INTRANASAL VIRULENCE OF PNEUMOCOCCI FOR MICE

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.