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.