THE TRANSMISSION OF DISEASE. 
687 
size of the draft horse and Shetland pony, the constant color 
and markings of the Hereford cattle, the intelligence of some 
breeds as compared to the stupidity of others, the docility of 
some families as compared to the irritability and viciousness, 
amount in some to actual ferocity, of others. Gluttony and 
daintiness are family characteristics ; strength, endurance and 
speed are well known hereditary propensities; speed in par¬ 
ticular is one of the best illustrations of the perpetuation and 
e x aggeration of a family trait by judicious mating we have. 
The American trotter has become a distinct breed of 
horses by long-continued judicious matings, and by careful 
education of the naturally acquired gifts. The healthy em¬ 
bryo develops into a normal foetus and after birth grows up 
to be a strong specimen of the type, but we believe that many 
slight variations in the embryonal protoplasmic structure 
occur that prove later in life to be the origin of many diseases. 
They may require exciting causes to make them develop, but 
the seeds of them were in the ovum from the time of its im¬ 
pregnation. This hypothesis enables us to account for many 
diseases otherwise obscure in their origin, and the difference 
in receptivity of infectious diseases in different families and 
individuals. Some breeds take them in a most virulent form, 
while others enjoy an almost natural immunity. 
All variations from the normal type are equally as trans¬ 
missible as the perfect ones, but variations developing after 
birth are far less so than the congenital ones. Those existing 
in the adult, due to environment, are transmissible, but far 
less so than inherited ones. The theory of the embryonal 
origin of disease was practically applied to tumors by Cou- 
heim, especially the cancers and the terratomata, and his 
views are quite generally accepted to-day. 
The following diseases may be mentioned as being due in 
many, if not most, cases to heredity, the seeds of them in the 
form of variations from the normal protoplasmic structure 
exist, and only require some stimulus to act as the exciting 
cause to produce them. The application of this exciting 
cause will produce the disease if the predisposition exist, but 
will not produce it if it does not exist. It may be delayed 
