AKT · Infections/Tropical, zoonotic & travellow yield

Toxoplasmosis

Toxoplasma gondii (protozoan) — cat faeces / undercooked meat; cats are the definitive host

Overview

Infection with the protozoan Toxoplasma gondii, acquired from cat faeces or undercooked meat. In the immunocompetent it is usually asymptomatic or a self-limiting mononucleosis-like illness. The two settings that matter: the immunocompromised (especially HIV with CD4 <100 → cerebral toxoplasmosis with ring-enhancing lesions) and congenital infection (primary maternal infection in pregnancy → the classic triad).

Recognise

Immunocompetent: usually asymptomatic, or a self-limiting glandular-fever-like illness (fever, lymphadenopathy, malaise) — Monospot-negative
Immunocompromised (HIV, CD4 <100): cerebral toxoplasmosis — headache, focal neurology, seizures, reduced consciousness; CT/MRI shows multiple RING-ENHANCING lesions (often basal ganglia)
Congenital (primary maternal infection in pregnancy): classic triad — intracranial calcification, hydrocephalus, chorioretinitis

Red flags

Cerebral toxoplasmosis in HIV → urgent treatment; the key differential is primary CNS lymphoma (both ring-enhancing)
Primary maternal infection in pregnancy → fetal risk → specialist management

Differentials & how to tell them apart

Primary CNS lymphoma (in HIV)also ring-enhancing — toxoplasmosis usually MULTIPLE lesions and responds to a treatment trial; lymphoma often single, EBV-positive CSF, PET-avid

EBV/CMV mononucleosisthe immunocompetent glandular-fever-like differential — serology

Other congenital (TORCH) infectionsCMV, rubella — overlapping congenital features; serology distinguishes

Investigations

Serology (IgM/IgG) in immunocompetent/pregnancy; in HIV — CT/MRI brain (multiple ring-enhancing lesions, often basal ganglia) + CD4 count; a response to an empirical treatment trial supports toxoplasmosis over CNS lymphoma; PCR/biopsy if uncertain; fetal/neonatal assessment for congenital infection.

Management

Immunocompetent → none; cerebral (HIV) → pyrimethamine+sulfadiazine+folinic acid + ART; pregnancy → specialist

1In the immunocompetent, toxoplasmosis is usually self-limiting (no treatment). In HIV with CD4 <100 and multiple ring-enhancing brain lesions, treat cerebral toxoplasmosis with pyrimethamine + sulfadiazine + folinic acid, plus ART.Gate: The key HIV differential is primary CNS lymphoma (both ring-enhancing) — toxoplasmosis is usually multiple lesions and improves on an empirical treatment trial; lymphoma is often single with EBV-positive CSF. Primary infection in pregnancy → specialist care (congenital risk).
2Co-trimoxazole prophylaxis in HIV with low CD4; specialist treatment for pregnancy/ocular disease; manage congenital toxoplasmosis (intracranial calcification, hydrocephalus, chorioretinitis).

Immunocompetent: usually no treatment — self-limiting; treat only if severe/ocular or in pregnancy

Cerebral toxoplasmosis (HIV): pyrimethamine + sulfadiazine (+ folinic acid) — plus ART; an empirical treatment trial that improves supports the diagnosis over CNS lymphoma; co-trimoxazole prophylaxis when CD4 <100–200

Pregnancy: specialist treatment (spiramycin ± pyrimethamine-sulfadiazine) — to reduce vertical transmission/fetal damage

Ocular toxoplasmosis: specialist therapy — chorioretinitis

Key points

Toxoplasma gondii (cat faeces/undercooked meat). Immunocompetent → self-limiting (often Monospot-negative mononucleosis). HIV CD4 <100 → cerebral toxoplasmosis (MULTIPLE ring-enhancing lesions, basal ganglia) → pyrimethamine+sulfadiazine+folinic acid; differential = CNS lymphoma (toxo improves on treatment trial). Congenital triad: intracranial calcification + hydrocephalus + chorioretinitis.

Monitor & prognosis

Treatment response (radiological/clinical), CD4/prophylaxis in HIV, fetal/neonatal assessment in pregnancy.

Benign in the immunocompetent; serious cerebral disease in HIV; congenital infection causes lasting damage.

Source: BHIVA; cross-ref HIV (above), neurology, O&G (congenital)