Molecular diagnosis and typing of Trypanosoma cruzi populations and lineages in cerebral Chagas disease in a patient with AIDS

JM BURGOS, S BEGHER, JM FREITAS, M BISIO, T DUFFY, J ALTCHEH, R TEIJEIRO, H LOPEZ ALCOBA, F DECCARLINI, H FREILIJ, MJ LEVIN, J LEVALLE, AM MACEDO, AG SCHIJMAN

AMERICAN JOURNAL OF TROPICAL MEDICINE AND HYGIENE

AMER SOC TROP MED & HYGIENE

Año: 2005 p. 1016 - 1018

0002-9637

Trypanosoma cruzi DNA was amplified from an intracranial biopsy and peripheral blood of an HIV patient with encephalitis; this episode was indicative of AIDS and congenital Chagas disease. The analysis of a microsatellite locus revealed a multiclonal parasite population at the brain lesion with a more complex minicircle signature than that profiled in blood using restriction fragment length polymorphism (RFLP)-PCR and low stringency single primer (LSSP) PCR. Interestingly, different sublineages of T. cruzi II were detected in blood and brain by means of spliced-leader and 24s alpha ribosomal-DNA amplifications. Quantitative-competitive PCR monitored the decrease of parasitic load during treatment and secondary prophylaxis with benznidazole. The synergy between parasiticidal plus antiretroviral treatments probably allowed the patient a longer survival than usually achieved in similar episodes. This is the first case report demonstrating a differential distribution of natural parasite populations and sublineages in Chagas disease reactivation, showing the proliferation of cerebral variants not detectable in peripheral blood.DNA was amplified from an intracranial biopsy and peripheral blood of an HIV patient with encephalitis; this episode was indicative of AIDS and congenital Chagas disease. The analysis of a microsatellite locus revealed a multiclonal parasite population at the brain lesion with a more complex minicircle signature than that profiled in blood using restriction fragment length polymorphism (RFLP)-PCR and low stringency single primer (LSSP) PCR. Interestingly, different sublineages of T. cruzi II were detected in blood and brain by means of spliced-leader and 24s alpha ribosomal-DNA amplifications. Quantitative-competitive PCR monitored the decrease of parasitic load during treatment and secondary prophylaxis with benznidazole. The synergy between parasiticidal plus antiretroviral treatments probably allowed the patient a longer survival than usually achieved in similar episodes. This is the first case report demonstrating a differential distribution of natural parasite populations and sublineages in Chagas disease reactivation, showing the proliferation of cerebral variants not detectable in peripheral blood.