THE BACILLUS OF TYPHOID FEVER. 345 



during the lifetime of the patients, and is found in greater abun- 

 dance in those cases which terminate fatally at an early date. It is 

 not a putrefactive organism, and is not developed in the tissues post 

 mortem, although it has been shown by Frankel and Simmonds that 

 it multiplies rapidly in the spleen after death, up to the time that 

 putrefactive decomposition commences. This is quite in accord with 

 what we should a priori have expected, in view of the facts relat- 

 ing to the propagation of typhoid fever. These facts indicate that 

 the disease in question is due to a microorganism which is capable of 

 multiplication external to the human body in a variety of organic 

 media, at comparatively low temperatures, and that it is widely dis- 

 tributed. From the endemic prevalence of the disease over vast 

 areas of the earth's surface we may infer that it is induced by a 

 hardy microorganism. Eberth's bacillus complies with all of these 

 conditions. 



There are numerous facts which indicate that the development of 

 an attack of typhoid and the severity of the symptoms depend to 

 some extent upon the quantity of the infectious material introduced 

 into the alimentary canal. Milk or water which has been infected 

 directly by the discharges of typhoid patients is especially danger- 

 ous, and there is reason to believe that repeated or concentrated 

 doses of such infectious material may be effective when a single 

 draught of the contaminated fluid, or a greater degree of dilution, 

 would be innocuous. 



Again, we have evidence that the typhoid germs may become 

 effective as a result of certain favorable circumstances relating to the 

 individual or to his environment. Those agencies which reduce the 

 vital resisting power of the tissues, and especially exposure to the 

 emanations from putrefying material, to sewer gas, to vitiated air in 

 overcrowded and ill- ventilated apartments, etc., are recognized as 

 favorable to the development of typhoid fever where the specific 

 cause is present. All these facts seem to accord with the experi- 

 mental evidence which indicates that the pathogenic power of the 

 bacillus of Eberth depends upon the formation of a poisonous 

 ptomaine rather than upon a special facility for multiplying in the 

 tissues of a living animal. Indeed, it seems quite probable that its 

 power to invade living animal tissues depends upon the toxic action 

 of this ptomaine ; or, it may be, of other ptomaines produced under- 

 certain circumstances in the body in excess or introduced from with- 

 out. Such toxic agents may serve, when the specific germ is intro- 

 duced into the intestine in comparatively small numbers, to give it 

 the mastery over the vital resisting power of the tissues subject to in- 

 vasion, and thus to induce an attack of the disease. ' 



1 The above account of researches relating to the etiology of typhoid fever is from 

 27 



