ANIMAL HEAT 601 



slowly than normal bioplasm. This increased, and to some 

 extent perverted, metabolism, 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 



(1) 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 constant 

 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 remains to ask whether the rise of temperature is anything 

 more than a superficial and, so to speak, an accidental circum- 

 stance. The orthodox view for many ages has undoubtedly been 

 that the increase of temperature is in itself a serious part of the 

 pathological process, a symptom to be fought with and, if 

 possible, removed. And, indeed, it is not denied by anyone 

 that the excessive rise of temperature seen in some cases of 

 febrile disease (to 43 C., or even to 45) is, apart from all other 

 changes, a most imminent danger to life, unless, as is sometimes 

 the case (in influenza, e.g., where a temperature of 44 has been 

 observed), the high temperature lasts only a short time. Experi- 

 mental heat paralysis, a condition in which all voluntary and 

 reflex movements are abolished, is produced in frogs by raising 

 the internal temperature to about 34 C. On cooling, the animal 

 recovers. A similar condition can be induced in mammals, but, 

 of course, at a higher temperature. The central nervous system 

 succumbs before the peripheral structures. The superior cervical 

 ganglion in the cat or rabbit loses the power of transmitting 

 nerve impulses at 50 C. But some evidence has been brought 

 forward, mostly from the field of bacteriology, to support the 

 idea that in infective processes the rise of temperature is of the 

 nature of a protective mechanism, that the fever is, indeed, a 

 consuming fire, but a fire that wastes the body, to destroy the 

 bacteria. The streptococcus of erysipelas, for example, does 

 not develop at 39 to 40 C., and is killed at 39*5 to 41 C., and 

 erysipelas infections in rabbits are less virulent if the body-tem- 

 perature be artificially raised. Anthrax bacilli, kept at 42 to 

 43 C. for some time, are attenuated, and when injected into 

 animals confer immunity to the disease. Heated for several 

 days to 41 to 42 C., pneumococci render rabbits immune to 

 pneumonia, and in rabbits in which ' puncture ' fever has been 



