Feb. io, 1923 
Genetics of Bunt Resistance in Wheat 
449 
superfluous receptors becoming detached from the cell. These are 
called amboceptors because they have two haptophorous groups, and 
in the immunizing process they act as links to bind the invading cells 
to the complements which are normally present and which, when so 
united to the foreign cells, are able to destroy them by means of a 
zymotoxic or toxophore group. The amboceptor with its complement 
constitutes a cytotoxin, hemolysin, or bacteriolysin. Other detached 
receptors act as antitoxins, as agglutinins, or as precipitins. Toxins 
have a haptophorous group by which they combine with antitoxins, 
and a toxophorous group to which their injurious effects are due. A 
toxin which has lost its toxophorous group, as by heating, is called a 
toxoid. A complement which has lost its zymotoxic group is a com- 
plementoid and an amboceptor that has lost one of its haptophorous 
groups is called an amboceptoid. The presence of a foreign cytotoxin 
leads to the presence of an anticytotoxin, which may act on the ambo¬ 
ceptor or on the complement. 
Whether Ehrlich’s or similar theories can be extended to account for 
all the complex phenomena of reistance and immunity in plants and 
animals remains for the future to decide. Like the hypotheses in physics 
and chemistry, it offers a shorthand method for explaning the facts. It 
helps to make a clearer understanding of the phenomena of both natural 
and acquired resistance and immunity and also explains in a logical way 
the change in the virulency of organisms, in so far as there is any expla¬ 
nation at present. For example, as Walker (59, p . J4) has shown the 
pathogenic organisms themselves may be immunized against immune 
serums by cultivating them in media containing increasing portions of 
the immune serums. 
It is not too much to suppose, therefore, that pathogenic organisms 
themselves are subject to contagious diseases, suffer from malnutrition, 
and benefit by becoming acclimated, in response to the same laws that 
operate in higher organisms. Changes in virulency can probably be ex¬ 
plained as the interaction of these factors in the majority of cases; but 
the plasticity or heterozygous character of some forms offer the possi¬ 
bility of genetical change by selection. The brief time required for each 
generation in many of the lower forms and the large numbers produced 
would make this a quick and permanent method of adapting an organ¬ 
ism to its environment. Since, in general, the lower forms are more 
constant or stable than the higher forms, it is probable that such genetic 
change by selection is very limited. 
From the foregoing discussion it seems that disease-resistance pheno¬ 
mena in both plants and animals are due to the same general causes. 
The hosts of a given parasite may vary both morphologically and physi¬ 
ologically; and according to their physico-chemical complex react di¬ 
versely in their irritability and response to such factors as temperature, 
moisture, light, nutrition, and poison. The same organism will react 
differently to the same stimuli at different stages in its development. 
In so far as the subject has been studied, the parasite or disease-causing 
organism seems to vary also, and according to the same laws that govern 
the host. Added to this, the host is changed within certain limits, chemi¬ 
cally, by its food supply and other external stimuli, such as other dis¬ 
eases or mechanical injury. The parasite probably has its diseases and 
is no doubt changed chemically by them and also by its changing food 
supply. In the delicate balance between these two organisms, host and 
