BACTERIAL ANAPHYLAXIS 



If we leave out of consideration bacteria which, like the diph- 

 theria bacillus, produce true secretory poisons, it would be the ability 

 to gain a foothold in the body, the degree of invasive power, the pre- 

 dilection in the choice of a path of entrance, and the specific local 

 accumulation upon which the speed and quantity of anaphylatoxin 

 production and absorption would depend, and which consequently 

 would give character to variations in the clinical pictures of different 

 diseases. Besides simplifying considerably our comprehension of 

 bacterial toxemia this point of view again brings out the great im- 1 

 portance of the work of Vaughan, and of Vaughan and Wheeler, 

 on the non-specific poisonous fraction obtained by hydrolysis of bac- 

 terial and other proteins. 



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 microorganisms 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 microorganism 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, 



