The protozoan parasite Toxoplasma gondii is capable of infecting all warm blooded animals; however, the consequences of infection are very variable between different species of animal. Marsupials and New World monkeys, which have evolved largely separately from the cat, the definitive host of the parasite, are among the most vulnerable species where infection with T. gondii can prove fatal. In more resistant species such as humans and sheep, infection is generally unapparent, provoking only mild symptoms; thereafter the host remains infected for life. However, when the immune system is compromised, such as in the immunologically immature fetus, infection with the parasite can have very serious consequences. Much of the work examining host immune responses has been done using experimentally infected mice. While there are many advantages in using this experimental model, care should be taken in extrapolating results from mice to other species. Mice are extremely vulnerable to the consequences of infection with T. gondii., and their use to further our understanding of congenital toxoplasmosis may not be ideal, as fetal infection can occur in successive pregnancies. This is not the case in rats or sheep; they are more resistant to the disease and therefore may provide a more relevant model for human congenital toxoplasmosis. Studies of host immune responses have emphasised the importance of the cytokine interferon gamma (IFN gamma) in resistance to T. gondii. The efficiency of induction of this cytokine may be critical for determining the outcome of the host-parasite relationship.