Toxoplasmosis

In immunocompetent individuals, infection is most often asymptomatic (80-90%). When symptoms do occur, after an incubation period of <2 weeks, they are typically mild and nonspecific, resembling a mononucleoside-like illness. Common features include low-grade fever, generalized lymphadenopathy, myalgias, and sore throat.

One thing you should remember is ocular toxoplasmosis which can occur in immunocompetent patients and can be postnatally acquired (unilateral) or occur as a reactivation following congenital transmission (bilateral) and can be sight-threatening. Of note, ocular involvement is rare in immunocompetent individuals, except in cases of congenital toxoplasmosis. Ocular lesions are characterized by focally necrotic chorioretinitis (posterior uveitis) - described as white-ish foci (active tachyzoites) and scarring. Lesions are also called salt and pepper - salt (tachyzoites) and pepper (scarring). Tend to self-heal within a few months.

To learn more about ocular toxoplasmosis, we recommend this website: Ocular Toxoplasmosis: A Refresher - American Academy of Ophthalmology

Figure 4. Toxoplasma retinopathy showing active and scarred lesions

Figure 5. Toxoplasma retinopathy showing scar

In contrast, immunocompromised individuals are at risk for reactivation of latent infection as mentioned. This is particularly seen in patients with uncontrolled HIV/AIDS (CD4+ T-lymphocyte counts <100 cells/mm3) and in transplant recipients receiving immunosuppressive therapy. For example, individuals following allogeneic bone marrow transplant are at risk of fulminant forms of the disease in the event of a primary infection during the aplastic phase. The most important manifestation to remember is encephalitis. Other manifestations include: pulmonary manifestations (pneumonitis), cardiac involvement (myocarditis), and, in rare cases, fulminant disseminated disease.

1. Necrotizing encephalitis: characterized by focal neurological deficits, seizures, and altered mental status. Neuroimaging may reveal ring-enhancing lesions. Although classically described in the corticomedullary junction or in the basal ganglia, lesions can occur anywhere in the brain.
2. Pulmonary manifestations (e.g., pneumonitis): characterized by fever, cough, dyspnea. Chest imaging can reveal diffuse or patchy ground-glass opacities (can resemble Pneumocystis). Can progress to ARDS.

Congenital toxoplasmosis occurs when Toxoplasma gondii is transmitted from mother to fetus during pregnancy via transplacental passage of tachyzoites. Vertical transmission is most likely when maternal infection is acquired during pregnancy; infection prior to conception does not result in transmission (except in very rare exceptions). The severity of congenital disease is generally greater when infection occurs earlier in gestation (first trimester); however, it is more likely to occur when infection occurs later in gestation (third trimester).

Clinical manifestations of congenital toxoplasmosis vary widely from asymptomatic to severe CNS damage. Classic findings in the newborn include chorioretinitis, hydrocephalus, intracranial calcifications, and long-term neurodevelopmental impairment. Symptomatic neonates may also present with systemic features such as rash, hepatosplenomegaly, jaundice, anemia, and lymphadenopathy.

Note: acutely infected pregnant women are typically asymptomatic (~80%); however, they may still present with any of the previously discussed manifestations, such as mononucleosis-like syndrome or retinitis.

Figure 6. Intracranial calcifications in a newborn with congenital toxoplasmosis