420 INFECTION AND RESISTANCE 



To support this assumption Friedberger points out the similarity 

 in the clinical manifestations of several diseases in which the inciting 

 bacteria are biologically very different, but in which the distribution 

 and invasive properties are alike. For instance, lobar pneumonia 

 caused by the pneumococcus is clinically very similar to that "caused 

 by the Friedlander bacillus, though the micro-organisms inciting 

 them are extremely unlike each other. He draws a similar parallel 

 between true cholera and cholera nostras, and we may add another 

 striking example in the great similarity existing clinically between 

 the various forms of acute and subacute septicemia in which a defi- 

 nite bacteriological diagnosis can rarely be made except by blood 

 culture. 



Conversely the same micro-organism may call forth diseases 

 which clinically apart from the purely local manifestations are very 

 dissimilar, according to the localization and distribution of the 

 bacteria. 



Granted that we accept this view, then the subsidence of the 

 disease might depend merely upon limitation of the supply of an- 

 tigen, as the increasing bactericidal action of the blood constituents 

 comes into play, and upon the consequent diminution of the anaphy- 

 latoxin. For, as the bacteria diminish and the sensitizer increases, a 

 changed proportion between them is established which, finally, as 

 experiment has shown, results in a failure of anaphylatoxin produc- 

 tion. For, although experiments have shown that, within a wide 

 latitude of relative proportions of bacteria and antibody, anaphyla- 

 toxin can be formed, beyond this range an excess of one or the other 

 element eventually will prevent their formation. 



Infectious disease, then, according to this point of view, repre- 

 sents merely the reaction of the body against a foreign protein, the 

 bacteria. These gain a foothold in the body, and at first, during the 

 so-called incubation time, cause no symptoms, since the slight amount 

 of bacterial destruction with correspondingly slight cleavage of the 

 bacterial protoplasm liberates too small an amount of anaphylatoxin 

 to incite noticeable deviations from the normal condition. As these 

 slight quantities of bacterial cleavage products are absorbed, however, 

 a reactionary formation of specific antibody occurs. Meanwhile, 

 also, the foreign protein increases and is distributed by bacterial 

 growth. In consequence of these parallel processes changes of pro- 

 portion between the reacting substances are created and a constantly 

 greater amount of anaphylatoxin is liberated and the disease pro- 

 gresses. This may kill the patient if the proportions become such 

 that the amount of poison formed exceeds the lethal dose. At any 

 rate, the symptoms may vary and fluctuate according to the relations 

 maintained between the reacting bodies, modified somewhat by the 

 supply of alexin or complement. If recovery is to take place the 

 amount of antibody (sensitizer, amboceptor) may become so great 



