Toxoplasmosis

Summary

Parasitic infection caused by Toxoplasma gondii
Typically asymptomatic in immunocompetent individuals
Can cause severe complications in immunocompromised patients and congenital infections

Pathophysiology

Caused by the protozoan parasite Toxoplasma gondii
Transmission:
- Ingestion of undercooked meat containing tissue cysts
- Consumption of food or water contaminated with oocysts shed in cat feces
- Transplacental transmission from mother to fetus
Life cycle:
- Definitive hosts: Felids (domestic and wild cats)
- Intermediate hosts: Warm-blooded animals, including humans
Tachyzoites invade host cells and replicate, leading to cell lysis and spread

Worldwide distribution
Seroprevalence:
- Varies by geographic region and cultural practices
- Estimated 30-50% of global population infected
Higher risk groups:
- Immunocompromised individuals (HIV/AIDS, organ transplant recipients)
- Pregnant women
- Individuals with frequent exposure to cats or raw meat

Serology:
- IgG and IgM antibodies
- IgG avidity test to determine timing of infection
PCR:
- Detection of T. gondii DNA in blood, cerebrospinal fluid, or amniotic fluid
Histopathology:
- Tissue biopsy with characteristic findings
Clinical presentation:
- Often asymptomatic in immunocompetent individuals
- Flu-like symptoms in acute infection
- Severe manifestations in immunocompromised patients (encephalitis, pneumonitis)
- Congenital toxoplasmosis: hydrocephalus, intracranial calcifications, chorioretinitis

Central Nervous System:
- CT:
- Multiple ring-enhancing lesions
- Cerebral oedema
- Hydrocephalus (in congenital cases)
- MRI:
- T1: Hypointense lesions
- T2: Hyperintense lesions with surrounding oedema
- Post-contrast: Ring-enhancing lesions
Ocular:
- Ultrasound: Hyperechoic foci in vitreous
- Fluorescein angiography: Active chorioretinitis
Congenital:
- Intracranial calcifications
- Ventriculomegaly
- Cortical atrophy

Case 1Case 2

50-year-old patient presented with a new diagnosis of HIV with a CD4 count of 50.
MRI showed multple large right frontal lesions with peripheral enhancement, diffusion restriction and petechial haemorrhage.
With differential diagnosis of lymphoma, the diagnosis of toxoplasmosis was made after a right frontal biopsy.

Patient with a new diagnosis of HIV (CD4 count of <50) presented with headache and right sided weakness.
MRI showed many peripherally/irregularly enhancing lesions in both cerebral hemispheres and the cerebellum.
Toxoplasma serology was positive.

Immunocompetent individuals:
- Often self-limiting, no treatment required for mild cases
Immunocompromised patients and severe cases:
- Pyrimethamine + sulfadiazine + leucovorin
- Alternative: Trimethoprim-sulfamethoxazole
Pregnant women:
- Spiramycin (to prevent fetal transmission)
- Pyrimethamine + sulfadiazine + leucovorin (if fetal infection confirmed)
Congenital toxoplasmosis:
- Pyrimethamine + sulfadiazine + leucovorin for 12 months
Ocular toxoplasmosis:
- Antiparasitic therapy + corticosteroids

Differential Diagnosis	Differentiating Feature
HIV encephalopathy	Lack of focal lesions on imaging; diffuse white matter changes
Primary CNS lymphoma	Single lesion more common; intense contrast enhancement
Brain abscess	Ring-enhancing lesion with restricted diffusion on MRI
Neurocysticercosis	Multiple small cystic lesions; calcifications in chronic stage
Tuberculoma	Thick-walled lesions; basal meningeal enhancement
Progressive multifocal leukoencephalopathy (PML)	No contrast enhancement; subcortical white matter involvement
Cryptococcosis	Gelatinous pseudocysts in basal ganglia and perivascular spaces; T2 hyperintense cystic lesions with minimal enhancement
Cerebral metastases	Multiple lesions at grey-white matter junction; ring or nodular enhancement; surrounding vasogenic oedema
Acute disseminated encephalomyelitis (ADEM)	Bilateral, large confluent white matter lesions; may involve basal ganglia; no ring enhancement
Neurosarcoidosis	Leptomeningeal enhancement; hilar lymphadenopathy on chest imaging