Invasion of the Salivary Glands of the Fly.—Long, slender trypanosomes from the proventriculus pass forward into the hypopharynx. They then pass back along the salivary ducts, about sixteen to thirty days after the fly’s feed. The trypanosomes reach the salivary glands as long, slender forms. In the glands they become shorter and broader, attach themselves to the surrounding structures, and assume the crithidial facies (fig. 30, c, d). As crithidial forms they remain attached to the wall and multiply in the glands. These crithidial stages differentiate into the short, broad trypanosome forms, capable of swimming freely (fig. 30, e).
Miss Robertson considers the development in the main gut to be indifferent multiplication, and that salivary fluid seems necessary to stimulate trypanosomes to the apparently essential reversion to the crithidial type. The second development in the salivary gland is the essential feature. The short, stumpy forms of trypanosomes (fig. 30, e) finally produced in the salivary glands are alone infective. No conjugation of trypanosomes occurs in the fly. Only about 5 per cent. of captive tsetse flies fed on trypanosome-infected blood become infective, but they probably remain infective for the rest of their lives.
J. G. Thomson and Sinton (1912)64 have obtained in cultures the various trypanosome forms of T. gambiense seen in the fly’s main gut.
Duke (1912)65 found T. gambiense in a species of antelope, the situtunga (Tragelaphus spekei), on Damba Island in Victoria Nyanza. Wild G. palpalis could be infected therefrom. The antelope may then act as a sleeping sickness reservoir in that district, but men are apparently the chief reservoir.
Trypanosoma nigeriense, Macfie, 1913.66
Macfie has recently (August, 1913) described a human trypanosome from the Eket district of Southern Nigeria. It is common in young people. The disease produced does not seem to be of a virulent type in Nigeria, and does not occur in epidemic form. In the early stages the glands of the neck are enlarged. In the later stages—cases of which are rarer—lethargy appears. The parasite is a polymorphic trypanosome, morphologically almost indistinguishable from T. gambiense, though it may be slightly shorter. Macfie recorded the occurrence in his preparations of a few trypanosomes appearing to have a flagellum free during their whole length. Some of the parasites, as seen in a sub-inoculated guinea-pig, are very small (8 µ long). Other trypanosomes have their nuclei displaced somewhat anteriorly. This parasite may only be a variety of T. gambiense. The parasite is perhaps spread by Glossina tachinoides.
Trypanosoma rhodesiense, Stephens and Fantham, 1910.
The parasite was found in the blood of a young Englishman who had contracted sleeping sickness in the Luangwa Valley, North-eastern Rhodesia, in the autumn of 1909. The patient had never been in an area infested with Glossina palpalis.
(1) Morphology.—The morphology of the parasite in man and sub-inoculated rats was studied by Stephens and Fantham in 1910.67 They pointed out a morphological peculiarity in the presence of certain trypanosomes with posterior nuclei in sub-inoculated animals, that is, parasites in which the nucleus (trophonucleus) was situated towards the posterior or aflagellar end, close up to or even beyond the blepharoplast or kinetic nucleus (fig. 31, 4, 5). When the nucleus was beside the blepharoplast, the former was seen to be kidney-shaped (fig. 31, 4). The posterior nuclear forms were of the stout and stumpy variety, and about 6 per cent. of the stumpy forms were found to have their nuclei displaced from the centre. The anterior or flagellar end of these trypanosomes often contained chromatoid granules. T. rhodesiense varies in length from 12 µ to 39 µ68; short stumpy forms vary from 13 µ to 21 µ, intermediate forms from 21 µ to 24 µ, and long, slender forms from 25 µ onwards. The average length is 24·1 µ.
Fig. 31.—Trypanosoma rhodesiense. 1, Long narrow form; 2–4, nucleus passing to posterior (aflagellar) end; 5, nucleus quite posterior. × 1,800. (After Stephens and Fantham.)
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 190769 in connection with T. gambiense. Fantham70 (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. Thomson71 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. Thomson72 (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