Strain differentiation and population biology

Restriction fragment length polymorphism (RFLP) provides a method for identifying genomic DNA differences between parasites of different isolates or between or among organisms of phylogenic proximity, and has also been applied to T. gondii (Cristina et al. 1991a,b; Sibley and Bootroyd 1992b) Using RFLP on polymerase chain reaction-amplified specific single copy genes obtained from different RH lines showed unique patterns, except in three isolates cloned from the same line (Howe and Sibley 1994).

Sequencing of the sag1 gene after amplification has shown that mouse-virulent and -avirulent isolates can be destinguished by mutations in the 3 region (Rinder et al. 1995) Strain differences between different isolates of T. gondii have been established by isoenzyme electrophoresis (Barnert et al. 1988; Dardé et al. 1988) and by immunological methods (Ware and Kasper 1987), and the relationship between isoenzyme pattern (zymodemes) and pathogenicity (virulence) has been described (Dardé et al. 1988, 1992). Furthermore, differences in chromosome size between different isolates have been demonstrated by pulse-field gel electrophoresis (Candolfi et al. 1989).

Strain-specific differences between different isolates of T. gondii have been demonstrated by immunoblot, immune-precipitation with antisera, isoenzyme analysis, and DNA typing techniques (Ware and Kasper 1987; Barnert et al. 1988; Weiss et al. 1988; Bülow and Boothroyd 1991). Polymorphism seems to be limited and for the few single loci examined in detail, only two alleles have been identified (Boothroyd and Sibley 1993). Virulent stains can now be differentiated from avirulent strains by their reactivity with certain monoclonal antibodies (Gross et al. 1991; Bohne et al. 1993), and random amplified polymorphic DNA (RAPD) polymerase chain reaction can distinguish between mouse-virulent and -avirulent strains (Guo et al. 1997).

Recent evidence suggests that the host may harbour different strains of T. gondii, and it has been hypothesized that only those hosts harbouring strains with the ability to induce Toxoplasma encepalitis are able to develop this manifestation during immunosuppression (Araujo et al. 1997).

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