History and exam

Key diagnostic factors

common

presence of risk factors

Key risk factors include immune suppression (drug-induced, HIV infection or other immune deficiencies), infection during pregnancy, being living in a high-risk area, exposure to cat faeces, and ingestion of undercooked or raw meat.

chorioretinitis

Most cases of toxoplasmic chorioretinitis result from congenital infection that does not become clinically apparent until after reactivation in the eye. However, outbreaks of acute chorioretinitis associated with water contamination have been reported.[34]

While the presence of lesions in the fundus should raise suspicion for toxoplasmosis, proof that Toxoplasmais the cause of such disease is often lacking.

Appearance of inflammatory lesions is not unique to toxoplasmosis, and the differential diagnosis should be considered.

focal neurological deficit

Symptom of encephalitis.

Other diagnostic factors

common

blurry vision

Symptom of chorioretinitis.

slurred speech

Symptom of encephalitis.

headache

Symptom of encephalitis.

unsteady gait

Symptom of encephalitis.

confusion

Symptom of encephalitis.

uncommon

fever

May be seen with encephalitis or disseminated disease.

lymphadenopathy

May be seen in symptomatic infection.

fetal microcephaly

May indicate infection has been transmitted to the fetus.

fetal intracranial calcification

May indicate infection has been transmitted to the fetus.

fetal hydrocephalus

May indicate infection has been transmitted to the fetus.

fetal intrauterine growth restriction

May indicate infection has been transmitted to the fetus.

seizure

Symptom of encephalitis.

malaise

May be seen in symptomatic infection; toxoplasmosis should be considered in patients who are immunosuppressed.

hepatitis

May occur in patients who are immunosuppressed.

pneumonitis

May occur in patients who are immunosuppressed.

myocarditis

May occur in patients who are immunosuppressed.

Risk factors

strong

immunosuppression

Immunosuppression (drug-induced, as with anti-rejection medications for solid organ or stem cell transplant recipients, and corticosteroids or immune modulators for autoimmune diseases, or due to immune deficiencies such as HIV infection) can lead to re-activation of latent infection or symptomatic de novo infection.

Risk for symptomatic disease in HIV infection increases when the CD4+ T lymphocyte count falls below 200 cells/microlitre. Patients with CD4 counts <50 cells/microlitre are at greatest risk.[24] Seropositive patients with a diagnosis of AIDS have a 12% to 47% 12-month incidence ofToxoplasma encephalitis without chemoprophylaxis.

Risk among solid organ transplant recipients is greatest for heart transplants.[25]  Risk also exists for allogeneic stem cell transplant recipients.[26] 

Use of post-transplant prophylaxis with trimethoprim/sulfamethoxazole in both solid organ and allogeneic stem cell recipients significantly reduces the risk of disseminated toxoplasmosis.

exposure during pregnancy

Transplacental transmission results only when a seronegative woman acquires toxoplasmosis during pregnancy. Seropositive women who become pregnant usually do not transmit toxoplasmosis to their children unless they are severely immunosuppressed (e.g., because of AIDS or treatments for systemic lupus erythematosus) and even in those cases transmission is rare. A woman who has a documented seroconversion should wait at least 6 months before becoming pregnant.[27]​ Risk of transmission to the fetus if the mother acquired new infection increases with trimester (9% to 14% risk in first trimester, 59% to 70% risk in third trimester), but the severity of the manifestations of infection falls with each trimester.[28][29]​​

residence in a high-risk area

Exposure is more common in warm climates and at lower elevations. Exposure is common in Central and South America because of water contamination, leading to an increased risk of chorioretinitis, even in patients with intact immune systems. Exposure is also common in France and some other European countries because of ingestion of undercooked infected meat.

ingestion of undercooked or raw meat

Poses a risk for exposure, not necessarily for symptomatic disease (unless immunosuppressed or exposed during pregnancy).

exposure to cat faeces

Poses a risk for exposure, not necessarily for symptomatic disease (unless immunosuppressed or exposed during pregnancy).

weak

heavy exposure to soil

Poses a risk for exposure.

ingestion of unwashed unpeeled raw fruits and vegetables

Poses a risk for exposure.

occupational exposure

This could occur with technicians working in a Toxoplasma research lab, or veterinarians. Although studies show exposure to cat faeces is a risk, they are unclear on the risk associated with cat exposure. Cats shed oocysts in their faeces during acute infection, and then only intermittently after initial exposure. Oocysts become infectious only after 1 to 4 days of environmental exposure. Oocysts do not stick to fur as do some other parasites, and cats' grooming generally removes all oocysts before they become infective.

Use of this content is subject to our disclaimer