Stannus and Yorke (1911) observed T. rhodesiense in animals inoculated from a case of sleeping sickness in Nyasaland. Sir D. Bruce and his colleagues73 have shown (1912) that T. rhodesiense is the parasite usually found in man and in animals sub-inoculated from cases of sleeping sickness in Nyasaland. It has since been found in German East Africa and Portuguese East Africa, while Ellacombe has described a case from North-western Rhodesia.
(3) Serum Reactions.—Interesting experiments on this subject were performed during 1911 and 1912 by various French investigators.
(a) Action of Immune Serum (Mesnil and Ringenbach)74: (1) A goat was infected with T. rhodesiense. Twenty-two days later its serum mixed with T. rhodesiense was injected into a mouse. Result: Protection. (2) The serum mixed with T. gambiense was injected into a mouse. Result: Infection.
(b) Action of Baboon Serum.—Contrary to T. gambiense, T. rhodesiense is very susceptible to human and baboon sera. Mesnil and Ringenbach75 showed that a dose of 1 c.c. of baboon (Papio anubis) serum cured mice infected with T. rhodesiense. In the same dose it acted very feebly on T. gambiense.
(c) Action of Human Serum.—1 c.c. of human serum cured T. rhodesiense mice in three out of four cases; on T. gambiense mice there was no appreciable effect.
Laveran and Nattan-Larrier76 have shown the same, namely, that human sera act on T. rhodesiense, but are quite without action on T. gambiense.
(d) Trypanolytic Reactions.—Mesnil and Ringenbach77 have also shown that the sera of animals (man, monkey and guinea-pig) infected with T. gambiense are trypanolytic for the homologous trypanosome, that is, T. gambiense, but have no action on the heterologous trypanosome, that is, T. rhodesiense.
(4) Cross Immunity Experiments.—(a) Mesnil and Ringenbach78 immunized a monkey (Macacus rhesus) against T. gambiense. It was inoculated with T. rhodesiense on June 7, 1911; on June 27 trypanosomes appeared, the infection being slight; on July 4 it died. A control died in ten and a half days.
(b) Laveran79 immunized a goat and mice against T. gambiense. When they had acquired a solid immunity, they were inoculated with T. rhodesiense. They became infected like the controls.
(c) Laveran and Nattan-Larrier80 immunized a ram against T. brucei, it subsequently became infected with T. rhodesiense.
(d) Laveran81 immunized a ram and a sheep against different strains of T. brucei. Inoculated with T. rhodesiense they both acquired acute infections and died. Conclusion: T. rhodesiense is not T. brucei.
When the converse set of experiments is tried, namely, immunizing an animal against T. rhodesiense, and then inoculating with T. gambiense, the difficulty immediately arises that it is impossible to immunize an animal against T. rhodesiense, owing to its virulence. But a partial and transitory immunity to T. rhodesiense can be obtained by treating the infected animal with drugs, such as arsenophenylglycin. The results, so far as they go, seem to show that an animal immunized against T. rhodesiense is immune not only to T. rhodesiense, but also to T. gambiense, a fact which, according to Mesnil and Léger, does not invalidate the specificity of T. rhodesiense, but tends to show that the two trypanosomes are closely related.
(5) Mode of Transmission and Reservoir.—Kinghorn has shown that T. rhodesiense is transmitted by Glossina morsitans in which it undergoes development. Kinghorn and Yorke82 found that about 16 per cent. of the wild game examined in Northern Rhodesia was naturally infected with T. rhodesiense. The wild game examined included waterbuck, hartebeest, mpala, bushbuck and warthogs. One native dog near the Nyasaland border was found infected, but not domestic stock. Taute doubts whether T. rhodesiense really occurs in wild game. Approximately 3·5 per cent. of the tsetse flies fed on infected animals may become permanently infected with T. rhodesiense, and capable of infecting clean animals. Furthermore, a tsetse fly when once infective probably remains infective for the rest of its life.
Kinghorn and Yorke, however, have shown that climatic conditions, namely, those of temperature, also affect the infectivity of the tsetse fly, as the ratio of flies capable of transmitting T. rhodesiense to those incapable of transmitting the virus is 1 : 534 in hot valley districts (e.g., Nawalia, Luangwa Valley, temperature 75° to 85° F.), while on elevated plateaux (e.g., Ngoa, on the Congo-Zambesi watershed, temperature 60° to 70° F.) the ratio falls to 1 : 1312.
Mechanical transmission by the tsetse fly does not occur, if a period of twenty-four hours has elapsed since the infecting meal.
Developmental Cycle in the Fly.—The period which elapses between the infecting feed of the flies and the date on which they become infective varies from eleven to twenty-five days in the Luangwa Valley, according to Kinghorn and Yorke. Attempts carried out at laboratory temperature on the Congo-Zambesi plateau, during the cold season, to transmit T. rhodesiense by means of G. morsitans were always unsuccessful. The developmental cycle of the trypanosome in the fly is influenced by the temperature to which the flies are subjected (as stated above). The first portion of the developmental cycle proceeds at the lower temperatures (60° to 70° F.), but higher temperatures are necessary for the completion of the development of the trypanosome. Kinghorn and Yorke found that the trypanosomes may persist in the fly, at an incomplete stage of their development, for at least sixty days when the climatic conditions were unfavourable.
The first portion of the developmental cycle of the trypanosome takes place in the gut of the fly. Invasion of the salivary glands of the tsetse is secondary to that of the intestine, but is necessary for the infectivity of the fly. A relatively high mean temperature, 75° to 85° F., is essential for the passage of the trypanosomes into the salivary glands and the completion of their development therein.
Kinghorn and Yorke83 state that the predominant type of trypanosome in the intestine of infected G. morsitans was a large broad form, quite different from that which is most common in the salivary glands. The trypanosome in the glands resembles the short form seen in the blood of the vertebrate host. The authors quoted state that both the intestinal and salivary gland forms of infective G. morsitans are virulent when inoculated into healthy animals.
Bruce and colleagues84 have quite recently (June, 1914) published an account of their investigations of T. rhodesiense in G. morsitans in Nyasaland. (Incidentally it may be remarked that Bruce considers T. rhodesiense to be identical with a polymorphic strain of T. brucei—see pp. 83, 94). The development of T. rhodesiense takes place in the alimentary canal and salivary glands, not in the proboscis, of the tsetse fly. In feeding experiments with laboratory bred flies, as well as with a few wild flies, fed on infected dogs or monkeys, only 8 per cent. of the flies were found to be infected on dissection. Of such infected flies, however, only some allow of the complete development of the trypanosomes within them, in other words only about 1 per cent of the flies become infective. The length of time which elapses before a fly becomes infective varies from fourteen to thirty-one days, averaging twenty-three days, when kept at 84° F. (29° C.). The dominant intestinal type of flagellate in the fly is that seen in the proventriculus, which contains many long, slender trypanosomes. These proventricular forms find their way to the salivary glands, wherein crithidial and encysted forms are seen. They change into “blood forms,” which are short, stumpy trypanosomes and are infective. “The infective type of trypanosome in the salivary glands—corresponding to the final stage of the cycle of development—is similar to the short and stumpy form found in the blood of the vertebrate host.” The cycle is thus very similar to that of T. gambiense in G. palpalis (fig. 30).
Culture.—J.