Toxoplasmosis
Written 15th August 2020 - Last Update 30th August 2026
Toxoplasmosis
Toxoplasma gondii — acquired from cat faeces (kitty litter/garden soil/contaminated water) and from undercooked or raw meat. Cats are the only definitive host; the parasite is endemic in Australia, not an imported infection. Most infections in immunocompetent people are asymptomatic or a mild, self-limited illness — fever, tender cervical lymphadenopathy, malaise — and the prognosis is excellent with no long-term effects. A high index of suspicion is needed, as the disease is under-recognised and under-reported.
Two groups matter clinically:
- Pregnancy — one of the TORCH infections; congenital toxoplasmosis causes serious eye (chorioretinitis → blindness) and brain damage. Advise pregnant women to avoid cat litter/soil and undercooked meat. (Can also be transmitted in breast milk.) See the womens-health TORCH page.
- Immunocompromise — reactivation of latent infection causes disease, most often toxoplasmic encephalitis (ring-enhancing brain lesions). Risk is driven by the degree of immunosuppression, not exposure history.
When to suspect it, and which test
- Take a full exposure history (cat faeces, undercooked meat, gardening/soil) but don’t let a negative one exclude the diagnosis — the parasite is also acquired from contaminated food/water without cat contact.
- Consider toxoplasmosis in anyone with fever and cervical lymphadenopathy, and in any immunosuppressed patient with new CNS signs, seizures, or visual change.
- Serology (IgM and IgG) is the primary test in immunocompetent patients — IgM appears from around day 5, IgG from 1–2 weeks. Serology is unreliable in immunosuppressed patients, who may not mount an antibody response.
- PCR (blood or other body fluid) is used in immunosuppressed patients with suspected CNS, pulmonary, or disseminated disease.
- CT/MRI brain in suspected cerebral toxoplasmosis typically shows multiple ring-enhancing lesions in the cortex, periventricular areas, basal ganglia, and thalami; MRI is preferred over CT.
- In HIV, reactivation risk rises sharply once CD4 <100 cells/µL, and can be as high as 30% in seropositive patients not on prophylaxis.
Referral
Refer immunocompetent patients with organ involvement (e.g. chorioretinitis) to the relevant specialist (ophthalmology). Immunosuppressed patients with suspected reactivation need infectious diseases input for diagnosis, treatment, and prophylaxis decisions.
Treatment (toxoplasma encephalitis — eTG)
Pyrimethamine (200 mg first dose, then 50 mg daily — 75 mg if >60 kg) + calcium folinate 15 mg daily, for 6 weeks, PLUS either:
- sulfadiazine 1–1.5 g 6-hourly, or
- clindamycin 600 mg 6-hourly.
Alternatively, co-trimoxazole (trimethoprim+sulfamethoxazole) as a single agent. Follow with maintenance/secondary prophylaxis (sulfadiazine + pyrimethamine + folinate; clindamycin replaces sulfadiazine if sulfa-allergic) until immune reconstitution. In HIV, primary prophylaxis (co-trimoxazole) is indicated once CD4 <100 cells/µL.