dilated upstream of an infection (causing redness and heat) and constricted downstream while capillary permeability to the affected tissue is increased, resulting in a net loss of blood plasma into the tissue - giving rise to edema or swelling. The swelling distends the tissues, compresses nerve endings, and thus causes pain.

The cellular component involves the movement of white blood cells from blood vessels into the inflamed tissue. The white blood cells, or leukocytes, take on an important role in inflammation; they extravasate (filter out) from the capillaries into tissue, and act as phagocytes, picking up bacteria and cellular debris. They may also aid by walling off an infection and preventing its spread.

If inflammation of the affected site persists, released cytokines IL-1 and TNF will activate endothelial cells to upregulate receptors VCAM-1, ICAM-1, E-selectin, and L-selectin for various immune cells. Receptor upregulation increases extravasation of neutrophils, monocytes, activated T-helper and T-cytotoxic, and memory T and B cells to the infected site.

Neutrophils are characteristic of inflammation in the early stages - they are the first cells to appear in an infected area, and any section of recently inflamed (within a couple of days or so) tissue viewed under a microscope will appear packed with them. They are easily identified by their multilobed nuclei and granular cytoplasm and perform many important functions, including phagocytosis and the release of extracellular chemical messengers. Neutrophils only live for a couple days in these interstitial areas, so if the inflammation persists for a longer duration then they are gradually replaced by longer lived monocytes

Various leukocytes are involved in the initiation and maintenance of inflammation. These cells can be further stimulated to maintain inflammation through the action of adaptive cascade through lymphocytes: T cells, B cells, and antibodies. These inflammation cells are:

Mast cells which release histamine and prostaglandin in response to activation of stretch receptors. This is especially important in cases of trauma.
Macrophages which release TNF-α, IL-1 in response to activation of toll-like receptors

The outcome in a particular circumstance will be determined by the tissue in which the injury has occurred, and the injurious agent that is causing it.

There are four possible results to inflammation:

Resolution, the complete reconstitution of damaged tissue, does not usually occur in the body.
Connective tissue scarring. Some 24 hours after inflammation in a wound first occurs, the wound healing response will commence. This response involves the formation of connective tissue to bridge the gap caused by injury, and the process of angiogenesis, the formation of new blood vessels, to provide nutrients to the newly formed tissue. Often healing can not occur completely and a scar will form; for example after laceration to the skin, a connective tissue scar results which does not contain any specialised structures such as hair or sweat glands.
abscess formation - primarily in infections by pyogenic bacteria
Ongoing or chronic inflammation. If the injurious agent continues, chronic inflammation will ensue. This process, marked by inflammation lasting many days, months or even years, may lead to the formation of a chronic wound. Chronic inflammation is characterised by a dominating presence of macrophages in the injured tissue, which extravasate via the same methods discussed above (ICAM-1 VCAM-1). These cells are powerful defensive agents of the body, but the toxins they release (including reactive oxygen species) are injurious to the organism's own tissues as well as invading agents. This is why chronic inflammation is almost always accompanied by tissue destruction. Finally, an abscess, or a collection of pus, can form in chronic inflammation.

When inflammation overwhelms the whole organism, systemic inflammatory response syndrome (SIRS) is diagnosed. When it is due to infection, the term sepsis is applied. Vasodilation and organ dysfunction are serious problems that may lead to septic shock and death.

With the discovery of interleukins, another concept of systemic inflammation developed. Although the processes involved are identical, this form of inflammation is not confined to a particular tissue but involves the endothelium (lining of blood vessels) and many other organ systems. High levels of several inflammation-related markers such as IL-6, IL-8, and TNF-α are associated with obesity [1][2]. These levels are reduced in association with increased levels of antiinflammatory molecules within four weeks after patients begin a very low calorie diet [3]. The role of systemic inflammation as a cause and/or result of insulin resistance and atherosclerosis is the subject of intense research. It has little direct bearing on clinical care.

WIKIPEDIA

 

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Curiously some people can experience a decrease in body temperature as a reaction to some infections. I am one of those weird birds that start at sub-normal and go even lower at the onset of infection; starting antibiotics will cause the temperature to cycle above my normal and then drop to sub-normal until the infection is gone. That each peerson will react differently to disease is what makes the science of medicine so very complex.

 

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In case the OP wants a simpler and more direct answer, there is a tendency for single celled organisms to have a lower tolerence for temperature than the cells of multcellular organisms. (Like people) Increased body temp slows the devision of many disease bacteria, give the immune system a little more of an advantage.

 

metabolism is increased to produce more cells to fight of infection, all of this requires release of energy for creation, and as we know most of energy in any process is wasted to thermal energy. Its a problem of efficiency of human body.

 

Phagocytic cells detect the bacteria (pathogens) and release chemicals (pyrogens) that artificially elevate body temperature. This is intended to speed up the immune system and weaken / kill the bacteria; after which, the phagocytes eat them.

 

the body heats up... to kill the germs...

if you eat garlic... at the first signs of being sick... it can stimulate your immune systm to respond ..... within a 1/2 hour.... and you will develop a fever,, long before your body would have normally developed one.


i eat garlic when ever i feel ill for the past 10 years... and as such, i have never been sick after eating alot of raw garlic.... it works.

-MT

 

tablariddimn: Your entire well-worded thesis explains the "inflammation process," but does not answer the question. Why a fever? Why the increase in body temperature? You appear to be the best qualified to answer his question.

 

its because germs.. prefer. 85 degrees... and they can just survive in 98.6....
but when the temp gets to 100-105... its very difficult and alot die...
at 106... all bacteria and germ stuff can die...

problem is... humans die at 106.5... thus the reason fever can kill.

use the garlic.

-MT

 

Valich:

Temperature is regulated in the hypothalamus. Substances that induce fever are called pyrogens. These are both external or exogenous, such as the bacterial substance LPS, and internal or endogenous. The endogenous pyrogens (such as interleukin 1) are a part of the innate immune system, produced by phagocytic cells, and cause the increase in the thermoregulatory set-point in the hypothalamus. The endogenous pyrogens may also come directly from tissue necrosis.



The brain ultimately orchestrates heat effector mechanisms. These may be

increased heat production by increased muscle tone, shivering and hormones like epinephrine and thyroid hormones, or,
prevention of heat loss, such as vasoconstriction or crawling under a blanket.
The autonomic nervous system may also activate brown adipose tissue to produce heat (=non-exercise associated thermogenesis, also known as non-shivering thermogenesis), but this seems mostly important for babies. Increased heart rate and vasoconstriction contribute to increased blood pressure in fever.

Types
Pyrexia can be classed as

low-grade: 38 - 39 °C (99.5 - 102.2 °F)
moderate: 39 - 40 °C (102.2 - 104 °F)
high-grade: more than 40 °C or 104 °F
Hyperpyrexia: 107.6°F (42° C) or more.
The latter is clearly a medical emergency because it approaches the upper limit compatible with life.

Most of the times, fever types can't be used to find the underlying cause. However, there are specific fever patterns that may occasionally hint the diagnosis:

Pel-Ebstein fever is a specific kind of fever associated with Hodgkin disease, being high for one week and low for the next week and so on. However, there is some debate ([1]) wether this truely exists.
Typhoid fever may show a specific fever pattern, with a slow stepwise increase and a high plateau.
In malaria, there may be a fever with a periodicity of 48 hours (tertian fever) or 72 hours (quartan fever, indicating Plasmodium vivax). These patterns may be less clear in travelers.
Febricula[1] is a mild fever of short duration, of indefinite origin, and without any distinctive pathology.

Causes

Fever is a common symptom of many medical conditions:

infectious disease, e.g. common cold, HIV, malaria, infectious mononucleosis, gastroenteritis, etc..
Immunological diseases like lupus erythematosus, sarcoidosis, inflammatory bowel diseases, etc..
Tissue destruction, which can occur in hemolysis, surgery, infarction, crush syndrome, rhabdomyolysis, cerebral hemorrhageetc..
Drug fever
directly caused be the drug (e.g. progesterone, chemotherapeutics causing tumor necrosis)
as an adverse reaction to drugs (e.g. antibiotics, sulfa drugs, etc.)
after drug discontinuation, like with heroin withdrawl
Cancers such as Hodgkin disease (with Pel-Ebstein fever)
Metabolic disorders like gout, porphyria, etc..
Thrombo-embolic processes (i.e. pulmonary embolism, deep venous thrombosis)
Persistent fever which cannot be explained after repeated routine clinical inquiries, is called fever of unknown origin.


Is fever useful?
The mainstream medical answer is: no. That is: there is no definitive proof in warm-blooded species (and certainly not in humans) in vivo that they recover more rapidly from infections due to fever.

Of course, there is evidence that hints a possible role for the usefulness (and therefore, evolutionary role, from a Darwinistic point of view) of fever. It does have an effect in cold-blooded species, and there are certainly some important immunological reactions that are speeded up by temperature. Possibly, some pathogens with strict temperature preferences could be hindered.


Treatment
Fever should not necessarily be treated. Fever is an important signal that there's something wrong in the body, and it can be used for follow-up. Fever might help the immune system or hinder specific pathogens, but this is generally considered of little importance. Moreover, not all fevers are of infectious origin.

Most people take medication against fever because it causes discomfort. Fever increases heart rate and metabolism, thus potentially putting an additional strain on elderly patients, patients with heart disease, etc. This may even cause delirium. Therefore, potential benefits (if any) must be weighed against risks in these patients. In any case, fever must be brought under control in instances when fever escalates to hyperpyrexia, and tissue damage is imminent.

Treatment of fever should primarily be based on lowering the setpoint, but facilitating heat loss may contribute. The former is accomplished with antipyretics. Heat loss may be an effect of heat conduction, convection, radiation or evaporation (=sweating, perspiration). This may be particularly important in babies, to whom it is best not to give to much drugs. However, when someone would use water that is too cold, this induces vasoconstriction and prevents adequate heat loss.


WIKIPEDIA

 

yeah... doctors will always cool the body... to prevent the over heating that a bad infection can cause...

i.e.. the body wants to reach 106... to kill the germs and save the body...


but its not a perfect system.... and if 106.5 is reached.. humans die.


fever... is a good thing... but anything over 104 is a danger and a doctor must act.......

since in fact... the body just needs more time to win the war... not more temp.


-MT

 

Can't vasodilation and increased blood flow due to inflammation or infection raise temperature in acute stages?

Some infections in latent stages may not show that.

Much details are given on following link;http://www.merck.com/mmhe/sec17/ch188/ch188d.html

 

tablariddim: Thanks for the superb reply. Very informative.

Is fever useful? From an evolutionary perspective one would think that it must be. You state that "the endogenous pyrogens are a part of the innate immune system." Possible the additional heat facilitates their production?