To clarify the mechanisms of infection and immunity of mouse typhoid, an experiment was carried out using several strains of mice. A highly virulent strain of Salmonella enteritidis was used as an infective agent. The strains of mice used were C57BL/6, CF#1, CFW, ddN, SM and dd/Ks strain. The last strain is an inbred one raised in our laboratory from one parent of ddN mouse by full sib-matings and selecting the mice highly susceptible to the infection with S. enteritidis. The results obtained were as follows:
1) C57BL/6, CF#1 and dd/Ks strains were uniformly highly susceptible to the intraperitoneal infection with S. enteritidis, but CFW, ddN and SM strains were not so susceptible as the former three strains.
2) To the intrastomachal inoculation with S. enteritidis C57BL/6 and dd/Ks strains were as susceptible as to the intraperitoneal infection, but CE#1 strain, though it was highly susceptible to the intraperitoneal infection, showed only a low degree of susceptibility to the intrastomachal inoculation. CFW, ddN and SM strains showed nearly the same low grade of susceptibility to the intrastomachal inoculation as to the intraperitoneal infection.
3) The acquired immunity with heat-killed vaccine to the intraperitoneal infection could not be attained by C57BL/6 and dd/Ks strains that were both highly susceptible to the infection, but in CF#1 strain a fairly good state of immunity was attained despite its high susceptibility to the intraperitoneal infection. CFW, ddN and SM strains that were not so susceptible to the infection attained a good state of immunity to the intraperitoneal infection by the inoculation with heat-killed vaccine. An attenuated live vaccine conferred a fairly good state of immunity on all the strains.
4) No correlation between the grade of antibody response to the vaccine and that of immunity to the infection could be observed.
5) The peculiar attitude shown by CF#1 strain in the intrastomachal infection and in the immunity experiment with heat-killed vaccine was discussed as follows considering the course of the infection. In the course of mouse typhoid there would be two major streams of infection, one would be bacterial multiplication in septic form and the other would be bacterial multiplication in the organs in which the infected bacteria resided. If the high susceptibility to the intraperitoneal infection of CF#1 strain was due to the septic bacterial multiplication rather than the bacterial multiplication in the organs, the effect of heat-killed vaccine in CF#1 strain would be conspicious, because very effective prevention with heat-killed vaccine against the septic bacterial multiplication had been observed in our study described elsewhere. Furthermore the low susceptibility to the intrastomachal infection of CF#1 strain could be explained by the same assumption, because the major determinant of the outcome of the intrastomachal infection would be the bacterial multiplication in the organs which would be less sevire in the infection of CF#1 strain.
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