Abstract

The influence of specific immunity upon the course of infection may vary considerably with different species of plasmodia and different mammalian hosts harbouring the same species of parasite. Certain infections, for example P. knowlesi in rhesus monkeys, lead to a rapidly progressive parasitaemia and almost inevitably to a fatal outcome so that the immune response is ineffective unless animals are protected initially by drug therapy. In other instances, including many examples of primate and avian malaria, infection is followed by clinical immunity associated with continuing low-grade infection, occasional parasitaemia and relapse after splenectomy. This 'non-sterilizing' response was analysed in detail by SERGENT (1963) and called premunition. Finally, certain infections, such as P. berghei in the rat and P. cynomolgi bastianellii in man, produce a parasitaemia of comparatively short duration followed by long-lasting specific resistance during which no living organisms can be demonstrated by sub-inoculation or following splenectomy; after challenge of such immune individuals, parasites are rapidly killed--usually within about 2 days. This type of response has been referred to as 'sterilizing' immunity. The occurrence of these diverse responses to specific malarial infections implies that our present knowledge of the underlying immune mechanisms, which is restricted to a limited number of host-parasite combinations, is probably not applicable to all malarial infections.

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