392 HOST-PARASITE RELATIONSHIPS 



Fig. 51. Mortality of mice from Salmonella 



20r 



20 r 



UJ 



a 



LU 



o 40r ™ 



20 



ix 10 



l i 



5 10 15 20 

 DAYS SURVIVED 



V\ 5 



^ 2x10 



5 10 15 20 

 DAYS SURVIVED 



Mortality (percentage frequency) from S. typhimnrium for mice of the unselected 

 population (left) and mice selected eleventh generations for resistance (right). 



numbers of survivors. In fact the numbers of mice dying in the selected cohort are so 

 few as to give them the appearance of random deaths. 



Analysis of pathogenesis in the resistant mice of the eleventh generation would re- 

 quire a notably higher number of invading organisms than when mice of the original 

 population were under study. In fact it is doubtful if the investigator could obtain 

 the same syndrome by only adjusting the initial numbers of the invading S. typhimurium 

 11C organisms. 



Heavy reliance must be placed on data of this kind in the methodologic design 

 of all infectious disease experiments. The information, however, has greater significance 

 in that it is indicative of how at least some of the different pathogen genotypes may 

 induce their effects. Increase in numbers of inoculated organisms of the same line 

 would increase the dosages of any substance generated by these organisms that may be 

 inimical to the hosts. Increased dosages lead to more severe morbid reactions. Pure 

 lines of the pathogen, when selected, often as apparent mutations, occurring within 

 the same original parental line, are often characterized by differences in virulence of 

 entirely similar patterns to those discussed above, even though a fixed number of organ- 

 isms are inoculated into each host. This suggests that, at least in some instances, 

 the genotypic differences in the pathogen act as quantity controls on the same substance 

 or capacity within the given mutant lines rather than in necessarily creating entirely 

 new products detrimental to the host genotypes. 



