Home Economics American Trypanosomiasis Chagas Disease, Second Edition: One Hundred Years of Research
Vertical transmission of Trypanosoma cruzi in other mammals
Vertical transmission in the natural mammal reservoir of Trypanosoma cruzi
The vertical transmission in mammals involved in the sylvatic cycle of T. cruzi (see Chapter 11, Ecological aspects of Trypanosoma cruzi: wild hosts and reservoirs) has to be considered as a possible complementary mode, beside vector transmission, of maintaining the parasite reservoir. It does not seem involved in the natural infection of the opossum Didelphis marsupialis in endemic areas.137 Vertical transmission has been observed in some eutherian mammals naturally infected, as dogs, bats,138-140 and nonhuman primates living in wild conditions or primate centers.141,142 There is no evidence that chronic maternal T. cruzi infection causes fetal loss in nonhuman primates.143 However, the importance of this vertical mode in the transmission of T. cruzi has not been evaluated on a large scale.
Vertical transmission in experimental infection with Trypanosoma cruzi
Guinea pigs were historically the first mammals to be studied for such transmis- sion,144,145 and one study documents vertical transmission of T. cruzi in dogs.146
Experiments in mice show acute infection inducing high rates of fetal resorptions and/or pup mortality, in relation to high blood parasite- and TNF-a-levels.147-150 Indeed, no or rare maternal—fetal transmissions are observed regardless of the time the parasites were inoculated, before or during gestation of mice and rats.109,147,149,151-160 However, transmission can occur when a blockade of
placental phagocytic activity or placental lesions are induced.161’162 Two works (by the same team) found transmission being associated with the virulent RA (TcVI)- and not with the CA1 or K98 (TcI)-T. cruzi strains.149’159 Other studies reported high percentages of positive PCR (see section: Detection of neonatal infection (0—4 weeks after birth)) in offspring of mice chronically infected with TcI, TcIV’ or TcV’ but congenital infection (with live parasites) was not demonstrated in such pups.163’164 A recent work of our team110 studied congenital transmission from mouse dams acutely or chronically infected with the T. cruzi strains X10 (TcI), Y (TcII), and Tulahuen (TcVI). It showed that congenital infection (detected by blood microscopic examination in offspring submitted to cyclophosphamide- induced immunosuppression in order to activate possible cryptic infection) occurred in approximately 4% of living pups born to dams acutely infected with Y or Tulahuen strains’ but not with X10 strain and not in those born to chronically infected animals. Interestingly’ this study also shows that (1) parasitemias in transmitting dams are higher than in nontransmitting animals (see section: Parasitic load during pregnancy and transmission of congenital infection); (2) re-inoculation of parasites during gestation in chronically infected mice’ strongly increases pup mortality (see section: Other fetal/neonatal factors susceptible to interfere with the development of congenital Chagas disease); and (3) PCR detection of parasitic DNA is unrelated to congenital infection (see section: Detection of neonatal infection (0—4 weeks after birth)). Parasites were not found in rat AF160 and postnatal transmission by murine milk was not observed37’160’165 (see section: Possible transmission routes of Trypanosoma cruzi parasites). Interestingly’ a study showed that the administration of the trypanocidal drug benznidazole to pregnant rats is able to cross the placenta and reach the fetus.166
So’ despite experimental data confirming some bioclinical observations’ mice and rats display lower yield of maternal—fetal parasite transmission than humans and do not bring relevant information on the T. cruzi-DTU-congenital infection relationship. Although they have hemochorial placentas like humans’ their layer architecture (labyrinthine interdigitation into the murine decidua vs. the villous structure of human placenta; see section: The hematogenous transplacental route: strengths and weaknesses of the trophoblastic barrier) and/or their maternal—fetal blood flow interrelations are different’ in addition to their shorter duration of gesta- tion.38 This makes it difficult to extrapolate data obtained from these animals to the maternal—fetal transmission occurring in human and should encourage further studies in nonhuman higher primates.
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