MICROBIC VIRULENCE AND HOST SUSCEPTIBILITY IN PARATYPHOID-ENTERITIDIS INFECTION OF WHITE MICE : III. THE IMMUNITY OF

L T Webster1

  • 1Laboratories of The Rockefeller Institute for Medical Research.

Insights

Mice surviving an initial dose of paratyphoid-enteritidis bacilli show increased resistance to subsequent bacterial challenges and mercury bichloride. This resistance is linked to strain pathogenicity, not just antigen similarity, highlighting non-specific host defense factors.

Area of Science:

  • Immunology
  • Microbiology
  • Host-Pathogen Interactions

Background:

  • Understanding non-specific host resistance mechanisms is crucial for developing effective countermeasures against bacterial infections.
  • Previous studies suggest that prior exposure to certain pathogens can modulate host immunity.

Purpose of the Study:

  • To investigate the impact of a preliminary oral dose of Salmonella enterica serovar Typhimurium (paratyphoid-enteritidis bacilli) on the resistance of mice to subsequent challenges.
  • To determine if this induced resistance is specific to the challenge strain or a more general phenomenon.

Main Methods:

  • Mice were administered a preliminary oral dose of paratyphoid-enteritidis bacilli.
  • Survival rates and resistance were assessed following subsequent oral or intraperitoneal challenges with homologous or heterologous bacterial strains and mercury bichloride.
  • The role of strain pathogenicity and antigenic similarity was evaluated.

Main Results:

  • Mice surviving the preliminary dose exhibited enhanced resistance to a second oral dose of a similar mouse typhoid strain.
  • This resistance was more dependent on the pathogenicity of the preliminary strain than its antigenic similarity.
  • Pre-exposed mice also showed increased resistance to lethal oral doses of mercury bichloride.
  • Mice that resisted or recovered from the initial infection were more resistant to a lethal intraperitoneal challenge.
  • Conversely, mice developing chronic infections succumbed readily to a second dose.

Conclusions:

  • Host resistance mechanisms involve significant non-specific factors that vary individually.
  • Preliminary exposure to paratyphoid-enteritidis bacilli can induce a state of enhanced, non-specific resistance in mice.
  • The degree of resistance is influenced by the pathogenicity of the initial bacterial strain and the host's response, rather than solely antigenic mimicry.