CHEMOTAXIS 63 



staphylococci, bacillus sub tills, bacillus coli communis, anthracis, 

 prodigiosus, proteus vulgaris, etc.). 



Buchner, to whom we owe so much of our information on this sub- 

 ject, was the first to suggest that the chemotactic influences which 

 are here manifestly at work, are referable to bacterial proteins, and he 

 emphasized that abscess formation is the outcome not so much of 

 the presence of living organisms, but of their dead bodies and the con- 

 tained proteins. According to Buchner, moreover, the proteins of all 

 bacteria are positively chemotactic, no matter whether the organisms 

 in question are otherwise pathogenic or not. 



Of the mechanism by which negative chemotaxis is brought to 

 bear upon leukocytes we know even less than of the production of 

 positive chemotaxis. That the virulence of the organism plays an 

 important role in this connection is, as I have already indicated, 

 undoubted. We could imagine that those organisms which have 

 developed a certain degree of passive resistance in consequence of 

 capsule formation, are less liable to opsonification and that in 

 consequence phagocytosis either does not occur at all or does so 

 only to a limited extent. In such a case, however, we could hardly 

 speak of negative chemotaxis. 



A beautiful example of its actual occurrence, however, is afforded 

 if the attempt is made to increase the aggressivity of certain organ- 

 isms (in the sense of Bail) by passage through the peritoneal cavity 

 of a series of animals, and transferring with the bacteria some of the 

 peritoneal exudate. It will then be noted that whereas the exudate 

 in the first animal is rich in leukocytes and poor in bacteria, 

 most of which are found within the cells, and whereas a systemic 

 invasion has not taken place, the latter is demonstrable at the end 

 of the series and simultaneously we find the peritoneal cavity filled 

 with a thin serous fluid which is swarming with bacteria, but is 

 almost free from leukocytes. Evidently there were strongly positive 

 chemotactic influences at work in the beginning of the series, while 

 at the end negative chemotaxis controls the situation. 



The problem then seems to resolve itself into a question of differ- 

 ence between the material injected into the first as compared with the 

 last animal of the series. The bacteria per se can here be left out of 

 sight, as the same result is obtained if for each injection the original 

 culture is employed. The only point of difference then is the absence 

 of aggressive exudate in the first animal of the series and its presence 



