| 18th | Top neurological disorders |
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An analog medical thermometer showing a temperature of 38.7 °C or 101.7 °F |
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| ICD-10 | R50. |
|---|---|
| ICD-9 | 780.6 |
| DiseasesDB | 18924 |
| eMedicine | med/785 |
| MeSH | D005334 |
Fever (also known as pyrexia or controlled hyperthermia[1]) is a common medical sign characterized by an elevation of temperature above the normal range of 36.5–37.5 °C (98–100 °F) due to an increase in the body temperature regulatory set-point.[2] This increase in set-point triggers increased muscle tone and shivering.
As a person's temperature increases there is generally a feeling of cold despite an increasing body temperature. Once the new temperature is reached there is a feeling of warmth. A fever is one of the body's immune responses which attempts to neutralize a bacterial or viral infection. A fever can be caused by many different conditions ranging from benign to potentially serious. With the exception of very high temperatures, treatment to reduce fever is often not necessary; however, antipyretic medications can be effective at lowering the temperature, and this may improve the affected person's comfort.
Fever differs from uncontrolled hyperthermia[1], usually just referred to as hyperthermia, in that hyperthermia is an increase in body temperature over the body's thermoregulatory set-point, due to excessive heat production and/or insufficient thermoregulation.
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| Temperature Classification | |
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| Normal | 36.5–37.5 °C (98–100 °F)[3] |
| Hypothermia | <35.0 °C (95.0 °F)[4] |
| Fever | >37.5–38.3 °C (100–101 °F)[1][5] |
| Hyperthermia | >37.5–38.3 °C (100–101 °F)[1][5] |
| Hyperpyrexia | >40.0–41.5 °C (104–107 °F)[6][7] |
A wide range for normal temperatures have been found.[5] Fever is generally agreed to be present if:
In healthy adult men and women the range for oral temperature is 33.2–38.2 °C (92–101 °F), for rectal it is 34.4–37.8 °C (94–100 °F), for tympanic membrane it is 35.4–37.8 °C (96–100 °F) and for axillary it is 35.5–37.0 °C (96–99 °F).[9]
People develop higher temperatures with activities but this is not considered a fever as the set-point is normal. Elderly people have a decreased ability to generate body heat, so even a low-grade temperature may represent a serious underlying illness.
The pattern of temperature changes may occasionally hint at the diagnosis:
A neutropenic fever, also called febrile neutropenia, is a fever in the absence of normal immune system function. Because of the lack of infection-fighting neutrophils, a bacterial infection can spread rapidly and this fever is therefore usually considered a medical emergency. This kind of fever is more commonly seen in people receiving immune-suppressing chemotherapy than in apparently healthy people.
Febricula[11] is a mild fever of short duration, of indefinite origin, and without any distinctive pathology.
Bad for you.
Hyperthermia occurs from a number of causes including heatstroke, neuroleptic malignant syndrome, malignant hyperthermia, stimulants such as amphetamines and cocaine,idiosyncratic drug reactions, and serotonin syndrome.
A fever is usually accompanied by sickness behavior which consists of lethargy, depression, anorexia, sleepiness, hyperalgesia, and the inability to concentrate.[12][13][14]
Fever is a common symptom of many medical conditions:
Persistent fever which cannot be explained after repeated routine clinical inquiries, is called fever of unknown origin.
As fever is a prominent symptom of many diseases, in humans and animals, it will often appear in the common appellation of diseases.
Temperature is ultimately regulated in the hypothalamus. A trigger of the fever, called a pyrogen, causes a release of prostaglandin E2 (PGE2). PGE2 then in turn acts on the hypothalamus, which generates a systemic response back to the rest of the body, causing heat-creating effects to match a new temperature level.
In many respects, the hypothalamus works like a thermostat.[15] When the set point is raised, the body increases its temperature through both active generation of heat and retaining heat. Vasoconstriction both reduces heat loss through the skin and causes the person to feel cold. The liver produces extra heat. If these measures are insufficient to make the blood temperature in the brain match the new setting in the hypothalamus, then shivering begins, to use muscle movements to produce more heat. When the fever stops, and the hypothalamic setting is set lower, the reverse of these processes (vasodilation, end of shivering and nonshivering heat production) and sweating are used to cool the body to the new, lower setting.
This contrasts with hyperthermia, in which the normal setting remains, and the body overheats through undesirable retention of excess heat or over-production of heat.[15] Hyperthermia is usually the result of an excessively hot environment (heat stroke) or an adverse reaction to drugs. Fever can be differentiated from hyperthermia by the circumstances surrounding it and its response to anti-pyretic medications.
A pyrogen is a substance that induces fever. These can be either internal (endogenous) or external (exogenous) to the body. The bacterial substance lipopolysaccharide (LPS), present in the cell wall of some bacteria, is an example of an exogenous pyrogen. Pyrogenicity can vary, as in extreme examples some bacterial pyrogens known as superantigens can cause rapid and dangerous fevers. Depyrogenation may be achieved through filtration, distillation, chromatography, or inactivation.
Cytokines (especially interleukin 1) are a part of the innate immune system, are produced by phagocytic cells, and cause the increase in the thermoregulatory set-point in the hypothalamus. Other examples of endogenous pyrogens are interleukin 6 (IL-6), and tumor necrosis factor-alpha.
These cytokine factors are released into general circulation where they migrate to the circumventricular organs of the brain due to easier absorption caused by the blood-brain barrier's reduced filtration action there. The cytokine factors then bind with endothelial receptors on vessel walls, or interact with local microglial cells. When these cytokine factors bind, the arachidonic acid pathway is then activated.
One model for the mechanism of fever caused by exogenous pyrogens includes LPS, which is a cell wall component of gram-negative bacteria. An immunological protein called lipopolysaccharide-binding protein (LBP) binds to LPS. The LBP–LPS complex then binds to the CD14 receptor of a nearby macrophage. This binding results in the synthesis and release of various endogenous cytokine factors, such as interleukin 1 (IL-1), interleukin 6 (IL-6), and the tumor necrosis factor-alpha. In other words, exogenous factors cause release of endogenous factors, which, in turn, activate the arachidonic acid pathway.
PGE2 release comes from the arachidonic acid pathway. This pathway (as it relates to fever), is mediated by the enzymes phospholipase A2 (PLA2), cyclooxygenase-2 (COX-2), and prostaglandin E2 synthase. These enzymes ultimately mediate the synthesis and release of PGE2.
PGE2 is the ultimate mediator of the febrile response. The set-point temperature of the body will remain elevated until PGE2 is no longer present. PGE2 acts on neurons in the preoptic area (POA) through the prostaglandin E receptor 3 (EP3). EP3-expressing neurons in the POA innervate the dorsomedial hypothalamus (DMH), the rostral raphe pallidus nucleus in the medulla oblongata (rRPa) and the paraventricular nucleus (PVN) of the hypothalamus . Fever signals sent to the DMH and rRPa lead to stimulation of the sympathetic output system, which evokes non-shivering thermogenesis to produce body heat and skin vasoconstriction to decrease heat loss from the body surface. It is presumed that the innervation from the POA to the PVN mediates the neuroendocrine effects of fever through the pathway involving pituitary gland and various endocrine organs.
The brain ultimately orchestrates heat effector mechanisms via the autonomic nervous system. These may be:
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.
There are arguments for and against the usefulness of fever, and the issue is controversial.[16][17] There are studies using warm-blooded vertebrates[18] and humans[19] in vivo, with some suggesting that they recover more rapidly from infections or critical illness due to fever. A Finnish study suggested reduced mortality in bacterial infections when fever was present.[20]
Theoretically, fever can aid in host defense.[16] There are certainly some important immunological reactions that are sped up by temperature, and some pathogens with strict temperature preferences could be hindered.[21] Fevers may be useful to some extent since they allow the body to reach high temperatures, causing an unbearable environment for some pathogens. White blood cells also rapidly proliferate due to the suitable environment and can also help fight off the harmful pathogens and microbes that invaded the body.[citation needed]
Research[22] has demonstrated that fever has several important functions in the healing process:
Fever should not necessarily be treated.[24] Most people recover without specific medical attention.[25] People are generally advised to keep adequately hydrated. Oral rehydration solutions or water are generally used for this purpose. Excessive water may lead however to hyponatremia. Some limited evidence supports the use of tepid sponging.[26] If the temperature reaches the level of hyperpyrexia aggressive cooling is required.[27]
The antipyretics ibuprofen is effective in treating a fever.[28] It is more effective than acetaminophen / paracetamol in children however both may be used together,[29] safely.[30] The effectiveness of acetaminophen by itself is questionable.[31] Ibuprofen is also superior to aspirin,[32] which is not usually recommended in children due to the risk of Reye's syndrome.
Pyrexia is from the Greek pyretos meaning fire. Febrile is from the Latin word febris, meaning fever, and archaically known as ague.
Fever is an important feature for the diagnosis of disease in domestic animals. The body temperature of animals, which is taken rectally, is different from one species to another. For example, a horse is said to have a fever at 38.5 °C, while a cow is said to have a fever at 39.6 °C.[citation needed]
In species that allow the body to have a wide range of "normal" temperatures, such as camels, it is sometimes difficult to determine a febrile stage.
<ref> tag; no text was provided for refs named EM01; see Help:Cite error.
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| A
Fever by |
O ! DO not die, for I shall hate
All women so, when thou art gone,
That thee I shall not celebrate,
When I remember thou wast one.
But yet thou canst not die, I know;
To leave this world behind, is death;
But when thou from this world wilt go,
The whole world vapours with thy breath.
Or if, when thou, the world's soul, go'st,
It stay, 'tis but thy carcase then;
The fairest woman, but thy ghost,
But corrupt worms, the worthiest men.
O wrangling schools, that search what fire
Shall burn this world, had none the wit
Unto this knowledge to aspire,
That this her feaver might be it?
And yet she cannot waste by this,
Nor long bear this torturing wrong,
For more corruption needful is,
To fuel such a fever long.
These burning fits but meteors be,
Whose matter in thee is soon spent;
Thy beauty, and all parts, which are thee,
Are unchangeable firmament.
Yet 'twas of my mind, seizing thee,
Though it in thee cannot perséver;
For I had rather owner be
Of thee one hour, than all else ever.
| This work published before January 1, 1923 is in the public domain worldwide because the author died at least 100 years ago. |
| Medical warning! This article is from the 1911 Encyclopaedia Britannica. Medical science has made many leaps forward since it has been written. This is not a site for medical advice, when you need information on a medical condition, consult a professional instead. |
FEVER (Lat. febris, connected with fervere, to burn), a term generally used to include all conditions in which the normal temperature of the animal body is markedly exceeded for any length of time. When the temperature reaches as high a point as 106° F. the term hyperpyrexia (excessive fever) is applied, and is regarded as indicating a condition of danger; while, if it exceeds 107° or 108° for any length of time, death almost always results. The diseases which are called specific fevers, because of its being a predominant factor in them, are discussed separately under their ordinary names. Occasionally in certain specific fevers and febrile diseases the temperature may attain the elevation of IIO -112° prior to the fatal issue. For the treatment of fever in general, see Therapeutics.
Every rise of temperature is due to a disturbance in the heat-regulating mechanism, the chief variable in which is the action of the skin in eliminating heat (see Animal Heat). Although for all practical purposes this mechanism works satisfactorily, it is not by any means perfect, and many physiological conditions cause a transient rise of temperature; e.g. severe muscular exercise, in which the cutaneous eliminating mechanism is unable at once to dispose of the increased amount of heat produced in the muscles. Pathologically, the heat-regulating mechanism may be disturbed in three different ways: ist, by mechanical interference with the nervous system; 2nd, by interference with heat elimination; 3rd, by the action of various poisons.
1. In the human subject, fever the result of mechanical interference with the nervous system rarely occurs, but it can readily be produced in the lower animals by stimulating certain parts of the great brain, e.g. the anterior portion of the corpus striatum. This leads to a rise of temperature with increased heat production. The high temperature seems to cause distintegration of cell protoplasm and increased excretion of nitrogen and of carbonic acid. Possibly some of the cases of high temperature recorded after injuries to the nervous system may be caused in this way; but some may also be due to stimulation of vaso-constrictor fibres to the cutaneous vessels diminishing heat elimination. So far the pathology of this condition has not been studied with the same care that has been devoted to the investigation of the third type of fever.
2. Fever may readily be produced by interference with heat elimination. This has been done by submitting dogs to a temperature slightly below that of the rectum, and it is seen in man in Sunstroke. The typical nervous symptoms of fever are thus produced, and the rate of chemical change in the tissues is accelerated, as is shown by the increased excretion of carbonic acid. The protoplasm is also injured and the proteids are broken down, and thus an increased excretion of nitrogen is produced and the cells undergo degenerative changes.
3. The products of various micro-organisms have a toxic action on the protoplasm of a large number of animals, and among the symptoms of this toxic action one of the most frequent is a rise in temperature. While this is by no means a necessary accompaniment, its occurrence is so general that the term Fever has been applied to the general reaction of the organism to the microbial poison. Toxins which cause a marked rise of temperature in men may cause a fall in other animals. It is not the alteration of temperature which is the great index of the severity of the struggle between the host and the parasite, but the death and removal to a greater or lesser extent of the protoplasm of the host. In this respect fever resembles poisoning with phosphorus and arsenic and other similar substances. The true measure of the intensity of a fever is the extent of disintegration of protoplasm, and this may be estimated by the amount of nitrogen excreted in the urine. The increased disintegration of protoplasm is also indicated by the rise in the excretion of sulphur and phosphorus and by the appearance in the urine of acetone, aceto-acetic and (-oxybutyric acids (see Nutrition). Since the temperature is generally proportionate to the intensity of the toxic action, its height is usually proportionate to the excretion of nitrogen. But sometimes the rise of temperature is not marked, while the excretion of nitrogen is very decidedly increased. When the temperature is sufficiently elevated, the heat has of itself an injurious action on the protoplasm, and tends to increase disintegration just as when heat elimination is experimentally retarded. But the increase due to rise of temperature is small compared to that produced by the destructive action of the microbial products. In the beginning of a fever the activity of the metabolism is not increased to any marked extent, and any increase is necessarily largely due to the greater activity of the muscles of the heart and respiratory mechanism, and to the muscular contractions which produce the initial rigors. Thus the excretion of carbon dioxide - the great measure of the activity of metabolism - is not usually increased, and there is no evidence of an increased combustion. In the later stages the increased temperature may bring about an acceleration in the rate of chemical change; but this is comparatively slight, less in fact than the increase observed on taking muscular exercise after rest. The rise of temperature is primarily due to diminished heat elimination. This diminished giving off of heat was demonstrated by means of the calorimeter by I. Rosenthal, while E. Maragliano showed that the cutaneous vessels are contracted. Even in the later stages, until defervescence occurs, heat elimination is inadequate to get rid of the heat produced.
The toxic action is manifested not only by the increased disintegration of protoplasm, but also by disturbances in the functions of the various organs. The activity of the digestive glands is diminished and appetite is lost. Food is therefore not taken, although when taken it appears to be absorbed in undiminished quantities. As a result of this the patient suffers from inanition, and lives largely on his own fats and proteids, and for this reason rapidly emaciates. The functions of the liver are also diminished in activity. Glycogen is not stored in the cells, and the bile secretion is modified, the essential constituents disappearing almost entirely in some cases. The production of urea is also interfered with, and the proportion of nitrogen in the urine not in the urea increases. This is in part due to the increased disintegration of proteids setting free sulphur and phosphorus, which, oxidized into sulphuric and phosphoric acids, combine with the ammonia which would otherwise have been changed to urea. Thus the proportion of ammonia in the urine is increased. Concurrently with these alterations in the functions of the liver-cells, a condition of granular degeneration and probably a state of fatty degeneration makes its appearance. That the functional activity of the kidneys is modified, is shown by the frequent appearance of proteoses or of albumen and globulin in the urine. Frequently the toxin acts very markedly on the protoplasm of the kidney epithelium, and causes a shedding of the cells and sometimes inflammatory reaction. The muscles are weakened, but so far no satisfactory study has been made of the influence of microbial poisons on muscular contraction. A granular and fatty degeneration supervenes, and the fibres waste. The nervous structures, especially the nerve-cells, are acted upon, and not only is their functional activity modified, but they also undergo structural changes of a chromatolytic nature. The blood shows two important changes - first, a fall in the alkalinity due to the products of disintegration of protoplasm; and, secondly, an increase in the number of leucocytes, and chiefly in the polymorpho-nuclear variety. This is best marked in pneumonia, where the normal number is often increased twofold and sometimes more than tenfold, while it is altogether absent in enteric fever.
An interesting general modification in the metabolism is the enormous fall in the excretion of chlorine, a fall far in excess of what could be accounted for by inanition, and out of all proportion to the fall in the sodium and potassium with which the chlorine is usually combined in the urine. The fevered animal in fact stores chlorine in its tissues, though in what manner and for what reason is not at present known.
Authorities. - Von Noorden, Lehrbuch der Pathologie des Stewechsels (Berlin, 1893); Metabolism and Practical Medicine, vol. ii., article "Fever" by F. Kraus (1907); Dr A. Rabe, Die modernen Fiebertheorien (Berlin, 1894); Dr G. B. Ughetti, Das Fieber, trans. by Dr R. Teuscher (Jena, 1895); Dr M. Lbvit, "Die Lehre von Fieber," Vorlesungen fiber allgemeine Pathologie, erstes Heft (Jena, 1897); Louis Guinon, "De la fievre," in Bouchard's Traite de pathologie generale, t. iii. 2nd partie (Paris, 1899); Sir J. B. Sanderson, "The Doctrine of Fever," in Allbutt's System of Medicine, vol. i. p. 139 (London, 1896). (D. N. P.)
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<< Feuilleton |
(Deut 28:22; Mt 8:14; Mk 1:30; Jn 4:52; Acts 28:8), a burning heat, as the
word so rendered denotes, which attends all febrile attacks. In all
Eastern countries such diseases are very common. Peter's wife's
mother is said to have
suffered from a "great fever" (Lk 4:38), an instance of Luke's professional exactitude in
describing disease. He adopts here the technical medical
distinction, as in those times fevers were divided into the "great"
and the "less."
what mentions this? (please help by turning references to this page into wiki links)
| http://www.biology-online.org/dictionary/Febricula">http://www.biology-online.org/dictionary/Febricula - Febricula - definition from Biology-Online.org |
http://www.biology-online.org">Biology-Online.org - Life Science Reference - Biology Online |
| http://www.quackwatch.org/11Ind/airola.html">The Legacies of Paavo Airola |
http://www.pediatricweb.com/seattle/bartarticle.asp?tArticleID=1025">What to do if your child has a fever - Child Health Advice | Child Health & Safety | Seattle Children's Hospital |
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