Trypanosoma cruzi — the causative agent of Chagas' disease — is a protozoan parasite that has life cycle stages in both mammalian and insect hosts. Different genetic forms of T. cruzi are known, but it has been thought that its propagation has been primarily clonal, without gene exchange between clones of different genotypes. In the February 27 Nature, Michael Miles and colleagues at the London School of Hygiene and Tropical Medicine, demonstrate that T. cruzi do exchange genes, and that the mechanisms of exchange are multiple and unusual (Nature, 421:936-939, February 27, 2003).

Miles et al. isolated two T. cruzi clones from the Amazon basin, transfected each with a different antibiotic resistance gene, and passaged the parasites together through a complete life cycle. When they were re-isolated from mammalian cells, multiple lines of offspring showed double antibiotic resistance, indicating gene exchange had occurred. But the antibiotic resistance genes were not the only genes exchanged: various offspring showed gene loss, gene fusion, recombination, and gene amplification, as well as exchange and loss of mitochondrial genotypes. Phylogenetic analysis of natural populations indicated "unequivocal evidence of genetic recombination" in these organisms as well.

The authors note that recovery of hybrids from mammalian cells may indicate that exchange takes place there. Infection with T. cruzi in vertebrates is often life-long, meaning hybrids may be subject to repeated and prolonged selective pressure within the vertebrate host. The genetic exchange mechanisms found in this single-celled organism "may also operate in phylogenetic groups close to the origins of eukaryotes," they conclude.