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 by[96] (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.