The incidence of congenital CMV infection ranges from 0.2% to 2.

2% with average
1% of all live births with higher rates among populations with a lower economic standard of
living. The risk for fetal infection is greatest with maternal primary CMV infections (30%)
and much less likely with recurrent infection (less than 1%). After the first year of life, the
prevalence of infection depends on group activities which is infection rate 50-80% during
childhood.1

CMV infection has two forms of transmission such as maternal and horizontal.2
Transmission sources of CMV include saliva, breast milk, cervical and vaginal secretions,
urine, semen, tears, blood products and organ allographs. There are three main mechanisms for
developing acquired CMV such as contamination with blood and body fluids during vaginal
birth, transmission of the virus during blood product administration and most commonly via
breastfeeding.3 CMV transmission by younger children is facilitated by the prolonged duration
of viral excretion in both saliva and urine. For children younger than 2 years of age who
acquired a CMV infection postnatally, CMV is excreted for an average of 18 months (range 6
to 40 months). In contrast, viral excretion in urine and saliva of healthy older children who a
primary CMV infection usually occurs for only a few days to several weeks, although some
individuals may excrete the virus for longer periods.4

The effects of CMV infection may vary from a congenital syndrome to an

asymptomatic course. In approximately 5% of infants CMV becomes clinically manifest with
damage to many organs including the liver, spleen, brain, eye and inner ear.5 (Level of
Evidence 3) Congenital infection causes neurologic and hematologic damage and
developmental defects which are evident at birth in 10% of infected babies.6 The sign and
symptoms of CMV infection vary with age, route of transmission and immunocompetence of
the patient. In infants and young children, primary CMV infection occasionally causes
pneumonitis, hepatomegaly, hepatitis and petechial rahes.1,7 In older children symptoms
resembling mild acute viral hepatitis or infectious mononucleosis may occur but often infection
is asymptomatic or result in only a mild non-specific febrile illness.7
In symptomatic forms of acquired CMV, the first signs are observed at the age of 2-3
months.8 Opthalmologic examination reveals chorioretinitis and or optic atrophy in
approximately 10% of symptomatic infants.9 (Level of Evidence 2) In Soomro study,
symptomatic of CMV infection such as fever (97%) and pruritis (93.9%). Microcephaly was
noticed in 57.6% in this study.10 (Level of Evidence 2) In this case, there are microcephaly
that assessed from 2 months years old represent of CMV symptoms. The patient also
diagnosed with CVI and had a 3 months evaluation control. In the Samileh study, CMV
infection which is IgM positive was detected in 34.7% of sensorineural hearing loss cases with
mean age 40 months.(Level of Evidence 3) A hearing loss had an adverse effect on the
development of language and communication skill.12 In Smiechura et al, there was 23%
sensorineural hearing loss in the gorup of children with congenital CMV and there no
sensorineural hearing loss in the gorup of children with acquired CMV. This study concluded
that all the children with congenital and acquired CMV should be monitored and assessed
throughtout their lifetime by an audiologist.13 (Level of Evidence 2) The clinical complication
of CMV can be divided into direct and indirect effect. CMV pneumonia is clearly the most

serious complication and rare manifestations include retinitis and encephalitis.13

Radiographic findings in the brain are abnormal in approximately 50-70% of children with
symptomatic infection in birth. The most finding is intracranial calcifications, with ventricular
dilatation, cysts and lenticulostriate vasculopathy occuring in varying proportions.9 In this
case, calcification was obtained from the brain MSCT

Approximately 6-12% of seropositive mothers transmit CMV by contaminated

cervical-vaginal secretion and 40% by breast milk to their infants, who usually remain
asymptomatic and do not exhibit sequelae. Premature and ill aterm infants may have
neurologic sequelae and psychomotor retardation. However, the risk for hearing loss,
chorioretinitis and microchepaly does not appear to be increased.1 The fetal infection may
cause the interruption of pregnancy, prematurity, low birth weight in full term newborns and
several congenital malformations such as inguinal hernia, cleft palate, dental abnormalities,
polycyctic kidneys, mitral and pulmonary stenosis, atrial and ventricular defect and atresia of
the biliary ducts.14 In this case, the mother had no prior CMV serologic test. During perinatal
period the patient had low birth weight but no congenital malformation was found

Diagnosis of active CMV infection is best confirmed by virus isolation from urine,
saliva, bronchoalveolar washings, breast milk, cervical secretion, buffy coat, and tissues
obtained by biopsy. Several methods are used for rapid quantitative detection of CMV
antigens and quantitative PCR assays are also available.1 A primary infection is confirmed by
seroconversion or the simultaneous detection of immunoglobin IgM and IgG antibodies with
low functional avidity.15 In this case both CMV IgG and IgM antibodies were positive.

Treatment of children with congenital CMV infection with ganciclovir

recommended.5,15,17 Ganciclovir is a drug whose effectiveness against CMV has been
proven.18 (Level of Evidence 1) Ganciclovir combined with intravenous immunoglobulin
(IVIG) has been used to treat life-threatening CMV infections. Two publihed regimens are
ganciclovir (7.5mg/kg/day devided every 8 hour intravena for 14 days) with CMV IVIG
(400mg/g on day 1, 2 and 7 and 200mg/kg on day 14) or ganciclovir 7.5mg/kg/day divided
every 8 hour intravena for 20 days with IVIG 500mg/kg every other day for 10 doses. 1,19 That
treatment followed by maintenance dosing for 3-4 weeeks. Treatment should be continued until
resolution of symptoms and negativation of viral load.19 When CMV infection is diagnosed in
the first year of life, treatment with ganciclovir is recommended and its associated with
diminished occurance of sensorineural hearing loss.17 (Level of Evidence 3) Prolonged
treatment of 3 months may yield better virologic and perhaps also clinical and biochemical
result, as suggested by Nigro et al.22 (Level of Evidence 1) Toxicity with ganciclovir is frequent
and often severe and includes neutropenia, thrombocytopenia, liver dysfuction, reduction in
spermatogenesis and gastrointestinal and renal abnormalities.1 A randomized controlled study
with ganciclovir (6mg/kg/dose every 12 hour intravena for the first 6 week of life) concluded that
treatment both prevents hearing deterioration and improves or maintains normal hearing
function at 6 months of age and may prevent hearing deterioration that occurs after 1 year of
age.1 A randomized study of oral valganciclovir is under way to compare the effiency of 42
days of treatment with 6 months of treatment. In addition, treated patients with a 6 week course
decreased in viral load of 0.7 log viral DNA copies/mL in urine. Toxicity of valganciclovir is
similar to that ganciclovir with 38% of subjects developing neutropenia.21 (Level of Evidence
1) In this case, the child received valganciclovir for 6 weeks.
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