Acquired immunity to Plasmodium vinckei in mice

Abstract

Plasmodium vinckei infections, which usually kill mice within 7 days, can be terminated in the majority of cases by a single injection of chloroquine phosphate equivalent to 10 mg/100 g body weight. After such drug treatment the parasites disappear from the blood for 6–11 days, after which a recrudescence with a low peak occurs. Most animals overcome this second parasitaemia and the parasites finally disappear completely. After recovery, mice exhibit an immune response to a challenge infection and, after a short period of parasitaemia during which a low peak is reached, the animals recover completely. This immunity, once acquired, apparently persists for the lifetime of the host. The establishment of the immune state depends on the period of patent parasitaemia during the primary infection and the longer this period the greater is the chance of a solid immunity developing. Immunity may be exhibited by mice treated with chloroquine as early as the 3rd day of infection. Killed parasites have no immunizing effect. Mice splenectomized before infection are capable of an immune response, and mice splenectomized after radical cure are also able to overcome a challenge infection. In both these cases more than one injection of chloroquine is required. The immunity produced in mice is that of the true sterile type, equivalent to that produced against P. berghei in rats, and is species-specific, conferring no resistance to infection with P. berghei. P. vinckei infections in mice provide a useful immunological model for laboratory studies. The immune response is predictable and easy to induce, and this parasite is therefore superior to P. berghei for immunological studies. Attention is drawn to the fact that in P. vinckei the infection is brought under control by the immune response and not by the antimalarial drug; therefore this ought to be taken into consideration in the assessment of drug trials.