Toxoplasma gondii was first described by Nicolle in 1909 in a North African rodent, Ctenodactylus gondii. The pathogen derives its species name from this. It is a unicellular parasite that is very widespread in nature and can infect many animal species. It is localised and replicates in practically all nucleated cells. The parasite has 3 principal forms: (1) banana-shaped trophozoites (hence the generic name “toxon” = bow) which reproduce asexually in nucleated cells, (2) intracellular dormant cysts with bradyzoites. In the cells the parasite forms cysts that are held in check by the immune system. The parasite thus remains present in the body, especially in muscle cells and in the brain, throughout the animal’s life. (3) oocysts that are the result of the parasite’s sexual cycle in the intestine of the cat. These oocysts can survive in the outside world for several months. If tissue cysts are present the parasite can become active again due to diminished activity of the immune system.

People are infected primarily via cat faeces or by eating contaminated and insufficiently cooked meat. In adults with an intact immune system Toxoplasma usually causes few problems, apart from occasional lymph node swelling and/or hepatitis. Reactivated parasites can attack the brain and retina in immunodepressed persons. Headache, neurological problems, blindness and focal cerebral lesions can occur. Such focal lesions can lead to epileptic fits. A favourable clinical response to anti-toxoplasmosis therapy is suggestive of cerebral toxoplasmosis (a good clinical response usually occurs within 2 weeks). Cerebral biopsy and PCR (Polymerase chain reaction) can be performed if there is doubt about the diagnosis. Toxoplamosis is an infection that can be prevented by prophylactic therapy. Cerebral localisations of lymphomas as well as tuberculomas can resemble cerebral toxoplasmosis.