Location: Animal Parasitic Diseases LaboratoryTitle: Population genetics, diversity and spread of virulence in Toxoplasma gondii) Author
Submitted to: Book Chapter
Publication Type: Book / Chapter
Publication Acceptance Date: 11/2/2011
Publication Date: 8/21/2012
Citation: Rosenthal, B.M., Ajioka, J.W. 2012. Population genetics, diversity and spread of virulence in Toxoplasma gondii. In: David, L.S., Howlett, B.J., Heitman, J., editors. Evolution of Virulence in Eukaryotic Microbes. Boston, MA: Wiley-Blackwell. p. 231-245. Interpretive Summary:
Technical Abstract: Globally, an estimated third of the human population harbors infection with Toxoplasma gondii, a single-celled eukaryotic parasite belonging to the phylum Apicomplexa (Dubey, 2010). Most infected persons are unaware of, and evidently unharmed by, the parasite cysts established in their muscles and/or neurological tissues. Nonetheless, this parasite has recently been ranked second in importance among all foodborne pathogens in the United States, causing over 300 deaths, 4,000 hospitalizations, and costing nearly 3 billion dollars annually in the United States alone (Batz et al., 2011) and although available evidence argues that most instances of human infection induce little if any harm, the full clinical spectrum of chronic infection remain incompletely understood (Weiss and Dubey, 2009, Henriquez et al., 2009). Infections acquired during pregnancy, and in persons with compromised cell-mediated immunity, pose marked health risks (Dubey, 2010). Concern for the health of pregnant mothers and their babies, and for the health of persons with HIV/AIDS, motivates efforts to minimize the consequences of infection with this ubiquitous parasite. These efforts have included successful establishment of in vitro and animal models of infection which have uncovered marked phenotypic differences among isolates and evolutionary lineages of T. gondii (Boothroyd, 2009, Sibley, 2009). Outbred mice, for example, survive experimental exposure to various isolates of T. gondii to very different extents, enabling fruitful research into the heritable basis of differences in ‘virulence ’ (as discussed below). Such work gains relevance in the light of epidemiological evidence that recognizably atypical parasite genotypes are responsible for outbreaks of particularly severe disease (Khan et al., 2006b).