1 70 RELATIONS OF BACTERIA TO DISEASE. 



the reaction of the body against the irritant. This question 

 has still to be settled, and all that we can do is to adduce 

 certain facts bearing on it. Thus in diphtheria and tetanus, 

 where toxic action leading to degeneration plays such an 

 important part, fever may be a very subsidiary feature, except 

 in the terminal stage of the latter disease ; and in fact in diph- 

 theria profoundly toxic effects may be produced without the least 

 interference with heat regulation. On the other hand, in bac- 

 terial disease, where defensive and reparative processes predom- 

 inate, fever is rarely absent, and it is nearly always present when 

 an active leucocytosis is going on. In this connection it may be 

 remarked that several observers have found that, when a relatively 

 small amount of the dead bodies of certain bacteria are injected 

 into an animal, fever occurs ; while the injection of a large amount 

 of the same is followed by subnormal temperatures and rapidly 

 fatal collapse. It might appear as if this indicated that the 

 occurrence of fever had a beneficial effect, but this is one of 

 the points at issue. Certainly such an effect is not due to the 

 bacteria being unable to multiply at the higher degrees of tem- 

 perature occurring in fever, for this has been shown not to be the 

 case. Whether the increase of bodily temperature indicates the 

 occurrence of changes, e.g. in the way of the production of bacteri- 

 cidal bodies, etc., is a question, and all attempts made hitherto 

 towards its solution have been unsuccessful. On the one hand, 

 it is stated that the maintaining, during an illness due to bacteria, 

 of an animal's body at its normal temperature by means of anti- 

 pyretics favours its recovery ; and on the other hand it has been 

 found that the placing of such an animal in an atmosphere at a 

 temperature above its normal also favours recovery. It is evident 

 that the experiments are not parallel, and, in fact, that from the 

 latter no conclusion can be drawn, as the additional factor of the 

 condition of the heat-regulating mechanism, when the bodily 

 temperature rises, is also introduced. If we consider the site of 

 the heat production in fever we again are in difficulties. It might 

 appear as if the tissue destruction, indicated by the occurrence of 

 fatty degeneration, would lead to heat development, but frequently 

 excessive heat production with increased proteid metabolism 

 occurs without any discoverable changes in the tissues ; and 

 further, in phosphorus poisoning there is little fever with great 

 tissue destruction. The increased work performed by the heart 



