Curative Benznidazole treatment in the acute stage of Trypanosoma cruzi infection prevents the development of chronic cardiac fibrosis

Tue10  Apr05:30pm(15 mins)
Stream 1 - Edward Llwyd 0.26 Biology Main


A F Francisco1; S Jayawardhana1; M C Taylor1; M Lewis1; J M Kelly1
1 Department of Pathogen Molecular Biology, London School of Hygiene and Tropical Medicine, Keppel Street, London, WC1E 7HT., UK


The insect-transmitted protozoan parasite Trypanosoma cruzi is the causative agent of Chagas disease (CD), and infects 5-8 million people in Latin America. CD is characterised by an acute phase, which is partially resolved by the immune system, but then develops as a chronic infection. Approximately 30% of those infected with T. cruzi develop chronic stage pathology, but this can take decades to become symptomatic. Because of this, and with difficulties in demonstrating parasitological cure, it has been difficult to assess the extent to which anti-parasitic therapy can prevent the development of pathology. We sought to address this question using highly sensitive bioluminescent imaging methodology and murine models BALB/c and C3H/HeN infected with CL Brener and JR strain, respectively. We monitored heart inflammation and fibrosis, two widely markers of cardiac pathology. This in vivo imaging procedure has a limit of detection of 100-1000 parasites, and facilitates the real-time tracking of parasite burden in individual mice during chronic infections. These experiments demonstrated that curative benznidazole treatment early in murine T. cruzi infections prevents the development of cardiac fibrosis. Treatment during the chronic stage can also block pathology, but the effectiveness of this varies between infection models. If these findings are extendable to humans, it will imply that widespread chemotherapeutic intervention targeted at early stage infections could play a crucial role in reducing CD morbidity at a population level.   

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