Trypanosoma (Herpetosoma) rangeli Tejera, 1920: intracellular amastigote stages of reproduction in white mice

The 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) various tissues were taken for sectioning and staining. The heart was most intensely 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 trypomastigotes 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 results with those reported for other Herpetosoma suggest study of the taxonomic position of T. rangeli

Geographical Distribution of Trypanosoma cruzi Genotypes in Venezuela

Chagas disease is an endemic zoonosis native to the Americas and is caused by the kinetoplastid protozoan parasite Trypanosoma cruzi. The parasite is also highly genetically diverse, with six discrete typing units (DTUs) reported TcI – TcVI. These DTUs broadly correlate with several epidemiogical, ecological and pathological features of Chagas disease. In this manuscript we report the most comprehensive evaluation to date of the genetic diversity of T. cruzi in Venezuela. The dataset includes 778 samples collected and genotyped over the last twelve years from multiple hosts and vectors, including nine wild and domestic mammalian host species, and seven species of triatomine bug, as well as from human sources. Most isolates (732) can be assigned to the TcI clade (94.1%); 24 to the TcIV group (3.1%) and 22 to TcIII (2.8%). Importantly, among the 95 isolates genotyped from human disease cases, 79% belonged to TcI - a DTU common in the Americas, however, 21% belonged to TcIV- a little known genotype previously thought to be rare in humans. Furthermore, were able to assign multiple oral Chagas diseases cases to TcI in the area around the capital, Caracas. We discuss our findings in the context of T. cruzi DTU distributions elsewhere in the Americas, and evaluate the impact they have on the future of Chagas disease control in Venezuela

Attenuation of virulence by culture in tissues

Trypomastigotes of the ’Brazil’ strain of Trypanosoma cruzi were cultured in Vero and fish (Pimephales promelas) cells at 30 and 37 C. Those harvested from 37 C Vero cell cultures killed all inoculated C3H mice no matter how long the cultures had been maintained. Those harvested from 120-day 30 C Vero and fish cultures killed only 1 out of 10 mice each, indicating attenuation of virulence. When the surviving mice were later challenged with Vero-cultured trypomastigotes known to be lethal to controls, only 2 of the 18 animals developed even light parasitaemias, indicating previous immunization by the attenuated parasites. Varying the number of attenuated trypomastigotes cultured at 30 C for 30 days at most delayed the rise of parasitaemia. Possible mechanisms of these phenomena are discussed

Trypanosoma cruzi in the anal glands of urban opossums: I- isolation and experimental infections

Opossums (Didelphis marsupialis) captured in intensely urbanized areas of the city of Caracas, Venezuela, were found infected with Trypanosoma cruzi. The developmental cycle of trypomastigote-epimastigote-metacyclic infective trypomastigote, usually occurring in the intestine of the triatomine vector, was taking place in the anal odoriferous glands of the opossums. Material from the glands, inoculated in young, healthy opossums and white mice by different routes, subcutaneously, intraperitoneally, orally, and into the eye, induced T. cruzi infections in all animals. Parasitemia, invasion of cardiac and skeletal muscle, and intracellular multiplication of amastigotes were observed. Inoculation of metacyclics from anal glands, cultured in LIT medium, gave equivalent results. All opossums survived; all mice died. Excreta of opossums may thus transmit Chagas' disease by contamination, even in urban areas where insect vectors are not present

Biological properties of Metatrypomastigotes of Trypanozoma cruzi from the anal glands of urban Didelphis marsupialis

Metacyclic trypomastigotes of Trypanosoma cruzi from the anal glands of naturally infected urban Didelphis and cultures derived from these were inoculated i.p., orally, and into the eyes of juvenile opossums. The marsupialis parasite could develop ill blood, tissues, and anal glands. The blood forms of these infections colonized Rhodrtius (Hemiptera, Reduviidae, Triatominae) employed for xenodiagnosis. NMRI mice were infected by the same routes by 6 metacyclics from the same sources. All mice died with parasitemias up to 10 6/ml blood, while all opossums survived 3 with parasitemias no higher than 103 /ml. Opossums showed limited cardio - and myotropism. While mice were extensively parasitized, in addition, in the smooth muscle of the intestines and lung, and in the liver. The continuing presence of in the anal glands close to the excretory orifices would suggest transmission of the disease by T. cruzi contamination