In human meningococcal infection the mechanism of the transition from asymptomatic carriage to invasive disease is unknown, partly due to the lack of an effective animal model that mimics all stages of the human disease. Therefore, we have endeavoured to develop a model for the human infection by instilling a suspension of Neisseria meningitidis into the nostrils of infant mice and subsequently determining the numbers of organisms in the nasal passages, lungs, blood and brains. Intranasal (i.n.) instillation resulted in consistent nasal colonisation which usually developed into a lung infection. In many cases the lung infection preceded bacteraemia, which occasionally resulted in death of the mice. The severity of the infection and the transition to bacteraemia were enhanced by intraperitoneal (i.p.) treatment of the mice with iron dextran or human transferrin. A N. meningitidis strain that was avirulent in an i.p. infection was also avirulent following i.n. infection. The requirement for lung colonisation to precede bacteraemia and the need for i.p. injection of iron compounds limit the use of i.n. infection of the infant mouse as a model for human meningococcal disease. However, various aspects of meningococcal virulence can be examined using this model.