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Host-parasite relations in mouse typhoid
Abstract:
The development of acquired resistance to Salmonella typhimurium has been studied in mice infected intravenously with small numbers of streptomycin-sensitive or streptomycin-resistant organisms. By the 14th day of a primary infection the mouse develops a mechanism capable of destroying completely a super infecting dose of organisms, but is unable to eliminate organisms of the primary infection. The latter are constantly returned to the circulation from necrotic foci at the sites of implantation. Passive transfer of serum from actively infected or vaccinated animals, and immunization with heat-killed organisms, increase the capacity of the host to clear organisms from the blood, but do not interfere to any significant extent with their subsequent multiplication in the tissues. It is concluded that the resistance of actively infected animals depends on a nonhumoral mechanism capable of destroying organisms from endogenous or exogenous sources.
Insights
Mice develop resistance to Salmonella typhimurium infection, clearing superinfecting bacteria but not primary infections. This resistance relies on a non-serum-based mechanism, crucial for controlling bacterial loads.
Area of Science:
- Immunology
- Microbiology
- Infectious Diseases
Background:
- Salmonella typhimurium infections establish persistent foci in mice.
- Acquired resistance mechanisms in mice against S. typhimurium are not fully understood.
Purpose of the Study:
- To investigate the development of acquired resistance to Salmonella typhimurium in a mouse model.
- To elucidate the mechanisms underlying resistance to primary and superinfections.
Main Methods:
- Intravenous infection of mice with streptomycin-sensitive or resistant S. typhimurium.
- Monitoring bacterial clearance from blood and tissues.
- Assessing the impact of passive serum transfer and heat-killed organism immunization.
Main Results:
- Mice developed a mechanism by day 14 to clear superinfecting S. typhimurium doses.
- Primary infection organisms persisted due to necrotic foci, despite enhanced blood clearance via serum transfer or immunization.
- Humoral immunity (serum transfer, immunization) improved bacterial clearance from blood but not tissue multiplication.
Conclusions:
- Acquired resistance in actively infected mice involves a nonhumoral mechanism.
- This mechanism effectively destroys organisms from both endogenous and exogenous sources.
- Resistance is primarily cell-mediated or tissue-based, not dependent on circulating antibodies for complete pathogen elimination.