Related Experiment Video
Updated: Jun 19, 2026
Characterization of Inflammatory Responses During Intranasal Colonization with Streptococcus pneumoniae
Published on: January 17, 2014
INTRANASAL VIRULENCE OF PNEUMOCOCCI FOR MICE
1Laboratories of The Rockefeller Institute for Medical Research.
Abstract:
1. Smooth colony pneumococci fresh from human beings, instilled in small doses into the nasal passages of special mice raised under standard conditions, brought about a characteristic infection and this spread to healthy contacts inciting in them the carrier state or fatal infection. 2. Differences in individual host response to the same dose of a given culture ranged from a complete refractory or nasopharyngeal carrier state, or a local cervical lymphadenitis, to fatal lobular or lobar pneumonias with or without pleurisy, empyema, and pericarditis, and acute fatal septicemia. 3. Pneumococci exhibited consistent individual strain differences with respect to ability to infect, when instilled intranasally into mice, and also differences in the spread to contacts. Degree of intranasal virulence paralleled demonstrable ability to spread to contacts. 4. Degree of intranasal virulence of strains did not parallel intraperitoneal virulence in 50 per cent of strains-high intranasal was accompanied by either high or moderate intraperitoneal virulence, and low intranasal by high, moderate, or low intraperitoneal virulence. 5. Type III strains were of relatively high intranasal and intraperitoneal virulences; Type II strains mostly low in intranasal but high or moderate in intraperitoneal virulence; Type I strains all low in intranasal but either high or moderate in intraperitoneal virulence. Most strains of other types were low both in intranasal and intraperitoneal virulences. 6. The intranasal virulence of pneumococci was not enhanced by animal passage. Nasal passage reduced the intranasal virulence to zero but did not affect intraperitoneal virulence, colony form, and agglutinative specificity. Passage by the intraperitoneal method maintained the characteristic level of intranasal virulence for a period, increased intraperitoneal virulence in some instances, but did not affect colony form or agglutinative properties.
Insights
Pneumococci infection in mice shows strain-specific virulence and transmission. Host response varies from carrier state to fatal pneumonia, with intranasal virulence correlating with spread to contacts.
Area of Science:
- Microbiology
- Infectious Diseases
- Immunology
Background:
- Streptococcus pneumoniae (pneumococci) are a leading cause of bacterial pneumonia and sepsis.
- Understanding pneumococcal virulence and transmission is crucial for developing effective prevention and treatment strategies.
Purpose of the Study:
- To investigate the intranasal virulence and transmissibility of different pneumococcal strains in a mouse model.
- To examine the relationship between intranasal and intraperitoneal virulence.
- To assess the impact of animal passage on pneumococcal virulence characteristics.
Main Methods:
- Instillation of smooth colony pneumococci from human sources into the nasal passages of mice.
- Observation of infection development, spread to healthy contacts, and host responses.
- Comparison of intranasal and intraperitoneal virulence across different pneumococcal serotypes (Types I, II, and III).
- Evaluation of the effects of nasal and intraperitoneal passage on virulence.
Main Results:
- Intranasal pneumococcal instillation caused characteristic infections and spread to contacts, leading to carrier states or fatal outcomes.
- Significant variation in host response, ranging from asymptomatic carriage to severe pneumonia and septicemia.
- Pneumococcal strains exhibited consistent differences in intranasal virulence and transmissibility, with intranasal virulence paralleling spread to contacts.
- Intranasal virulence did not consistently correlate with intraperitoneal virulence; Type III strains were highly virulent by both routes, while Type I and II showed varied virulence profiles.
- Animal passage did not enhance intranasal virulence; nasal passage reduced it to zero, while intraperitoneal passage maintained it for a period.
Conclusions:
- Pneumococcal virulence and transmission are strain-dependent and influenced by the route of infection.
- The mouse model effectively demonstrates pneumococcal pathogenesis, host variability, and transmission dynamics.
- Intranasal virulence is a key factor in pneumococcal spread, but does not fully predict systemic pathogenicity.
