THE LIMITS OF SERUM-THERAPY. 753 



selves digested and converted into useful secretions, one of 

 which is fibrinogen, its phosphorus being acquired from the 

 alkaline phosphates of the plasma. 



This exemplifies an exceedingly beautiful provision of 

 Nature,, if examined closely. Indeed, leucocytosis, when not in- 

 hibited as it is in typhoid fever, being commensurate with the 

 degree of intoxication (the adrenal system acting as touch- 

 stone, as it were, for the morbid process) the fibrinogen derived 

 from the bacteria ingested by the surplus of phagocytes is evi- 

 dently intended to supply the needs of the febrile process, thus 

 avoiding a derangement of the general mechanism of all func- 

 tions. As it is only inhibited to a marked extent in typhoid 

 fever, however, it becomes evident that in all other febrile 

 processes and intoxications that are not sufficiently severe to 

 overwhelm the adrenal system and cause immediate insuffi- 

 ciency (in which bacteria penetrate the blood-stream) the addi- 

 tional fibrinogen required for the febrile process is obtained at 

 the expense of the bacilli ingested by the surplus of phago- 

 cytes, besides that acquired from proteids; the trypsin through 

 overactivity of the spleno-pancreatic system; the oxidizing sub- 

 stance through overactivity of the adrenal system. In other 

 words, the dominant triad of the protective process is always 

 available in diseases in which pathogenic organisms penetrate 

 into the blood. On the whole, it seems clear to us that: 



When leucocy to genesis is not inhibited: 



1. The plasma is provided with the three agencies, fibrin- 

 ogen, trypsin, and oxidizing substance, that enable it to dissociate 

 the bacteria that phagocytes do not ingest and digest. 



2. The bacteria ingested by phagocytes are converted in 

 these cells into peptones, myosinogen, and fibrinogen, the phos- 

 phorus being derived from the alkaline salts of the plasma. 



8. The system is thus supplied with the surplus of fibrin- 

 ogen required to sustain the febrile process, even though the proteids 

 obtained from the intestinal canal by the cells be small. 



When leucocytogenesis is inhibited to any marked extent, as 

 it is in typhoid fever: 



1. The absorption of proteids from the intestinal canal 

 and phagocytosis are correspondingly reduced and the formation 

 of fibrinogen is inadequate. 



