Preparing for an epidemic of limited health literacy: weathering the perfect storm.
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ABSTRACT:
SUBMITTER: Parker RM
PROVIDER: S-EPMC2517979 | biostudies-other | 2008 Aug
REPOSITORIES: biostudies-other
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Project description:Coronavirus disease 2019 (COVID-19) accounts for over 180,000 deaths in the USA. Although COVID-19 affects all racial ethnicities, non-Hispanic Blacks have the highest mortality rates. Evidence continues to emerge, linking the disproportion of contagion and mortality from severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2), a result of adverse social determinants of health. Yet, genetic predisposition may also play a credible role in disease transmission. SARS-CoV-2 enters cells by interaction between SARS-CoV-2 spike protein and the receptor molecule angiotensin converting enzyme 2 (ACE2) expressed on the surface of the target cells, such that polymorphisms and the expression level of ACE2 influence infectivity and consequent pathogenesis of SARS-CoV-2. Genetic polymorphisms in other multiple genes, such as acetylcholinesterase (AChE) and interleukin-6, are also closely associated with underlying diseases, such as hypertension and type 2 diabetes mellitus, which substantially raise SARS-CoV-2 mortality. However, it is unknown how these genetic polymorphisms contribute to the disparate mortality rates, with or without underlying diseases. Of particular interest is the potential that genetic polymorphisms in these genes may be influencing the disparity of COVID-19 mortality rates in Black communities. Here, we review the evidence that biological predisposition for high-risk comorbid conditions may be relevant to our ability to fully understand and therefore address health disparities of COVID-19 deaths in Blacks.
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Project description:AimsOur aim is to identify important attributes of major diseases that shape how they are perceived by the public.Methods and resultsFour focus groups among members of the public were recruited, in March and October 2016, and used semistructured discussion to explore important attributes of cancer, heart disease, stroke, dementia, mental illness, and infectious disease. Common themes were identified by using inductive thematic analysis.Five themes were identified: fear, impact on family and friends, hope, detection, and prevention. Fear of cancer includes not only fear of death but also of aggressive treatments. Loss of dignity is feared in dementia, while infectious disease raises fear of uncontrollable "plague"; in contrast, people with mental illness may themselves be seen as a potential threat. The impact of cancer and its treatment on family and friends was described as intense and all-consuming, even for those not involved directly in caring; with dementia and stroke, the family impact is taking on care, including funding, over the long term with little expectation of improvement. Hope is a major theme in cancer and stroke recovery, linked with the need to take action, often expressed in aggressive language of "fighting," but seen as futile in dementia. Detection difficulties for "silent" cancers mean that real treatment opportunities are missed; cardiovascular and infection risk, however, are seen as easy to identify and act on, whereas mental illness and dementia are seen as poorly diagnosed and with limited treatment options. Prevention awareness is high for cardiovascular disease and infection, lower for cancer, and limited for dementia and mental health.ConclusionAlthough themes overlap across diseases, the specific concerns are different and each condition has a unique profile. Quantifying the relative importance of these themes could allow their incorporation in decision-making, not only when they occur as a named disease but also in any relevant condition.
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Project description:Simulation studies are often used to predict the expected impact of control measures in infectious disease outbreaks. Typically, two independent sets of simulations are conducted, one with the intervention, and one without, and epidemic sizes (or some related metric) are compared to estimate the effect of the intervention. Since it is possible that controlled epidemics are larger than uncontrolled ones if there is substantial stochastic variation between epidemics, uncertainty intervals from this approach can include a negative effect even for an effective intervention. To more precisely estimate the number of cases an intervention will prevent within a single epidemic, here we develop a 'single-world' approach to matching simulations of controlled epidemics to their exact uncontrolled counterfactual. Our method borrows concepts from percolation approaches, prunes out possible epidemic histories and creates potential epidemic graphs (i.e. a mathematical representation of all consistent epidemics) that can be 'realized' to create perfectly matched controlled and uncontrolled epidemics. We present an implementation of this method for a common class of compartmental models (e.g. SIR models), and its application in a simple SIR model. Results illustrate how, at the cost of some computation time, this method substantially narrows confidence intervals and avoids nonsensical inferences. This article is part of the theme issue 'Modelling infectious disease outbreaks in humans, animals and plants: epidemic forecasting and control'. This theme issue is linked with the earlier issue 'Modelling infectious disease outbreaks in humans, animals and plants: approaches and important themes'.
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Project description:Cytokine storm syndromes require rapid diagnosis and treatment to limit the morbidity and mortality caused by the hyperinflammatory state that characterizes these devastating conditions. Herein, we discuss the current knowledge that guides our therapeutic decision-making and personalization of treatment for patients with cytokine storm syndromes. Firstly, ICU-level supportive care is often required to stabilize patients with fulminant disease while additional diagnostic evaluations proceed to determine the underlying cause of cytokine storm. Pharmacologic interventions should be focused on removing the inciting trigger of inflammation and initiation of an individualized immunosuppressive regimen when immune activation is central to the underlying disease pathophysiology. Monitoring for a clinical response is required to ensure that changes in the therapeutic regimen can be made as clinically warranted. Escalation of immunosuppression may be required if patients respond poorly to the initial therapeutic interventions, while a slow wean of immunosuppression in patients who improve can limit medication-related toxicities. In certain scenarios, a decision must be made whether an individual patient requires hematopoietic cell transplantation to prevent recurrence of disease. Despite these interventions, significant morbidity and mortality remains for cytokine storm patients. Therefore, we use this review to propose a clinical schema to guide current and future attempts to design rational therapeutic interventions for patients suffering from these devastating conditions, which we believe speeds the diagnosis of disease, limits medication-related toxicities, and improves clinical outcomes by targeting the heterogeneous and dynamic mechanisms driving disease in each individual patient.
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Project description:BackgroundSevere acute respiratory syndrome coronavirus 2 (SARS-CoV-2) recently emerged in Wuhan, Hubei-China, as responsible for the coronavirus disease 2019 (COVID-19) and then spread rapidly worldwide. While most individuals remain asymptomatic or develop only mild symptoms, approximately 5% develop severe forms of COVID-19 characterized by acute respiratory distress syndrome (ARDS) and multiple-organ failure (MOF) that usually require intensive-care support and often yield a poor prognosis.SummaryThe pathophysiology of COVID-19 is far from being completely understood, and the lack of effective treatments leads to a sense of urgency to develop new therapeutic strategies based on pathophysiological assumptions. The exaggerated cytokine release in response to viral infection, a condition known as cytokine release syndrome (CRS) or cytokine storm, is emerging as the mechanism leading to ARDS and MOF in COVID-19, thus endorsing the hypothesis that properly timed anti-inflammatory therapeutic strategies could improve patients' clinical outcomes and prognosis. Key Messages: The objective of this article is to explore and comment on the potential role of the promising immunomodulatory therapies using pharmacological and nonpharmacological approaches to overcome the dysregulated proinflammatory response in COVID-19.
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Project description:ObjectivesST11 KPC-producing Klebsiella pneumoniae (Kp) is highly prevalent in China. We investigated the inter- and intra- host transmission and evolution characteristics of ST11 KPC-producing Kp.MethodsA retrospective study was conducted in a hospital. The clinical data and antimicrobial resistance (AMR) phenotypes were collected. Whole genome sequencing was performed. The transmission route was reconstructed by combining single nucleotide polymorphisms (SNPs) with the clinical information. Hypervirulent Kp (HvKp) was defined as the presence of some combination of peg-344, iroB, iucA, rmpA, or rmpA2.ResultsFifty-eight Kp strains isolated from thirty-five patients were enrolled. The information of one isolate was missing. The mean age of the patients was 74.3 ± 18.0 years, and 18 (50.0%) were female. Fifteen patients (41.7%, 15/36) presented with poor prognosis. All the strains were identified as ST11, and 57 strains harbored blaKPC-2. Two distinguished clades were identified based on the 1,325 high quality SNPs. In clade 1, carbapenem-resistant (CR)-hvKp accounted for 48.3% of the strains (28/58), which mostly presented as KL64 subclones, whereas CR-classical Klebsiella pneumoniae (cKp) commonly possessing KL47 were clustered in Clade 2. One CR-hvKp strain might have originated from the CR-cKp strain from within-host evolution. Even worse, a prolonged transmission of CR-hvKp has led to its spread into healthcare institutes.ConclusionTwo endemic subclones of ST11 KPC-producing Kp, KL64-CR-hvKp and KL47-CR-cKp, were transmitted in parallel within the hospital and/or the healthcare institute, suggesting that the ongoing genomic surveillance should be enhanced.
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Project description:BackgroundCarbapenem resistance is a critical healthcare challenge worldwide. Particularly concerning is the widespread dissemination of Klebsiella pneumoniae carbapenemase (KPC). Klebsiella pneumoniae harboring blaKPC (KPC-Kpn) is endemic in many areas including the United States, where the epidemic was primarily mediated by the clonal dissemination of Kpn ST258. We postulated that the spread of blaKPC in other regions occurs by different and more complex mechanisms. To test this, we investigated the evolution and dynamics of spread of KPC-Kpn in Colombia, where KPC became rapidly endemic after emerging in 2005.MethodsWe sequenced the genomes of 133 clinical isolates recovered from 24 tertiary care hospitals located in 10 cities throughout Colombia, between 2002 (before the emergence of KPC-Kpn) and 2014. Phylogenetic reconstructions and evolutionary mapping were performed to determine temporal and genetic associations between the isolates.ResultsOur results indicate that the start of the epidemic was driven by horizontal dissemination of mobile genetic elements carrying blaKPC-2, followed by the introduction and subsequent spread of clonal group 258 (CG258) isolates containing blaKPC-3.ConclusionsThe combination of 2 evolutionary mechanisms of KPC-Kpn within a challenged health system of a developing country created the "perfect storm" for sustained endemicity of these multidrug-resistant organisms in Colombia.
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Project description: Not available
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Project description:A subset of patients with severe COVID-19 develop profound inflammation and multi-organ dysfunction consistent with a "Cytokine Storm Syndrome" (CSS). In this review we compare the clinical features, diagnosis, and pathogenesis of COVID-CSS with other hematological CSS, namely secondary hemophagocytic lymphohistiocytosis (sHLH), idiopathic multicentric Castleman disease (iMCD), and CAR-T cell therapy associated Cytokine Release Syndrome (CRS). Novel therapeutics targeting cytokines or inhibiting cell signaling pathways have now become the mainstay of treatment in these CSS. We review the evidence for cytokine blockade and attenuation in these known CSS as well as the emerging literature and clinical trials pertaining to COVID-CSS. Established markers of inflammation as well as cytokine levels are compared and contrasted between these four entities in order to establish a foundation for future diagnostic criteria of COVID-CSS.
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