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a zoonosis, which afflicts a variety of small mammals. The parasite is transmitted among its hosts by hematophagus reduvild bugs. Human disease occurs, when the bugs establish a habitat in human dwellings (191). Currently, there are 18-20 million people infected and another 40 million people are at risk of acquiring the disease (192). T. cruzi differs from other trypanosomes in that it has an intracellular amastigote stage in cardiac muscle and other tissues as well as trypomastigote forms in the circulating blood (193). The trypomastigotes are approx. 20 Âľm in length. The nucleus is generally centrally positioned and the large oval kinetoplast is located posteriorly. In stained blood films they characteristically assume a C or U shape. The infective stage of T. cruzi is the metacyclic trypomastigote. It is 15 Âľm in length and possesses a single nucleus and flagellum. The disease is transmitted by reduvild bugs of Rhidnius spp. or Triatoma spp. etc. (194). Infection occurs shortly after an infected bug bites an individual. Its feces contain the infective trypomastigotes. The host experiences a mild itching sensation and rubs the trypomastigotes into the bite wound. Trypomastigotes enter a wide variety of cells and transform into amastigotes. The amastigote is 3-5 Âľm in diameter and does not possess an external flagellum. The host becomes hypersensitive to the parasite as the result of the cellular destruction at the site of initial infection. Some amastigotes transform into trypomastigotes and after being released into the peripheral blood, they infect other sites in the body. The bug becomes infected, when it takes a blood meal from an individual harbouring trypomastigotes. Trypomastigotes transform into epimastigotes within the midgut of the bug. Epimastigotes differentiate into metacyclic trypomastigotes within the hindgut. This is the infective stage of the parasite (195). The entry of T. cruzi into human body is accompanied by inflammation at the point of entry. If this occurs in the eye there may be conjunctivitis, unilateral palpebral oedema and satellite adenopathy. Manifestations of generalised infection occur with fever, tachycardia, lymphadenopathy and oedema. The acute congenital phase may be symptomless or may be associated with jaundice, skin haemorrhages and neurological signs. After 2-4 months the acute clinical manifestation disappears and the disease enters the chronic phase, generally starting with a long period of clinical latency, which lasts 10-30 years or throughout life. After this period many infected patients present manifestations related to the involvement of certain organs such as heart, oesophagus, colon and nervous system. Heart involvement is the major aspect of chagas disease because of its characteristics, frequency and consequences, and is also the source of most controversies. About 20-30 % of the total chagasic population in endemic areas has symptomless heart disease and these patients may live for many years. Heart disease worsens in some of them, with increasing arrythmias or heart failure (196). The drugs used for the treatment of American trypanosomiasis are nifurtimox and benznidazole (197).