from Wikipedia, the free encyclopedia
Classification according to ICD-10
R50.9 Fever, unspecified
ICD-10 online (WHO version 2019)

The Fever (Latin fever ) or pyrexia is a state of increased core body temperature with a mismatch between chemical heat production and physical heat emission, the most accompanying the defense against invading viruses , live microorganisms or other as alien recognized substances occur and certain as associated with, in particular Malignant tumors , trauma or, less often, inflammation processes caused by other causes . The associated processes are based on complex physiological reactions, which include a pyrogen-mediated , regulated and limited increase in the core body temperature that is actively brought about by the organism. The latter arises as a result of a temperature setpoint change in the hypothalamic heat regulation center, i.e. it is based on increased excitation and excitability of the heat center in the diencephalon by pyrogenic substances. Fever is an example of a regulated change in homeostasis . A clinical thermometer is used to measure, determine, evaluate the progression or to exclude the increased body temperature associated with a fever .


The word "fever" goes back to the Middle High German vieber (also biever , biefer ), from Old High German fiebar , verifiable since the 9th century and borrowed from the Latin febris , actually "heat".

The word “pyrexia” from ancient Greek πύρεξ (ις) , pýrex (is) , “have a fever”, goes back to the Greek πυρετός , pyretós , “burning heat”, “fever”. Compare pyr , "fire", and from it " pyrogenic ", " causing fever".

Temperature regulation

Contrary to a common misunderstanding, fever is in most cases not the cause of illness, but part of the body's response to illness. The frequent practice of symptomatically lowering a fever above a certain level in order to avert supposed harm to the patient, often does not correspond to the state of research in fever physiology. Instead of routinely lowering the fever above a certain temperature, it is recommended that symptomatic therapy be based on the state of health and secondary risks of the fever for certain patient groups.

Fever is fundamentally different from the unregulated conditions of hyperthermia . No pyrogens are involved in these , which is why drug antipyretic therapy remains ineffective. The temperature remains elevated, although the organism tries to lower its temperature at the limit of its counter-regulatory possibilities. Such overheating can occur in the case of excessive warming from the environment and / or in the context of vigorous physical exercise, and rarely in the case of disturbed temperature regulation in the context of neurological diseases or malignant hyperthermia .

Fever is one of the most common times for advice in a general or pediatric practice.


The ability of multicellular organisms to form fever-like reactions as part of the innate immune response is probably around 600 million years old, highly conserved in evolution and predominantly successful: It occurs in mammals , reptiles , amphibians , fish as well as some invertebrates (invertebrates) up to towards the insects and usually leads to improved survival or healing of various infections. Animals of the same temperature and cold blood change their behavior as part of a fever reaction in order to reach the higher body temperature required by the fever reaction (looking for a warmer environment, etc.), animals of the same temperature also have more efficient physiological possibilities to increase their body temperature. The same antipyretics that inhibit the physiological fever reaction in animals of the same temperature, suppress e.g. B. the targeted search for a warmer place in the event of an infection.

Normal core body temperatures and temperature ranges for fever

Core body temperatures and fever
species Basal temperature / ° C Temperature with fever / ° C
human 36.0-37.2 37.9-41.4
horse 37.5-38.2 38.3-39.3
dog 38.1-39.2 39.3-42.2
cat 38.0-39.0 39.4-40.9
pig 39.3-39.9 40.5-41.1
rat 37.9-38.2 38.6-39.4
mouse 36.5-37.2 37.8-39.3
Dove 39.7-40.7 41.0-41.5
lizard 34.0-37.0 39-42
frog 25-28 35-39

Fever physiology

Fever is normal thermoregulation at a higher level

Typical course of a fever.
The green line shows the target value, the red line the actual core temperature.

The uppermost thermoregulatory center is the regio praeoptica of the hypothalamus : Here afferent signals run e.g. B. of heat and cold receptors from the skin of the whole body together. The temperature information from the periphery is compared with the central temperature information and integrated; the result is a thermoregulatory response controlled from here with one of the two following goals:

  • Loss of heat (inhibition of the sympathetic nervous system with the consequence of peripheral vasodilation and warming of the skin as well as sweating, panting in dogs, etc.) or
  • Heat production and conservation (activation of the sympathetic nervous system with peripheral vasoconstriction and skin cold, inhibition of sweating to prevent heat drainage, and also shivering ( chills ) and activation of the metabolism to produce more heat).

Furthermore, behavior in the hypothalamus is influenced by the perception of self-heat (changing clothes, looking for a different environment, etc.). In the case of a normal pyrogen-induced fever reaction, these regulatory mechanisms work in exactly the same way, so they are only possible with an intact preoptic region of the hypothalamus. Therefore, when the temperature rises feverishly, you freeze and feel cold on your hands and feet. On the other hand, you feel warm or even sweat when the temperature drops again after the fever (or when you are given an antipyretic drug).

Development of the rise in fever

Simplified after, (W): heat-sensitive neuron; (C): cold-sensitive neuron; (I) temperature-insensitive neuron, see text for further description

There are various neurons in the praeoptica region of the hypothalamus : around 30% are heat-sensitive (that is, they fire faster when the temperature rises), over 60% do not react to temperature changes, and less than five percent are cold-sensitive. It is assumed that the so-called temperature setpoint is created by comparing the neuron activity of the temperature-insensitive neurons with the heat-sensitive neurons. In particular, the activity of the cold-sensitive neurons is heavily dependent on excitatory and inhibitory input from neighboring neurons, while the heat-sensitive neurons mainly receive input from the periphery. The heat-sensitive neurons become more active from a certain temperature and ultimately trigger a regulation that causes the body to emit more heat.

These heat-sensitive neurons can be inhibited by so-called pyrogens , which then shifts the normal regulatory equilibrium in the thermoregulatory center. Some of these pyrogens belong to the acute phase proteins that occur during inflammation . An idea of ​​the interdependencies of the various pyrogens was gained primarily through animal experiments with fever production, especially with injected lipopolysaccharides (components from the wall of gram-negative bacteria ). This exogenous pyrogen leads mainly in monocytes , mediated among other things by the CD14 receptor , to an increased formation of endogenous pyrogens, starting with tumor necrosis factor (TNF), interleukin-8 and traces of interleukin-1 and a little later for significant amounts of interleukin-6 . The latter correlates best with the course of the fever itself. This formation of endogenous pyrogens in monocytes stimulated by lipopolysaccharides is somewhat slower (and more limited in time for TNF and interleukin-8) than at 42 ° C (a temperature just above the natural temperature limit) at 37 ° C. Tumor necrosis factor can also have a fever-limiting property depending on the context. When lipopolysaccharides are injected as exogenous pyrogen or interleukin-1β as endogenous pyrogen in the experiment, a uniform, bimodal increase in fever results. A first fever peak begins quickly and lasts 30–60 minutes. It is caused by the fact that interleukin-1β activates the neutral sphingomyelinase via its interleukin-1 receptor , which catalyzes the formation of soluble C2 ceramide . Ceradmid inhibits the heat-sensitive neurons. It was also hypothesized that this first increase in fever was mediated by the vagus nerve, but attempts at this point gave inconsistent results.

At the same time, interleukin-1β stimulates the increased transcription of cyclooxygenase-2 initially in the macrophages , which increasingly forms prostaglandins, especially prostaglandin E2 , which reaches the hypothalamus via the circumventricular organs and causes the onset of the second rise in fever. Then the cyclooxygenase-2 in the endothelial cells of the hypothalamus itself is stimulated, which leads to a central increase in prostaglandin E 2 production . The resulting prostaglandin-E 2 can get into the brain and then ultimately induce a longer-lasting increase in fever via its EP3 receptor with a maximum about three hours after the appearance of interleukin-1β, also via the inhibition of heat-sensitive neurons. In this way, heat-emitting processes (peripheral vasodilation, sweating, etc.) are inhibited and furthermore the inhibition of the heat-sensitive neurons on the cold-sensitive neurons is canceled. This then leads to the build- up of heat and even chills. All in all, the result is a stereotypical and reproducible bimodal fever rise until the new regulatory equilibrium is established. Overall, fever is the result of finely tuned communication between the organism's immune system and its nervous system.

Limiting the rise in fever

In the event of an acute fever reaction, the human body temperature (especially in children) rises rapidly to values ​​between 40 and 41.4 ° C, but almost never above this, regardless of the cause of the fever or the location of the temperature measurement. Under normal conditions, the body must therefore be able to regulate and limit a fever reaction effectively before it becomes dangerous by itself. If this were not the case, the phenomenon of the fever reaction would not have been able to establish itself evolutionarily. However, the processes of fever development have been researched for much longer and therefore more is known about them than about the processes of fever limitation by the organism itself.

The body can limit its fever response with the help of a number of endogenous anti-pyrogens. These include:

Regulators at the cytokine level

  • Interleukin-1β antagonist: This suppresses the fever-inducing effect of interleukin-1β. It is formed in the locally inflamed tissue with a delay to interleukin-1β and then appears in the blood in higher concentrations than interleukin-1 itself.
  • Interleukin-10 : Inhibits the formation of tumor necrosis factor, interleukin-1 , interleukin-2 and interleukin-6 in antigen-presenting cells such as e.g. B. monocytes and dendritic cells and thus indirectly the activation of T lymphocytes . IL-10 inhibits the activation of cyclooxygenase-2 by lipopolysaccharides in monocytes and thus fever reactions. It is involved in the development of immune tolerance.
  • Tumor necrosis factor: Traditionally, TNF-α is viewed as a pyrogen rather than an anti-pyrogen (see above). This is because injections of tumor necrosis factor cause a fever. Furthermore, it appears as one of the first cytokines in serum when lipopolysaccharides are injected for experimental fever production. If, however, higher doses of lipopolysaccharides are injected, a fever does not occur immediately, but rather a brief phase of hypothermia . This phase of hypothermia does not arise if the effect of the tumor necrosis factor is blocked. Overall, the results on the effect of TNF on suppression and / or induction of fever are inconclusive.

Prostaglandin derivatives


  • Endocannabinoid system : By activating the centrally located cannabinoid receptor 1 , a febrile reaction caused by lipopolysaccharides can be suppressed; the interleukin-6 production associated with the fever is also suppressed. The exact mechanism leading to this is unclear. It is interesting that a breakdown product of paracetamol combines with arachidonic acid to form a bioactive N-acylamine AM404 , which also activates cannabinoid receptor 1. Paracetamol must therefore be viewed as an indirectly acting cannabinoid mimetic.
  • Nitric oxide : Nitric oxide is formed by various isoforms of the enzyme NO synthase and activates a guanylate cyclase, which increases cGMP levels in the target cells. In the cells of the brain, nitric oxide has an inhibiting effect on heat generation and promotes heat distribution and thus overall a temperature reduction in general and also in the fever reaction.


  • Glucocorticoids (hormones of the adrenal cortex) are released to an increased extent during various types of stress, including infection. On the one hand, they counteract the fever in the periphery by inhibiting the release of cytokines. On the other hand, a direct central antipyretic effect could also be demonstrated.
  • Melanocortins : This group of central peptide hormones (melanocyte-stimulating hormones and ACTH ) is very diverse, complex and context-dependent in vegetative regulatory processes such as hunger, satiety, urge to move, energy homeostasis and thus also temperature regulation. They suppress the fever reaction via the central melanocortin-4 receptor . They also inhibit the biological activity of TLR-4 , which otherwise mediates the effect of lipopolysaccharides in macrophages. In the non-febrile organism, melanocyte-stimulating hormones tend to increase the body temperature; the melanocortin-3 receptor may be involved here. In contrast, the MC4R mediates the pyrogen-induced loss of appetite, which is often associated with a febrile inflammatory reaction, as does tumor cachexia .
  • In addition to their peripheral effect as thirst hormones, antidiuretic hormones ( vasopressin ) are also a centrally acting neuropeptide : Here it is involved in the regulation of the adenohypophysis and central pathways of the autonomic nervous system as well as in connections between the limbic system and the hypothalamus. It is increasingly released during fever reactions and limits them (via the V1 receptor) and alleviates them. (For this reason, among other things, one often finds hyponatremia in highly inflammatory diseases such as pneumonia or sepsis , which, among other things, indirectly indicates to what extent the body has already activated its antipyretic regulation).
  • Estrogen and progesterone can limit fever and inhibit the parallel released interleukin-1β as well as lead to a lower formation of cyclooxygenase-2 in the hypothalamus. Furthermore, the release of vasopressin in the brain (which in turn lowers fever) is influenced by the presence of these hormones there. It is possible that the fever response is suppressed in pregnant women close to the due date and in newborns.
  • Melatonin : This hormone is involved in the sleep-wake regulation. It lowers fever, the cytokine level in the serum and prostaglandins excreted in the urine and increases cortisol secretion. These effects suggest that the daily fluctuation of fever (often higher in the evening than in the morning) could have something to do with the effects of melatonin on the overall hormonal balance.

Fever and heat shock response

Before denaturation of cell proteins, e.g. B. at elevated temperature, cells protect themselves through the heat shock response. This is an evolutionarily ancient and highly conserved process that occurs in all living things right down to bacteria. The heat shock proteins thus formed have a wide range of functions, one of the main tasks being to facilitate the correct folding of denatured proteins. This function contributes significantly to cell survival under stress conditions. The genes for the heat shock proteins have been preserved throughout evolution, although new possibilities have arisen for the more highly developed organisms to deal with environmental stressors. The relationship between the evolutionarily old heat shock response and the evolutionarily more recent fever response can be viewed as an example of how newer processes use earlier developed processes. Examples of the complex relationships between fever and heat shock response are:

  • The threshold for a heat shock response is around 4 ° C above the normal level of elevated temperature; this threshold is lowered by cytokines, such as those found in fever, so that in the event of a fever the body is better protected from protein denaturation than when the temperature is off other reasons would rise.
  • Fever stimulates a heat shock response of many fever-causing bacteria, the resulting bacterial heat shock proteins strongly stimulate the macrophages of the host organism in the inflammation focus and thereby improve its innate defense.
  • The heat shock proteins produced by the host also stimulate its own immune functions via the CD14 receptor .
  • On the other hand, the expression of heat shock proteins is regulated by certain transcription factors , the heat shock factors ; but at the same time inhibit the transcription of z. B. Interleukin-1β or tumor necrosis factor .
  • Heat shock proteins can form complexes with many other proteins (from bacteria or from the host). These complexes can stimulate or inhibit the immune system, depending on the context. You play e.g. B. also play a role in the manifestation of autoimmune diseases .

Modulation of the inflammatory process

Many features of neutrophilic granulocytes , the macrophages and lymphocytes , which are important for the defense against infections such. B. mobility, phagocytic ability , radical formation , multiplication, antibody formation, etc. are increasingly observable at temperatures of 38 to 41 ° C and decrease again at temperatures above 41 ° C. Fever, for example, promotes T lymphocytes , which point to infection sites, by changing their surface proteins. And thermal stress (TS) in the fever range of 38 to 40 ° C plays an active role in the control of lymphocyte migration to secondary lymphoid organs or foci of inflammation. TS regulates integrins and selectins , which are important cell adhesion molecules and play a role in mediating lymphocyte traffic. Fever induces the expression of heat shock protein 90 ( HSP90 ), which is then selectively bound to the lymphocyte surface and clustered to promote vascular adhesion through focal adhesion kinase RhoA signaling. The HSP90 is only induced at a temperature above 38.5 ° C. The HSP90 level can then last for 48 hours even if the temperature returns to normal.

Defense against infection

For most infections - from a simple cold to life-threatening sepsis - it has been shown that fever-lowering measures can usually make the course of the disease more complicated and prolong it. This applies both within clinical studies and in (animal) experimental settings, for viral, bacterial and parasitic diseases. Some examples are given in the table below:

species infection Antipyresis Result year Ref.
lizard experimental sepsis with the bacterium Aeromonas hydrophila varied ambient temperature 34 to 42 ° C or salicylic acid significantly better survival at 40 to 42 ° C than at 34 to 38 ° C or without than with salicylic acid 1975, 1976
goldfish experimental sepsis with the bacterium Aeromonas hydrophila varied ambient temperature better survival in higher temperature 1977
Rabbits experimental sepsis with the bacterium Pasteurella multocida Salicylic acid significantly poorer bacterial defense under salicylic acid 1981
human Sepsis from bacteria or fungi Influence of body temperature among other influencing factors on survival The likelihood of survival increases with body temperature 1983, 1997
mouse experimental pneumonia with pneumococci Acetylsalicylic acid twice as poor survival and poorer defense against infection in the lungs under acetylsalicylic acid 1984
human Study in children aged one to twelve with chickenpox Paracetamol or placebo longer duration of illness on paracetamol 1989
human experimental rhinitis with rhinovirus Acetylsalicylic acid , paracetamol , ibuprofen increased nasal swelling, prolonged virus excretion, suppressed antibody formation with acetylsalicylic acid and paracetamol 1990
human uncomplicated malaria Paracetamol Parasites stay longer in the blood with paracetamol 1997
mouse experimental peritonitis with klebsiae Body temperature 37.5 or 39.7 ° C due to different warm surroundings better survival and bacterial defense at a warmer body temperature 2000
human Patient with a fever in a trauma intensive care unit Randomized study: aggressive antipyresis from 38.5 ° C or feverish up to 40 ° C Study discontinued due to increased mortality in the antipyresis group 2005
Mouse, chicken experimental flu (meta-analysis) Acetylsalicylic acid , paracetamol , diclofenac slightly increased flu mortality under antipyresis 2010
human Critically ill patients with fever (> 48h intensive care unit) with and without sepsis Prospective observational study: fever with / without antipyresis and mortality Antipyresis increases mortality only in patients with sepsis 2012

There are also studies that could not determine any disease-prolonging effect of fever-lowering measures in infectious diseases. However, lowering the fever does not usually reduce the effect of an infectious disease. However, lowering the fever can alleviate secondary problems in some patient groups. Such results and clinical experience, as well as increasing knowledge of the physiology of fever, make the routine use of antipyretics in fever z. B. in intensive care units. What is required today is a therapy that is oriented towards the individual treatment goals; Lowering the temperature as an end in itself is not an absolute treatment goal for fever. However, a single temperature increase to over 38.5 ° C or twice to over 38 ° C within 12 hours in immunosuppressed patients with neutropenia (granulocyte count below 500–1000 / µL) should be treated immediately with antibiotics.

Febrile convulsions, epileptic fits

Febrile seizures occur in (1%) - 6% - (14%) (depending on the population group) of all children aged one to five; the mechanisms by which they occur are poorly known. It is believed that affected children have a complex inherited disposition for febrile seizures. A hypothesis currently being pursued in this regard is that this system could be a mutation of a seizure-inhibiting GABA receptor that has temperature-dependent properties. In contrast to a presumption often expressed in textbooks, antipyretics do not significantly prevent febrile seizure relapse. Endogenous pyrogens can lower the brain's seizure threshold. These are, for example, tumor necrosis factor -alpha, interleukin-1 beta and interleukin-6 , which lead to fever by stimulating cyclooxygenase-2 with a subsequent increase in prostaglandin E2 . A lower fever only inhibits cyclooxygenase-2, but not the release of these pyrogens. However, an increased temperature itself can inhibit the release of these pyrogens. This may also explain why lowering the fever does not prevent febrile seizures.

Patients with epilepsy must be differentiated from those with febrile convulsions. Since there are many different types of epilepsy, the influence of fever and high temperature on seizure activity is different: it can be increased or it can remain the same. In some cases, however, the seizure activity can temporarily decrease due to a fever.

Influence of fever in the first year of life on asthma and allergy

Repeated episodes of fever in the first year of life (which mostly occur due to respiratory infections) are associated with a higher prevalence of early onset , non-allergic asthma . However, allergic sensitization and asthma that started later occur less often after more frequent febrile episodes in the first year of life. It seems important that the febrile episodes occur before an allergic sensitization has occurred. Only episodes of fever between the seventh and twelfth month of life seem to protect against atopic predisposition , and a sufficient fever> 39 ° C is also important. In contrast, airway infections in the first year of life generally seem to increase the frequency of asthma (see e.g.). In these studies, however, the influence of antibiotics and antipyretic measures, e.g. B. accounted for by paracetamol ; the latter has an asthma-promoting effect. Children from families with an anthroposophical lifestyle receive fewer antibiotics and antipyretics, among other things, and have fewer asthma and allergies.

Fever and cancer

Since cancer diagnosis and treatment became a science in the 19th century, rare cases of "inexplicable" spontaneous cures have been reported time and again . Many of these cases are preceded by a high febrile illness. This was successfully used therapeutically before the chemotherapy era, e.g. B. with the fever generated by an injected bacterial extract. While in the chemotherapy and radiation era from the 1950s it was the opinion that the body had no means of its own to fight cancer cells, the connection between fever and cancer cure has been more systematically investigated since the 1990s. Meanwhile, it is undisputed that fever, especially if it is high, may help the immune system fight cancer better. In practical oncology, such considerations must be combined with the aim of alleviating unpleasant situations for the patient.

Since cancer is a long-dormant disease, this is also possible in the run-up to a manifest cancer, i.e. preventive. This explains why episodes with febrile infections are less common in the history of cancer patients. This could be shown clearly for the melanoma risk , for example .

Fever to fight syphilis

Before the introduction of the first effective syphilis remedy in the 1910s - arsphenamine (Salvarsan) - people suffering from syphilis were infected with malaria , a disease characterized by severe fever. The high fever killed the syphilis bacteria quite reliably. In particular, patients with syphilis in the late stage, in which neurological and psychiatric symptoms appear, were treated in this way. The realization that syphilis can be cured with malaria-induced fever attacks led to the Nobel Prize for Medicine for the Austrian psychiatrist Julius Wagner-Jauregg .

Other symptoms that may be accompanied by the “fever” symptom

Fever always occurs as part of a complex physical inflammatory reaction that can vary in severity. The overall symptoms are always influenced by the underlying disease, so it is difficult to attribute individual symptoms to the fever in each case. However, the following symptoms often occur together with febrile illnesses:

  • Symptoms directly related to temperature regulation:
    • When the fever rises, freezing, cold hands and feet with possibly already warm head, possibly muscle tremors and chills. Possibly. Marbled skin with poor blood circulation and reduced capillary refill (if you briefly press the skin on the back of your hand, for example, the white spot persists for more than two to three seconds).
    • When the fever goes down, heat, possibly sweating, reddening of the skin, vasodilatation in the body periphery. In this context, circulatory lability with dizziness when standing up and a possible risk of collapse .
  • Symptoms related to the general acceleration of the metabolism in fever:
    • Increase in pulse rate (ten heartbeats per minute more per 1 ° C increase in body temperature, so-called " Liebermeister rule ")
    • Increase in breathing rate
  • Symptoms that often accompany the febrile inflammatory reaction because they are triggered by similar physiological processes:
    • Loss of appetite, headache and body aches
    • Sensitivity to pain, increased sensitivity to light and noise, sensitivity to touch
  • Central nervous symptoms:
    • Febrile seizures in children from six months to six years of age
    • Fatigue, weakness, insomnia, nightmares
    • Unclear, "glassy" look, shiny eyes
    • Disturbances in perception, restlessness, states of confusion up to hallucinations ("fever delirium" or "feverish delirium")
  • Possibly. Symptoms of dehydration when not drinking enough (which is necessary if you have a fever):
    • decreased and concentrated urine
    • dry and coated tongue , chapped and chapped lips
    • increased thirst
    • Weight loss
    • constipation

Fever pattern

In the course of the fever, a distinction is made between the rise in temperature (stage incrementi), the heat or altitude stage (fastigium) and the fall in fever (stage decrementi). The course of the fever curve (graphic representation of the fever temperature as a function of time) can provide information about the cause of the fever (e.g. pathogens), but it cannot be relied on alone for a diagnosis. Traditionally, the following fever patterns (fever types) were grouped into diagnostically useful groups (according to):

  • Continuous fever (Febris continua; persistent fever, daily fever, permanent fever): Fever that remains constant for four days or more with daily fluctuations less than or maximum 1 ° C, with more than 39 ° C: can e.g. B. indicate lobar pneumonia , rickettsiosis , typhoid, or tularemia . If there is a daily difference of up to 1.5 ° C, it is referred to as remittent Febris .
  • Intermittent fever (Febris intermittens): Very fluctuating fever with feverless intervals, often with normal temperatures in the morning and fever peaks in the evening, with rapid increases in fever with chills. This can indicate local purulent infections from which germs repeatedly spread into the bloodstream, such as B. endocarditis or osteomyelitis . Also for acute brucellosis , malaria , salmonellosis or miliary tuberculosis .
  • Alternating fever (Febris recurrens): Fever with fever-free days e.g. B. in malaria .
  • Double-peaked fever: After a few days of fever, there is a brief decrease in temperature with a second, usually higher, fever peak. This is a typical pattern for viral diseases such as B. measles , yellow fever , flu or dengue fever .
  • Pel-Ebstein fever: periods of about one week with fever and similarly long fever-free episodes with repetition of the cycle. This could indicate Hodgkin lymphoma or brucellosis .
  • Undulating fever ( Febris undulans ): The disease caused by Brucella .


Feeling with the hand

The temperature of the forehead and torso can be roughly estimated by hand. In addition, by feeling the hands and feet, one can judge whether the patient is freezing (heat concentration when the temperature rises) or whether he is warm (the heat is redistributed by the body, the temperature will then no longer rise quickly).

Parents can safely rule out (higher) fevers in their children by feeling the temperature. If you suspect a fever, you should take the temperature anyway.

Temperature measurement

Body temperature can be measured with different measuring devices and at different locations.

Measuring equipment

Traditionally, measurements were made with mercury thermometers . However, because of the mercury it contains and the glass construction, damaged thermometers pose a health risk. Since April 2009, the sale of mercury thermometers has been banned within the EU, with the exception of the scientific and medical field. Mercury is increasingly being replaced by non-toxic gallium . It is a peak value thermometer, which means that the highest value during the measurement remains in the display. The metal column must therefore be shaken down before measuring again.

Such analog thermometers have the advantage over modern digital thermometers that they do not require electricity. Digital thermometers have a higher breaking strength, enable faster measurements and often offer a memory function for displaying previous measurement results. They are also easier to use thanks to an acoustic signal at the end of the measurement process and easy readability.

Ear thermometer

The pyrometric measurement of infrared radiation , mostly with ear thermometers, is becoming increasingly popular . Because of the high measuring speed, this is particularly popular for measuring children, but is also increasingly being used in general practices and hospitals. Modern digital thermometers often only need 60 seconds and signal that the measurement process is complete. Digital ear thermometers often only need a few seconds to perform the measurement.

In terms of price, analog and digital thermometers are roughly on par with minor deviations. Ear thermometers are 10 to 40 times more expensive, depending on the model. A cost factor that must also be taken into account with ear thermometers is the replaceable plastic shells, which should avoid direct skin contact with the device.

Measuring points

Body temperature can be measured sublingually (in the mouth), rectal (in the anus), auricular (in the ear), vaginal (in the vagina), inguinal (in the groin) or axillary (in the armpit), with the value measured rectally being the Body core temperature is closest. A measurement on the forehead is also possible for orientation. Using infrared measuring devices , this is e.g. B. in disease control, also possible over a distance. The rectal measurement is the most reliable - especially for babies and toddlers up to four years of age - and the measured temperature is the highest in comparison. The temperature under the tongue is around 0.3–0.5 ° C lower and that under the armpits around 0.5 ° C and is relatively unreliable.

When measuring in the ear is pyrometric , i. H. based on the temperature-dependent infrared radiation, the temperature of the eardrum is measured. This measuring method is fast and in principle accurate, but delivers incorrectly low values in the event of incorrect operation due to incorrect angulation and obstruction of the ear canal due to cerumen . More modern devices offer technical possibilities to recognize this.

In order not to falsify the measurement by cooling, the measuring device should first be warmed up to approximately body temperature. With high-quality ear thermometers, the tip is electrically heated to 37 degrees before the measurement. When measuring in the mouth, you should not have consumed any cold food or drinks within 15 minutes.

In intensive care medicine, the temperature is often measured via a urinary catheter with a thermistor or via a thermistor catheter in an artery (which is also used to measure cardiac output ). Mouth and armpits are too unreliable.


With a fever, the fluid requirement is increased, so it is particularly important to ensure that there is sufficient fluid intake. In the first phase (see symptoms ), in which chills are often felt, heat loss from the body should be avoided. Fever reduction through heat dissipation, e.g. B. calf wrap is i. d. Usually only makes sense if the target value is also lowered with suitable medication. Cooling measures are also useful at extremely high temperatures. B. Ice packs placed in the groin. A person with a fever does not necessarily have to keep bed rest, as there is currently no evidence of a positive effect of bed rest. Physical rest, i.e. avoidance of physical and mental overexertion, is recommended. If you feel dizzy, your ability to drive is impaired.

"Antipyretic therapy" means treatments to lower febrile body temperatures. There are various indications for antipyretic therapy. Above all, a reduced subjective well-being with a fever speaks for the use of an antipyretic therapy, whereby antipyretic drugs often also have an analgesic effect. But also the avoidance of undesirable metabolic effects in fever, such as B. dehydration or undesirable cardiovascular effects in fever, z. B. tachycardia , are indications. Children and the elderly in particular are sensitive to high fever; febrile seizures may occur in young children , especially after a rapid rise in fever.

Before using an antipyretic therapy, however, one should also consider arguments that speak against the use of an antipyretic therapy. In this way, one loses the fever as a diagnostic parameter, whereby a delay in therapeutic decisions is theoretically conceivable.

Anti-fever drugs ( antipyretics ) are z. B. acetylsalicylic acid , ibuprofen , paracetamol or metamizole . The willow bark used in naturopathic medicine contains salicin , which is metabolized in the body to salicylic acid and has a similar effect to acetylsalicylic acid. Treatment by dissipating body heat, such as B. calf wraps , torso rubbing bath, descending bath tub or irrigator (enemas) are used in complementary medicine. Even in intensive care being treated if necessary by heat dissipation, then usually with the help of filled with ice water pouches for. B. be placed in the bar. In contrast to medicinal fever lowering, there is no normalization of the temperature setpoint, so that the body tries to counteract the external cooling, which is associated with high energy consumption. Therefore, these measures only make sense if they are treated with medication.

Raising the temperature to fight fever

According to supporters of complementary procedures , increasing the temperature is also suitable for combating fever. Above all, increasing footbaths , teas and saunas are recommended. There is no proof of effectiveness for these measures; Especially when taking a sauna there is a risk of a life-threatening rise in temperature.

Causal treatment of fever

If the pathogen is known (or likely), the cause of the fever can be treated: Treatment with antibiotics is used for a bacterial fever. If the fever is caused by fungi, antifungal drugs help ; in some viral infections can antivirals are used.

See also

Web links

Wiktionary: Fever  - explanations of meanings, word origins, synonyms, translations

Individual evidence

  1. ^ PA Mackowiak: Physiological rationale for suppression of fever. In: Clin Infect Dis . 31, Suppl 5, 2000, pp. S185-S189, PMID 11113022 .
  2. a b W. Kozak u. a .: Molecular mechanisms of fever and endogenous antipyresis. In: Ann NY Acad Sci. 917, 2000, pp. 121-134, PMID 11268336 .
  3. Vglo. for example Jürgen Martin: The 'Ulmer Wundarznei'. Introduction - Text - Glossary on a monument to German specialist prose from the 15th century. Königshausen & Neumann, Würzburg 1991 (= Würzburg medical-historical research. Volume 52), ISBN 3-88479-801-4 (also medical dissertation Würzburg 1990), p. 118.
  4. ^ F. Kluge: Etymological dictionary of the German language . 24th edition.
  5. Dictionary.com (English)
  6. ^ HJ Thompson: Fever: a concept analysis. In: J Adv Nurs. 51 (5), 2005, pp. 484-492. PMID 16098165 .
  7. ^ A b T. Reckert: Advice on dealing with fever and reducing feverish anxiety. In: Pediatrician. 42/43, 2011, pp. 695-698.
  8. According to W. Fink, G. Haidinger: The frequency of health disorders in 10 years of general practice. In: Z. Allg. Med. 83 (3), 2007, pp. 102-108. Quoted from What family doctors mainly deal with. In: MMW update. Med. 149th volume, no. 16, 2007.
  9. a b c d e J. D. Hasday, IS Singh: Fever and the heat shock response: distinct, partially overlapping processes. In: Cell Stress Chaperones. 5 (5), Nov. 2000, pp. 471-480, PMID 11189454 .
  10. ^ Roche Lexicon Medicine . 5th edition. Urban & Fischer Verlag, Munich 2003, ISBN 3-437-15156-8 , pp. 615 Entry on "Fever" .
  11. a b c d J. A. Boulant: Role of the Preoptic-Anterior Hypothalamus in Thermoregulation and Fever. In: Clin Infect Dis. 31, 2000, pp. 157-161. PMID 11113018
  12. S. Rivest et al. a .: How the Blood Talks to the Brain Parenchyma and the Paraventricular Nucleus of the Hypothalamus During Systemic Inflammatory and Infectious Stimuli. In: Proc Soc Exp Biol Med. 223 (1), 2000, pp. 22-38.
  13. a b c J. Roth u. a .: Molecular aspects of fever and hyperthermia. In: Neurol Clin. 24 (3), August 2006, pp. 421-439. PMID 16877116
  14. J. Koncar-Zeh: The influence of hyperthermia on the intracellular expression of proinflammatory cytokines in human monocytes. Medical dissertation. University Clinic for Anaesthesiology and Operative Intensive Care Medicine at Martin Luther University Halle-Wittenberg, 2005.
  15. M. Sanchez-Alavez et al. a .: Ceramide mediates the rapid phase of febrile response to IL-1β . In: PNAS . 103 (8), 2006, pp. 2904-2908. PMID 16477014
  16. ^ AA Steiner et al. a .: Cellular and Molecular Bases of the Initiation of Fever . In: PLoS Biology . 4 (9), 2006, p. E284.
  17. B. Kis et al. a .: Effects of LPS stimulation on the expression of prostaglandin carriers in the cells of the blood-brain and blood-cerebrospinal fluid barriers. In: J Appl Physiol . 100 (4), Apr 2006, pp. 1392-1399. Epub 2005 Dec 1.
  18. M. Lazarus a. a .: EP3 prostaglandin receptors in the median preoptic nucleus are critical for fever responses. In: Nat Neurosci . 10 (9), September 2007, pp. 1131-1133. Epub 2007 Aug 5.
  19. ^ Roche, Lexicon of Medicine. 5th edition. 2003, p. 615 entry on "Fever"
  20. ^ PA Mackowiak: Concepts of fever. In: Arch Intern Med 158 (17), 1998, pp. 1870-81. PMID 9759682 .
  21. PA Mackowiak, YES Boulant: Fevers glass ceiling. In: Clin Infect Dis. 22 (3), 1996, pp. 525-536, PMID 8852974 .
  22. a b c d e f g h i j J. Roth: Endogenous Antipyretics. In: Clin Chim Acta. 371 (1-2), 2006 Sep, pp. 13-24. Epub 2006 Mar 6. PMID 16549059
  23. ^ G. Grütz: New insights into the molecular mechanism of Interleukin-10-mediated immunosupression. In: Journal of Leukocyte Biology. Volume 77, January 2005, pp. 3-15.
  24. K. Benamar et al. a .: A Novel Role of Cannabinoids: Implication in the Fever Induced by Bacterial Lipopolysaccharide . In: J Pharmacol Exp Ther . 320 (3), March 2007, pp. 1127-1133. Epub 2006 Dec 28.
  25. A. Bertolini et al. a .: Paracetamol: New Vistas of an Old Drug. In: CNS Drug Reviews . 12 (3-4), 2006, pp. 250-275. doi : 10.1111 / j.1527-3458.2006.00250.x
  26. ^ A b c J. B. Tatro, PS Sinha: The Central Melanocortin System and Fever. In: Annals New York Academy of Sciences. 994, 2003, pp. 246-257. PMID 12851323 .
  27. J. Dong et al. a .: Effects of electrical stimulation of ventral septal area on firing rates of pyrogen-treated thermosensitive neurons in preoptic anterior hypothalamus from rabbits. In: Life Sci . 80 (5), January 9, 2007, pp. 408-413. PMID 17054999 .
  28. A. Mouihate et al. a .: Suppression of fever at near term is associated with reduced COX-2 protein expression in rat hypothalamus. In: Am J Physiol Regul Integr Comp Physiol. 283, 2002, pp. R800-R805.
  29. Martin E. Feder, Gretchen E. Hofmann: Heat-shock proteins, molecular chaperones, and the stress response: Evolutionary and Ecological Physiology. In: Annual Review of Physiology. 61, 1999, pp. 243-282, doi: 10.1146 / annurev.physiol.61.1.243 .
  30. ^ A b F.J. Quintana, IR Cohen: Heat Shock Proteins as Endogenous Adjuvants in Sterile and Septic Inflammation. In: The Journal of Immunology. 175, 2005, pp. 2777-2782.
  31. Tracy Hampton PhD: Fever Induces a Molecular Homing Response in Immune Cells During Infection. In: JAMA Network. May 7, 2019, accessed May 12, 2019 .
  32. MJ Kluger et al. a .: Fever and survival. In: Science . 188 (4184), April 11, 1975, pp. 166-168. PMID 1114347 .
  33. ^ HA Bernheim, MJ Kluger: Fever: effect of drug-induced antipyresis on survival. In: Science. 193 (4249), Jul 16, 1976, pp. 237-239. PMID 935867 .
  34. ^ JB Covert, WW Reynolds: Survival value of fever in fish. In: Nature . 267, May 5, 1977, pp. 43-45.
  35. ^ LK Vaughn et al. a .: Effects of antipyresis on bacterial numbers in infected rabbits. In: Brain Res Bull. 7 (2), Aug 1981, pp. 175-180. PMID 7272797 .
  36. MP Weinstein u. a .: The clinical significance of positive blood cultures: a comprehensive analysis of 500 episodes of bacteremia and fungemia in adults. II. Clinical observations, with special reference to factors influencing prognosis. In: Rev Infect Dis. 5 (1), Jan-Feb 1983, pp. 54-70. PMID 6828812 .
  37. MP Weinstein u. a .: The clinical significance of positive blood cultures in the 1990s: a prospective comprehensive evaluation of the microbiology, epidemiology, and outcome of bacteremia and fungemia in adults. In: Clin Infect Dis. 24 (4), April 1997, pp. 584-602. PMID 9145732 .
  38. AL Esposito: Aspirin impairs antibacterial mechanisms in experimental pneumococcal pneumonia. In: Am Rev Respir Dis. 130 (5), Nov 1984, pp. 857-862. PMID 6238561 1984.
  39. ^ S. Jefferies: "Systematic review and meta-analysis of the effects of antipyretic medications on mortality in Streptococcus pneumoniae infections" . In: Postgrad Med J. 88, 2012, pp. 21-27. PMID 22121249
  40. TF Doran et al. a .: Acetaminophen: more harm than good for chickenpox? In: J Pediatr. 114 (6), Jun 1989, pp. 1045-1048. PMID 2656959 .
  41. NMH Graham et al. a .: Adverse effects of aspirin, acetaminophen, and ibuprofen on immune function, viral shedding, and clinical status in rhinovirus-infected volunteers. In: J Infect Dis . 162 (6), Dec 1990, pp. 1277-1282. PMID 2172402 .
  42. ^ CH Brandts: Effect of paracetamol on parasite clearance time in Plasmodium falciparum malaria. In: The Lancet . (9079) September 6, 1997, pp. 704-709. PMID 9291905 .
  43. Q. Jiang et al. a .: Febrile Core Temperature Is Essential for Optimal Host Defense in Bacterial Peritonitis . In: Infection and Immunity. March 2000, pp. 1265-1270, Volume 68, No. 3.
  44. CI Schulmann u. a .: The effect of antipyretic therapy upon outcomes in critically ill patients: a randomized, prospective study. In: Surg Infect (Larchmt). 6 (4), 2005, pp. 369-375. PMID 16433601
  45. S. Eyers et al. a .: The effect on mortality of antipyretics in the treatment of influenza infection: systematic review and meta-analysis. In: JR Soc Med. 103 (10), 2010, pp. 403-411. PMID 20929891 , PMC 2951171 (free full text).
  46. BH Lee et al. a .: Association of body temperature and antipyretic treatments with mortality of critically ill patients with and without sepsis: multi-centered prospective observational study. In: Crit Care. 16 (1), 2012, p. R33. PMID 22373120 , PMC 3396278 (free full text)
  47. M. Ryan, MM Levy: Clinical review: Fever in intensive care unit patients. In: Critical Care. 7, 2003, pp. 221-225.
  48. U. Brüderlein u. a .: Fever in intensive care medicine. In: Anästhesiol Intensivmed Emergency Med Schmerzther. 41, 2006, pp. E8-E18, doi: 10.1055 / s-2006-925295 .
  49. Y. Launey et al. a .: Clinical review: Fever in septic ICU patients - friend or foe? In: Crit Care. 15 (3), 2011, p. 222. PMID 21672276 , PMC 3218963 (free full text)
  50. ^ Marianne Abele-Horn: Antimicrobial Therapy. Decision support for the treatment and prophylaxis of infectious diseases. With the collaboration of Werner Heinz, Hartwig Klinker, Johann Schurz and August Stich. 2nd, revised and expanded edition. Peter Wiehl, Marburg 2009, ISBN 978-3-927219-14-4 , pp. 41-48 ( fever with immunosuppression ).
  51. JQ Kang et al. a .: Why Does Fever Trigger Febrile Seizures? GABAA Receptor 2 Subunit Mutations Associated with Idiopathic Generalized Epilepsies Have Temperature-Dependent Trafficking Deficiencies . In: The Journal of Neuroscience. 26 (9), March 1, 2006, pp. 2590-2597.
  52. ^ A. El-Radhi, W. Barry: Do antipyretics prevent febrile convulsions? In: Arch Dis Child . 88 (7), July 2003, pp. 641-642. PMID 12818921 .
  53. T. Strengell et al. a .: Antipyretic Agents for Preventing Recurrence of Febrile Seizures - Randomized Controlled Trial. In: Arch Pediatr Adolesc Med. 163 (9), 2009, pp. 799-804. PMID 19736332
  54. ^ MA Galic: Cytokines and brain excitability. In: Front Neuroendocrinol. 33 (1), 2012, pp. 116-125. PMID 22214786 , PMC 3547977 (free full text)
  55. J. Koncar-Zeh: The influence of hyperthermia on the intracellular expression of proinflammatory cytokines in human monocytes . Dissertation. 2005, DNB 983130833 .
  56. ^ H. Siemes, BFD Bourgeois: Seizures and epilepsies in children and adolescents . Thieme Verlag, Stuttgart 2001, ISBN 3-13-127031-4 , p. 43.
  57. E. von Mutius u. a .: Frequency of infections and risk of asthma, atopy and airway hyperresponsiveness in children. In: Eur Respir J. 14, 1999, pp. 4-11.
  58. M. Calvani et al. a .: Fever episodes in early life and the development of atopy in children with asthma. In: Eur Respir J. 20, 2002, pp. 391-396.
  59. ^ LK Williams et al. a .: Timing and intensity of early fevers and the development of allergies and asthma. In: J Allergy Clin Immunol. 116 (1), July 2005, pp. 102-108.
  60. P. Nafstad et al. a .: Early Respiratory Infections, Asthma, and Allergy: 10-Year Follow-up of the Oslo Birth Cohort. In: Pediatrics. Volume 116, No. 2, August 2005, pp. E255 – e262.
  61. AL Kozyrskyj u. a .: Increased Risk of Childhood Asthma From Antibiotic Use in Early Life. ( Memento of July 26, 2008 in the Internet Archive ) In: Chest. 131, 2007, pp. 1753-1759.
  62. R. Beasley et al. a .: Association between paracetamol use in infancy and childhood, and risk of asthma, rhinoconjunctivitis, and eczema in children aged 6-7 years: analysis from Phase Three of the ISAAC program. In: Lancet. 372 (9643), Sep 20, 2008, pp. 1039-1048. PMID 18805332 .
  63. ^ BE Del-Rio-Navarro et al. a .: Study of the Relationship Between Acetaminophen and Asthma in Mexican Children Aged 6 to 7 Years in 3 Mexican Cities Using ISAAC methodology. (PDF; 78 kB). In: J Investig Allergol Clin Immunol. Volume 18 (3), 2008, pp. 194-201.
  64. JS Alm: Atopy in children of families with an anthroposophic lifestyle. In: Lancet. 353 (9163), May 1, 1999, pp. 1485-1488. PMID 10232315 .
  65. E. Göhring: The perfect storm of the cytokines. Active fever therapy with MBV - Coley's Toxins. 2nd Edition. Epubli, Berlin 2016, ISBN 978-3-7375-2266-3 .
  66. U. Hobohm: Fever and cancer in perspective. In: Cancer Immunol Immunother . 50, 2001, pp. 391-396, PMID 11726133 .
  67. ^ S. Dalal, DS Zhukovsky: Pathophysiology and Management of Fever. In: The Journal of Supportive Oncology. 4, 2006, pp. 9-16, PMID 16444847 .
  68. ^ U. Hobohm: Fever therapy revisited . (PDF; 90 kB). In: British Journal of Cancer . 92, 2004, pp. 421-425.
  69. KF Kölmel: Infections and melanoma risk: results of a multicentre EORTC case-control study. European Organization for Research and Treatment of Cancer. In: Melanoma Res. 9 (5), 1999, pp. 511-519, PMID 10596918 .
  70. Hans von Kress (ed.): Müller - Seifert . Pocket book of medical-clinical diagnostics. 69th edition. Verlag von JF Bergmann, Munich 1966, pp. 4–6 ( body temperature ), here: p. 6.
  71. a b P. A. Mackowiak u. a .: Concepts of fever: Recent Advances and Lingering Dogma. In: Clin Infect Dis. 25 (1), Jul 1997, pp. 119-138, PMID 9243046 .
  72. Georg Sticker : Hippokrates: The common diseases first and third book (around the year 434-430 BC). Translated, introduced and explained from the Greek. Johann Ambrosius Barth, Leipzig 1923 (= Classics of Medicine. Volume 29); Unchanged reprint: Central antiquariat of the German Democratic Republic, Leipzig 1968, p. 115 f. ( Persistent fever with a three-day increase in malaria and typhus).
  73. Hans von Kress (ed.): Müller - Seifert . Pocket book of medical-clinical diagnostics. 69th edition. Published by JF Bergmann, Munich 1966, p. 6.
  74. Y.-W. Li, L.-S. Zhou, X. Li: Accuracy of Tactile Assessment of Fever in Children by Caregivers: A Systematic Review and Meta-analysis. In: Indian Pediatr. 54, 2017, pp. 215-221, PMID 28159951 .
  75. Health tip : fever. ( Memento of September 28, 2007 in the Internet Archive ) (PDF)
  76. internisten-im-netz.de
  77. Ihr-apotheken-ratgeber.de