ABSTRACT
Background: Household overcrowding is associated with increased risk of infectious diseases across contexts and countries. Limited data exist linking household overcrowding and risk of COVID-19. We used data collected from the Virus Watch cohort to examine the association between overcrowded households and SARS-CoV-2.
ABSTRACT
Objective: Paediatric neurologists are concerned about the risk of COVID-19 in children with demyelinating disorders receiving immunomodulatory treatment. To investigate this, we collected data via the UK Childhood Neuro-Inflammatory Disorders (UK-CNID) network of the British Paediatric Neurology Association (BPNA). Methods: Survey of paediatric neurologists managing unvaccinated UK children (<18 years) with a demyelinating disorder (multiple sclerosis [MS];neuromyelitis optica spectrum disorder [NMOSD] and myelin oligodendrocyte glycoprotein antibody disease [MOGAD]) on immunomodulatory therapy with SARS-CoV-2 infection confirmed by reverse transcriptase-polymerase chain reaction (RT-PCR) of nasopharyngeal swabs between March and December 2020. Results: Of 151 UK children (MS 98, MOGAD 37, NMOSD 16) with a median age of 9 years (range 6-18y), with a demyelinating disorder, nine (6.0%) had a positive PCR for SARS-CoV-2. Five had MS and four MOGAD. Four were from south Asian or south-east Asian, four were White and one was mixed White and south Asian. Seven children had COVID-19 symptoms;two were asymptomatic. Two required a brief hospital admission for typical COVID-19 respiratory symptoms and the remaining five had mild symptoms including fever, rash, cough and headache. One with MOGAD, treated with azathioprine, developed transverse myelitis 12 days after COVID-19 onset. She recovered fully with a course of corticosteroids. MS patients were on following disease modifying therapies;dimethylfumarate (n=2), fingolimod (n=1);natalizumab (n=1) and ocrelizumab (n=1). MOGAD cases were on the following immune therapy: combination of oral prednisolone and intravenous immunoglobulin (n=2), prednisolone steroids (n=1) and azathioprine (n=1). Conclusions: In contrast to adult patients, who often have underlying co-morbidities and advanced neurological disabilities, we have identified that children treated for demyelinating disorders appear to have a milder COVID-19 course. Whilst the number of children treated for demyelinating disorders that developed COVID-19 is low, the overall mild course described may provide reassurance to neurologists, patients and family members.
ABSTRACT
Background: Many neuroinflammatory disorders including autoimmune and post-infectious encephalitis are observed to have a seasonal variation. We evaluated changes in the incidence of neuroinflammatory disorders in association with the COVID-19 pandemic, hypothesising that social distancing and changes in health behaviour would lead to a reduction in infection-triggered conditions. Methods: In this single institution retrospective study, we reviewed all children admitted during the COVID-19 pandemic between March 2020 and March 2021, identifying those with new onset and non-COVID associated acute demyelinating syndrome (ADS), multiple sclerosis (MS), Guillain-Barre syndrome (GBS), autoimmune encephalitis (AE) and post-infectious encephalitis (PIE). Incidences were compared with the three years pre-pandemic (2017-2020). Two-tailed p-values were calculated from z-scores for 2020 to 2021 with respect to the 2017 to 2020 distributions. Results: The number of children admitted with AE during the COVID-19 pandemic (2020-2021) was 3, compared to 7.67 (annual mean during 2017-2020) representing a 61% decline (p<0.001). PIE decreased by 30% from a mean of 10 to 7 (p=0.26). Whereas, GBS, ADS and MS were not statistically significant with 3, 6 and 10 admissions during the pandemic compared to a mean of 3.33, 8.33 and 9.33 admissions in 2017 to 2020, respectively. Conclusion: The significant decrease in the incidence of AE during the COVID-19 pandemic suggests that disruptions to seasonal endemic infection transmission by changes in social mixing and health behaviours can modify the link between infection and autoimmune encephalitides. However, incidence of other neuroinflammatory conditions typically presumed to have an infectious trigger such as GBS and ADS was not reduced, suggesting infectious triggers may either be less important in the aetiology of these conditions or that this link is more complex and cannot be observed within the epoch of behavioural change. Autoimmune induction may indeed involve longer lags from infection, require a second infection and be influenced by other environmental and genetic factors.