Toxoplasmosis is a disease caused by the obligate intracellular parasite Toxoplasma gondii. Transmission occurs either through ingestion of cysts found, for example, in raw meat or cat feces, or from mother to fetus through the placenta. The clinical presentation depends on the patient's immune status: In immunocompetent individuals, 90% of cases are harmless and asymptomatic, with the remaining 10% displaying mild mononucleosis-like symptoms. In immunosuppressed patients (e.g., those who are HIV-positive), infection may result in cerebral toxoplasmosis (headache, confusion, focal neurological deficits) or toxoplasmic chorioretinitis (eye pain, reduced vision). Treatment is indicated for immunosuppressed patients, infected mothers, congenital toxoplasmosis, and immunocompetent patients with more severe symptoms. The treatment of choice is usually a combination of pyrimethamine, sulfadiazine, and leucovorin (folinic acid), with the exception of new infections during pregnancy, which are treated with spiramycin.
For the congenital variant and how to manage infection in pregnant women, see “.”
- In the US: ∼ 10% of adults
- In some tropical climates: up to 95%
Epidemiological data refers to the US, unless otherwise specified.
- Pathogen: Toxoplasma gondii, an obligate intracellular, single-celled protozoan
Route of transmission
Oral ingestion: The oocysts are excreted in the feces of cats (final host) and are orally ingested by other mammals such as humans, hoofed animals, and birds (intermediate hosts). Primary modes of transmission include the following:
- Cat feces
- Raw or insufficiently cooked meat (most common)
- Unpasteurized milk (especially goat milk)
- Transplacental transmission: see toxoplasmosis in pregnancy
- Via organ transplantation or blood transfusion
- Oral ingestion: The oocysts are excreted in the feces of cats (final host) and are orally ingested by other mammals such as humans, hoofed animals, and birds (intermediate hosts). Primary modes of transmission include the following:
- Incubation time: 5 days to 3 weeks 
- Immunocompetent patients: typically primary infection 
- Immunosuppressed patients (e.g., patients with AIDS): primary infection or reactivation in previously infected individuals 
- Serology 
- PCR using, e.g.:
- Additional diagnostics, e.g.:
- Indications include immunosuppression; , pregnancy, and severe infection (e.g., active ocular toxoplasmosis).
- Treatment of choice
- For details, including dosages, see:
Immunocompetent patients do not usually require treatment.
- A necrotizing encephalitis affecting immunocompromised individuals that is caused by reactivation of T. gondii
- The most common neurological disorder associated with AIDS
Clinical features 
A definitive diagnosis requires the presence of clinical features, biopsy findings of T. gondii, and ≥ 1 mass lesion seen on imaging. Empiric treatment is usually initiated based on typical clinical features and currently available imaging and serology results. 
- Imaging: CT or MRI with contrast
- CSF: pleocytosis, ↑ protein, PCR positive for T. gondii 
- Serology: IgM and IgG antibody tests 
- Biopsy: may be required if treatment fails and/or to differentiate from other diagnoses 
Treatment of cerebral toxoplasmosis 
See “Approach to undifferentiated neurological symptoms in patients with HIV” for initial management of this patient group.
- Preferred regimen 
- Treatment duration: at least 6 weeks, followed by chronic maintenance therapy
- Supportive treatment 
- Disposition: Admission, potentially to a critical care unit, is usually required.
Primary CNS lymphoma is a differential diagnosis of cerebral toxoplasmosis. Until this differential is ruled out, avoid glucocorticoids, as they can alter neuroimaging and biopsy findings and may delay a diagnosis.
Prophylaxis for HIV patients 
- ABCDE assessment and treatment as required
- Management of acute seizures and status epilepticus
- Evaluate for and manage .
- Consult infectious diseases.
- Basic laboratory studies (e.g., BMP, CBC)
- Toxoplasma serology
- CT/MRI head with contrast
- Lumbar puncture for toxoplasma PCR and to rule out meningitis
- HIV testing including CD4 count
- Initiate .
- Consider admission, potentially to critical care unit.
Clinical features 
- Visual impairment, floaters, scotomas
- Defects in the visual field at the site of inflammation
- Pain (but may be painless in some patients)
- Optic atrophy or macular scar formation can progress to blindness.
- Typically self-limited in immunocompetent patients
- Frequently recurrent in immunocompromised patients
- Retinochoroiditis juxtapapillaris (Jensen disease): visual field defects caused by retinochoroidal lesions adjacent to the optic disc 
- Adjunctive tests: PCR or antibody titers of ocular fluid if the diagnosis is uncertain