THE CAUSATION OF DISEASE. 1 77 



the various cells of the body and their respective environments," 

 and disease in such an organism consists of the sum of the 

 abnormal inter-actions. 



Owing to the mutual inter-action of tissue upon tissue in a 

 multicellular organism it very rarely happens that disease in 

 such an organism remains strictly localized to one tissue. 

 When disease of one tissue leads to morbid action in another, 

 it is by modifying its cell-E. Such an abnormal cell-E 

 may be spoken of as a secondary mal-E, while one which 

 occurs independently of any previous morbid action may be 

 said to constitute a primary mal-E. External violence and 

 indigestible food constitute forms of primary mal-E ; the pre- 

 sence of nitrogenous sewage in the cell-spaces in renal disease, 

 and the diminution of oxygen in phthisis, are examples of 

 secondary mal-E. 



When the vital processes of a multicellular organism are more 

 or less universally thrown out of gear by disease in some one 

 part, we may define the disease as " the morbid inter-action of 

 the primary mal-E and the tissue primarily affected, plus all 

 those morbid inter-actions of the secondary mal-E's and the 

 tissues secondarily affected." The name of the disease connotes 

 the sum of these morbid inter-actions. 



In studying a disease in a multicellular organism, our object 

 should be to discover the tissue primarily affected and the 

 exact nature of the morbid E, and to assign to each, as far as 

 possible, its exact share in causation. We can never entirely 

 exclude 8 from causation, but when we are able to satisfy 

 ourselves that the E is distinctly abnormal, and that the S 

 is perfectly normal (a very difficult task in many cases, owing 

 to the difficulty of defining a normal S or E), we may, for 

 all practical purposes, attribute the entire causation to E. 

 But when the morbid process is facilitated by some peculiar 

 structural weakness, practical account must be taken of this 

 latter, and, according to our ability to gauge accurately the 

 degree of structural weakness and the intensity of environmental 

 abnormality, in that same proportion is our knowledge of the 

 causation perfect. 



Having fixed upon the primarily erring tissue, and 

 assigned to S and E their relative share in causation, it is 



