American Trypanosomiasis (Chagas Disease)

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Chapter: Pharmaceutical Microbiology : Protozoa

Chagas disease begins as a localized infection that is followed by parasitaemia and colonization of internal organs and tissues. Infection may first be evidenced by a small tumour (chagoma) on the skin.


AMERICAN TRYPANOSOMIASIS (CHAGAS DISEASE)

 

Chagas disease begins as a localized infection that is followed by parasitaemia and colonization of internal organs and tissues. Infection may first be evidenced by a small tumour (chagoma) on the skin. Symptoms of the disease include fever, oedema and myocarditis (infection of the heart muscle) with or without heart enlargement, and meningoencephalitis in children. The acute disease is frequently subclinical and patients may become asymptomatic carriers; this chronic phase may result, after 10–20 years, in cardiopathy. Chagas disease is transmitted by several genera of triatomine bugs (Triatoma, Rhodnius and Panstrongylus) and in nature the disease exists among wild mammals and their associated triatomines. Human trypanosomiasis is seen in almost all countries of the Americas, including the southern USA, but the main foci are in poor rural areas of Latin America.

 


 

 

T. cruzi exhibits two cell types in vertebrate hosts, a blood form termed a trypomastigote, and in the tissues (mainly heart, skeletal and smooth muscle, and reticuloendothelial cells) the parasite occurs as an amastigote (Figure 6.3). Trypomastigotes ingested when the insect takes a blood meal from an infected host transform into epimastigotes in the intestine. Active reproduction occurs and in 8–10 days metacyclic trypomastigote forms appear which are flushed out of the gut with the faeces of the insect. These organisms are able to penetrate the vertebrate host only through the mucosa or abrasions of the skin; hence, transmission does not necessarily occur at every blood meal. Within the vertebrate the trypomastigotes transform into amastigotes, which, after a period of intracellular multiplication at the portal of entry, are released into the blood as trypanosomes; these invade other cells or tissues, becoming amastigotes again.


 

The pathology of the infection is associated with inflammatory reactions in infected tissues. These can lead to destruction of the infected tissue and if it involves heart tissue this can cause acute myocarditis. Parasite enzymes may also cause cell and tissue damage. In the absence of parasites, an autoimmune pathological process seems to be mediated by T lymphocytes (CD4+) and by the production of certain cytokines:

these induce a polyclonal activation of Blymphocytes and the secretion of large quantities of autoantibodies.

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