Shamez Ladhani (United Kingdom)
St George's, University of London Paediatric Infectious Diseases Research GroupAuthor Of 2 Presentations
HERPES SIMPLEX VIRUS IN INFANTS UNDER 90 DAYS OF AGE: INTERIM RESULTS OF THE 2019-2021 BRITISH PAEDIATRIC SURVEILLANCE UNIT (BPSU) STUDY
Abstract
Backgrounds:
Neonatal herpes simplex virus (HSV) infection is a rare but dangerous condition. A recent study suggests that the UK incidence may have increased since the last national surveillance study in 2007. Rising numbers of cases may support the wider use of empirical treatment. Postnatal transmission is thought to account for ~10% of cases. More information about this disease is required to inform future prevention and treatment strategies.
Methods
Analysis of questionnaires completed for the current British Paediatric Surveillance Unit neonatal HSV study was conducted. Semi-anonymised patient identifiers allow removal of duplicate cases. The study was extended from 25 months to 30 months to capture additional data on changing trends during the COVID-19 pandemic. Interim results are reported here.
Results:
228 cases were notified July 19 - Dec 2021. 159 questionnaires were completed and basic data on 111 cases was available after duplications and incomplete records were removed. 29.7% were premature, 26.1% died. Full data analysed on the first 80 cases (July 19-April 21) show: 27.0% were premature, 26.9% had disseminated disease and mortality was 71.0% in disseminated disease. 23.8% of babies with disseminated disease had no fever at presentation. Treatment was delayed by more than one day in 60%. Case notifications reduced during UK lockdown periods.
Conclusions/Learning Points:
UK incidence of neonatal HSV disease has increased since the last BPSU study. Mortality remains high and presenting features are non-specific. Absence of fever at presentation demonstrates that HSV should not only be considered in febrile infants. Falling numbers of reported cases during periods of social distancing and strict public hygiene measures may highlight the importance of postnatal transmission. Follow-up focusing on disease recurrence and long-term complications at 12 and 24 months is ongoing.
LOWER RISK OF MULTISYSTEM INFLAMMATORY SYNDROME IN CHILDREN (MIC-S) WITH THE DELTA VARIANT OF SARS-COV-2
Abstract
Backgrounds:
Multisystem Inflammatory Syndrome in Children (MIS-C, also known as PIMS-TS) typically occurs 2-6 weeks after exposure to SARS-CoV-2. Early estimates suggested a risk of MIS-C of 1 in 3-4000 infected children. Whether this risk is sustained with new SARS-CoV-2 variants remains unknown.
Methods:
We utilised prospective data from the NHS South Thames Paediatric Network (STPN), which manages all cases of MIS-C amongst 1·5 million children in South-East England, to assess trends over time. We compared MIS-C cases with two independent SARS-CoV-2 infection datasets. We used publicly available UK Health Security Agency case numbers weighted to child population distributions according to area population estimates from the Office for National Statistics (ONS). To avoid bias due to evolving testing behaviour, we also compared MIS-C cases to community infection rates, obtained from the ONS COVID-19 Infection Survey, which randomly selects individuals for fortnightly PCR tests. All three datasets were normalised to the peak of the Alpha wave, and plotted against time. MIS-C cases were plotted 40 days prior to hospitalisation, corresponding to the best fit of rising SARS-CoV-2 infection and MIS-C cases during the Alpha wave.
Results:
Compared with the Alpha wave, we found fewer cases of MIS-C relative to SARS-CoV-2 infections during both initial and subsequent Delta waves. This relative reduction continued into the Omicron wave.
Conclusions/Learning Points:
Re-infection rates with the Alpha or Delta variants and vaccination rates were very low during the Delta wave. As a result, lower MIS-C rate relative to SARS-CoV-2 infections during the Delta wave is unlikely to be explained by population level immunity from prior infection or vaccination. It is most likely due to viral mutations in key antigenic epitopes responsible for triggering the hyperinflammatory response observed with MIS-C.