Toxoplasmosis

Introduction

Central nervous system (CNS) toxoplasmosis is an opportunistic infection caused by the intracellular protozoan parasite Toxoplasma gondii . This parasite may be acquired in utero or through the ingestion of infected meat or cat feces, as cats are its definitive host. While T. gondii infects a large portion of the population, it uncommonly causes significant disease in immunocompetent individuals. T. gondii typically causes disease in immunocompromised patients, such as in the setting of HIV/AIDS when the CD4 count has dropped below 100 cells per microliter. With the advent of modern HAART therapy, the prevalence of toxoplasmosis in HIV/AIDS patients has dramatically decreased in developed countries. The clinical manifestations of CNS toxoplasmosis are nonspecific, with the most common presenting symptoms being headache, lethargy, fever, and focal neurologic signs. Chorioretinitis is the most common manifestation of congenital toxoplasmosis, which may also cause seizure, hydrocephalus, and psychomotor delay. Many individuals in the general population are seropositive for toxoplasma. Consequently, the clinical diagnosis of toxoplasmosis can be a dilemma. As a result, imaging is vital in establishing a presumptive diagnosis.

Imaging Findings

In congenital toxoplasmosis, calcifications are common, which may involve the subcortical and periventricular white matter, basal ganglia, and cortex ( Fig. 8.1 ). Subcortical cysts, volume loss, and hydrocephalus can also be seen. Cranial ultrasound is often the first imaging study obtained, although CT or MRI is helpful for further evaluation.

In immunocompromised patients, CNS toxoplasmosis typically presents as multiple lesions with a predilection for the deep gray nuclei and gray-white matter junctions but occasionally presents as a solitary lesion ( Fig. 8.2 ). The imaging features are associated with necrotizing encephalitis on pathology ( Fig. 8.3 ). MRI of the brain including intravenous contrast is the imaging modality of choice for evaluating patients with suspected toxoplasmic encephalitis. Classically, the lesions have ring-like peripheral enhancement with an eccentric mural nodule, referred to as an “eccentric target sign” ( Fig. 8.4 ). However, the ring enhancement can be diminished or absent when a patient’s CD4 count is very low. The lesions are usually centrally hypoattenuating on CT and T1 hypointense on MRI. The lesions may be T2 hyperintense to isointense internally depending on the level of organizing necrotic component. There may be mural hyperattenuation on CT or T1 hyperintensity on MRI secondary to subacute hemorrhage or increased protein content. The lesions demonstrate surrounding hypoattenuation on CT or T2 hyperintensity on MRI compatible with vasogenic edema. Toxoplasmosis lesions typically show decreased cerebral blood volume on perfusion imaging.