‘Virulence’ of Toxoplasma gondii in humans

Abstract number: 1133_6

Dardé M.-L., the CRB ToxoBS group 

The majority of Toxoplasma gondii strains have been grouped into 3 main genotypes, called type I, II, and III. Recently, multilocus studies revealed the existence of atypical and recombinant genotypes. The relationship between isolate genotype and virulence is well described in the mouse model, but is more difficult to approach in humans due to the opportunistic behaviour of this parasite. For instance, in France, where the isolates are systematically collected and typed (Biological Resource Centre, ToxoBS group), the vast majority of congenital toxoplasmoses are due to type II, whatever the clinical outcome (foetal death, neurological involvement, chorioretinitis, or subclinical toxoplasmosis), the main prognosis factor remaining the stage of pregnancy at the time of infection. Whether this predominance of type II in congenital toxoplasmosis is due to its predominance in humans and animals in France or to a higher tendency to cross the placental barrier remains to be determined. The very few type I or atypical strains isolated from congenital toxoplasmosis are found in severe disease, notably disseminated toxoplasmosis, suggesting a role for the strain genotype in the pathogenesis of these forms. In immunocompetent patients, the ‘serotyping’ method has never been applied to large series of asymptomatic patients, so the strains responsible for about 80% of toxoplasmic infections in humans are still unknown. The classical lymphadenopathies seem to be due to type II strains, but more severe acquired toxoplasmosis or ocular toxoplasmosis are associated with atypical or type I strains. In immunodeficient patients, the 3 main types, principally type II, but also atypical or recombinant strains, were detected. These studies were performed mainly in some European countries and U.S.A. and the situation might well be different in other continents as suggested by the higher genetic diversity – and pathogenicity – of isolates in French Guiana or Brazil, or by the frequency of recombinant genotypes detected in African patients. Physiopathological and immunological aspects of the behaviour of the different Toxoplasma genotypes in humans are totally ignored. All our hypothesis (widespread parasite dissemination in organs for type I strains, cyst formation and reactivation with type II strains) are derived from mouse experimental toxoplasmosis and studies are needed to better understand the influence of strain genotype on human toxoplasmosis.