Chagas' disease.

Diagnosis of Parasitic Diseases: Old and New Approaches

“…For many years, microscopy has been the only tool available for the detection of parasites through inspection of blood smears [10][11][12][13][14], tissue specimens [15][16][17], feces, lymph node aspirates [18,19], bone marrow [20], and even cerebrospinal fluid [21]. However, sample preparation for direct observation is time-consuming, labour intensive, and proper diagnosis depends on qualified laboratory technicians.…”

Genetic epidemiology of trypanosoma cruzi infection and Chagas disease

“…The most commonly used method to assess the cardiac lesions associated with Chagas' disease is electrocardiography (39). The cardiac form of Chagas' disease is evidenced in electrocardiograms by conduction abnormalities including bradyarrhythmias, premature ventricular contractions, and bundle-branch block, particularly right bundle-branch block (13,14,40). The rarer digestive form is characterized by development of megacolon and/or megaesophagus with symptoms that may include abdominal pain, chronic constipation with the maximum number of days between bowel movements being 10 (71% of cases of megacolon) to 30 or more (14% of cases of megacolon), difficulty swallowing, gastroesophageal reflux, and chest pain not related to cardiac disease (13,(41)(42).…”

“…The parasite is transmitted to humans by reduviid bugs (genera Triatoma, Rhodnius, and Panstrongylus) when feces deposited after a blood meal come in direct contact with mucosa, conjunctiva, or open wounds in the host (12)(13). Active vector control programs have been implemented throughout Latin America, but despite these efforts the disease remains the leading cause of heart disease in that area of the world (11,14). While transmission of new infections has been reduced, an estimated 16-18 million individuals are currently infected and over a hundred million are considered at risk for infection (15)(16)(17).…”

Avaliação da participação da galectina-1 na evolução da infecção experimental aguda por Trypanosoma cruzi

“…A miocardite aguda é um processo inflamatório no tecido cardíaco que é parte essencial da resposta protetora do hospedeiro contra a infecção (BRENER & GAZZINELLI, 1997 , 1972;ANDRADE, 1985;TANOWITZ et al, 1992); e a forma digestiva é caracterizada por apresentar um aumento de no tamanho do esôfago (megaesôfago) e/ou cólon (megacólon) (EARLAM, 1972;ADAD et al, 1991). É certo, porém, que a reação inflamatória depende de linfócitos T sensibilizados, tendo em vista que em camundongos atímicos infectados por T. cruzi não há resposta inflamatória no miocárdio, a despeito de um intenso parasitismo tecidual (GONÇALVES- DA-COSTA et al, 1984).…”

“…Baseado nestas observações sugere-se que a miocardite na fase aguda seja totalmente dependente de linfócitos T sensibilizados contra antígenos de T. cruzi (RIBEIRO-DOS-SANTOS et al, 1985). O processo inflamatório gerado após a infecção por T. cruzi, ou miocardite, é caracterizado por um infiltrado de células mononucleares, destruição das fibras miocárdicas e acúmulo de fibras de colágeno ao redor dos miócitos (ANDRADE, 1985;TANOWITZ et al, 1992;TALVANI et al, 2000;ROSSI, 1991). Esse infiltrado mononuclear crônico é constituído principalmente de linfócitos T (95%), predominantemente células T CD8 + , e poucos macrófagos (HIGUCHI et al, 1993;DOS SANTOS et al, 2001).…”