What is toxoplasmosis?

Toxoplasmosis is an infection caused by Toxoplasma gondii — an intracellular protozoan parasite that infects approximately one-third of the global human population. In immunocompetent adults, primary infection is usually asymptomatic (occasionally causes cervical lymphadenopathy resembling glandular fever); the parasite then forms latent cysts in the brain and muscle that persist for life. Disease is severe in two groups: the developing fetus (congenital toxoplasmosis) and immunocompromised individuals (toxoplasmic encephalitis).

How do humans get toxoplasmosis?

Three main routes: (1) Cat contact: domestic cats shed Toxoplasma oocysts in faeces for 1-3 weeks after primary infection — oocysts become infectious in 1-5 days and survive in soil for months. Humans ingest oocysts through cat litter handling, gardening, or contaminated water. (2) Undercooked/raw meat: tissue cysts in pork, lamb, venison and other meats are killed by thorough cooking to ≥66°C. (3) Congenital: primary infection during pregnancy → transplacental transmission.

How dangerous is toxoplasmosis in pregnancy?

Primary T. gondii infection acquired during pregnancy can be transmitted to the fetus — causing congenital toxoplasmosis. Risk of transmission increases with gestational age; severity of fetal damage is worst with first-trimester infection. Severe congenital toxoplasmosis causes: chorioretinitis (leading to visual impairment — may not manifest until childhood); hydrocephalus; intracranial calcifications; intellectual disability; deafness; seizures. In France, routine antenatal Toxoplasma serology and monthly monitoring for seronegative pregnant women is standard, with spiramycin treatment for maternal infection.

What is toxoplasmic encephalitis and who gets it?

Toxoplasmic encephalitis (TE) occurs when latent T. gondii brain cysts reactivate in the context of severe immunosuppression — primarily HIV patients with CD4 <100 cells/μL (the threshold below which immune control of latent Toxoplasma is insufficient). TE causes multiple ring-enhancing brain lesions typically in the basal ganglia — presenting with fever, headache, confusion, focal neurological deficits and seizures. It is an AIDS-defining illness. TE can also occur in organ transplant recipients, lymphoma patients, and others on high-dose immunosuppression.

How is toxoplasmosis treated?

Acute congenital toxoplasmosis: pyrimethamine + sulfadiazine + folinic acid for 12 months. Maternal primary infection during pregnancy: spiramycin (reduces vertical transmission risk); if fetal infection confirmed on amniocentesis: switch to pyrimethamine + sulfadiazine + folinic acid. Toxoplasmic encephalitis in HIV: pyrimethamine + sulfadiazine + folinic acid for 6 weeks (acute phase), then maintenance therapy until CD4 >200 sustained on ART. Clindamycin can substitute for sulfadiazine. TMP-SMX is an alternative for TE and prophylaxis.

What is the cat-human transmission risk?

Only cats that have recently acquired Toxoplasma (by eating infected prey) shed oocysts — for approximately 1-3 weeks. The risk from a typical indoor cat that does not hunt is minimal. High-risk exposures: handling cat litter of cats that hunt; gardening in contaminated soil; eating raw/undercooked meat. Pregnant women and immunocompromised individuals should: wear gloves for cat litter changes (or have someone else do it); wear gloves for gardening; and cook meat thoroughly.

Does toxoplasmosis affect behaviour?

There is intriguing but contested evidence that latent T. gondii infection may subtly affect human behaviour — possibly through dopamine dysregulation in the brain. Studies suggest associations between seropositivity and reaction time changes, increased risk-taking, and associations (in ecological studies) with schizophrenia risk. The magnitude of effects is small, the mechanisms are hypothetical, and causality is unproven. T. gondii does affect the behaviour of infected rodents dramatically (making them attracted to cat urine — facilitating the parasite's completion of its lifecycle), but whether similar effects occur in humans at population-relevant scale is unproven.

How does GMJ News cover toxoplasmosis?

GMJ News covers WHO toxoplasmosis data, congenital toxoplasmosis prevention, toxoplasmic encephalitis in HIV, TMP-SMX prophylaxis, chorioretinitis management and prevention in pregnancy. Toxoplasmosis is directly relevant to PHIG's infectious disease and HIV programmes and to the Georgian Medical Journal's clinical coverage.

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Toxoplasmosis

Q: How is toxoplasmosis treated?

Acute congenital toxoplasmosis: pyrimethamine + sulfadiazine + folinic acid for 12 months. Maternal primary infection during pregnancy: spiramycin (reduces vertical transmission risk); if fetal infection confirmed on amniocentesis: switch to pyrimethamine + sulfadiazine + folinic acid. Toxoplasmic encephalitis in HIV: pyrimethamine + sulfadiazine + folinic acid for 6 weeks (acute phase), then maintenance therapy until CD4 >200 sustained on ART. Clindamycin can substitute for sulfadiazine. TMP-SMX is an alternative for TE and prophylaxis.

GMJ News knowledge hub · last reviewed September 2026 · Georgian Medical Journal

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Toxoplasmosis — caused by the intracellular protozoan Toxoplasma gondii — infects an estimated one-third of the global human population (approximately 2.5-3 billion people), making it arguably the most successful parasite in history; while most infections in immunocompetent adults are asymptomatic, toxoplasmosis is devastating in two vulnerable groups: congenital infection (affecting approximately 1-2 million infants per year, causing chorioretinitis, hydrocephalus, intellectual disability and deafness) and immunocompromised patients (toxoplasmic encephalitis is an AIDS-defining illness, causing life-threatening brain abscesses in HIV patients with CD4 <100 cells/μL) (WHO).

Key messages

One-third of global population infected

Toxoplasma gondii infects approximately one-third of the global population — approximately 2-3 billion people — making it one of the most prevalent human parasites; while most infections are asymptomatic in immunocompetent adults, toxoplasmosis causes devastating disease in two groups: fetuses and immunocompromised patients (WHO).

Cats are the definitive host

Domestic and wild cats are the only definitive hosts for T. gondii — shedding infectious oocysts in faeces for 1-3 weeks after primary infection. Oocysts survive in soil for months to years. Humans are infected through cat litter/soil contact, undercooked meat (tissue cysts) or raw produce.

Congenital toxoplasmosis — devastating

Primary Toxoplasma infection during pregnancy causes congenital toxoplasmosis — affecting approximately 1-2 million infants per year. Severe sequelae (chorioretinitis, hydrocephalus, intellectual disability, deafness) occur particularly with first-trimester infection. Spiramycin (primary infection) and pyrimethamine + sulfadiazine + folinic acid (fetal infection confirmed) are treatments.

AIDS-defining illness

Toxoplasmic encephalitis — reactivation of latent Toxoplasma infection in HIV patients with CD4 <100 cells/μL — is an AIDS-defining illness causing life-threatening brain abscesses. Symptoms: confusion, focal neurological deficits, fever, headache. Treated with pyrimethamine + sulfadiazine + folinic acid, with TMP-SMX prophylaxis when CD4 <200.

Brain cysts are permanent

Once acquired, T. gondii forms latent bradyzoite cysts in brain, muscle and other tissues that persist for life. These cysts are resistant to all available drugs and are the source of reactivation in immunosuppression. Immunocompetent people maintain lifelong latent infection — controlled by the immune system without symptoms.

Seroprevalence varies widely by geography

Toxoplasma seroprevalence ranges from approximately 10-20% in the UK and USA to approximately 80% in France, Brazil and parts of Africa — reflecting dietary practices (raw/undercooked meat consumption) and cat density. France's high seroprevalence is linked to eating raw/rare meat.

Key statistics

~2-3B

people infected globally (~1/3 of world population)

WHO

1-2M

congenital toxoplasmosis cases/year

WHO/TORCH

<100

CD4 cells/μL threshold for toxoplasmic encephalitis risk

WHO mhGAP

10-80%

seroprevalence range by country

WHO

Cats

only definitive host — shedding oocysts

WHO

TMP-SMX

prophylaxis for HIV+ patients with CD4 <200 prevents TE

WHO/BHIVA

Toxoplasma gondii seroprevalence (%) in adult general population by region — WHO/published studies

Source: Published seroprevalence studies. Very high in France, Brazil, parts of Africa; lower in UK, USA.

Glossary of key terms

Toxoplasma gondii
WHOAn obligate intracellular protozoan parasite — one of the most successful parasites in nature. Three life stages: tachyzoites (rapidly replicating — during acute infection); bradyzoites (slowly replicating, within tissue cysts — latent infection); and oocysts (sexually produced in cats, shed in faeces — environmentally resistant).

Congenital toxoplasmosis
WHOVertical transmission of T. gondii from mother to fetus — only occurs during primary maternal infection during pregnancy. Risk of transmission increases with gestational age (10% first trimester → 60% third trimester); severity is inversely related (first trimester infection causes worst outcomes). Sequelae: chorioretinitis, hydrocephalus, intracranial calcifications, intellectual disability, deafness.

Toxoplasmic encephalitis (TE)
WHO/BHIVAReactivation of latent Toxoplasma brain cysts in severely immunocompromised patients (HIV CD4 <100, organ transplant recipients, lymphoma). Causes ring-enhancing brain lesions with oedema on CT/MRI, typically in the basal ganglia. Treated with pyrimethamine + sulfadiazine + folinic acid (6 weeks acute, then maintenance). Empirical treatment is often started based on clinical-radiological diagnosis without biopsy.

Pyrimethamine + sulfadiazine
WHO EMLThe combination treatment for toxoplasmosis — pyrimethamine inhibits dihydrofolate reductase; sulfadiazine inhibits dihydropteroate synthase. Folinic acid supplementation is essential to prevent pyrimethamine-induced bone marrow suppression. Clindamycin can substitute for sulfadiazine if intolerant. Treatment duration for TE: 6 weeks, then maintenance until CD4 >200 with ART.

TMP-SMX prophylaxis
WHO/BHIVA/EACSTrimethoprim-sulfamethoxazole (co-trimoxazole) — one double-strength tablet daily — prevents toxoplasmic encephalitis and PCP in HIV patients with CD4 <200. One of the most important preventive interventions in HIV care. WHO recommends TMP-SMX prophylaxis for all HIV-positive individuals with CD4 <200 in LMICs regardless of Toxoplasma serostatus.

Chorioretinitis
WHO/OphthalmologyEye inflammation from Toxoplasma reactivation in the retina — the most common cause of chorioretinitis in immunocompetent patients in endemic areas. Causes painless visual floaters, photophobia and scotoma. Typically self-limiting in immunocompetent patients; treatment (pyrimethamine + sulfadiazine + steroids) for vision-threatening lesions.