Natural resistance and host specificity

Toxoplasma gondii strains may vary in their pathogenicity in a given host. Certain strains of mice are more susceptible than others (Suzuki et al. 1993; McLeod et al. 1984), and appear to be regulated, at least in part, by H-2- and H-13-linked genes ( Jones and Erb 1985). However, more recently, genes of the H-2 and D/L locus have been implicated in the regulation of the development of brain cysts and T. gondii encephalitis (Brown and McLeod 1990; Suzuki et al. 1991). At least five genes are involved in the regulation of T. gondii infection in mice (McLeod et al. 1989; Blackwell et al. 1993). In mice T. gondii can be transferred during pregnancy from the mother to the litter (Beverley 1959); Toxoplasma gondii infection in rhesus monkeys has been described as a model for congenital toxoplasmosis

(Schoondermark et al. 1993).

Most mammals and birds can be infected with T. gondii. The natural resistance to infection varies between species. In general, mice are more susceptible than rats are (Jacobs 1956). The severity of infection in individual mice within the same strain may vary (Suzuki et al. 1989), and certain host species are genetically resistant to clinical toxoplasmosis.

For example, adult rats do not become ill while young rats can die because of toxoplasmosis. Mice of any age are susceptible to clinical T. gondii infection. Adult dogs are resistant whereas puppies are fully susceptible. Cattle and horses are amongst the most-resistant intermediate hosts for clinical toxoplasmosis, in contrast to certain marsupials and new-world monkeys, which are the most susceptible to infection (Dubey and Beattie 1988).

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