Parasitology 3: Ms. Freeman

Toxoplasma gondii

Most likely, this patient acquired toxoplasmosis some time ago while in Liberia. Toxoplasmosis is most often acquired through the ingestion of the organism in contaminated soil, water, or food or in undercooked meat from an animal infected with Toxoplasma. Clear infection rates can be difficult to establish since most acute infections are asymptomatic, so seroprevalence is often used as a surrogate. Seroprevalence of Toxoplasmosis is higher in countries outside of the United States, with rates of seropositivity decreasing relative to economic development. Across all countries, seroprevalence increases with age likely correlating with cumulative exposure risk over time. 

Acute toxoplasmosis infection is often asymptomatic. When symptomatic, the most common manifestation is regional or generalized lymphadenopathy. When generalize symptoms (fever, malaise, headache) are present, the syndrome can mimic mononucleosis.

There are two infectious stages to humans:

1. Oocysts: The product of sexual reproduction, which are excreted in the feces of the definitive host (felines). These structures are highly contagious and may remain viable in the environment for many years in the soil or water.
2. Bradyzoites are the structures that form when a mammal is infected with oocysts that invade across the GI lumen and encyst in tissues. When this occurs in animals meant for food, undercooked meat containing bradyzoites infects the human.

• Immunosuppression. In particular, advanced cell-mediated immunodeficiency related to AIDS is the most common risk factor for reactivation disease, manifested as CNS infection.
• Developing fetuses also have limited immune response to Toxoplasmosis, and primary infection in a pregnant woman can lead to congenital toxoplasmosis (T in TORCH).

Image findings of Cerebral Toxoplasmosis and Neurocysticercosis have many overlaps and can manifest as “ring-like lesions” on CT and MRI.

In general, lesions of neurocysticercosis have a clear cystic structure (a “hole”) compared to Toxoplasma, which tends to be more mass-like. The peri-lesional edema (enhancement) is more variable in neurocysticercosis, with very old lesions without active organism having little to no ring-enhancement.

CNS Toxoplasmosis is classically associated with significant edema. Both agents can cause obstructive hydrocephalus. In the case of neurocysticercosis, this is due to a cyst physically obstructing outflow. In CNS toxoplasmosis, hydrocephalus is usually associated with massive edema.