FEVER, a term generally used for conditions in which the normal temperature of the animal body is raised for any length of time. This normal varies in different animals, and in man is 98.4°. When the temperature reaches Io6° in man the term hyperpyrexia (excessive fever) is applied. The patient's condition then is very serious and if it exceeds or Io8° death results except in some cases of sun- or heat-strokes. Occasionally the temperature rises to I I0°–I I 2 ° immediately before death. (For the treatment of fever in general see THERAPEUTICS). (For the specific fevers see SMALLPDX, SCARLET FEVER, TYPHOID FEVER, etc.).
Pathology.—Every rise of temperature is due to a disturbance in the heat-regulating mechanism, the chief variable of which is the action of the skin in eliminating heat (see ANIMAL HEAT) This mechanism works satisfactorily but not instantaneously, and many physiological conditions cause a transient rise of tempera ture ; e.g. severe muscular exercise, in which the cutaneous mech anism is unable at once to dispose of the increased amount of heat produced in the muscles. Pathologically, it may be disturbed in three different ways: 1st, by mechanical interference with the nervous system; 2nd, by interference with heat loss; 3rd, by the action of various poisons.
I.—In man, fever the result of mechanical interference with the nervous system rarely occurs, the nearest approach being haem orrhage into the basal ganglia or pons, but it can readily be pro duced in 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 disintegration 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 are caused in this way; but some may also be due to stimulation of vasoconstrictor fibres to the cutaneous vessels diminishing heat loss.
3.—Many bacterial toxins and a few chemical substances cause a rise of temperature when injected in small doses and a fall when the dose is large. In all instances they lead to destruction of protein. Hence, the true measure of the intensity of a fever is not merely the temperature attained but the extent of disintegra tion of protoplasm. This may be estimated by the amount of nitrogen excreted in the urine, by a rise in the excretion of sulphur and phosphorus and by the appearance in the urine of acetone, aceto-acetic and (3-oxybutyric acids (see NUTRITION). Further, a high temperature has of itself an injurious action on the proto plasm, and tends to increase disintegration just as when heat loss is experimentally retarded, though the increase is small compared to that produced by the destructive action of tile microbial pro ducts. In the early stage of fever (rigors) the rise of temperature is primarily due to deficient heat loss, though increased production plays its part, and even in the later stages until defervescence occurs, heat loss is inadequate to get rid of the heat produced. The mechanism of increased heat production in fever is uncertain. In part, no doubt, it is due to increased muscular activity but in part it may be due to stimulation of the heat-producing centre by the products of tissue disintegration.
Probably as the result of toxic action fever is accompanied by disturbances in the functions of various organs. The activity of the digestive glands is diminished and appetite is lost. Food is not taken, the patient suffers from inanition, lives largely on his own fats and proteids, and rapidly emaciates. Glycogen is not stored in the liver cells, and bile is modified, the essential con stituents disappearing almost entirely in some cases. The produc tion of urea is interfered with, and the proportion of non-urea nitrogen in the urine 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. Con currently with these alterations in the functions of the liver-cells, granular, and probably fatty degeneration, make their appearance. That the functional activity of the kidneys is modified, is shown by the frequent occurrence of proteoses or of albumen and glob ulin in the urine. Frequently the toxin causes a shedding of the renal epithelium. The muscles are weakened, granular and fatty degeneration supervene, and the fibres waste. The nervous struc tures, especially the nerve-cells, suffer functionally and structur ally. The blood shows a fall in alkalinity and variation in the number of leucocytes, chiefly, the polymorphonuclear variety. Thus in pneumonia, the normal number is often increased twofold and sometimes more than tenfold, while the numbers are often re duced in enteric fever.