Toxoplasma gondii is a ubiquitous coccidian parasite
- Oocysts -excreted in cat faeces (the definitive host) - ingestion initiates infection
- Tachyzoites, which multiply intra-cellularly
- Tissue cysts (mainly brain and muscle) - viable parasites in the brain and striated muscles throughout the life of the host.
Toxoplasmosis infection - via GI tract, multiplication in GI tract, via blood & lymphatics to organs. Normally immune response eradicate disease at this stage. In immunocompromised, no inflammatory stage and infection remains chronic.
- Most frequent form of disease (seen in 1/4 AIDS patients)
- Insidious onset drowsiness/coma
- Focal neurology (particularly language difficulties)
- Cranial nerve signs (hemianopia, aphasia, cranial nerve palsies)
- Low grade pyrexia
Differential Dx CNS Toxoplasmosis
- Chronic meningitis (esp. fungi / syphilis)
- Encephalitis (esp. CMV or HSV)
- Brain mets
- Primary CNS lymphoma
- Progressive multi-focal leukoencephalopathy
- Rising serum IgG (± IgM)
- Ab response muted in HIV
- T gondii isolated from CSF
- PCR detection of T gondii DNA
Multiple bilateral, hypodense lesions
Possible mass effect
Lesions = ring or homogenous enhance
Occasionally diffuse pattern
Is more sensitive in disclosing multiple lesions
If single lesion found, lymphoma more likely than toxoplasmosis. Beware missing metastatic lesions.
Multiple lesions may be incorrectly interpreted as multiple metastases in patients without a known history of HIV infection, so HIV and CNS toxoplasmosis must be considered in individuals with these findings and HIV risk factors.
- Toxoplasmosis treatment is often empiric
- Cotrimoxazole (trimethoprim-sulfamethoxazole)
- Or triple therapy with pyrimethamine, sulfadiazine, and folinic acid.