Brumpt found that T. cruzi could live in Cimex lectularius, C. boueti, and Ornithodorus moubata. The Cimex fæces may be infective. Blacklock found multiplication of the parasite in C. lectularius.
Culture.—The trypanosome can be cultivated on Novy-MacNeal’s blood agar, and the cultural forms resemble those described in the bug.
Possible Reservoir.—Chagas thinks that probably the armadillo or “tatu” (Dasypus novemcinctus) may be the reservoir of T. cruzi. He also thinks that Triatoma geniculata is a transmitter; it lives in the burrows of the armadillo. Other carriers may be Triatoma infestans and T. sordida.
Clinical Features.—The trypanosomiasis of Brazil, produced by T. cruzi and spread by Triatoma spp. has received various names, such as oppilação, canguary, parasitic thyroiditis, and coreotrypanosis. It is also known as the human trypanosomiasis of Brazil, South American trypanosomiasis, and Chagas’ disease.
Chagas88 reports two principal forms—acute and chronic. The acute infection is rare, and is characterized by increase in the volume of the thyroid gland, pyrexia, a sensation of crackling in the skin, enlarged lymphatic glands in the neck, axilla, etc., while the liver and spleen are increased in volume. Sclerosis of the thyroid gland is found at autopsy and fatty degeneration of the liver. During an attack of fever, trypanosomes are found in the blood. The acute form was only observed in children.
In the chronic form Chagas reports several varieties: (a) A pseudo-myxœdematous form, occurring in most cases, especially up to the age of 15. There is hypertrophy of the thyroid gland or at least signs of hypothyroidism, general hypertrophy of glands, disturbance of heart rhythm, and nervous symptoms. (b) The myxœdematous form is characterized by similar symptoms, especially by considerable swelling of the thyroid body, and myxœdema of the subcutaneous cellular tissue; sometimes there is a true pachydermic cachexia. (c) In the nervous form there are motor disturbances, aphasia, disturbances of intelligence or signs of infantilism, athetosis of the extremities and idiocy. There are also paralytic symptoms of bulbar origin, disturbances of mastication, phonation and deglutition, and in some cases convulsive attacks. (d) The cardiac form, characterized by disturbance of the heart rhythm. In all these forms the parasite is found at autopsy in the nervous substance, brain, bulb and heart.
Vianna (1911)89 has studied the histopathology of the disease. Some of the chief points are: in the heart muscle destruction of the sarcoplasm, followed by interstitial myocarditis; in the central nervous system invasion of the neuroglia cells and inflammatory reaction; in the suprarenal capsule invasion of medulla or cortex; inflammatory reaction can also be seen in the kidneys, the hypophysis and thyroid gland.
Recently Chagas states90 that “schizotrypanosomiasis” has been found in a child 15 to 20 days old, and that Trypanosoma cruzi has also been found in a fœtus—the mother being infected with the trypanosome. The trypanosomiasis can, then, be transmitted hereditarily.
Trypanosoma lewisi, Kent, 1881.
The trypanosome has a nucleus somewhat displaced anteriorly, about one-third of the way from the anterior (flagellar) end of the body, a relatively straight edge to the undulating membrane, and a rod-shaped blepharoplast (fig. 37, A). It averages about 25 µ long and 1·5 µ broad.
Much attention has been devoted in recent years to the elucidation of the life history of the rat parasite, Trypanosoma lewisi. It is usually non-pathogenic to its host. It has been shown that the trypanosome can be transmitted from rat to rat by the rat-flea, Ceratophyllus fasciatus, and by Ctenocephalus canis (the so-called dog-flea). (See also p. 92). The flagellate may also persist, but doubtfully develop, in the rat-louse, Hæmatopinus spinulosus. These researches may now be summarized.
Fig. 37.—Trypanosoma lewisi, from rat’s blood. a, ordinary form; b, small form; c, d, stages in equal binary fission; e, elongate form (longocaudense type), resulting from division as seen in d; f, unequal binary fission; g, h, multiple fission into four and eight; i, small form; j, binary fission of small form; K, division rosette. × 2,000. (After Minchin and Thomson.)
Life Cycle in the Vertebrate Host.—After infection of a rat, the trypanosomes usually appear in the animal’s blood in five to seven days. This incubation period applies either to a natural or an artificial infection. The trypanosomes first observed in the rat’s blood are diverse in form (fig. 37), being small, medium and large in size. This diversity is explained by the rapid multiplication taking place. A trypanosome may divide by equal longitudinal fission (fig. 37, C, D), but more commonly multiple fission occurs (fig. 37, G, H), and is unequal. Rosette forms are produced, in which the parent form can be recognized by its long flagellum (fig. 37, H) and attached to it are daughter individuals, smaller in size, from which flagella are growing. Minchin and J. D. Thomson (1912) find that the daughter forms may be set free sometimes with a crithidia-like facies (fig. 37, I), the blepharoplast being anterior but near to the nucleus. The daughter forms, when set free, may themselves divide by binary or multiple fission, in the latter case forming rosettes (fig. 37, K). Rosette forms were described by Moore, Breinl and Hindle in 1908.
Lingard, some years ago, described as a distinct species, T. longocaudense, certain forms with markedly elongate posterior ends (fig. 37, E). According to Minchin, “these forms appear to arise by binary fission” (fig. 37, D). These long drawn-out forms “are of constant occurrence and very numerous at a certain stage of the multiplication period.” It is about the eighth or tenth day after infection that the multiplication of T. lewisi is at its maximum in the rat’s blood. About the twelfth or thirteenth day the trypanosomes seen in the blood appear uniform. According to Minchin (1912)91 the rat “gets rid of its infection entirely sooner or later, without having suffered, apparently, any marked inconvenience from it, and is then immune against a fresh infection with this species of trypanosome.” There is, then, a cycle of development in the vertebrate host. Minchin notes that the records of the pathogenicity of T. lewisi in rats, causing their death, need further investigation.
T. lewisi inoculated into dormice (Myoxus nitela) and jerboas may become pathogenic thereto.
Carini found cysts in the lungs of rats infected with T. lewisi. He thought the cysts were schizogonic stages of the trypanosome, comparable with those found in the lungs of animals sub-inoculated with T. cruzi. Delanoë (1912)92 has found, however, that such cysts, containing eight vermicules, occurred in rats uninfected with T. lewisi. Delanoë concludes that the pneumocysts are independent of T. lewisi, and represent a new parasite, Pneumocystis carinii. The pneumocysts may be allied to the Coccidia, and must be considered when investigating the life-cycle of a trypanosome in a vertebrate host. Some of the stages of T. cruzi may possibly be of this nature.
Life-cycle in the Invertebrate Host.—This occurs in fleas, and has been investigated in considerable detail by Minchin and Thomson in Ceratophyllus fasciatus, and by Nöller in Ctenocephalus canis and Ctenopsylla musculi.
When infected rat’s blood is taken up by the flea, the parasites pass with the ingested blood direct to the mid-gut of the Siphonapteran. In the flea’s stomach they multiply in a somewhat remarkable manner, namely, by penetration of the cells of the lining epithelium, and division inside the epithelial cells. Inside these lining cells the trypanosomes first grow to a large size and then form large spherical bodies, within which nuclear multiplication occurs (fig. 38, A-F). Any one of these large spherical bodies contains at first a number of nuclei, blepharoplasts and developing flagella, the original flagellum still remaining attached for a time. The cytoplasm then divides into daughter trypanosomes which are contained within an envelope, formed by the periplast of the parent parasite. Inside the periplast envelope are a number of daughter trypanosomes “wriggling very actively; the envelope becomes more and more tense, and finally bursts with explosive suddenness, setting free the flagellates, usually about eight in number, within the host-cell” (fig. 38, F). The daughter forms escaping from the host cell into the stomach lumen of the flea are fully formed, long trypanosomes.
Fig. 38.—Trypanosoma lewisi. Developmental stages from stomach of rat flea. O, ordinary blood type; A-F, stages occurring in gut-epithelium of flea, when the trypanosome becomes rounded and undergoes multiplication, forming in F eight daughter trypanosomes; G, type of trypanosome resulting from such division which passes back to the rectum. × 2,000. (After Minchin.)
The trypanosomes (fig. 38, G) pass into the flea’s rectum. The next phase is a crithidial one. The parasites become pear-shaped, in which the blepharoplast (kinetic nucleus) has travelled anteriorly past the nucleus towards the flagellum (fig. 39). The crithidial forms attach themselves to the wall of the rectum, and multiply by binary fission (fig. 39, D). A stock of parasites is thus formed which, according to Minchin and Thomson, “persist for a long time in the flea—probably under favourable conditions, for the whole life of the insect” (fig. 39, A–I).
From the crithidial forms of the rectum, according to Minchin, small infective trypanosomes arise by modification morphologically (fig. 39, J–M). The flagellum grows longer and draws out more the anterior part of the body, the blepharoplast migrates posteriorly, behind the nucleus, and carries with it the flagellar origin. These trypanosomes are small, but broad and stumpy (fig. 39, N), and can infect a rat. Minchin and Thomson formerly considered that the small, stumpy, infective trypanosomes pass forwards from the rectum into the stomach, and “appear to be regurgitated into the rat’s blood when the flea feeds.” However, the small infective trypanosomes were previously described by Swellengrebel and Strickland.93 They may be found in the flea’s fæces. Nöller (1912)94 has found that the development of T. lewisi proceeds quite well in the dog flea (Ctenocephalus canis) in Germany. Wenyon confirms this, and states that the human flea, Pulex irritans, and the Indian rat-flea, Xenopsylla cheopis, are also able to serve as true hosts for T. lewisi.
Fig. 39.—Trypanosoma lewisi. Developmental stages from rectum of rat-flea. A, early rectal form; C, D, division of crithidial form; E, group of crithidial forms; F–I, crithidial forms without free flagella, some becoming rounded; J–M, transitional forms to trypanosome type seen in N, which represents the final form in the flea. × 2,000. (After Minchin.)
Nöller stated that rats were not infected with T. lewisi by infective fleas biting them, but by the rats licking up the fæces passed by the fleas while feeding. This is not in agreement with Minchin and Thomson’s earlier views of regurgitation, which, apparently, they have now abandoned.95 Wenyon (1912) confirms Nöller’s experiments. He took a dog flea, containing infective trypanosomes in its fæces, and allowed it to feed on a clean rat. The fæces of the flea, passed while feeding, were carefully “collected on a cover glass and taken up in culture fluid with a fine glass pipette.” The contents of the pipette were discharged into the mouth of a second clean rat. Injury to the rat’s mouth was carefully avoided. The first rat, on which the infective flea was fed, did not become infected, while the second rat, in whose mouth infective flea fæces were placed, became infected in six days.
When infective forms of T. lewisi have been developed within the gut of a rat flea, they may enter and infect the vertebrate host by96 (a) being crushed and eaten by the rodent; (b) the rat may lick its fur on which an infected flea has just passed infective excrement; or (c) the rat may lick, and infect with flea excrement, the wound produced by the bite of the flea.
The time taken for the full development of T. lewisi in the flea is about six days. The intracellular phase is at its height about the end of the first day; the crithidial phase, in the flea’s rectum, begins during the second day; the stumpy, infective trypanosomes are developed in the rectum about the end of the fifth day.
Wenyon97 writes that, “the fleas, when once infected with T. lewisi, remain infected for long periods, for though many small infective trypanosomes are washed out of the gut at each feed, those that remain behind multiply to re-establish the infection of the hind gut. Further, the infection is still maintained even if the flea is nourished on a human being, so that fresh human blood does not appear to be destructive to the infective forms in the flea.”
The best method of controlling fleas during experiments is that due to Nöller. He adopted the method of showmen who exhibit performing fleas, and secure them on very fine silver wire.
Of fleas fed on an infected rat only about 20 per cent. become infective. About 80 per cent. are immune. If fleas are examined twenty-four hours after feeding, trypanosomes will be found in all, so that many of the parasites are destined to degenerate.
It may be of interest to note that Gonder98 (1911) has shown that a strain of T. lewisi resistant to arsenophenylglycin loses its resistance after passage through the rat-louse, Hæmatopinus spinulosus. These experiments suggest that physiological “acquired characters” may be lost by passage through an invertebrate host.
Trypanosoma brucei, Plimmer and Bradford, 1899.
Trypanosoma brucei was discovered by Sir D. Bruce in 1894 in cattle in Zululand and was named T. brucei by Plimmer and Bradford in 1899 in honour of its discoverer. This trypanosome is of considerable economic importance, as it is responsible for the fatal tsetse fly disease, or “nagana,” in cattle, horses and dogs. The disease is widely distributed in Africa and is transmitted from host to host by the tsetse, Glossina morsitans, and other species of Glossina. The virus is maintained in nature in certain big game, such as wildebeest, bushbuck and koodoo, which thus act as living reservoirs of disease from which the tsetse may become infected. These reservoir hosts are not injured, apparently, by the presence of the parasites.
T. brucei is rapidly fatal to the small laboratory animals, such as rats and mice. Horses, asses and dogs practically always succumb to its attacks, while a very small number of cattle recover from “nagana.” The disease is characterized by fever, destruction of red blood corpuscles, severe emaciation and by an infiltration of coagulated lymph in the subcutaneous tissue of the neck, abdomen and extremities giving a swollen appearance thereto. The natural reservoirs in which T. brucei has been long acclimatized are unaffected by the trypanosomes, while the newer hosts, such as imported cattle in Africa, are rapidly destroyed by their action.
The general morphology and life history in the vertebrate host is that of a typical trypanosome (fig. 40). Its length is from 12 µ to 35 µ, its breadth from 1·5 µ to 4 µ. Multiplication by longitudinal division proceeds in the peripheral blood (fig. 26), while latent, leishmaniform bodies are produced in the internal organs.
Bruce and colleagues99 have quite recently (June, 1914) described the development of a Zululand strain of T. brucei in G. morsitans. The tsetse flies were bred out in Nyasaland. In vertebrate blood the brucei strain was polymorphic. The development was like that found for T. gambiense in G. palpalis (fig. 30), and by Bruce and colleagues for T. rhodesiense in G. morsitans in Nyasaland. Long trypanosomes were found in the proventriculus of the tsetse. Crithidial, rounded or encysted, and immature “blood forms” occurred in the salivary glands; and finally infective, stumpy, “blood forms” were differentiated in the salivary glands. The period of development of T. brucei in G. morsitans takes about three weeks, and then the fly becomes infective. Bruce believes that T. rhodesiense of Nyasaland and T. brucei of Zululand are the same, their cycles of development in G. morsitans being “marvellously alike.” (But see Laveran, p. 80.)
T. brucei has been cultivated with difficulty by Novy and MacNeal, using blood agar. The best treatment for nagana is arsenic in some form.
It is probable that more than one trypanosome has been confused under the name T. brucei, more especially as the occurrence of many species of trypanosomes in various animals in Africa was not suspected until comparatively recent times. It has been shown by Stephens and Blacklock (1913) that the original Zululand strain of T. brucei was monomorphic, while the organism sent from Uganda, and at the time believed by Bruce to be the same as the Zululand trypanosome, has been found to be polymorphic, with morphological resemblances to T. rhodesiense. Stephens and Blacklock100 have suggested the name T. ugandæ for the polymorphic trypanosome, which, however, has marked resemblances with Trypanosoma pecaudi, and they are, perhaps, identical. T. pecaudi was the name given by Laveran101 in 1907 to the causal agent of “baleri” in equines and sheep in the French Sudan. T. pecaudi, which is dimorphic, is widely distributed in Africa. An extremely small number of both T. pecaudi and T. ugandæ have been shown to possess posterior nuclei. T. pecaudi is transmitted by various species of Glossina, and is said to develop in the gut and proboscis of the fly.
On the other hand, Bruce and colleagues (1914), examining a strain sent from Zululand in 1913, state that T. brucei is polymorphic. Bruce (1914) suggests that passage through laboratory hosts has influenced and altered the morphology of the parasite.
Trypanosoma evansi, Steel, 1885.
Syn.: Spirochæta evansi, Steel, 1885; Hæmatomonas evansi, Crookshank, 1886; Trichomonas evansi, Crookshank, 1886.
Trypanosoma evansi, first found by Evans in 1880, in India, is the causal agent of the disease known as “surra.” The malady affects more particularly horses, mules, camels and cattle in India and neighbouring countries, such as Burma and Indo-China. It occurs also in Java, the Philippines, Mauritius and North Africa. Elephants may be affected. A serious outbreak among cattle in Mauritius occurred in 1902, the disease being imported into the island. The symptoms are fever, emaciation, œdema, great muscular weakness and paralysis culminating in death.
T. evansi varies from 18 µ to 34 µ in length and 1·5 µ to 2 µ in breadth. It has a pointed posterior extremity, and, anteriorly, there is a free portion to the flagellum (fig. 41). It is possibly monomorphic, but a few broad forms occur. The trypanosome multiplies by longitudinal fission in the blood. Rounded leishmaniform stages occur in the spleen of the vertebrate host, which stages Walker102 (1912) considers to be phases of schizogony.
The parasite is transmitted in nature by various species of Tabanus and Stomoxys, though at present little is known of the life-history within these invertebrate hosts.
Dogs are said to contract the disease by feeding on animals dead of surra.
A variety of T. evansi is the cause of “mbori” in dromedaries in Africa (Sahara and Sudan). Another possible variety, or closely allied form, is T. soudanense, the causal agent of “el debab” in camels and horses in North Africa, especially Algeria and Egypt.
An extraordinary example of the possible infection of a human being with an animal trypanosome is recorded in the case of Professor Lanfranchi, of the Veterinary School, Parma. The Professor became infected with trypanosomes, although only nagana and surra were maintained in his laboratory, and he himself had never visited the tropics. He suffered from irregular attacks of fever and was œdematous, but his mind remained clear. The identification of the trypanosome from Lanfranchi’s blood has been a matter of great difficulty. Apparently Mesnil and Blanchard (1914)103 consider the strain found in the patient is almost indistinguishable in its reactions from T. gambiense, though the parasite is monomorphic. Lanfranchi considers that he was infected with T. evansi.
Trypanosoma equinum, Voges, 1901.
Syn.: Trypanosoma elmassiani, Lignières.
Trypanosoma equinum was found by Elmassian to be the cause of the fatal disease, “mal de caderas,” of horses and dogs, in South America (Paraguay, Argentine, Bolivia). The name refers to the fact that in the disease, as in other trypanosomiases, the hind quarters become paralysed. Cattle are refractory to inoculation.
T. equinum is about 22 µ to 24 µ long and about 1·5 µ broad (fig. 42). Although this trypanosome is very active, yet it is characterized by the blepharoplast (kinetic nucleus) being very minute or even absent, as the granule sometimes seen may be the basal granule of the flagellum.
The mode of transmission of T. equinum is not known with absolute certainty. Migone has shown that the parasite causes a fatal disease in the large South American rodent, the capybara (Hydrochœrus capybara). This animal appears to be a reservoir of the parasite. Dogs may become infected by eating diseased capybaras, and it is suggested that the infection is spread from the dogs to horses by the agency of fleas. Some authorities consider that T. equinum may be spread by various Tabanidæ and by Stomoxys. Neiva (1913)104 doubts all these modes of transmission in Brazil, and suggests Chrysops or Triatoma as vectors.
Trypanosoma equiperdum, Doflein, 1901.
Syn.: Trypanosoma rougeti, Laveran and Mesnil.
The malady of horses known as “dourine” or “mal du coït” is due to a trypanosome, T. equiperdum, discovered by Rouget in 1894. “Dourine”—also known as “stallion disease” or “covering disease”—is found among horses and asses in Europe, India, North Africa and North America. The trypanosome is transmitted by coitus, and so far as is known not by insect agency.
Fig. 43.—Trypanosoma equiperdum. × 2000 approximately. (Original. From preparation by Fantham.)
The progress of the disease may be considered under three periods. The period of œdema, when signs of œdema of the genitalia are seen. The œdema is generally painless and non-inflammatory. This period lasts about a month. It is succeeded by the period of eruption, which sets in about two months after infection. Circular œdematous areas (“plaques”), often about the size of a two-shilling piece, appear under the skin of the sides and hind quarters, and also, at times, under the skin of the neck, thighs and shoulders. The eruption is variable, but usually lasts about a week and leaves the animal in an enfeebled condition. Gland enlargement and swelling of the joints and synovia also may occur. The third period of the disease is described as that of anæmia and paralysis. The animal becomes very anæmic, emaciation is marked, superficial non-healing abscesses often form, and conjunctivitis and ulcerative keratitis can occur. Paralysis ensues, and in from two to eighteen months the animal dies. In the acute form of the disease the animal may die after the first period from acute paralysis.
It is difficult to find the trypanosomes in naturally infected animals, and they are best obtained from the plaques of the eruption. Apparently the parasite occurs more in the lymph than in the blood.
Ruminants are said to be refractory to this trypanosome.
T. equiperdum is about 25 µ to 28 µ in length on an average, but varies from 16 µ to 35 µ. Its cytoplasm is relatively clear, and does not show chromatic granules (fig. 43). It is stated to be monomorphic.
It has been shown recently by Blacklock and Yorke (1913)105 that there is another trypanosome giving rise to dourine in horses. This trypanosome is dimorphic (resembling T. pecaudi and T. ugandæ), and is named T. equi. Previously T. equiperdum and T. equi had been confused.
Uhlenhuth, Hübner and Worthe have demonstrated the presence of endotoxins in T. equiperdum. These endotoxins may be set free by trypanolysis.
Trypanosoma theileri, Bruce, 1902.
This parasite, 60 µ to 70 µ long, and 4 µ to 5 µ broad, is distinguished for its large size, though it is not so large as T. ingens from Uganda oxen, whose length may be 72 µ to 122 µ, and breadth 7 µ to 10 µ. The posterior end of T. theileri is drawn out. Small forms of the flagellate are known, 25 µ to 53 µ in length. Probably other forms of the parasite have the nucleus posterior, and these flagellates were formerly separated as T. transvaaliense (Laveran, 1902). Myoneme fibrils may be seen on its body. The pathogenicity of this organism is doubtful, it was formerly thought to be the causal agent of “gall-sickness” in cattle in South Africa. T. theileri also occurs in Togoland, German East Africa, and Transcaucasia. Allied or identical parasites occur in cattle in India.
Trypanosoma theileri, specific to cattle, is perhaps transmitted by the fly Hippobosca rufipes in South Africa.
Trypanosoma hippicum, Darling, 1910.
Trypanosoma hippicum causes the disease of mules known as “murrina.”106 It was found in mules imported to Panama from the United States. It can live in other equines. The parasite varies from 18 µ to 28 µ in length, and is from 1·5 µ to 3 µ broad. Its undulating membrane is little folded. The trypanosome has a noticeable blepharoplast. It can penetrate mucous membranes, and it is thought that the trypanosome may be transmitted during coitus. It may also be spread mechanically by species of Musca, Sarcophaga and Compsomyia, sucking the wounds of infected animals and carrying over the trypanosomes to wounds on healthy ones.
Endotrypanum schaudinni, Mesnil and Brimont, 1908.
This organism was discovered in the blood of a sloth (Cholœpus didactylus), in South America (French Guiana).107 It possesses special interest, in that the best known form of the organism is endoglobular, inhabiting the erythrocytes of the sloth. A free trypanosome in the same animal was considered to be different from the endoglobular form, which was somewhat like a peg-top, and possessed a short flagellum. Darling108 (November, 1914) has seen the organism in Panama. He describes free crithidial forms in shed blood, but not in the blood-stream of the sloth.
Trypanosoma boylei, Lafont, 1912.
This is a parasite of the Reduviid bug, Conorhinus rubrofasciatus. The insect attacks man in Mauritius, Réunion and other places. Lafont infected rats and mice by intraperitoneal injection with the gut-contents of infected bugs. Trypanosomes appeared in the mice. Other flagellate types were assumed by the parasites in the bug.
Monomorphic Trypanosomes.
A number of trypanosomes, characterized by relative uniformity in size and structure, may be considered under this heading. They occur in cattle, sheep, goats and horses in Africa, especially West Africa. Morphologically, they are characterized by the posterior (aflagellar) part of the body being swollen, while the anterior part narrows. The nucleus is central and situated at the commencement of the narrowing of the body. The blepharoplast is almost terminal, the undulating membrane is narrow and not markedly folded, so that the flagellar border lies close to or along the body. The flagellum may or may not possess a free portion.
Some recent workers have considered that T. brucei (Zululand strain) and T. evansi are also monomorphic, but they do not exhibit the general characteristics outlined above. T. brucei and T. evansi have already been considered separately.
The monomorphic trypanosomes, as defined above, include:—
Trypanosoma vivax, Ziemann, 1905.
This trypanosome109 occurs in cattle, sheep and goats, and was first found in the Cameroons. It is fatal to cattle. Equines are also affected. Antelopes are the possible reservoirs of the trypanosome. It is probably transmitted by Glossina palpalis and other tsetse flies. Its movement is very active. It possesses a free flagellum (fig. 45) and it averages 23 µ to 24 µ in length. T. cazalboui (Laveran, 1906)—the causal agent of “souma” in bovines and equines in the French Sudan—is probably synonymous with T. vivax.
Trypanosoma capræ (Kleine, 1910) is allied, but is somewhat broader and more massive. It was found in goats in Tanganyika.
Trypanosoma congolense, Broden, 1904.
Probable synonyms.—Trypanosoma dimorphon, Laveran and Mesnil, 1904; Trypanosoma nanum, Laveran, 1905; Trypanosoma pecorum, Bruce, 1910; Trypanosoma confusum, Montgomery, 1909.
This trypanosome causes disease among horses (e.g., Gambia horse sickness), cattle, sheep, goats, pigs, and dogs. It is widely distributed in Central Africa (e.g., Gambia, Congo, Uganda, Nyasaland), the strain probably being maintained naturally in big game. It is transmitted by various Glossinæ, and perhaps by Tabanus and Stomoxys. It is said to develop in the gut and proboscis of Glossina palpalis and G. morsitans. The trypanosome averages 13 µ to 14 µ in length and has no free flagellum (fig. 46). It is about 2 µ broad. Formerly T. nanum and T. pecorum were said to differ in their pathogenicity, the former being said not to infect the smaller laboratory animals. Yorke and Blacklock (1913), however, consider that the virulence varies and that these trypanosomes are probably the same.
The T. dimorphon originally obtained by Dutton and Todd (1903) in Gambian horse sickness has been shown to be a mixture of T. vivax and T. congolense.
Trypanosoma simiae (T. ignotum) is like T. congolense. It averages 17·5 µ long. It is virulent to monkeys and pigs.
Trypanosoma uniforme, Bruce, 1910.
This trypanosome was found in oxen in Uganda.110 It can be inoculated to oxen, goats and sheep, but is refractory to dogs, rats and guinea-pigs. It has been found in antelopes. It resembles T. vivax, but is smaller (fig. 47), averaging 16 µ in length. A free flagellum is present. It is transmitted by Glossinæ.
Many other trypanosomes occur in mammals, while birds, reptiles, amphibia (fig. 48) and fish also harbour them. The discussion of these forms does not come within the scope of the present work. They are dealt with in Laveran and Mesnil’s “Trypanosomes et Trypanosomiases,” 2nd edit., 1912.
General Note on Development of Trypanosomes in Glossina.
Before concluding the account of trypanosomes, it may be of interest to remark that several African trypanosomes develop in various species of Glossina, and are found in different parts of the alimentary tract and in the proboscis. Thus (a) T. vivax, T. uniforme and T. capræ develop in the fly’s proboscis (labial cavity and hypopharynx) only; (b) T. congolense, T. simiæ and T. pecaudi develop first in the gut of the fly and then pass forward to its proboscis; and (c) T. gambiense and T. rhodesiense develop first in the gut and later invade the salivary glands of the tsetse. The proboscis or the salivary glands in such cases are termed by Duke111 the anterior station of the trypanosome, wherein it completes its development.
Adaptation of Trypanosomes.
These flagellates may exhibit power of adaptation to changes of environment, such as those due to the administration of drugs, change of host, etc. A few examples of such mutations may be briefly considered:—
(1) Blepharoplastless Trypanosomes.—T. brucei may become resistant to pyronin and oxazine. Accompanying this drug resistance is a change in morphology, namely, the loss of the blepharoplast (Werbitzki).112 A race or strain of blepharoplastless trypanosomes may be thus produced which retains its characteristic feature after as many as 130 passages (Laveran).113 Oxazine is the more powerful drug, and it acts directly on the blepharoplast. (Compare the natural blepharoplastless character of T. equinum.)
(2) Reference has been made on p. 93 to the experiments of Gonder, who showed that a strain of T. lewisi rendered resistant to arsenophenylglycin lost its resistance after passage through the rat louse. This is in marked contrast with the retention of drug resistance during passage by inoculation from rat to rat.
(3) T. lewisi from the blood of a rat when transferred to a snake seems largely to disappear, as very few flagellates are seen. When blood from the snake is inoculated into a clean rat, then trypanosomes reappear in the rat, but they are not all like those originally inoculated. It seems certain that, in such a case, changes in form and virulence of the trypanosome have occurred. Similar experiments were made with T. brucei from rats to adders and other animals and back to rats. Changes in the form and virulence of T. brucei occurred.
These interesting experiments were performed by Wendelstadt and Fellmer.114
Genus. Herpetomonas, Saville Kent, 1881.
Herpetomonas is a generic name for certain flagellates possessing a vermiform or snake-like body, a nucleus placed approximately centrally, and a blepharoplast (kinetic nucleus) near the flagellar end. There is no undulating membrane (fig. 49, a). The organisms included in this genus certainly possess one flagellum, while according to Prowazek (1904) Herpetomonas muscæ-domesticæ, the type species, possesses two flagella united by a membrane. Patton,115 Porter116 and others affirm, however, that the biflagellate character of H. muscæ-domesticæ (from the gut of the house-fly) is merely due to precocious division. The matter is further complicated by the generic name Leptomonas, given by Kent in 1881, to an uniflagellate organism found by Bütschli in the intestine of the Nematode worm, Trilobus gracilis. This parasite, Leptomonas bütschlii, has not yet been completely studied. Until these controversial points relating to the identity or separation of Herpetomonas and Leptomonas have been satisfactorily settled, we may retain the better known name Herpetomonas for such uniflagellate, vermiform organisms. However, the name Leptomonas, having been used by Kent two pages earlier in his book (“Manual of the Infusoria”) than Herpetomonas, would have priority if the two generic names were ultimately shown to be synonymous.
A full discussion of these interesting and important flagellates hardly comes within the purview of the present work; brief mention can only be given here to certain species.
The Herpetomonads occur principally in the digestive tracts of insects, such as Diptera and Hemiptera. They are also known in the guts of fleas and lice, but are not confined to blood-sucking insects. One example, H. ctenocephali (Fantham, 1912)117 occurs in the digestive tracts of dog fleas, Ctenocephalus canis, in England, France, Germany, Italy, India, Tunis, etc. It is a natural flagellate of the flea, and might easily be confused with stages of blood parasites in the gut of the dog flea. Dog fleas are stated by Basile to transmit canine kala-azar, which is believed to be the same as human infantile kala-azar. Confusion is further likely to arise since herpetomonads pass through pre-flagellate, flagellate and post-flagellate or encysted stages; pre- and post-flagellate stages being oval or rounded and Leishmania-like. The post-flagellate stages are shed in the fæces, and are the cross-infective stages by means of which new hosts are infected by the mouth. The possible presence of such natural flagellates must always be considered when experimenting with fleas, lice, mosquitoes, etc., as possible vectors of pathogenic flagellates like Leishmania and Trypanosoma. H. pediculi (Fantham, 1912) occurs in human body lice.118 See further remarks on pp. 107, 112.