Certain regular periods occur in the course of the trypanosomiasis when few or no flagellate trypanosomes are found in the peripheral blood of the patient or of the sub-inoculated animal. These periods can be explained in terms of morphology, for the trypanosomes are capable of assuming a non-flagellate form in the internal organs of the host, particularly in the lungs and in the spleen. Such forms are known as “latent” or “resting” forms. The term “latent body” was first used by Moore and Breinl in 1907[69] in connection with T. gambiense. Fantham[70] (1911) has described the process of formation of latent from motile forms and the reconversion of the latent bodies into active flagellates. Fresh preparations of splenic blood or lung blood containing trypanosomes were made. A trypanosome gradually withdrew or cast off its flagellum, concentrated its cytoplasm, and became more or less elongate oval. Nucleus and blepharoplast approached one another and came to lie more or less side by side. Then an opaque line often made its appearance around the nuclear area and differentiated as a slight envelope or covering, the cytoplasm external to this merely degenerating. The small, oval, refractile body (fig. [29], d—f) thus formed was a non-flagellate latent body, 2 µ to 4 µ in diameter, like Leishmania or the non-flagellate, multiplicative forms of T. cruzi (fig. [34]), and remains temporarily inactive in the internal organs of the host. After this period of inactivity, the non-flagellate body, recuperated by its rest, begins to elongate again. The nuclei separate. From a small vacuole-like portion the flagellum differentiates and forces out the ectoplasm, which assumes the form of the undulating membrane with its flagellar border. Subsequent growth results in the production of the typical trypanosome form, which re-enters the circulating blood and multiplies by longitudinal binary fission. Division of the parasite prior to the formation of a latent body may occur and division of the latent forms themselves is known, though less common. Consequently latent bodies, like the flagellate forms themselves, show diversity in size. The blepharoplast of the latent bodies is sometimes less well marked than in Leishmania (see fig. [29], d-f). Laveran’s views on these bodies have already been given on p. [74].
(2) Animal Reactions.—The posterior nuclear trypanosomes were found in all sub-inoculated animals, such as rats, guinea-pigs, dogs, mice, Macacus, rabbits and horses, but were not seen in the human patient, as few trypanosomes occurred in his peripheral blood. R. Ross and D. Thomson[71] found a periodic, cyclical variation in the number of the parasites in the patient’s blood from day to day, the cyclical period being about a week (fig. [32]). Fantham and J. G. Thomson[72] (1911) found a similar periodic, cyclical variation in the trypanosomes in the blood of sub-inoculated rats, guinea-pigs and rabbits. On counting the parasites in the blood of similar animals inoculated with T. gambiense, they established, by enumerative methods, that T. rhodesiense was more virulent than T. gambiense, while Yorke also showed this marked virulence of T. rhodesiense in practically all laboratory animals. In other words the duration of infection in the case of T. rhodesiense was shorter. It was also found that T. rhodesiense was resistant to atoxyl. The patient, from whom the original strain was obtained, died about nine months after the probable date of infection. Some patients infected with T. rhodesiense have died in an even shorter period, such as four or five months.
In sheep and goats T. rhodesiense causes an acute disease, marked by high fever, œdema of the face, and keratitis, as shown by Bevan and others, death resulting after a relatively short period. T. gambiense gives rise, in these animals, to no symptoms except fever, which may be overlooked. T. rhodesiense produces keratitis in dogs.
Fig. 32.—Chart showing daily counts of number of trypanosomes per cubic millimetre of peripheral blood from a case of Rhodesian sleeping sickness. (After R. Ross and D. Thomson.)
Stannus and Yorke (1911) observed T. rhodesiense in animals inoculated from a case of sleeping sickness in Nyasaland. Sir D. Bruce and his colleagues[73] 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 Ringenbach[75] 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.