Chagas’ disease is a protozoan infection caused by Trypanosoma cruzi and is mainly acquired by vectorial transmission in endemic areas, when infected excreta of Triatominae bugs are inoculated into the sting site or neighbouring mucous membranes of the victim. The insect vector acquires the disease from feeding on infected animals (wild and domestic) and harbours the parasite in the gastrointestinal tract. Less common mechanisms of transmission include transfusion, congenital transmission, organ transplantation, laboratory accident, breast feeding, or oral contamination (1). Multiplication of the parasite through its amastigote form is obligatory in the intracellular milieu. It initially occurs within cutaneous macrophages, followed by rupture of the infected cells and subsequent release of trypomastigote forms in the blood stream, and then invasion of remote sites (2) Parasite multiplication may occur in every tissue, but neat predilection is observed towards the myocardium, skeletal and smooth muscle, and the nervous system. When transmitted by the insect vector, skin swelling produces the typical entry lesions known as chagomas (3).