The mouse was found to be natively susceptible to Listeria monocytogenes. Its susceptibility was attributed to the capacity of the organism to survive and multiplying in host macrophages. During the first 3 days of a primary infection the bacterial populations of spleen and liver were found to increase at a constant rate. On the 4th day of infection the host became hypersensitive to Listeria antigens and at the same time bacterial growth ceased. A rapid inactivation of the organism ensued. Convalescent mice were resistant to challenge, but no protective factor could be found in their serum. Histological evidence suggested that acquired resistance was the result of a change occurring in the host's mononuclear phagocytes. When challenged in vitro, the macrophages of convalescent mice were found to resist infection with Listeria monocytogenes. Listeria-resistant cells appeared during the course of infection at a time which corresponded with the development of the antibacterial mechanism in the spleen. They persisted for as long as the antibacterial mechanism remained intact in this organ. This period of absolute resistance to Listeria lasted about 3 weeks. Thereafter, the host remained hypersensitive but unable to inactivate a challenge inoculum of Listeria. However, it remained capable of producing an accelerated response to reinfection. This was thought to depend upon an ability to generate a new population of resistant cells from a residuum of specifically sensitized macrophages or macrophage precursors still surviving in the tissues as a result of the immunological activation which occurred during the primary infection.
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