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