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Published on: July 24, 2016
Congenital Cytomegalovirus among Children with Cerebral Palsy
Hayley Smithers-Sheedy1, Camille Raynes-Greenow2, Nadia Badawi3
1Marie Bashir Institute for Infectious Diseases and Biosecurity, Sydney Medical School, The University of Sydney, Sydney, New South Wales, Australia; The Children's Hospital at Westmead, Westmead, New South Wales, Australia; Cerebral Palsy Alliance, Sydney Medical School, The University of SydneySydney, New South Wales, Australia.
Insights
Congenital cytomegalovirus (CMV) infection, detected via newborn screening cards (NBSC), is common in children with cerebral palsy (CP). This study found CMV DNA in 9.6% of CP cases, linked to epilepsy but not spasticity patterns.
Area of Science:
- Virology
- Neurology
- Pediatrics
Background:
- Congenital cytomegalovirus (CMV) infection is a leading non-genetic cause of cerebral palsy (CP).
- Early detection of congenital CMV infection is crucial for understanding its role in neurodevelopmental disorders.
- Newborn screening cards (NBSC) offer a potential retrospective method for identifying congenital CMV exposure.
Purpose of the Study:
- To determine the prevalence of cytomegalovirus (CMV) DNA in newborn screening cards (NBSC) of children diagnosed with cerebral palsy (CP).
- To compare CMV DNA detection rates across different spastic subtypes of CP.
- To analyze demographic and clinical characteristics of children with CP associated with congenital CMV infection.
Main Methods:
- A retrospective observational study analyzed patient records and NBSCs from children with CP (birth years 1996-2014) in Australia.
- Nested polymerase chain reaction (PCR) was used to detect CMV DNA in NBSCs, with positive results validated by real-time PCR.
- Data on clinical characteristics, including spasticity patterns and epilepsy, were extracted from CP registers and rehabilitation services.
Main Results:
- Of 323 children with available NBSCs, 9.6% tested positive for CMV DNA, with 8.7% confirmed by a second PCR method.
- CMV DNA detection in NBSCs was significantly associated with the presence of epilepsy in children with CP.
- No significant association was found between CMV DNA detection and sex or spasticity subtypes in children with CP.
Conclusions:
- Congenital CMV infection, indicated by CMV viremia in the newborn period, is highly prevalent in children with cerebral palsy.
- Further research is warranted to elucidate the mechanisms by which congenital CMV contributes to the development of CP.
- Retrospective analysis of NBSCs is a viable method for assessing the role of congenital CMV in CP etiology.
Objectives:
To determine the proportion of children with cerebral palsy (CP) and cytomegalovirus (CMV) DNA detected retrospectively in their newborn screening cards (NBSC), to compare the proportion of children with CMV DNA in their NBSC across spastic subtypes of CP, and to compare the sex and other characteristics of children with CP and CMV detected on their NSBC with those in whom CMV DNA was not detected.
Study Design:
Retrospective observational study. Data were extracted from patient records on children with CP (birth years 1996-2014) from 2 Australian state CP registers and state-wide paediatric rehabilitation services with consent. NBSCs were retrospectively analyzed for CMV DNA by nested polymerase chain reaction (PCR) using primers against gB. Positive samples were validated using real time PCR for CMV UL83.
Results:
Of 401 children recruited, 323 (80.5%) had an available NBSC. Of these, 31 (9.6%; 95% CI, 6.8-13.3) tested positive for CMV DNA by nested PCR for CMV gB, of whom 28 (8.7%; 95% CI, 6.1-12.2) also had CMV DNA detected by real-time PCR for CMV UL83. Detection of CMV DNA was significantly associated with epilepsy, but not with clinical or epidemiologic characteristics, including sex and pattern of spasticity.
Conclusions:
CMV viremia in the newborn period, indicating congenital CMV infection, is highly prevalent among children with CP. Further research is needed to investigate the mechanisms and contribution of congenital CMV to the causal pathways to CP.
