Virulent strains of Toxoplasma gondii comprise a single clonal lineage

Abstract

The protozoan Toxoplasma gondii is a prevalent parasite in wild and domestic animals worldwide, being transmitted through the food chain by carnivorous feeding and scavenging. Toxoplasma normally divides asexually to yield a haploid form that can infect virtually any vertebrate but it also has a well defined sexual cycle that occurs exclusively in cats. Toxoplasma has become important as an often fatal opportunistic pathogen in patients with AIDS, although the 15-85% of adult human populations that are chronically infected with T. gondii are typically asymptomatic. Infections in immunocompromised hosts have variable outcomes. For example, only 30 to 50% of AIDS patients that are chronically infected with the parasite develop toxoplasmic encephalitis and only about half of acute maternal infections result in congenital disease of the newborn. T. gondii strains differ in their virulence in animals, but the extent to which different strains are related has not been determined. Here we analyse 28 strains from a variety of hosts on five continents and find that the ten virulent strains have an essentially identical genotype, whereas the nonvirulent strains are moderately polymorphic. These data strongly suggest that virulent strains of T. gondii originated from a single lineage which has remained genetically homogeneous despite being globally widespread, and despite the ability of this organism to reproduce sexually.

Toxoplasma gondii, “new” genotypes and virulence

“…Multilocus and multi-chromosome genotyping of isolates from South America, Asia and Africa with PCR-RFLP or microsatellite markers revealed that the majority of them possess type I, II or III alleles (mainly I and III), identical to those found in the three major lineages, but these have segregated differently among the loci analyzed. These isolates, presenting different mixtures of classical alleles can be considered as T he first genotyping studies on Toxoplasma gondii strains, performed on a limited number of laboratory strains and isolates mainly from France or from USA, lead to the description of a clonal population structure with three main lineages, designated as type I, II and III, related to mouse-virulence (Dardé et al, 1988(Dardé et al, , 1992Sibley & Boothroyd, 1992;Howe & Sibley, 1995). But genotypes not belonging to the three main lineages were found predominant in other continents where the population structure of Toxoplasma was more complex, with a higher genetic diversity than initially described.…”

Rhoptries: an arsenal of secreted virulence factors

“…Several recent studies have taken advantage of these tools and the highly clonal population structure of Toxoplasma [30], to map genes in the parasite that control important phenotypic differences between parasite lineages. These studies have lead to the important discovery that ROP proteins play vital roles in modulating host cell signaling and parasite virulence.…”

K24T. gondiiisolate is a hybrid and has the virulence of lineage I isolates

“…For 850, primers were: 5'-AAGGACCTGGTAACAGTCC-3' and 5'-TCAAG-GCTTGGATGTTTCG-3 '. The conditions of PCR referred to by Sibley & Boothroyd (1992), were optimised to: 40 cycles of 94° C for 1 min. 50° C for 2 min, and 72° C for 2 min.…”

“…The virulence of the strains is usually determined on the basis of lethal dose of tachyzoites (Cruz, 1989). On the basis of lethal doses and tachyzoite virulence for mice different strains of T. gondii were divided into two groups: virulent strains (LD100< 10 tachyzoites), which are able to cause acute lethal infection with ascites in mice, and avirulent strains (LD100 > 10 3 ), which cause chronic infection typical by the formation of tissue cysts in the brain of mice (Sibley & Boothroyd, 1992). Ferreira et al (2001) divided T. gondii isolates into three groups according to mortality and period of survival in mice infected with the dose of ten tachyzoites.…”

“…Pathogenicity of some strains increased after passage with parenteral inoculation in mice (Jacobs & Melton, 1954). A loss of ability to produce oocysts after the infection in cats was observed in the cases of increased pathogenicity (Frenkel el al., 1976 (Cristina et al, 1991;Cristina et al, 1995;Sibley & Boothroyd, 1992;Literâk et al 1998). …”