ABSTRACT
Background: On the 5th of April 2022, cases of adenovirus-induced hepatitis were reported in Scotland and then reached multiple parts of the world. While adenovirus normally presents with diarrhea, vomiting, and fever, these novel cases also resulted in the development of fulminant hepatitis in non-immunocompromised cases. Main body: The responsible pathogen “Adenovirus 41” is an enterovirus. Enteroviruses are spread by the fecal-oral route and are resistant to drying. As such, they predominate in sewage water. Hepatitis is normally restricted to poorer countries, yet this new wave seems to be confined to mostly high-income countries in Europe and the USA. These countries treat and recycle a higher percentage of sewage water. We also propose that the fulminant nature of this strain could be due to either a cross-species mutation or the general decrease in trained immunity post-COVID-19 lockdown. Short conclusion: Evidence strongly suggests that the link between these new hepatitis cases is recycled sewage water. This should warrant further investigations on the origin of this outbreak by re-visiting the role of recycled sewage water in causing such outbreak.
ABSTRACT
Prothrombotic states, similar to heparin-induced thrombocytopenia (HIT) in recipients of the ChAdOx vaccine, sounded alarm bells internationally. Equivalent episodes of HIT were detailed in several case reports of coronavirus disease 2019. This suggests a common pathogenesis and warrants a shift in the management of implicated cases.
ABSTRACT
Background: Coronavirus disease 2019 (COVID-19) emerged as a small outbreak in Wuhan rapidly progressing into the deadliest pandemic since the Spanish flu of 1918. The disease was deemed trivial in children, until the reporting, few days ago, of an emerging pediatric multi-inflammatory syndrome mimicking Kawasaki disease (KD). Main body: This report reveals that coronaviridae were implicated in induction of several post-infectious vasculitides, namely, KD, AHEI, and HSP. This occurs in genetically susceptible individuals to vascular inflammation. Shared genetic susceptibilities between KD and CoV include genes encoding for CD 40, HLAB-15:03, and ACE. This leads to augmented inflammation with hypersecretion of cytokines especially IL-6. Conclusion(s): The revealed relationships between KD and CoV can help to predict the risk of KD in COVID-19 patients through screening levels of upregulated cytokines. It might also signify that classic treatment of KD with IVIG might need to be replaced with anti-cytokine therapy in COVID-19 patients. Copyright © 2020, The Author(s).