The Inheritance of Factors Controlling Resistance in Mice Infected with Trypanosoma brucei rhodesiense

• Published in: The Journal of parasitology Vol. 81; no. 4; pp. 653 - 657
• Main Authors: Seed, J. R., Sechelski, J.
• Format: Journal Article
• Language: English
• Published: Lawrence, KS American Society of Parasitologists 01-08-1995
• Subjects: Animals; Antibodies; Biological and medical sciences; Crosses, Genetic; Experimental protozoal diseases and models; Female; Genes, Dominant; Hematocrit; Immunity, Innate - genetics; Inbred strains; Inbreeding; Infections; Infectious diseases; Male; Medical sciences; Mice; Mice, Inbred C3H; Mice, Inbred Strains; Parasitemia; Parasitemia - genetics; Parasitemia - immunology; Parasitic diseases; Phenotypes; Phenotypic traits; Protozoal diseases; Research Notes; Time Factors; Trypanosoma brucei rhodesiense - immunology; Trypanosome; Trypanosomiasis, African - genetics; Trypanosomiasis, African - immunology; Protozoa; Protozoal disease; Genetic inheritance; Rodentia; Parasite; Parasitosis; African sickness; Survival; Infection; Vertebrata; Experimental disease; Mammalia; Sensitivity resistance; Mouse; Pathogenic; Trypanosoma rhodesiense; Rhizoflagellata; Parasitemia; Trypanosoma brucei; Trypanosomiasis
• ISSN: 0022-3395; 1937-2345
• DOI: 10.2307/3283873

In crosses between 2 recombinant inbred strains of mice (B x H-2 and B x H-14), resistance to infection with Trypanosoma brucei rhodesiense as measured by survival time is suggested to be controlled by a dominant gene(s). In prior studies using the same clone of trypanosomes, but a different set of inbred mouse strains, it was demonstrated that resistance in H-2 congenic mice was a recessive trait. This work suggests that in mouse trypanosomiasis, the number of genes involved in resistance and their dominant or recessive nature will vary between different inbred mouse strains. There was a statistically significant difference between the survival times of animals with high or low antibody anti-trypanosome titers. Differences in survival time were not correlated with the height of the first parasitemia. There was, however, a strong negative correlation between the number of trypanosomes at the second peak in parasitemia and survival time. It is also suggested that the extent to which the host is immunosuppressed early in infection determines the ability to control the later peaks in parasitemia and, therefore, survival time.