Studies of antigenic variation in Trypanosoma vivax have been hindered by its low infectivity to laboratory hosts and difficulties in obtaining defined cloned populations. The recent isolation of mouse-infective T. vivax has partially overcome the first problem. We have developed a highly efficient cloning technique which has been applied to the isolation of a collection of 71 clones, representing 31 distinct variable antigen types, of mouse-infective T. vivax from Nigeria. This serodeme showed no cross-reaction with several T. brucei-group serodemes, but some cross-reaction with naturally occurring Kenyan T. vivax.

Two Trypanosoma vivax stocks from East Africa have been adapted to rats and mice. Adaptation was induced by rapid passage at two- to four-day intervals in sublethally irradiated rats. After 200 such passages, the two stocks gave rise to parasitemias of 10(9)-10(10) trypanosomes/ml in peripheral blood, and the infection was fatal in 90% of the rats. By passaging the rat-adapted T. vivax into normal mice at two- to three-day intervals for over 200 passages, the two stocks also became pathogenic to mice. One of the stocks was also capable of maintenance in non-irradiated rats. The two stocks displayed a marked degree of pleomorphism in irradiated and non-irradiated rats and mice. In the early rising parasitemia, the organisms were predominantly short, with a well formed undulating membrane, a pointed posterior end, and a large terminal kinetoplast. As parasitemia approached its peak, the organisms transformed into long, slender forms with an inconspicuous undulating membrane, an elongated posterior end, and a sub-terminal kinetoplast. The short forms associated with the early, rising parasitemia were more infective for mice than the long forms encountered at peak parasitemia. Although the two rodent-adapted stocks retained their pathogenicity for goats, neither the original stocks nor their corresponding rodent-adapted stocks could be cyclically transmitted by tsetse flies. The availability of these stocks will greatly facilitate investigations on East African T. vivax which would otherwise be difficult to carry out in experimental rodents.

Antigenic variation in the ILDar 1 serodeme of the naturally rodent-infective stock of West African Trypanosoma vivax has been investigated following cyclical transmission. The immunofluorescent and immune lysis tests were employed with a panel of 39 variant-specific mouse antisera. When antigenically homogeneous, or mixed, populations were transmitted by tsetse flies to goats, the first peak parasitaemias arising in the goats were antigenic mixtures (up to 9 major, and several minor variants being recognized in some cases) from which the ingested variant was absent. Although first peak parasitaemias in similarly infected goats showed some variants in common, there was no obvious relationship between the VAT profiles in different goats. When these populations were expanded in irradiated mice, VAT heterogeneity was maintained with a tendency towards the development of predominant variants in some, but not all, instances. Six additional variants, derived following the growth of bloodstream form ILDat 1.9 in 37 degrees C culture, were also represented in goat and mouse populations. Two further variants, isolated after cyclical development of ILDat 1.9-derived trypanosomes in vitro, were not present in the early parasitaemias in goats and mice.

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