Last data update: May 13, 2024. (Total: 46773 publications since 2009)
Records 1-7 (of 7 Records) |
Query Trace: Bowyer ME[original query] |
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Investigation and public health response to a COVID-19 outbreak in a rural resort community — Blaine County, Idaho, 2020 (preprint)
Dunne EM , Maxwell T , Dawson-Skuza C , Burns M , Ball C , Turner K , Hahn CG , Bowyer M , Carter KK , Hudson L . medRxiv 2021 2021.02.09.21251216 Blaine County, Idaho, a rural area with a renowned resort, experienced an outbreak of novel coronavirus disease (COVID-19). We undertook an epidemiologic investigation to describe the outbreak and guide public health action. Confirmed cases of COVID-19 were identified from reports of SARS-CoV-2-positive laboratory test results to South Central Public Health District.Information on symptoms, hospitalization, recent travel, healthcare worker status, and close contacts was obtained by medical record review and patient interviews. Viral sequence analysis was conducted on a subset of available specimens. During March 13–April 10, 2020, a total of 451 COVID-19 cases occurred among Blaine County residents (1,959 cases per 100,000 population). An additional 37 cases occurred in out-of-state residents. Among the 451 COVID-19 patients, the median age was 51 years (Interquartile range [IQR]: 37–63), 52 (11.5%) were hospitalized, and 5 (1.1%) died. The median duration between specimen collection and a positive laboratory result was 9 days (IQR: 4–10). Forty-four (9.8%) patients reported recent travel. Healthcare workers comprised 56 (12.4%) cases; 33 of whom worked at the only hospital in the county, leading to a 15-day disruption of hospital services. Of 562 close contacts monitored by public health authorities, 22 (3.9%) had laboratory-confirmed COVID-19 and an additional 29 (5.2%) experienced compatible symptoms. Sequencing results from 34 Idaho specimens supported epidemiologic findings indicating travel as a source of SARS-CoV-2, and identified multiple lineages among hospital workers. Community mitigation strategies included school and resort closure, stay-at-home orders, and restrictions on incoming travelers. COVID-19 outbreaks in rural communities can disrupt health services. Lack of local laboratory capacity led to long turnaround times for COVID-19 test results. Rural communities frequented by tourists should consider implementing restrictions on incoming travelers among other mitigation strategies to reduce COVID-19 transmission.Competing Interest StatementThe authors have declared no competing interest.Funding StatementNo external funding was received.Author DeclarationsI confirm all relevant ethical guidelines have been followed, and any necessary IRB and/or ethics committee approvals have been obtained.YesThe details of the IRB/oversight body that provided approval or exemption for the research described are given below:COVID-19 is a reportable disease under Idaho Department of Health and Welfare Rules, IDAPA 16.02.10. Case investigation, data collection, and analysis were conducted for public health purposes. This project was reviewed by the Center for Surveillance, Epidemiology, and Laboratory Services Human Subjects Contact at the Centers for Disease Control and Prevention (CDC). The project was determined to meet the requirements of public health surveillance covered by the U.S. Department of Health and Human Services Policy for the Protection of Human Research Subjects as defined in 45 CFR 46.102, and the decision was made that this project was nonresearch and did not require ethical review by the CDC Human Research Protection Office. Ethical approval was waived and informed consent was not required.All necessary patient/participant consent has been obtained and the appropriate institutional forms have been archived.YesI understand that all clinical trials and any other prospective interventional studies must be registered with an ICMJE-approved registry, such as ClinicalTrials.gov. I confirm that any such study reported in the manuscript has been registered and the trial registration ID is provided (note: if posting a prospective study registered retrospectively, please provide a statement in the trial ID field explaining why the study was not registered in advance).YesI have followed all appropriate research reporting guidelines and uploaded the relevant EQUATOR Network research reporting checklist(s) and other pertinent material as supplementary files, if applicable.YesSARS-CoV-2 sequence data have be n uploaded to the GISAID database, with accession numbers provided in S1 Table. Data on the estimated proportion of Blaine County residents staying at home are available at https://docs.safegraph.com/docs/social-distancing-metrics. Census block group data are available at https://data.census.gov/cedsci/. De-identified patient data are not publicly available for legal and ethical reasons. These data were collected as part of reportable disease surveillance under Idaho law, and not for research purposes. Due to the rural setting and relatively small population, there is a risk of reidentification of some patients included in the data set. De-identified data can be requested from the Idaho Division of Public Health by contacting the Bureau of Communicable Diseases Epidemiology Section at Epimail{at}dhw.Idaho.gov. https://www.gisaid.org/ |
Investigation and public health response to a COVID-19 outbreak in a rural resort community-Blaine County, Idaho, 2020.
Dunne EM , Maxwell T , Dawson-Skuza C , Burns M , Ball C , Turner K , Hahn CG , Bowyer M , Carter KK , Hudson L . PLoS One 2021 16 (4) e0250322 Blaine County, Idaho, a rural area with a renowned resort, experienced a COVID-19 outbreak early in the pandemic. We undertook an epidemiologic investigation to describe the outbreak and guide public health action. Confirmed cases of COVID-19 were identified from reports of SARS-CoV-2-positive laboratory test results to South Central Public Health District. Information on symptoms, hospitalization, recent travel, healthcare worker status, and close contacts was obtained by medical record review and patient interviews. Viral sequence analysis was conducted on a subset of available specimens. During March 13-April 10, 2020, a total of 451 COVID-19 cases among Blaine County residents (1,959 cases per 100,000 population) were reported, with earliest illness onset March 1. The median patient age was 51 years (interquartile range [IQR]: 37-63), 52 (11.5%) were hospitalized, and 5 (1.1%) died. The median duration between specimen collection and a positive laboratory result was 9 days (IQR: 4-10). Forty-four (9.8%) patients reported recent travel and an additional 37 cases occurred in out-of-state residents. Healthcare workers comprised 56 (12.4%) cases; 33 of whom worked at the only hospital in the county, leading to a 15-day disruption of hospital services. Among 562 close contacts monitored by public health authorities, laboratory-confirmed COVID-19 or compatible symptoms were identified in 51 (9.1%). Sequencing results from 34 specimens supported epidemiologic findings indicating travel as a source of SARS-CoV-2, and identified multiple lineages among hospital workers. Community mitigation strategies included school and resort closure, stay-at-home orders, and restrictions on incoming travelers. COVID-19 outbreaks in rural communities can disrupt health services. Lack of local laboratory capacity led to long turnaround times for COVID-19 test results. Rural communities frequented by tourists face unique challenges during the COVID-19 pandemic. Implementing restrictions on incoming travelers and other mitigation strategies helped reduce COVID-19 transmission early in the pandemic. |
Microglial activation and responses to vasculature that result from an acute LPS exposure
Bowyer JF , Sarkar S , Burks SM , Hess JN , Tolani S , O'Callaghan JP , Hanig JP . Neurotoxicology 2020 77 181-192 Bacterial cell wall endotoxins, i.e. lipopolysaccharides (LPS), are some of the original compounds shown to evoke the classic signs of systemic inflammation/innate immune response and neuroinflammation. The term neuroinflammation often is used to infer the elaboration of proinflammatory mediators by microglia elicited by neuronal targeted activity. However, it also is possible that the microglia are responding to vasculature through several signaling mechanisms. Microglial activation relative to the vasculature in the hippocampus and parietal cortex was determined after an acute exposure of a single subcutaneous injection of 2 mg/kg LPS. Antibodies to allograft inflammatory factor (Aif1, a.k.a. Iba1) were used to track and quantify morphological changes in microglia. Immunostaining of platelet/endothelial cell adhesion molecule 1 (Pecam1, a.k.a. Cd31) was used to visualize vasculature in the forebrain and glial acidic fibrillary protein (GFAP) to visualize astrocytes. Neuroinflammation and other aspects of neurotoxicity were evaluated histologically at 3 h, 6 h, 12 h, 24 h, 3 d and 14 d following LPS exposure. LPS did not cause neurodegeneration as determined by Fluoro Jade C labeling. Also, there were no signs of mouse IgG leakage from brain vasculature due to LPS. Some changes in microglia size occurred at 6 h, but by 12 h microglial activation had begun with the combined soma and proximal processes size increasing significantly (1.5-fold). At 24 h, almost all the microglia soma and proximal processes in the hippocampus, parietal cortex, and thalamus were closely associated with the vasculature and had increased almost 2.0-fold in size. In many areas where microglia were juxtaposed to vasculature, astrocytic endfeet appeared to be displaced. The microglial activation had subsided slightly by 3 d with microglial size 1.6-fold that of control. We hypothesize that acute LPS activation can result in vascular mediated microglial responses through several mechanisms: 1) binding to Cd14 and Tlr4 receptors on microglia processes residing on vasculature; 2) damaging vasculature and causing the release of cytokines; and 3) possibly astrocytic endfeet damage resulting in cytokine release. These acute responses may serve as an adaptive mechanism to exposure to circulating LPS where the microglia surround the vasculature. This could further prevent the pathogen(s) circulating in blood from entering the brain. However, diverting microglial interactions away from synaptic remodeling and other types of microglial interactions with neurons may have adverse effects on neuronal function. |
Summary of recommendations from the National Institute for Occupational Safety and Health Fire Fighter Fatality Investigation and Prevention Program, 20062014
Hard DL , Marsh SM , Merinar TR , Bowyer ME , Miles ST , Loflin ME , Moore PH . J Safety Res 2018 68 21-25 Introduction: The NIOSH Fire Fighter Fatality Investigation and Prevention Program (FFFIPP) conducts independent investigations of selected fire fighter line-of-duty deaths (LODD) and offers recommendations to prevent similar deaths. The purpose of the current study was to provide information on more recent FFFIPP recommendations and to determine if recommendations have changed over time. Methods: Fatality investigations completed from 2006 to 2014 were selected for this study with recommendations being assigned into twelve major categories when possible. The most frequently occurring recommendations were then rank ordered overall and then by medical and traumatic fire fighter LODD. Results: There were 1,067 total recommendations made in the published fire fighter investigative reports for both medical and trauma-related fire fighter fatalities for the period 2006–2014. Of these, 784 (73%) could be placed within one of the 12 categories noted previously. The top 10 recommendation categories overall were: 1. Medical screening, 2. Fitness and wellness program, 3. Training, 4. Medical clearance, 5. Standard Operating Procedures/Standard Operating Guidelines (SOPs/SOGs), 6. Incident command, 7. Strategy and tactics, 8. Communications, 9. Personal protective equipment and 10. Staffing. Conclusions: The leading recommendations from the NIOSH FFFIPP medical investigations between 2006 and 2014 did not change compared to those made between 1998 and 2005, with the exception of the addition of “medical clearance for duty”. There were changes for the traumatic injury leading recommendations for 2006–2014, with the major change being “training”, which was the leading FFFIPP recommendation for traumatic injuries for this time period. Practical applications: The intent of the FFFIPP is to influence fire departments and fire fighters to critically assess and evaluate situations/circumstances similar to those identified by NIOSH investigations and implement the recommendations offered to prevent additional fire fighter fatalities. |
Corticosterone and exogenous glucose alter blood glucose levels, neurotoxicity, and vascular toxicity produced by methamphetamine
Bowyer JF , Tranter KM , Sarkar S , George NI , Hanig JP , Kelly KA , Michalovicz LT , Miller DB , O'Callaghan JP . J Neurochem 2017 143 (2) 198-213 Our previous studies have raised the possibility that altered blood glucose levels may influence and/or be predictive of methamphetamine (METH) neurotoxicity. This study evaluated the effects of exogenous glucose and corticosterone (CORT) pretreatment alone or in combination with METH on blood glucose levels and the neural and vascular toxicity produced. METH exposure consisted of four sequential injections of 5, 7.5, 10, and 10 mg/kg (2h between injections) D-METH. The three groups given METH in combination with saline, glucose (METH+Glucose), or CORT (METH+CORT) had significantly higher glucose levels compared to the corresponding treatment groups without METH except at 3 h after the last injection. At this last time point, the METH and METH+Glucose groups had lower levels than the non-METH groups, while the METH+CORT group did not. CORT alone or glucose alone did not significantly increase blood glucose. Mortality rates for the METH+CORT (40%) and METH+Glucose (44%) groups were substantially higher than the METH (< 10%) group. Additionally, METH+CORT significantly increased neurodegeneration above all other treatments ( approximately 2.5-fold in the parietal cortex). Thus, maintaining elevated levels of glucose during METH exposure increases lethality and may exacerbate neurodegeneration. Neuroinflammation, specifically microglial activation, was associated with degenerating neurons in the parietal cortex and thalamus after METH exposure. The activated microglia in the parietal cortex were surrounding vasculature in most cases and the extent of microglial activation was exacerbated by CORT pretreatment. Our findings implicate elevated blood levels of glucose and hyperthermia in METH-induced neurotoxicity, neurovascular damage, and lethality, and that acute elevation of CORT exacerbates both neurotoxicity and neuroinflammation. |
Vascular-directed responses of microglia produced by methamphetamine exposure: indirect evidence that microglia are involved in vascular repair?
Bowyer JF , Sarkar S , Tranter KM , Hanig JP , Miller DB , O'Callaghan JP . J Neuroinflammation 2016 13 (1) 64 BACKGROUND: Brain microglial activations and damage responses are most commonly associated with neurodegeneration or systemic innate immune system activation. Here, we used histological methods to focus on microglial responses that are directed towards brain vasculature, previously undescribed, after a neurotoxic exposure to methamphetamine. METHODS: Male rats were given doses of methamphetamine that produce pronounced hyperthermia, hypertension, and toxicity. Identification of microglia and microglia-like cells (pericytes and possibly perivascular cells) was done using immunoreactivity to allograft inflammatory factor 1 (Aif1 a.k.a Iba1) and alpha M integrin (Itgam a.k.a. Cd11b) while vasculature endothelium was identified using rat endothelial cell antigen 1 (RECA-1). Regions of neuronal, axonal, and nerve terminal degeneration were determined using Fluoro-Jade C. RESULTS: Dual labeling of vasculature (RECA-1) and microglia (Iba1) showed a strong association of hypertrophied cells surrounding and juxtaposed to vasculature in the septum, medial dorsal hippocampus, piriform cortex, and thalamus. The Iba1 labeling was more pronounced in the cell body while Cd11b more so in the processes of activated microglia. These regions have been previously identified to have vascular leakage after neurotoxic methamphetamine exposure. Dual labeling with Fluoro-Jade C and Iba1 indicated that there was minimal or no evidence of neuronal damage in the septum and hippocampus where many hypertrophied Iba1-labeled cells were found to be associated with vasculature. Although microglial activation around the prominent neurodegeneration was found in the thalamus, there were also many examples of activated microglia associated with vasculature. CONCLUSIONS: The data implicate microglia, and possibly related cell types, in playing a major role in responding to methamphetamine-induced vascular damage, and possibly repair, in the absence of neurodegeneration. Identifying brain regions with hypertrophied/activated microglial-like cells associated with vasculature has the potential for identifying regions of more subtle examples of vascular damage and BBB compromise. |
Chronic exposure to corticosterone enhances the neuroinflammatory and neurotoxic responses to methamphetamine
Kelly KA , Miller DB , Bowyer JF , O'Callaghan JP . J Neurochem 2012 122 (5) 995-1009 Upregulation of proinflammatory cytokines and chemokines in brain ("neuroinflammation") accompanies neurological disease and neurotoxicity. Previously, we documented a striatal neuroinflammatory response to acute administration of a neurotoxic dose of methamphetamine (METH), i.e. one associated with evidence of dopaminergic terminal damage and activation of microglia and astroglia. When we used minocycline to suppress METH-induced neuroinflammation, indices of dopaminergic neurotoxicity were not affected but suppression of neuroinflammation was incomplete. Here, we administered the classic anti-inflammatory glucocorticoid, corticosterone (CORT), in an attempt to completely suppress METH-related neuroinflammation. METH alone caused large increases in striatal proinflammatory cytokine/chemokine mRNA and subsequent astrocytic hypertrophy, microglial activation and dopaminergic nerve terminal damage. Pretreatment of mice with acute CORTfailed to prevent neuroinflammatory responses to METH. Surprisingly, when mice were pretreated with chronic CORT in the drinking water, an enhanced striatal neuroinflammatory response to METH was observed, an effect that was accompanied by enhanced METH-induced astrogliosis and dopaminergic neurotoxicity. Chronic CORT pretreatment also sensitized frontal cortex and hippocampus to mount a neuroinflammatory response to METH. Because the levels of chronic CORT used are associated with high physiological stress, our data suggest that chronic CORT therapy or sustained physiological stress may sensitize the neuroinflammatory and neurotoxicity responses to METH. (Published 2012. This article is a US Government work and is in the public domain in the USA.) |
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