Background: Parechovirus-A3 (PeV-A3) is an emerging pathogen causing sepsis and meningoencephalitis in neonates and young infants. We previously reported that maternal antibodies against PeV-A3 are important to protect neonates and young infants from the infection. We showed that all neonates and infants who developed PeV-A3-related diseases had low neutralizing antibody titers (NATs) against PeV-A3 at the onset of disease, subsequently developed high NATs at 3 and 6 months of age. Subsequent changes in NATs against PeV-A3 in children who suffered from PeV-A3-related diseases are currently unknown. Additionally, their long-term neurological outcome is not well described in such population.
Methods: Subjects were PeV-A3-infected infants less than 4 months in Niigata, Japan during 2013-2014, and follow-up serum samples were obtained longitudinally from the patients at 3, 6 months, 1 and 3 years after the infection. NATs against PeV-A3 were measured using LLC-MK2 cells. Neurological outcomes of the patients were evaluated by their pediatricians at their study visits.
Results: We evaluated 45, 34, 33, 26, and 16 serum samples at onset, 3, 6 months, 1 and, 3 years after the infection, respectively. All 45 serum samples at onset had low NATs against PeV-A3 less than 1:32 which was regarded as a cutoff to prevent PeV-A3 infection. Subsequently, the NATs had elevated to the high level (≥1:512) after the infection in all patients. Three years after the infection, all patients except one achieved normal neurodevelopmental milestones. Only one patient who was diagnosed as severe status epileptics due to meningoencephalitis had developmental delay with difficulties in sitting and walking with support.
Conclusion: This study showed that NATs against PeV-A3 sustained high levels in patients who had severe PeV-A3-related diseases in their neonatal or young infantile periods. Neurological outcomes of the patients who suffered from PeV-A3-related diseases seem to be excellent, except for the case with complicated clinical course.
K. Watanabe, None
A. Saitoh, None