Organism: obligate intracellular protozoan parasite Toxoplasma gondii, can live in any cell except for nonnucleated RBCs; reservoirs in feces of house cat (felines are definite host)

Infection: ingestion of undercooked meat (eg, pork, free-range chicken) containing cysts or sporulated oocysts / transplacental transmission of trophozoites; acquired through blood transfusion + organ transplantation

• Disease remains dormant for as long as normal host immunity is maintained!

Forms:

1. Cyst (bradyzoite)
2. Trophozoite
3. Oocyst: uniquely found in intestinal mucosa of cat; outside cat it can survive for >1 year in warm moist soil

Hosts: birds, mammals, reptiles, cockroach, flea

Geographic exposure: France (75–90%) >Central America >urban USA (17–35%)

• 500 million persons infected with T. gondii worldwide!

Seropositivity: up to 20% of urban adults in USA; up to 90% of European adults

Transmission:

1. fecal-oral: fruits, vegetables, poorly cooked meat; children especially susceptible via house cat / litter box
2. hematogenous: blood transfusion

Spread: hematogenous

Histo: inflammatory solid / cystic granulomas (← glial mesenchymal reaction) surrounded by edema and microinfarcts (← vasculitis)

Affected tissue:

• Gray + white matter of brain
  • Most common cause of focal CNS infection mass effect in patients with AIDS!
• Retina: most common retinal infection in AIDS
• Alveolar lining cells (4%):
  mimics Pneumocystis carinii pneumonia
• Heart (rare):
  cardiac tamponade / biventricular failure
• Skeletal muscle
• asymptomatic; lymphadenopathy; malaise, fever

Toxoplasmosis is the most common opportunistic infection affecting the CNS in patients with AIDS!

1. AIDS INFECTION = toxoplasmic encephalitis
   = reactivation of a chronic latent infection in >95%
   • Most common cerebral mass lesion in AIDS!
   • 2–3 times more frequent than lymphoma!
   
   Incidence: 3–20–40% of AIDS patients; 20–70% of normal adult population is seropositive for antibodies
   Path: well-localized indolent granulomatous process / diffuse necrotizing encephalitis
   • fever, headaches, confusion, seizures (15–25%)
   • focal neurologic deficit of subacute onset (50–89%)
   • pseudotumor cerebri syndrome
   
   Location:
   1. basal ganglia (75%)
   2. subcortical at gray-white matter junction scattered throughout brain parenchyma
   3. NO involvement of corpus callosum / leptomeninges
   
   CT:
   • multifocal abscesses with a predilection for basal ganglia:
     • multiple / solitary (up to 39%) lesions <2 cm with nodular / thin-walled (common) ring enhancement
     • surrounding white matter edema
   • double-dose delayed CT scans with higher detection rate for multiple lesions (64–72%)
   • ± hemorrhage and calcifications after therapy
   
   MR:
   • multiple hypo- to isointense lesions on T2WI
   • T1 hyperintense lesion + hypointensity on GRE ← hemorrhage
   • prominent associated mass effect
   • marked edema
   • increased diffusivity related to underlying acellular core on DWI (opposite to pyogenic + fungal abscess)
   • nodular / ring enhancement
   • poorly defined peripheral enhancement = poor host response
   • HIGHLY SUGGESTIVE “eccentric target” sign (30%) = small enhancing nodule along lesion margin
   • diffuse cerebral volume loss (30%)
   
   MR spectroscopy:
   • lipid breakdown products without elevated choline levels
   
   Dx: improvement on antitoxoplasma therapy within 2–3 weeks / biopsy
   DDx: CNS lymphoma (single lesion, hyperattenuation, T2 hypointensity, restricted diffusion, periventricular location)
   • Multiple lesions suggest toxoplasmosis!
2. INTRAUTERINE INFECTION
   = devastating effects on fetal brain because maternal antibodies passed to child will be limited by blood-brain barrier
   Time of fetal infection: chances of transplacental transmission greater in late pregnancy
   Screening: impractical due to high false-positive rate
   • Toxoplasma gondii found in ventricular fluid
   • microcephaly, mental retardation, seizures; chorioretinitis
   • thickened vault, sutures apposed / overlapping
   • hydrocephalus → return to normal / persistent large head
   • intracerebral calcifications in posterior aspect of brain
   • multiple irregular nodular / cystlike / curvilinear calcifications in periventricular area + thalamus + basal ganglia + choroid plexus (= necrotic foci); bilateral; 1–20 mm in size; increasing in number + size (usually not developed by time of birth)
   
   OB-US (as early as 20 weeks MA):
   • sonographic findings in only 36%
   • evolving symmetric ventriculomegaly
   • intracranial periventricular + hepatic densities
   • increased thickness of placenta
   • ascites
   • Microcephaly is NOT a feature of toxoplasmosis!
     Dx: elevated toxospecific IgM levels in fetal blood

Dx: demonstration of elongated teardrop-shaped trophozoites in histologic sections of tissue

Rx: empiric therapy (pyrimethamine + sulfadiazine for 3 weeks)