1911 Encyclopædia Britannica/Fever
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 110°-112° prior to the fatal issue. For the treatment of fever in general, see Therapeutics.
Pathology.—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: 1st, 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 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.of cell protoplasm and increased excretion of nitrogen and of carbonic acid. Possibly some of the cases of high temperature recorded
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 β-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 Stoffwechsels (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. Lövit, “Die Lehre von Fieber,” Vorlesungen über allgemeine Pathologie, erstes Heft (Jena, 1897); Louis Guinon, “De la fièvre,” in Bouchard’s Traité de pathologie générale, 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.)