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Routes of maternal—fetal transmission of Trypanosoma cruzi

Possible transmission routes of Trypanosoma cruzi parasites

A possible mode of maternal—fetal transmission might be through parasites released into amniotic fluid (AF) (Fig. 23.1; see section: Histopathologic studies of placentas from infected or uninfected neonates).21,22 The latter might contaminate the fetuses by oral or pulmonary routes, or eventually by skin penetration (fetuses are bathing in AF and continuously absorbing it). Lung and skin infections with T. cruzi have been reported in macerated fetuses and stillborns.23,24 However, AF contains potent antimicrobial peptides25 and T. cruzi parasites are not found by microscopic observation and parasitic DNA is hardly detected in AF or aspirated gastric fluid content of infected asymptomatic newborns.26,27

Possible routes of maternal—fetal transmission of T

Figure 23.1 Possible routes of maternal—fetal transmission of T. cruzi. aIn case of huge parasite amounts in the placental intervillous space; bin case of moderate parasite amounts in the placental intervillous space.

Source: According to Carlier Y, Truyens C. Maternal-fetal transmission of Trypanosoma cruzi. In: Telleria J, Tibayrenc M, editors. American trypanosomiasis-Chagas disease. One hundred years of research. London, Burlington: Elsevier; 2010. p. 539—81.

The possibility of placental/fetal invasion directly from the uterine wall (transuterine route) remains to be determined, since T. cruzi amastigote nests are observed in placental deciduas of mothers having delivered infected neonates28 (Fig. 23.1).

Although outside of the scope of this chapter, it is interesting to mention the possible postnatal transmission of parasites through maternal milk by breast feeding. Only one report mentions a possible infant contamination during lactation.29 Another one indicates the presence of parasites in milk during maternal infection,30 but their detection might have been related to a contamination of collected milk with maternal blood.31 Others studies do not observe parasites in milk of infected women.32-34 Moreover, blood trypomastigotes, by contrast with metacyclic trypo- mastigotes expressing Tcgp82, can hardly adhere and migrate through the gastric mucin layer and survive into the gastric milieu.35,36

Whether fetal contamination with parasites coming from AF or uterine wall, and/or eventually by breast feeding remains a possibility in acute or reactivated infection,37 these routes are unlikely in chronic infection.

Placenta is therefore the key fetal organ facing the parasites present into the intervillous blood space and from which transmission depends. Such a route requires parasites to cross or skirt the trophoblastic barrier (first placental line of defense) (Fig. 23.1).

 
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