Introduction

Toxoplasma gondii is an obligate intracellular protozoon that was discovered in the gondi in 1908. In the1930s and 1940s toxoplasma was discovered to cause congenital disease in neonates (Sabin 1941) and severe disseminated disease in adults (Pinkerton & Henderson 1941). Subsequently toxoplasma was found to cause transient, nonsuppurative lymphadenopathy, usually in the head and neck regions, in immunocompetent patients (Remington et al. 1995). In the 1970s toxoplasma became appreciated as a cause of disease in iatrogenically immunosuppressed patients, primarily solid-organ transplant recipients. In the 1980s toxoplasma attained notoriety as the most common cause of encephalitis/brain abscess in acquired immunodeficiency syndrome (AIDS) patients.

Toxoplasma includes varied strains of differing virulence. Different animal species differ markedly in their resistance to toxoplasma infection, e.g. rats are highly resistant but mice are very susceptible, and some inbred strains of mice are more susceptible than others (Suzuki et al. 1989b). Cell-mediated immunity, activated macrophages, antibody and cytokines participate in host defence against toxoplasma, most frequently and extensively studied in murine models. Both CD8+ lymphocytes and CD4+ lymphocytes appear important for murine defence (Gazzinelli et al. 1991; Nagasawa et al. 1991; Subauste et al. 1991). CD8+ cells are cytotoxic for toxoplasma-infected cells and secrete interferon gamma. CD4+ cells are needed to effect drug cures in experimentally infected mice (Araujo 1992). Of the cytokines, interferon gamma has been studied most extensively.