Mouse mortality from a high Plasmodium berghei inoculum density may be due to immune suppression in the host

Abstract

Patients’ malaria parasite burden on hospital presentation has been implicated in human artemisinin monotherapy failure rather than any drug resistance-conferring genetic mutation in the infecting Plasmodium species. We investigated this observation using a mouse-Plasmodium berghei model at varying inocula abundance and monitored the pathogenesis without intervention. Three inoculums abundance levels were used: 107, 105and 103 highly parasitized blood (≥ 4000 parasites/µl). All 107 inoculum mice died within 12.7 days. The 103 inoculum and the 105 inoculum mice cleared their malaria parasitaemia between days 12 - 14 and between days 34 - 36 post-inoculation respectively. The 103inoculum and 105 inoculum mice had changes in baseline value of 1.71 and 2.02 in total white blood cells count between days 6 - 10 respectively, compared to 1.33 for the 107inoculum mice. Monocytes counts (cells/mm3) on day 6 was 223.3, 1254 and 40.7 for the 103 inoculum, 105 inoculum and 107 inoculum mice, while 152.5, 1073 and 477.5, respectively on day 10. Immunosuppression by the parasite might be the cause of the in appropriate immune response by 107 inoculum mice. Key words: Malaria, mice, parasite density, immune response, immune suppression.