Obligate intracellular protozoan infection (Toxoplasma gondii) — usually asymptomatic, but causes severe congenital disease and CNS lesions in immunocompromised hosts.
Also known as: toxoplasmosis, Toxoplasma gondii, congenital toxoplasmosis, CNS toxoplasmosis
Overview
Infection by Toxoplasma gondii, an obligate intracellular protozoan with cats as the definitive host. Humans are intermediate hosts, acquiring infection via ingestion of oocysts (cat feces, contaminated water/soil) or tissue cysts (undercooked meat). Lifelong latent infection persists in tissue cysts.
Epidemiology
Seroprevalence ~10-20% in US adults, higher in older adults and immigrants; up to 60-80% in parts of Europe and South America. Estimated 750,000-1.1 million new US infections yearly. Second leading cause of foodborne deaths in the US.
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Ingestion of undercooked or raw meat (especially pork, lamb, venison)
Cat litter exposure (especially outdoor cats); soil/garden contact without gloves
Unfiltered/untreated water in endemic areas
Pregnancy (highest risk if primary infection in second/third trimester)
Immunocompromise: HIV with CD4 <100, hematopoietic transplant, lymphoma
Pathophysiology
Ingested oocysts/cysts release sporozoites/bradyzoites that invade gut epithelium, transform into tachyzoites, and disseminate hematogenously. Cell-mediated immunity controls infection but does not eliminate tissue cysts (containing bradyzoites) in brain, muscle, eye, and heart. Reactivation occurs when CD4 cells decline (HIV) or with immunosuppression. Congenital transmission risk rises from ~10% in first trimester to ~80% in third trimester, but severity is inverse (severe disease more common with early transmission).
Congenital toxoplasmosis: classic triad of chorioretinitis, hydrocephalus, and diffuse intracranial calcifications; may also have seizures, hepatosplenomegaly, jaundice, microcephaly, IUGR; many asymptomatic at birth but develop chorioretinitis or learning disabilities later
Chorioretinitis on funduscopy: yellow-white focal retinal lesion with overlying vitreous inflammation
Focal CNS deficits, hemiparesis, papilledema
Congenital: hepatosplenomegaly, jaundice, blueberry-muffin rash, microcephaly or macrocephaly
Classic findings
AIDS patient with CD4 <100, headache, focal neuro deficit, and multiple ring-enhancing brain lesions on MRI in the basal ganglia or gray-white junction — toxoplasmosis until proven otherwise. Congenital infection: diffuse intracranial calcifications (vs. periventricular in CMV).
Differential diagnosis
CNS lymphoma (HIV) — Single lesion (toxoplasmosis usually multiple), no response to empiric anti-toxo therapy, positive EBV PCR in CSF; thallium SPECT positive (negative in toxo)
CMV/other TORCH (congenital) — Overlapping features; targeted serology and PCR
Glioma or metastasis — Less typical for HIV-stage 3; biopsy if no response to empiric therapy
Diagnostic workup
Diagnostic criteria
Clinical syndrome + serology/PCR + imaging. CNS toxoplasmosis in HIV often diagnosed empirically with response to therapy (2-week trial); biopsy if no improvement.
Labs
Toxoplasma IgG (lifelong) and IgM (acute; IgM can persist >1 year)
• Pyrimethamine 200 mg load then 50-75 mg PO daily + sulfadiazine 1-1.5 g PO QID + leucovorin 10-25 mg daily × 6 weeks induction
• Then chronic suppression at half doses until CD4 >200 × ≥6 months on ART
Alternative: TMP-SMX (effective and more accessible)
Pregnancy with primary infection: spiramycin to prevent fetal transmission; if fetal infection confirmed (amniotic fluid PCR), switch to pyrimethamine + sulfadiazine + leucovorin after 14 weeks gestation (avoid pyrimethamine in first trimester due to teratogenicity)
Congenital toxoplasmosis: pyrimethamine + sulfadiazine + leucovorin × 1 year
Toxoplasma IgM can persist >1 year — do not interpret a positive IgM as recent infection without IgG avidity testing.
In HIV with CD4 <100 + positive toxoplasma IgG, TMP-SMX prophylaxis prevents both PCP and toxoplasmosis.
Empiric anti-toxo therapy in HIV with ring-enhancing lesions — clinical/radiographic response within 2 weeks supports the diagnosis; failure → biopsy to evaluate for lymphoma.
Congenital intracranial calcifications: toxoplasmosis is diffuse; CMV is periventricular.
References
DHHS OI — Guidelines for the Prevention and Treatment of Opportunistic Infections in Adults and Adolescents with HIV — Toxoplasmosis section
CDC — Toxoplasmosis: Information for Healthcare Providers
Maldonado 2017 — AAP Diagnosis, Treatment, and Prevention of Congenital Toxoplasmosis in the United States (Pediatrics)
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