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Homeless shelter residents and staff may be at higher risk of SARS-CoV-2 infection. However, SARS-CoV-2 infection estimates in this population have been reliant on cross-sectional or outbreak investigation data. We conducted routine surveillance and outbreak testing in 23 homeless shelters in King County, Washington, to estimate the occurrence of laboratory-confirmed SARS-CoV-2 infection and risk factors during 1 January 2020–31 May 2021. Symptom surveys and nasal swabs were collected for SARS-CoV-2 testing by RT-PCR for residents aged ≥3 months and staff. We collected 12,915 specimens from 2,930 unique participants. We identified 4.74 (95% CI 4.00–5.58) SARS-CoV-2 infections per 100 individuals (residents: 4.96, 95% CI 4.12–5.91; staff: 3.86, 95% CI 2.43–5.79). Most infections were asymptomatic at the time of detection (74%) and detected during routine surveillance (73%). Outbreak testing yielded higher test positivity than routine surveillance (2.7% versus 0.9%). Among those infected, residents were less likely to report symptoms than staff. Participants who were vaccinated against seasonal influenza and were current smokers had lower odds of having an infection detected. Active surveillance that includes SARS-CoV-2 testing of all persons is essential in ascertaining the true burden of SARS-CoV-2 infections among residents and staff of congregate settings.
Convulsive status epilepticus (CSE) is a common neurological emergency. Our objectives were to study children with recurrent nonfebrile CSE to assess the evidence for focal origin.
Series of 18 children with recurrent CSE and intractable epilepsy were identified by chart review. Clinical, radiological, and EEG data were reviewed. Focal structural abnormalities were identified on MRI and CT images by one neuroradiologist who was unaware of the clinical details.
The patient's ages ranged between 6-22 years (mean 15.3, SD 4), and 67% were males. Most children (89%) had a severe cognitive and / or behavioural disorder. Most patients (89%) had multiple seizure types and 95% of these were partial seizures. Twelve (67%) children had at least one episode of CSE with focal features identified clinically. Focal brain abnormalities were detected on 18% and 55% of CTand MRI films respectively. Overall, 53% had a focal abnormality on structural neuroimaging. Interictal EEG revealed focal or multifocal abnormalities on at least one occasion in 94% and 22% of patients respectively. Overall, 17 patients had focal features on at least one EEG. Thirteen ictal EEGs were recorded on 11 (61%) patients. Ten (91%) of these recordings revealed a focal onset.
Many handicapped children with recurrent CSE have focal clinical, radiological, or electrographic features. This supports a focal origin for CSE in most children with intractable epilepsy.
Rett syndrome (RTT) is a severe neurodevelopmental disorder affecting females almost exclusively and is characterized by a wide spectrum of clinical manifestations. Mutations in the X-linked methyl-CpG-binding protein 2 (MECP2) gene have been found in up to 95% of classical RTT cases and a lesser proportion of atypical cases. Recently, mutations in another X-linked gene, CDKL5 (cyclin-dependent kinase-like 5) have been found to cause atypical RTT, in particular the early onset seizure (Hanefeld variant) and one female with autism. In this study we screened several cohorts of children for CDKL5 mutations, totaling 316 patients, including individuals with a clinical diagnosis of RTT but who were negative for MECP2 mutations (n = 102), males with X-linked mental retardation (n = 9), patients with West syndrome (n = 52), patients with autism (n = 59), patients with epileptic encephalopathy (n = 33), patients with Aicardi syndrome (n = 7) and other patients with intellectual disability with or without seizures (n = 54). In all, seven polymorphic variations and four de novo mutations (c.586C>T [p.S196L]; c.58G>C [p.G20R]; c.2504delC [p.P835fs]; deletion of exons 1 - 3) were identified, and in all instances of the latter the clinical phenotype was that of an epileptic encephalopathy. These results suggest that pathogenic CDKL5 mutations are unlikely to be identified in the absence of severe early-onset seizures and highlight the importance of screening for large intragenic and whole gene deletions.
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