Background
The burden of CMV-associated sensorineural hearing loss (SNHL) in populations with CMV seroprevalence approaching 100% is unknown. The purpose of this study was to assess the rate, associated factors and predictors of SNHL in CMV-infected infants identified by newborn screening in a highly seropositive maternal population.
Methods
Newborns with positive saliva CMV-DNA and confirmed by virus isolation in the first two weeks of life were enrolled in a prospective follow-up study to monitor hearing outcome.
Results
Of 12,195 infants screened, 121 (1%) were CMV-infected and 12 (10%) had symptomatic infection at birth. Hearing function could be assessed in 102/121 children who underwent at least one ABR testing at a median age of 12 months. SNHL was observed in 10/102 (9.8%; 95%CI: 5.1–16.7) children. Median age at the latest hearing evaluation was 47 months (12 to 84 months). Profound loss (>90dB) was found in 4/5 children with bilateral SNHL while all 5 children with unilateral loss had moderate to severe deficit. The presence of symptomatic infection at birth (OR 38.1; 95%CI: 1.6– 916.7) was independently associated with SNHL after adjusting for IUGR, gestational age, gravidity and maternal age. Among 10 infants with SNHL, six (60%) were born to mothers with non-primary CMV infection.
Conclusions
Even in populations with near universal immunity to CMV, congenital CMV infection is a significant cause of SNHL demonstrating the importance of CMV as a major cause of SNHL in children worldwide. As in other populations, SNHL is more frequently observed in symptomatic CMV infection.
Postnatal CMV infection acquired by exposure to raw maternal milk is very frequent among extremely premature newborns, being facilitated by high DNA-lactia and lower GA, regardless of maternally acquired neutralizing antibody levels. The association with advanced stages of ROP is a concern and needs to be further explored in larger studies.
We determined the risk of seroconversion in seronegative pregnant women living in a high seroprevalence population. Cytomegalovirus (CMV)-immunoglobulin G reactivity was determined at the 1st trimester in all women and sequentially for seronegative women. A total of 1915 of 1952 (98.1%; 95% confidence interval [CI], 97.4%-98.7%) women were seropositive, and 36 (1.8%; 95% CI, 1.3%-2.6%) were seronegative. Five of the 36-seronegative women seroconverted for a cumulative rate of 13.9% (95% CI, 4.8%-30.6%). Congenital CMV infection was diagnosed in 1 of 36 infants (2.8%; 95% CI, 0.5%-63.9%) born to seronegative women compared with 8 of 1685 (0.5%; 95% CI, 0.2%-1.0%) infants born to seropositive mothers. Even with a high risk of primary infection in seronegative women, most CMV-infected infants were born to women with pre-existing seroimmunity.
CMV shedding is relatively frequent in seropositive pregnant women. The association between virus shedding and caring for young children as well as crowded living conditions may provide opportunities for increased exposures that could lead to CMV reinfections in seropositive women.
Congenital cytomegalovirus (CMV) infection rates increase with maternal seroprevalence due to transmission from maternal non-primary infection. CMV seroprevalence estimates of pregnant women are needed for planning strategies against congenital CMV transmission. We aimed to determine the age-specific prevalence of serum antibodies for CMV in a representative age-stratified sample of unselected pregnant women from a Brazilian population. A total of 985 pregnant women, aged 12–46 years (median 24 years), were enrolled. Overall CMV seroprevalence was 97% (95% confidence interval 95.8–98.0), with age-specific (years) prevalence as follows: 12–19 (96.3%), 20–24 (97.7%), 25–29 (97.1%), and 30–46 (96.7%). CMV seroprevalence is almost universal (97%) and is found at similar levels in pregnant women of ages ranging from 12 to 46 years. Because high CMV seroprevalence is found even in women of a younger age in this population, this finding suggests that the majority of primary CMV infections occur early, in infancy or childhood. As a consequence, vaccines currently under development to prevent primary infection may not be a solution for the prevention of congenital CMV infection in this population.
We concluded that AMX-CLAV for 14 days did not change the clinical course of AECRS compared with placebo. The addition of an oral antibiotic to ongoing topical intranasal steroid spray may not provide additional benefit during management of AECRS.
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