International Mammalian Genome Society

logo18th International Mouse Genome Conference

17-22 October 2004, Seattle, USA


POSTER 94 - THE CAPACITY TO CONTROL OF ANEMIA DEVELOPMENT AND PARASITEMIA GROWTH IS UNDER DIFFERENT GENETIC MECHANISMS IN AFRICAN MURINE TRYPANOSOMOSIS

Naessens J 1, Mburu D 1, Noyes H 2, Kemp S 2, Gibson J 3, Iraqi I  1

1 International Livestock Research Institute (ILRI), Nairobi, Kenya, 2 University of Liverpool, Liverpool, United Kingdom, 3 University of New England, Armidale, Australia

The A/J (A) mouse strain is more susceptible to infection with African trypanosomes and die earlier than the more resistant C57BL/6 (BL6) mice, while BALB/c (BALB) is known to be intermediately susceptible. In an early study, trypanotolerance QTL associated with survival time, following infection with the disease, were mapped to chromosomes 17, 5 and 1, using two F2 resource populations (C57BL/6 x A/J and C57BL/6 x BALB/c), and designated as Tir1, Tir2 and Tir3, respectively. Subsequently, these QTL were fine mapped using F6 advanced intercross line (AIL) populations. After infections with Trypanosoma congolense, A/J mice developed a higher parasitemia than BL6 mice. In contrast, the BL6 mice never develop such high parasitemia, but start dying in late stages of the infection. Searching for more parameters, which might underline the variation in susceptibility of the different mouse strains, we recorded the kinetics of anemia development in the three mouse strains following infection with T. congolense. BL6 mice developed anemia within a week after infection, and this lack of red blood cells got more severe with time. A/J mice also developed anemia early on, but recovered once the first parasitemic wave subsided. It seems likely that A/J mice die from pathology related to high numbers of parasites in the body, while BL6 mice die from pathology correlated with severe anemia. BALB mice also developed a high parasitemia, but were even better than A/J mice to control their anemia. These data suggest that the capacity to control parasitemia and the capacity to limit anemia are two unrelated genetic mechanisms.

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