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Since Proom (1947), Cooper (1952), Andersen (1953) and Fisher (1955) published their work on the course of infection with Bordetella pertussis in the lungs of normal and immune mice as indicated by the number of viable bacilli in the lungs, it has become evident that infection in the lungs of mice is quite different from infection in the brain. Dolby & Standfast (1958) and Dolby (1958) showed that protection against challenge by the intranasal and intracerebral routes is governed by different antibodies operating in different ways. Standfast (1958) also showed that the potency of vaccines assayed by challenge by the lethal intranasal route is different from the potency assayed by the intracerebral route. Two types of challenge by the intranasal route have been used by different workers, a lethal (Burnet & Timmins, 1937; Standfast, 1958) and a sublethal (Fisher, 1955; Andersen & Bentzon, 1958). Andersen &Bentzon (1958), estimating the potency of pertussis vaccine by making lung smears from mice after sublethal infection by the intranasal route, obtained values similar to those from assays using the intracerebral route. The course of disease in both normal and protected mice after infection by the intranasal route is reported in this paper. The findings confirm and extend the results of previous workers, indicate that the lethal and sublethal intranasal challenges may be measuring two different antibodies, and suggest a mode of action of the antibody which protects mice against the lethal challenge by the intranasal route.

The intranasal infection of mice with Bordetella pertussis