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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.

Tests were made in vivo of the sensitivity or resistance to human plasma of many strains of polymorphic trypanosomes. Five strains of T. gambiense from Nigeria were tested and all were highly resistant. Fifteen strains of T. rhodesiense (isolated from man in East Africa) were tested and they showed great variation in their degree of resistance from high resistance (five strains) to only subresistance (two strains). Forty strains of T. brucei (isolated from animals or tsetse flies) were tested; 20 were sensitive, nine were doubtful (probably sensitive) and 10 were subresistant (i.e., probably only one of a million trypanosomes in them was resistant). One strain (ETAT 10, isolated from tsetse flies) was highly resistant. During this work, tests were made on 14 stains of T. brucei (isolated from animals or fly) which were recorded as having been tested on human volunteers. Six of these strains were sensitive to human plasma and none had infected volunteers. Seven strains were subresistant, and three had infected volunteers. One strain was highly resistant and had infected a laboratory worker. For practical purposes it is advisable to consider that if a strain of polymorphic trypanosomes is plasmasensitive, it is probably not infective for man; if a strain is at all plasma-resistant it is potentially infective for man; and if a strain is highly resistant then it is almost certainly infective for man.

Infection rates in sterile male Glossina morsitans centralis, G. austeni, G. palpalis palpalis, G.p. gambiensis, G. fuscipes fuscipes, G. tachinoides and G. brevipalpis for Trypanosoma vivax, T. congolense and T. brucei isolated from East and West Africa, were studied. Five groups of the sterile males, together with the five groups of sexually fertile males, of each of the respective species and subspecies were allowed to feed for 24 days on a Boran calf or goats infected with T. vivax or T. congolense, or with T. brucei for 34 days, after which they were dissected. The results showed that the infection of the pathogenic Trypanosoma species became better established in some tsetse species than in others. Also, the infection rates of T. vivax, T. congolense and T. brucei for sterile and sexually fertile males of any of the above Glossina did not differ significantly. These results indicate that releases of sterile male tsetse in the tsetse control programme will potentially increase the risk of trypanosomiasis during the period of tsetse releases in the affected areas, unless in the areas with low tsetse density the sterile male tsetse are rendered refractory to trypanosome infection prior to their releases while in the areas with medium to high tsetse densities, the resident tsetse populations are initially reduced with insecticides, traps and/or targets.

To determine if, as is the case with Trypanosoma brucei and T. congolense, serodemes of T. vivax could be distinguished on the basis of immunity to the metacyclic stages of the parasite, attempts were made to immunize goats by infection with infected tsetse, followed by chemotherapy or eventual 'self-cure'. Thirty goats were infected by tsetse with either clones or stocks of T. vivax from East or West Africa. Twenty-four goats were treated with diminazene aceturate (Berenil, Hoechst A.G.) 2-6 weeks after infection and 6 goats were allowed to self-cure. Infection, followed by treatment, induced immunity to a first homologous challenge by infected tsetse in only 2 of 24 goats (one immune to the East African stock, and the other to a clone of the West African stock). Immunity to a clone of the East African stock was induced in 3 or 4 animals after a second infection and treatment and in the fourth animal of the group following a third infection and treatment. One of 2 goats infected with the clone of the East African stock was immune to challenge at 16 weeks, following self-cure without treatment, and 1 of 4 goats infected with the parent stock was similarly immune when challenged at 40 weeks post-infection. Goats susceptible to infection with East African T. vivax showed evidence of partial immunity by delayed pre-patent periods and depressed parasitaemias after challenge. Goats infected with the relatively more virulent West African T. vivax were, however, completely susceptible to infection after homologous challenge, and showed only a slight delay in pre-patent period. A similar result was obtained in a further 8 goats primed and challenged by large numbers of tsetse (20 or 100 infected tsetse/goat) with the West African T. vivax. In further experiments using a very short treatment interval, infections following challenge were clearly shown to be the result of a lack of immunity rather than relapse following treatment. Lytic antibody activity to cultured metacyclic trypanosomes could not be detected during infection but such activity against bloodstream forms was detected after 2 weeks of infection. It is suggested that the primary reason for the erratic induction of immunity to T. vivax employing this methodology is the low number of metacyclics transmitted by infected tsetse, and thus poor antigenic stimulus encountered by goats upon tsetse challenge.