268 DISTURBANCES OF CIRCULATION 



proteoses, so that their inhibiting influence is no longer shown. 

 This corresponds to the observation of Kanthack l that immune 

 serum against venom neutralizes very effectively the anticoagu- 

 lating principle of venom ; an amount of antiserum altogether 

 insufficient to neutralize the toxic properties of venom will 

 neutralize its property of preventing clotting. The bacterial 

 products may also modify coagulation, and L. Loeb 2 has found 

 that different organisms are unequally effective in this respect, 

 Staphylococcus aureus being much more powerful in causing 

 coagulation than any others tested ; typhoid, diphtheria, tubercle, 

 and xerosis bacilli and streptococci being without any apparent 

 effect, while pyocyaneus, prodigiosus, and colon bacilli occupy 

 an intermediate position. Furthermore, after the organisms are 

 killed by boiling, this effect is greatly reduced, showing that it 

 does not depend merely upon the mechanical action of the 

 bacteria, but probably upon bacterial products contained in the 

 culture-media. 



After phosphorus-poisoning the blood may become non-coag- 

 ulable, which, Jacoby 3 found, was due to an absence of fibrino- 

 gen in the blood; this Jacoby attributed to a fibrinogen-destroying 

 ferment in the liver. As yet this is the only known example of 

 non-coagulability due to absence of fibrinogen, with the excep- 

 tion of Doyon's 4 similar finding in chloroform necrosis of the 

 liver. In other instances of decreased coagulability the fibrino- 

 gen is present, generally in normal amounts. After death the 

 blood becomes incoagulable because the fibrinogen is destroyed 

 through a process similar to that of fibrinolysis ; 5 this fibrinol- 

 ysis may be complete as early as ten hours after death. The 

 other proteids of the blood do not seem to be correspondingly 

 attacked. Thrombokinase is also scanty in cadaver blood, but 

 there seem to be no coagulation-inhibiting substances present. 



Pfeiffer 6 estimated the fibrin content of the blood in disease, 

 and found it increased in diseases with leucocytosis (pneumonia, 

 rheumatism, erysipelas, scarlet fever), except leukemia, where it 

 was normal ; in diseases without leucocytosis (typhoid, malaria, 

 nephritis), the fibrin was normal in amount. Stassano and 

 Billon 7 have, furthermore, shown that the amount of fibrin-fer- 



1 Cited by Lazarus-Barlow, p. 141. 



2 Jour. Med. Research, 1903 (10), 407. 



3 Zeit. physiol. Chem., 1900 (30), 175; also Doyon et aL, Compt. Eend. Soc. 

 Biol., 1905 (58), 493. 



.* Compt. Rend. Soc. Biol., 1905 (58), 704. 



5 Morawitz, Hofmeister's Beitr., 1906 (8), 1. 



6 Zeit. klin. Med., 1897 (33), 214 ; Cent. f. inn. Med., 1898 (19), 1. 



7 Compt. Rend. Soc. Biol., 1903 (55), 511. 



