IMMUNOLOGICAL CONTROL OF CHRONIC TRYPANOSOMA-BRUCEI-GAMBIENSE IN OUTBRED RODENTS

  • 1 January 1984
    • journal article
    • research article
    • Vol. 41  (4) , 335-342
Abstract
Recent human isolates of T. b. gambiense generally fail to become or remain patent in mice and rats. The purpose of this study was to determine if this was due to acquired immunity and if so which immunosuppressive method was the most efficient in raising parasitemia levels. Prior to infection, rats and mice were immunosuppressed by treatments with cobra venom factor, anti-lymphocyte sera, hydrocortisone acetate, cyclophosphamide, by splenectomy, or by lethal X-irradiation. While no parasites were detected in the blood of most untreated rodents for 30 days postinfection, all immunosuppressive procedures resulted in patent parasitemias in at least 50% of the treated animals. The most effective method, lethal X-irradiation, consistently caused fulminating infections typical of acute African trypanosomiasis. Cyclophosphamide had the same effect as X-irradiation in rats but was less effective in mice. Splenectomy allowed fulminating 1st peak parasitemias in two-thirds of the rodents while cobra venom factor and anti-lymphocyte sera in general allowed only low 1st peaks of parasitemia that were resolved within 10 days of infection. Hydrocortisone acetate allowed low grade and sporadically patent infections throughout the 30 day study. To determine if in untreated rodents, the parasites were eliminated or maintained in a subpatent state, rodents infected for 30-45 days were immunosuppressed with cyclophosphamide. Rats (50%) and mice (30%) developed patent parasitemias within 1 wk of immunosuppression suggesting that a majority of animals had eliminated the infection. The doubling time for T. b. gambiense in normal and immunosuppressed rodents was determined to be 2 times/day, one-half the rate of more virulent Trypanosoma brucei sspp. isolates. The parasite growth rate was the most likely factor in the effective host control of this parasite during the 1st peak of parasitemia. This experimental host-parasite relationship may be a model for the study of chronic African trypanosomiasis caused in humans by T. b. gambiense and in native ungulates by T. b. brucei and T. b. rhodesiense.