Toxoplasma gondii an obligate intracellular protozoan
is acquired perorally, transplacentally or rarely parenterally by transfusion
or transplantation (McLeod and Remington, 2004).
Newly infected cat and other felidae excrete infectious
toxoplasma oocysts in their feces. Human infection is usually acquired
by the oral route by eating undercooked or raw meat that contains cysts
or by ingestion of cysts.
Congenital infection may present as a mild or severe neonatal
disease with onset during 1st months of life or with sequelae or relapse
at any time and the manifestations include small for gestational age,
prematurity, peripheral retinal scars, persistent jaundice, chorioretinitis
and cerebral calcification (McLeod and Remington, 2004).
More than half of these are considered normal in the perinatal
period but almost all such children will have ocular involvement later
in life and retinochoroiditis is the most common ocular manifestation
of congenital toxoplasmosis. Other manifestations are convulsions, hydrocephalus,
microphthalmia, microcephaly, hepatosplenomegaly, nystagmus, visual impairment,
strabismus, developmental delay (McLeod and Remington, 2004). Ocular involvement
existed in 30% of treated children with congenital involvement (Kodjikian
and Fleury, 2006).
Ocular involvement in congenital toxoplasmosis is frequently
bilateral but acquired toxoplasmosis in old children and adult is generally
unilateral (Rosso et al., 2005; Kenneth et al., 2004).
The second most common symptom was microphthalmia and strabismus
(Vutova et al., 2002).
In two sibling bilateral macular lesions were consistent
with the diagnosis of congenital toxoplasmosis, there was considerable
evidence that the lesions were scars from toxoplasmic retinochoroiditis
(Stern and Roman, 1978).
The aim of this study was to describe a 10 month old infant
with toxoplasmosis that was presented with ocular involvement.
A 10 month old boy infant was referred to our department
owing of strabismus and nystagmus.
The infant had fever in 4th month of life and after 1 month
Epiphora, abnormal eye movement, strabismus, nystagmus, abnormal lip movement
(probably convulsions) is started. In fundoscopy salt and pepper in right
eye and several scars in left eye were seen and the patient referred to
me. In examination, the infant had strabismus in left eye and nystagmus
in both eyes. Jaundice, abnormal lip movement (probably convulsion), epiphora
and fever in 4th month were seen in the history, but the infant does not
have development delay.
CSF analysis was normal, toxoplasma Ab (IgM) = 5.9 and toxoplasma
EEG had abnormal wave and in Brain CT scan multiple calcification
in periventricular (bilaterally) and in subcortical area were seen.
According to the results, toxoplasmosis was diagnosed and
treatment was begun with pyrimethamine, Sulfadiazin, folinic acid, prednisolone
and pirimidon for convulsions.
He responded dramatically to the therapy and after 1 month,
the eye lesions were inactivated and there was no progression in eye involvement.
Toxoplasmosis can involve multiple organ system such as
the nervous system, ear, lung, heart, skeletal muscle, LAP, skin, liver,
kidney, bone, endocrine and any part of eye may be involved either unilaterally
or bilaterally including maculae, optic nerve and visual pathway in the
brain and visual cortex and glaucoma. Extraocular muscle may also be involved.
Ocular toxoplasmosis is a recurrent and progressive disease
that require multiple course of therapy. Our patient was well baby without
any gross problem at birth, but in 10 month of age ocular toxoplasmosis
was suggested by history of fever and epiphora that progress to nystagmus
and strabismus in 5 month, finding in brain CT scan (calcification) and
positive serology were seen at 10 month And soon the clinical response
to treatment were seen.
The diagnosis of toxoplasmosis can be established by isolation
of T. gondii from blood and etc. or by culture or serology such
as IgM-ELISA, IgA ELISA. PCR of amniotic fluid is the procedure of choice
for establishing the diagnosis of congenital toxoplasmosis and sensitivity
and specificity of this test are approximately 95% in 18 week of gestation.
IgG antibody titers of 1/4 to 1/64 are usual in older children with active
toxoplamic chorioretinitis. When the retinal lesions are characteristic
and serologic tests are positive the diagnosis is likely (McLeod and Remington,
At birth when a diagnosis of congenital toxoplasmosis is
suspected, the following studies should be performed: general, ophthalmologic
and neurologic examination, head CT scan, attempt to isolate T. gondii
from placenta and infant`s leukocytes from umbilical cord blood and buffy
coat, measurement of serum toxoplasma- specific IgG, IgM, IgA and IgE
antibodies and the total amount of IgM and IgG in serum, lumbar puncture
including analysis of CSF for cell, glucose, protein, toxoplasma-specific
IgG and IgM antibodies and total amount of IgG and PCR and inoculation
into mice. Presence of toxoplasma-specific IgM in CSF or local production
of specific IgG in CSF establishes the diagnosis of congenital cerebral
toxoplasma infection (McLeod and Remington, 2004).