Pediatric Toxoplasmosis Clinical Presentation

Updated: Sep 20, 2019
  • Author: Itzhak Brook, MD, MSc; Chief Editor: Russell W Steele, MD  more...
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Congenital toxoplasmosis is the consequence of transplacental hematogenous fetal infection by T gondii during primary infection in pregnant women. Primary infection in an otherwise healthy pregnant woman is asymptomatic in 60% of cases. Symptoms during pregnancy are frequently mild. The most common manifestations are fatigue, malaise, a low-grade fever, lymphadenopathy, and myalgias. Latent Toxoplasma infection with reactivation during pregnancy may lead to congenital infection only in immunocompromised women (most commonly, those with AIDS).

The classic triad of chorioretinitis, hydrocephalus, and intracranial calcifications cannot be used as a strict diagnostic criterion for congenital toxoplasmosis because a large number of cases would be missed. Congenital toxoplasmosis may occur in the following forms:

  • Neonatal disease

  • Disease occurring in the first months of life

  • Sequelae or relapse of previously undiagnosed infection

  • Subclinical infection

When clinically recognized in the neonate, congenital toxoplasmosis is very severe. Spontaneous abortions, prematurity, or still birth may result. Signs of generalized infection, such as the following, are usually present:

  • Intrauterine growth restriction

  • Fever

  • Chorioretinitis (usually bilateral)

  • Cerebral calcification

  • Abnormal cerebrospinal fluid (xanthochromia and pleocytosis)

  • Vomiting

  • Eosinophilia

  • Abnormal bleeding

  • Jaundice

  • Hepatomegaly

  • Splenomegaly

  • Lymphadenopathy

  • Rash

Neurologic signs are severe and always present. They include the following:

  • Microcephaly or macrocephaly

  • Bulging fontanelle

  • Nystagmus

  • Abnormal muscle tone

  • Seizures

  • Delay of developmental milestone acquisition

Most cases of chorioretinitis result from congenital infection, although patients are often asymptomatic until later in life. [7] Symptoms include blurred vision, scotoma, pain, photophobia, and epiphora. Impairment of central vision occurs when the macula is involved, but vision may improve as inflammation resolves. Relapses of chorioretinitis are frequent but are rarely accompanied by systemic signs or symptoms.

Late manifestations of untreated congenital toxoplasmosis can include chorioretinitis and neurologic abnormalities such as motor abnormalities, intellectual disability, and hearing loss. This can occur even when there are no clinical symptoms or findings at the time of birth.

Latent toxoplasmosis may reactivate in women with human immunodeficiency virus (HIV) and result in congenital transmission. Congenital toxoplasmosis in the infant with HIV appears to run a more rapid course than in infants without HIV.


Physical Examination

In subacute congenital toxoplasmosis, symptoms may not be observed in patients until some time after birth.

Lymphadenopathy is the most common form of symptomatic acute toxoplasmosis in immunocompetent individuals. Patients typically present with painless, firm lymphadenopathy that is confined to one chain of nodes (most commonly cervical nodes). The suboccipital, supraclavicular, axillary, and inguinal groups may also be involved.

Other physical manifestations include a low-grade fever, occasional hepatosplenomegaly, and a rash. Other findings include anemia, disseminated intravascular coagulation, hepatitis, cholestasis, hepatic calcifications, hepatomegaly, splenomegaly, jaundice, myocarditis, pneumonitis, premature birth, rashes (maculopapular, petechial, purpura, blueberry muffin rash), sepsislike illness, temperature instability, and thrombocytopenia.

Ophthalmologic examination reveals multiple yellow-white, cottonlike patches with indistinct margins located in small clusters in the posterior pole. Other ophthalmological findings include amblyopia; cataract; chorioretinitis; chorioretinal edema; chorioretinal edema, scars, and neovascular membrane; posterior hyaloid membrane iris detachment; leukocoria; macular or peripheral retinal lesions; microphthalmia or microcornea; nystagmus; papilledema; optical nerve atrophy; retinal detachment; strabismus; visual impairment; and vitritis.

Characteristically, a focal necrotizing retinitis develops that may atrophy and generate black pigment or that may be associated with panuveitis. Papillitis is usually indicative of CNS disease. Flare-up of congenitally acquired chorioretinitis is often associated with scarred lesions in proximity to the fresh lesions.

Because of multifocal involvement of the CNS, clinical findings widely vary. They include alterations in mental status, seizures, motor weakness, cranial nerve disorders, sensory abnormalities, cerebellar signs, meningismus, movement disorders, and neuropsychiatric manifestations in patients with immunocompromise. Other neurological findings include brain masses and calcifications, cerebrospinal fluid changes (pleocytosis, lymphocytosis, eosinophilia, elevated protein, low glucose), developmental delay, obstructive hydrocephalus, hypotonia, microcephaly or macrocephaly, palsies, and sensory hearing loss.