Fig. 46.—Trypanosoma congolense. × 2,000. (Original. From preparation by Fantham.)
Fig. 47.—Trypanosoma uniforme. × 2,000. (Original. From preparation by Fantham.)
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.
Fig. 48.—Trypanosoma rotatorium, from blood of a frog. × 1,400. (After Laveran and Mesnil.)
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.
Fig. 49.—a, Herpetomonas; b, Crithidia; c, Trypanosoma. (After Porter.)
Laveran and Franchini (1913–14)119 have recently succeeded in inoculating Herpetomonas ctenocephali, from the gut of the dog flea, intraperitoneally into white mice, and producing an experimental leishmaniasis in the mice. A dog was also infected. They have also succeeded in infecting mice with H. pattoni—a natural flagellate of