MECHANISM OF CONGENITAL CHAGAS DISEASE: EFFECTIVE INFECTION DEPENDS ON THE INTERPLAY BETWEEN TRYPANOSOMA CRUZI AND THE DIFFERENT TISSUE COMPARTMENTS IN THE CHORIONIC VILLI OF THE HUMAN PLACENTA

Abstract

American trypanosomiasis, or Chagas disease, a zoonosis caused by Trypanosoma cruzi (T. cruzi), is endemic in Latin America and ten million people are estimated to be infected (Araújo et al 2009, World Health Organization (WHO), 2010). In the past decades, Chagas disease has been increasingly detected in other non-endemic countries such as Canada, the United States of America, Australia, Japan and in Europe. The presence of Chagas disease outside Latin America is the result of population mobility, notably migration, but also from travelers returning from Latin America and in adopted children (Schmunis, 2007). Subsequent transmission occurs through transfusion, transplantation or vertical routes. More than 10 000 deaths are estimated to occur annually from Chagas disease; its incapacitating effects and mortality are ones of the biggest public-health problems in Latin America. The 10-year mortality rate may range from 9% to 85%, depending on the extent of the cardiac damage induced by the parasite (WHO, 2010). Chagas disease manifests first with an acute phase, lasting for about 2 months, characterized by high parasitaemia. Most cases are asymptomatic or present nonspecific symptoms. Then, it turns into a chronic phase, the parasites hiding in target tissues, especially in the heart and digestive muscles (WHO, 2010) and in case of pregnancy, also in the placenta (Bittencourt, 1976). During the chronic phase, different clinical manifestations may be observed: 1) the cardiac form; 2) the digestive form, particularly enlargement of the esophagus and the colon; and 3) a mixed form (cardiac plus digestive) (Rassi, 2006).