The relation between severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) infection and demyelinating Guillain‐Barre syndrome (GBS) has been defined. We aim to report the clinical features of a child with axonal GBS associated with SARS‐CoV‐2. A 6‐year‐old male presented with symmetric ascending paralysis progressed over a 4‐day course and 2 days of fever. He had bilateral lower and upper limb flaccid weakness of 1/5 with absent deep tendon reflexes. He had severe respiratory muscle weakness requiring invasive mechanical ventilation. On admission, SARS‐CoV‐2 returned as positive by real‐time polymerase chain reaction on a nasopharyngeal swab. Cerebrospinal fluid analysis showed elevated protein without pleocytosis. He was diagnosed with GBS associated with SARS‐CoV‐2 infection. The nerve conduction study was suggestive of acute motor axonal neuropathy. Ten consecutive therapeutic plasma exchange sessions with 5% albumin replacement followed by four sessions on alternate days were performed. On Day 12, methylprednisolone (30 mg/kg/day for 5 days) was given. On Day 18, intravenous immunoglobulin (2 g/kg/day) was given and repeated 14 days after due to severe motor weakness. On Day 60, he was discharged from the hospital with weakness of neck flexor and extensor muscles of 3/5 and the upper limbs and the lower limbs of 2/5 on home‐ventilation. Our patient is considered to be the youngest patient presenting with a possible para‐infectious association between axonal GBS and SARS‐CoV‐2 infection. The disease course was severe with a rapid progression, an earlier peak, and prolonged duration in weakness as expected in axonal GBS.

Background: The coronavirus disease 2019 pandemic was caused by the novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Although the predominant clinical presentation is a respiratory disease, neurologic manifestations are being recognized increasingly. Case Report: We report 2 children 9 years of age who developed acute disseminated encephalomyelitis-like disease associated with SARS-CoV-2. Seizures and encephalopathy were the main central nervous system symptoms. The cerebrospinal fluid analysis performed within the first week of disease onset showed elevated protein in both children with normal cell count and no evidence of infection including negative SARS-CoV-2 by antibody and polymerase chain reaction. Brain magnetic resonance imaging revealed T2A, fluid-attenuated inversion recovery cortical and subcortical hyperintensity without restricted diffusion consistent with acute disseminated encephalomyelitis–like disease. They received methylprednisolone followed by therapeutic plasma exchange. One of them showed complete clinical improvement and resolution in magnetic resonance imaging findings. The other developed laminar necrosis in brain magnetic resonance imaging and showed significant clinical improvement after therapeutic plasma exchange. He was positive for positive SARS-CoV-2 antibody in cerebrospinal fluid on day 55 of admission. They were both positive for SARS-CoV-2 antibodies in serum after 2 weeks. Conclusions: Our two cases highlight the occurrence of acute disseminated encephalomyelitis–like disease as a postinfectious/immune-mediated complication of SARS-CoV-2 infection.

Multisystem inflammatory syndrome in children (MIS-C) is a rare condition following SARS-CoV-2 infection associated with intestinal manifestations. Genetic predisposition, including inborn errors of the OAS-RNAseL pathway, has been reported. We sequenced 154 MIS-C patients and utilized a novel statistical framework of gene burden analysis, “burdenMC,” which identified an enrichment for rare predicted-deleterious variants in BTNL8 (OR = 4.2, 95% CI: 3.5–5.3, P < 10−6). BTNL8 encodes an intestinal epithelial regulator of Vγ4+γδ T cells implicated in regulating gut homeostasis. Enrichment was exclusive to MIS-C, being absent in patients with COVID-19 or bacterial disease. Using an available functional test for BTNL8, rare variants from a larger cohort of MIS-C patients (n = 835) were tested which identified eight variants in 18 patients (2.2%) with impaired engagement of Vγ4+γδ T cells. Most of these variants were in the B30.2 domain of BTNL8 implicated in sensing epithelial cell status. These findings were associated with altered intestinal permeability, suggesting a possible link between disrupted gut homeostasis and MIS-C-associated enteropathy triggered by SARS-CoV-2.

Background: Influenza is a common cause of hospital admissions worldwide, and an increase in influenza cases has been observed following the COVID-19 pandemic. Our study investigated the epidemiological and clinical characteristics of pediatric patients with influenza infection admitted to pediatric intensive care units (PICUs) in Istanbul, Turkey, following the COVID-19 pandemic. Methods: We conducted a retrospective study of pediatric patients with confirmed influenza infection who were admitted to 1 of the 11 PICUs in Istanbul, Turkey, between July 1, 2022, and June 30, 2024. Data on demographic characteristics, risk factors, clinical presentations, microbiological findings, complications and outcomes were systematically collected. Results: A total of 108 children diagnosed with laboratory-confirmed influenza required admission to the PICUs. Sixty-five (60.2%) were diagnosed with influenza A and 43 (39.8%) patients were diagnosed with influenza B. Epidemiologic and clinical characteristics were similar in both influenza types, oxygen saturation was significantly higher in the influenza A group compared to the influenza B group. Severe neurological manifestations, including seizures and encephalitis, were significantly more common in the Influenza A group. In contrast, patients with Influenza B demonstrated a higher incidence of gastrointestinal symptoms, such as nausea, vomiting and abdominal pain. Pneumonia, sepsis and/or multiorgan dysfunction and liver failure were significantly higher in influenza B. Mortality was observed solely in the Influenza B group, with six patients resulting in death, corresponding to a mortality rate of 14%. Conclusions: Influenza virus infection can cause serious multisystem complications such as acute respiratory distress syndrome and encephalitis. Influenza A can present with isolated or predominant neurological manifestations. Mortality may be more common in influenza B.