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Published on: December 10, 2013
Respiratory syncytial virus-associated mortality in a healthy 3-year-old child: a case report
A Gavotto1,2, A Ousselin3, O Pidoux3
1Pediatric and Congenital Cardiology Department, Arnaud de Villeneuve Hospital, Montpellier University Hospital Center, Montpellier, France.
Insights
Respiratory syncytial virus (RSV) can cause sudden cardiac death in children, even without comorbidities. This case highlights RSV-induced myoepicarditis and autonomic nervous system inflammation as potential causes of unexpected death.
Area of Science:
- Pediatric Cardiology
- Infectious Diseases
- Molecular Genetics
Background:
- Respiratory syncytial virus (RSV) is a leading cause of acute lower respiratory tract infections in children.
- Fatalities are most common in infants under six months or those with comorbidities.
Observation:
- A previously healthy 47-month-old girl experienced sudden cardiopulmonary arrest.
- Postmortem analysis revealed RSV, viral myoepicarditis, and inflammation of cardiac nerves and ganglia.
- A heterozygous mutation in myosin light chain 2 was identified, also present in healthy family members.
Findings:
- RSV infection was confirmed as the cause of death.
- Viral myoepicarditis and autonomic nervous system inflammation were implicated in the cardiac arrest.
- The role of the myosin light chain 2 mutation in this sudden death is uncertain.
Implications:
- RSV can lead to severe extrapulmonary manifestations, including fatal arrhythmias.
- This case underscores the importance of considering viral infections in unexplained pediatric sudden death.
- Further research is needed to understand the interplay between genetic predisposition and viral infections in sudden cardiac death.
Background:
Respiratory syncytial virus (RSV) is the most frequently identified pathogen in children with acute lower respiratory tract infection. Fatal cases have mainly been reported during the first 6 months of life or in the presence of comorbidity.
Case Presentation:
A 47-month-old girl was admitted to the pediatric intensive care unit following sudden cardiopulmonary arrest occurring at home. The electrocardiogram showed cardiac asystole, which was refractory to prolonged resuscitation efforts. Postmortem analyses detected RSV by polymerase chain reaction in an abundant, exudative pericardial effusion. Histopathological examination was consistent with viral myoepicarditis, including an inflammatory process affecting cardiac nerves and ganglia. Molecular analysis of sudden unexplained death genes identified a heterozygous mutation in myosin light chain 2, which was also found in two other healthy members of the family. Additional expert interpretation of the cardiac histology confirmed the absence of arrhythmogenic right ventricular dysplasia or hypertrophic cardiomyopathy.
Conclusions:
RSV-related sudden death in a normally developing child of this age is exceptional. This case highlights the risk of extrapulmonary manifestations associated with this infection, particularly arrhythmia induced by inflammatory phenomena affecting the cardiac autonomic nervous system. The role of the mutation in this context is uncertain, and it is therefore necessary to continue to assess how this pathogenic variant contributes to unexpected sudden death in childhood.
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