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Published on: July 24, 2016
Clinical features of respiratory syncytial virus bronchiolitis in an infant: rapid and fatal brain involvement
Paolo Bottino1, Rebecca Miglino2, Lisa Pastrone2
1A.O.U. "Citta della Salute e della Scienza di Torino", S.C. Microbiology and Virology U., Corso Bramante n. 88, 10126, Turin, TO, Italy. paolo.bottino@unito.it.
Insights
Respiratory Syncytial Virus (RSV) can cause severe neurological damage and sudden infant death, even without obvious brain injury signs. This case highlights the critical need to consider RSV
Area of Science:
- Pediatrics
- Virology
- Neurology
Background:
- Respiratory Syncytial Virus (RSV) is a primary cause of infant hospitalization and mortality globally, mainly through bronchiolitis and pneumonia.
- Emerging evidence highlights extrapulmonary manifestations of RSV, particularly neurological complications, necessitating evaluation even without overt signs of brain involvement.
Observation:
- A 40-day-old infant presented with severe RSV bronchiolitis, hypoxemia, and respiratory acidosis, initially improving with oxygen therapy.
- Clinical deterioration led to preparation for intubation, but the infant died; no neurological signs were evident during emergency care.
- Post-mortem examination revealed lung congestion, atelectasis, and significant brain white matter degradation with edema.
Findings:
- Autoptic analysis confirmed widespread RSV genome presence in respiratory, meningeal, pericardial, abdominal, lung, and brain tissues.
- The case demonstrates systemic RSV dissemination leading to fatal neurological damage and sudden infant death.
Implications:
- This case underscores the neurotropic potential of RSV and its role in sudden infant death, often underestimated.
- Clinicians must maintain a high index of suspicion for neurological involvement in severe RSV cases, irrespective of apparent neurological symptoms.
- Further research into RSV neurotropism is crucial for developing targeted interventions and improving infant outcomes.
Background:
Respiratory Syncytial Virus (RSV) infection is a significant cause of bronchiolitis and pneumonia, mostly responsible for hospitalization and infant death worldwide. However, in recent years the importance of extrapulmonary RSV manifestations, especially at neurological level, have become evident. Seizures, lethargy, ataxia and status epilepticus are suggestive of brain involvement, but also in their absence a direct neurological damage RSV-related need to be evaluated.
Case Presentation:
A 40-day old male infant was admitted to the Emergency Department with severe bronchiolitis and dyspnea. The patient was reported to be coughing for a week with a vomiting episode in the previous two days. The nasopharyngeal swab confirmed the diagnosis of RSV infection and blood gas test showed hypoxemia and respiratory acidosis. For these reasons, the patient was provided with oxygen therapy. A few hours later, after an initial improvement in clinical parameters, a worsening of respiratory dynamics occurred and the patient was prepared for endotracheal intubation, but in the meantime death occurred. During all the observation period in the Emergency Room, no signs of neuropathological damage were evident. Post mortem examination showed lungs congestion with alveolar atelectasis and white matter degradation with severe edema at brain level. Microbiological analysis performed on autoptic samples confirmed the presence of RSV genome in tracheobronchial aspirate, meningeal swabs, pericardic and abdominal fluids, lung and brain biopsies.
Conclusions:
RSV is usually associated with respiratory diseases, however, as reported by an increasingly number of studies, the systemic dissemination of virus during severe disease can lead to a sudden infant death. The clinical picture herein reported showed a severe bronchiolitis resulting in a fatal and underestimated cerebral involvement due to RSV neurotropic behaviour and underline the need for clinicians to pay more attention to neurological involvement of RSV infection, even in absence of cerebral damage evidence.
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