FEVER 68 T 



patient is really on a semi-starvation diet, the heat-equivalent of 

 which is not much more than half his heat-production. Yet it 

 has not been found possible to completely prevent the loss of 

 nitrogen by putting the fever patient on a diet rich in protein, or 

 on a diet containing a moderate amount of protein with a large 

 quantity of fat and carbo-hydrate, even when the total heat- value 

 of the diet is much in excess of the 32 or 33 calories per kilo of body- 

 weight which corresponds to the heat-production of a resting man. 

 Another suggestive fact is that the excessive excretion of nitrogen 

 does not run parallel with the rise of temperature in fever, but is 

 often most marked after the crisis. During the stage of defer- 

 vescence an enormous amount of urea is sometimes given off. In a 

 case of typhus, in the mixed urine of the third and fourth days after 

 the crisis, no less than 160 grammes of urea was found (Naunyn), or 

 nearly three times the normal amount for a man on full diet. Again, 

 when fever is caused by the injection of bacteria or their products, 

 the increase in the carbon dioxide eliminated and oxygen consumed 

 occurs even when the temperature is prevented from rising by cold 

 baths. It seems perfectly clear, then, that the increase of metab- 

 olism is, in many cases at least, a primary phenomenon of fever. 

 Its course and incidence, falling as it does so largely upon the 

 proteins, the steady loss of tissue nitrogen, and the inability of the 

 tissues to recoup their losses from the protein of the food or to 

 shield their own protein by burning more carbo-hydrate or fat, all 

 suggest that the cells are poisoned by toxic products of the infective 

 process. The poisoned bioplasm falls an easy prey to the hydro- 

 lysing and oxidizing agents always present in the tissues. It breaks 

 down more rapidly and builds itself up more slowly than normal 

 bioplasm. This increased, and to some extent perverted, metab- 

 olism, far from being occasioned by the febrile temperature, is quite 

 probably the cause of the thermo-regulative upset which we call fever. 

 For Mandel has shown (i) that one of the purin bases (xanthin) 

 causes fever in monkeys; (2) that the purin bases in the urine are 

 increased both in infective fevers and the so-called aseptic or surgical 

 fever that is, in cases where the temperature rises after such injuries 

 as extensive crushing of tissues without infection. There is a con- 

 stant relation between the height of the fever and the quantity of 

 purin bases excreted. The source of the purin bases in aseptic fever 

 is presumably the autolysis of the injured tissue, from which they 

 pass into the blood without being oxidized to uric acid. The xanthin 

 fever can be prevented by salicylates, though not by antipyrin. 



It has been very generally admitted that the chief seat of excessive 

 metabolism in fever is the muscles; but U. Mosso has stated that 

 cocaine fever the marked rise of temperature produced by injec- 

 tion of cocaine can be obtained in animals paralyzed by curara. 

 This, even if true, would not support the conclusion that a ' nervous 



i 



