Malaria is one of the most lethal
parasitic infections in the world. The lethality of the parasite depends on the rate of multiplication of the parasite within host erythrocytes. Different strains of the
malaria parasite often respond in a different way to the same strain of mice or vice versa. In the present study, we investigated the course of
infection of the
arteether-sensitive and
arteether-resistant Plasmodium vinckei parasites in Swiss albino AKR (inbred) and AJ (outbred) mice. The higher parasite burden and mortality were observed in the sensitive parasite-infected mice, whereas the
infection with the resistant parasite was non-lethal. Resistant parasite-infected mice developed a moderate level of
parasitemia that decreased gradually throughout the
infection. The microscopic examination suggests that the resistant parasite invades reticulocytes more efficiently than normocytes, regardless of the mouse strain examined. Since the reticulocytes are rare in blood circulation, it limits the increase in parasite proliferations, while
arteether-sensitive parasites can invade both mature normocytes and reticulocytes, resulting in the mortality of the mice. However, treatment with
phenylhydrazine in Swiss mice results in
reticulocytosis, which transforms the non-lethal resistant parasites to produce lethal
infections. Our findings demonstrate that the characteristic response during
infections with the
arteether-resistant strain is dependent on the availability of reticulocytes in peripheral blood circulation. We can use this model for identifying the interaction between host and
artemisinin derivative-resistant parasites.