ANTI-ENZYME IMMUNITY 297 



is able to elaborate its toxic products. It has been observed that the 

 plasma of a species of host (horse, rabbit and human) which is 

 susceptible to infection is clotted by the action of staphylococcal 

 factor; and the plasma of those species (guinea pig, and mouse) which 

 are resistant to infection do not respond to the clotting effect of 

 staphylococcal factor. In the latter case, the animals have been reported 

 to tolerate enormous doses of the same staphylococci, suggesting 

 that in the absence of clottable menstruum the bacteria are easily 

 phagocytized by leucocytes. 



Inhibition of the phagocytosis of staphylococci by leucocytes is 

 conceived as due to the formation of a fibrin envelope around the cocci. 

 The clotting of plasma in an environment containing cocci and leuco- 

 cytes produces compact masses, embedded in a fibrin matrix, forming 

 a mechanical obstacle to phagocytosis quite apart from the specific 

 mechanism of inhibition. Under these conditions leucocytes are en- 

 tangled and immobilized and are prevented from ingesting the cocci 

 which are clumped in the fibrin. Localization of a large number of 

 leucocytes in this manner produces abundant pus formation. 



The conversion of fibrinogen into fibrin on the surface of cocci 

 producing sticky surfaces and thereby the agglutination of cocci has 

 been demonstrated by the following observations. Birch-Hirschfeld 

 (1934) (cited by Cadness-Graves, et at. 1943) observed that thick 

 suspensions of staphylococci were rapidly clumped in human plasma. 

 Cadness-Graves, et al. made use of this observation and developed a 

 slide-test for rapid presumptive identification of potentially pathogenic 

 Staphylococcus aureus Qfyogenes'), or those staphylococcal strains 

 which produced clotting factor. Berger (1943) reported that all clotting 

 factor-producing staphylococci were agglutinated by solutions of fi- 

 brinogen. Those cocci which failed to produce this factor were not 

 affected. The clumping of pathogenic staphylococci in plasma is not a 

 true agglutination and no immune body is involved. He suggested that 

 the reaction is due to the ability of the cocci to form fibrin from fi- 

 brinogen on their surfaces and that this causes them to stick together. 

 According to Smith, Hale and Smith (1947) the inhibition of phago- 

 cytosis due to the protective barrier of fibrin formed around the cocci 

 as a result of clotting activity is a most important factor in the initiation 

 and establishment of infection. 



Smith and Hale (1944) reported that the non-clotting of the plasma 



