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The Puritan cleric blamed the resistance on Satan, but in fact issues of freedom-including arguments from Benjamin Franklin's brother, who was seeking to establish a free press-fueled the opposition to inoculation even in such a fervently religious environment so long ago.2 Colgrove and Samuel's focus on the power of ideas about freedom and rights is thus highly significant and should be of substantial interest to policymakers. In their conclusion, they correctly note that "[g]iven the grave public health threat posed by COVID-19 and the safety and efficacy of the available vaccines, compulsory measures are well justified from the standpoints of ethics, policy, and law" (p. 240). If this is all that history tells us, then the only real lesson we will learn is one that we likely already know: that we will, perhaps tragically, never be able to move toward a just and effective resolution of the fundamental paradox of a collectivist-oriented public health in a land of individual liberty.10 So what does "history" reveal here, or at least strongly predict?
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PURPOSE OF REVIEW: The novel severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the most critical public health challenge in recent history. In this report, we present a case of suspected acute hemorrhagic encephalitis with bilateral intracranial hemorrhages associated with coronavirus disease 2019 (COVID-19) infection. RECENT FINDINGS: A 48-year-old female COVID-19-positive patient developed acute changes in her neurologic status. A head CT with CT angiography demonstrated extensive bilateral parietal and occipital intraparenchymal hemorrhage with intraventricular extension and acute hydrocephalus. The patient was treated with an external ventricular drain, and a CSF sample was tested for SARS-CoV-2 but was found to be negative. SUMMARY: The underlying mechanism for developing acute hemorrhagic encephalitis in viral illnesses may be autoimmune in nature and warrants further investigation. The initial neurologic presentation of COVID-19-related hemorrhagic encephalitis is altered level of consciousness, which may prompt further neurologic examination and imaging to exclude this feature.
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BACKGROUND: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the cause of an ongoing pandemic, with increasing deaths worldwide. To date, documentation of the histopathological features in fatal cases of the disease caused by SARS-CoV-2 (COVID-19) has been scarce due to sparse autopsy performance and incomplete organ sampling. We aimed to provide a clinicopathological report of severe COVID-19 cases by documenting histopathological changes and evidence of SARS-CoV-2 tissue tropism. METHODS: In this case series, patients with a positive antemortem or post-mortem SARS-CoV-2 result were considered eligible for enrolment. Post-mortem examinations were done on 14 people who died with COVID-19 at the King County Medical Examiner's Office (Seattle, WA, USA) and Snohomish County Medical Examiner's Office (Everett, WA, USA) in negative-pressure isolation suites during February and March, 2020. Clinical and laboratory data were reviewed. Tissue examination was done by light microscopy, immunohistochemistry, electron microscopy, and quantitative RT-PCR. FINDINGS: The median age of our cohort was 73·5 years (range 42-84; IQR 67·5-77·25). All patients had clinically significant comorbidities, the most common being hypertension, chronic kidney disease, obstructive sleep apnoea, and metabolic disease including diabetes and obesity. The major pulmonary finding was diffuse alveolar damage in the acute or organising phases, with five patients showing focal pulmonary microthrombi. Coronavirus-like particles were detected in the respiratory system, kidney, and gastrointestinal tract. Lymphocytic myocarditis was observed in one patient with viral RNA detected in the tissue. INTERPRETATION: The primary pathology observed in our cohort was diffuse alveolar damage, with virus located in the pneumocytes and tracheal epithelium. Microthrombi, where observed, were scarce and endotheliitis was not identified. Although other non-pulmonary organs showed susceptibility to infection, their contribution to the pathogenesis of SARS-CoV-2 infection requires further examination. FUNDING: None.