No abstract

SUMMARYMale mice (NMRI strain) of 3 and 5 g were inoculated i. p. with 8 x 10 6 and 9 x 10 4 metatrypomastigotes/g harvested from a 12-day-old LIT culture of Try panosoma rangeli of the "Dog-82" strain. At regular intervals after inoculation, the animals were sacrificed and portions of heart, liver, spleen, lung, thigh, kidney, stomach, intestine, brain, sternum, and vertebral column were embedded in paraffin, sectioned, and stained with haematoxylin-eosin and Giemsa colopho¬ nium. Pathology was encountered in the first five tissues cited above. The sub cutaneous, periosteal, interstitial, and peribronchial connective tissues, and later the muscle cells of the heart, were heavily parasitized by amastigotes and trypo¬ mastigotes. The possible reasons for the decrease in tissue parasitosis at the same time that the parasitemia is reaching its peak, and for the low level of in flammation in the parasitized tissues, are discussed. The observations of other workers, as well as the results described here, indicate that certain strains of T. rangeli under certain conditions may well cause pathological alterations in mammals.

The Neotropical mammalian parasite Trypanosoma (Herpetosoma) rangeli Tejera, 1920 is difficult to study due to the scarcity of blood forms in the vertebrate host. High and persistent parasitemias (up to 7 times the original inoculum at the peak, and persisting for up to 2 wk) were obtained by i.p. inoculation of infant (6.0 g) male white mice (NMRI strain) with 15 X 10(3) trypomastigotes/g body weight from 12-day-old cultures of the "Dog-82" strain of T. rangeli. This strain was cultured 15 mo at ambient temperature in LIT medium, modified by substituting defibrinated adult rabbit blood for fetal calf serum. These results underlined the importance of host age and time of culture of the parasite as factors influencing levels of parasitemia. The abrupt decline in the parasitemias may be due to an early development of a strong immunological response. Negative xenodiagnoses with Rhodnius prolixus may be due either to sterile immunity in the host mice, or to the low susceptibility of the strain of Rhodnius used. Concurrent experiments established that the T. rangeli strain was not naturally contaminated with T. cruzi.

SUMMARYThe method, site, and stage of multiplication of Trypanosoma (Herpetosoma) rangeli Tejera, 1920 has not hitherto been known. "We have now observed many intracellular nests or pseudocysts, containing amastigotes and trypomastigotes of this parasite in the heart, liver, and spleen of suckling (5.0 g) male white mice (NMRI strain) inoculated i.p. with 9 x 10 4 metatrypomastigotes/g body weight from a 12-day-old culture of the "Dog-82" strain of T. rangeli. At the peak of parasitemia (1.9 x 10 6 trypomastigotes/ml blood, 3 days post-inoculation) va rious tissues were taken for sectioning and staining. The heart was most inten sely parasitized.The amastigotes were rounded or ellipsoidal, with a rounded nucleus and the kinetoplast in the form of a straight or curved bar; the average maximum diameter of 50 measured amastigotes was 4.2 p. Binary fission was seen in the nucleus and kinetoplast of some amastigotes; no blood trypomasti gotes were seen in division. The above characteristics, as well as the location of the pseudocysts in the tissues, are similar to T. cruzi. Comparison of these re sults with those reported for other Herpetosoma suggest study of the taxonomic position of T. rangeli.

Meta-trypomastigotes of Trypanosoma rangeli Tejera, 1920, harvested from LIT medium, were inoculated i.p. or s.c. into 6, 16, and 26 g NMRI mice, these representing increasing degrees of immunological maturity. In all cases, similar pleomorphic patterns were observed. Four morphobiometrically differentiable types of trypanosome were encountered in an overlapping temporal sequence. These observations, taken in comparison with those on pleomorphism in this and other species of Trypanosoma by other workers, are consistent with the hypothesis that the pleomorphic types represent the natural development of the parasite, rather than the result of the immune response of the mammal host. Small, slender trypanosomes prevalent at the onset of the parasitemia either reinvade the tissue cells for relatively limited subsequent generations of tissue reproduction, or else differentiate toward the forms that are only capable of colonizing the insect vector.