GENETICS OF INFECTIOUS DISEASES 389 



two males, one L and one S, may have pure L and hybrid progeny in the same litter. 

 Environmental conditions are common to all animals of a litter, each having the same 

 opportunity to receive immune bodies from the mother and to receive latent infection 

 from the parents. According to the genetic hypothesis, the L progeny should be nearly 

 1 00 per cent susceptible and the hybrids should show resistance as may be seen in table 

 62. According to the hypothesis of acquired immunity, the L and hybrid littermates 

 should be equally susceptible. 



The two types of progeny tested showed that the L mice of the litter were all 

 susceptible, whereas the hybrid mice of the same litter were resistant as expected of this 

 hybrid cross. The differences were highly significant. This technique offered a means 

 of showing that the concentration of genetic factors for resistance in the selected strain, 

 S, were truly significant whereas any factors for acquired immunity were without effect 

 when the disease was murine typhoid (S. typhimurium) . The results further substantiate 

 the earlier results as well as indicate a desirable technique for separating the genetic 

 basis for natural resistance to a disease from that due to factors for immunity harbored 

 by the mothers. 



EFFECT OF NUMBERS OF PATHOGENS ON SURVIVAL 



The effects of sheer numbers of organisms on the characteristics of a disease are 

 of interest particularly as such data help to understand the pathogenesis whereby 

 genotypes alter the phenotypic expressions of the disease. Schott 1167 utilized a host 

 population composed of a random selection of albino Mus musculus. They were infected 

 by intraperitoneal injections of different numbers of the same line of bacteria. The 

 survival for each dosage is shown in figure 49. 



Figure 49 shows that the survivals of the mice were greatly influenced by the num- 

 bers of organisms which they received. Animals which received the low dosage 

 (1 x 10 4 organisms) displayed a long incubation period followed by increased and then 

 decreased mortality. An appreciable number of animals survived the disease attack. 

 At the high exposures (1 x 10 7 organisms), the organisms rapidly overwhelmed the 

 hosts. There was practically no incubation period. The course of the disease ended 

 days earlier than those for the smaller dosages. Between these two extremes inter- 

 mediate effects were observed. The pathogen was S. typhimurium in mice but the data 

 are illustrative of what may be observed for all types of pathogens— chemical poisons, 

 viruses, bacteria, protozoa, and multicellular pathogens. The scales of dosage will 

 change with the material used, that is, with ricin a dose less than 0.001 mg. caused 

 sickness but few deaths, whereas a dose of 0.004 mg. resulted in deaths of nearly all 

 the treated mice, but the principle of mortality dependent on dose was maintained 

 throughout this range. In genetic studies of host-disease syndromes, the investigator 

 must stay within the limits of dosage set by the test curves for the particular material. 

 Experience shows that the preferable limits for resistance studies are those set by 



