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(American Journal of Pathology. 2000;156:1805-1809.)
© 2000 American Society for Investigative Pathology


Regular Articles

Genetic Characterization of Trypanosoma cruzi Directly from Tissues of Patients with Chronic Chagas Disease

Differential Distribution of Genetic Types into Diverse Organs

Annamaria R. Vago*, Luciana O. Andrade{dagger}, Adriana A. Leite{dagger}, Débora d’Ávila Reis*, Andrea M. Macedo{dagger}, Sheila J. Adad§, Sebastião Tostes, Jr.§, Maria da Consolação V. Moreira{ddagger}, Geraldo Brasileiro Filho{ddagger} and Sérgio D. J. Pena{dagger}

From the Departamento de Morfologia*
and Departamento de Bioquímica e Imunologia,{dagger}
Instituto de Ciências Biológicas, Belo Horizonte; the Faculdade de Medicina,{ddagger}
Universidade Federal de Minas Gerais, Belo Horizonte, Minas Gerais; and the Faculdade de Medicina do Triângulo Mineiro,§
Uberaba, Minas Gerais, Brazil

We have previously shown that a low-stringency single-specific primer–polymerase chain reaction (LSSP- PCR) is a highly sensitive and reproducible technique for the genetic profiling of Trypanosoma cruzi parasites directly in tissues from infected animals and humans. By applying LSSP-PCR to the study of the variable region of kinetoplast minicircle from T. cruzi, the intraspecific polymorphism of the kinetoplast-deoxyribonucleic acid (kDNA) sequence can be translated into individual kDNA signatures. In the present article, we report on our success using the LSSP-PCR technique in profiling the T. cruzi parasites present in the hearts of 13 patients with chagasic cardiopathy and in the esophagi of four patients (three of them with chagasic megaesophagus). In two patients, one with the cardiodigestive clinical form of Chagas disease and the other with cardiopathy and an esophageal inflammatory process, we could study both heart and esophagus and we detected distinct kDNA signatures in the two organs. This provides evidence of a differential tissue distribution of genetically diverse T. cruzi populations in chronic Chagas disease, suggesting that the genetic variability of the parasite is one of the determining factors of the clinical form of the disease.





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