ABSTRACT
Melioidosis, caused by the bacterium Burkholderia pseudomallei, is an uncommon infection that is typically associated with exposure to soil and water in tropical and subtropical environments. It is rarely diagnosed in the continental United States. Patients with melioidosis in the United States commonly report travel to regions where melioidosis is endemic. We report a cluster of four non-travel-associated cases of melioidosis in Georgia, Kansas, Minnesota, and Texas. These cases were caused by the same strain of B. pseudomallei that was linked to an aromatherapy spray product imported from a melioidosis-endemic area.
Subject(s)
Aromatherapy/adverse effects , Burkholderia pseudomallei/isolation & purification , Disease Outbreaks , Melioidosis/epidemiology , Aerosols , Brain/microbiology , Brain/pathology , Burkholderia pseudomallei/genetics , COVID-19/complications , Child, Preschool , Fatal Outcome , Female , Genome, Bacterial , Humans , Lung/microbiology , Lung/pathology , Male , Melioidosis/complications , Middle Aged , Phylogeny , Shock, Septic/microbiology , United States/epidemiologyABSTRACT
SARS-CoV-2 infections among vaccinated nursing home residents increased after the Omicron variant emerged. Data on booster dose effectiveness in this population are limited. During July 2021-March 2022, nursing home outbreaks in 11 US jurisdictions involving >3 infections within 14 days among residents who had received at least the primary COVID-19 vaccine(s) were monitored. Among 2,188 nursing homes, 1,247 outbreaks were reported in the periods of Delta (n = 356, 29%), mixed Delta/Omicron (n = 354, 28%), and Omicron (n = 536, 43%) predominance. During the Omicron-predominant period, the risk for infection within 14 days of an outbreak start was lower among boosted residents than among residents who had received the primary vaccine series alone (risk ratio [RR] 0.25, 95% CI 0.19-0.33). Once infected, boosted residents were at lower risk for all-cause hospitalization (RR 0.48, 95% CI 0.40-0.49) and death (RR 0.45, 95% CI 0.34-0.59) than primary vaccine-only residents.
Subject(s)
COVID-19 , United States/epidemiology , Humans , COVID-19/epidemiology , COVID-19/prevention & control , COVID-19 Vaccines , SARS-CoV-2 , Nursing Homes , Disease OutbreaksABSTRACT
Sepsis, life-threatening organ dysfunction secondary to infection, contributes to at least 1.7 million adult hospitalizations and at least 350,000 deaths annually in the United States. Sepsis care is complex, requiring the coordination of multiple hospital departments and disciplines. Sepsis programs can coordinate these efforts to optimize patient outcomes. The 2022 National Healthcare Safety Network (NHSN) annual survey evaluated the prevalence and characteristics of sepsis programs in acute care hospitals. Among 5,221 hospitals, 3,787 (73%) reported having a committee that monitors and reviews sepsis care. Prevalence of these committees varied by hospital size, ranging from 53% among hospitals with 0-25 beds to 95% among hospitals with >500 beds. Fifty-five percent of all hospitals provided dedicated time (including assigned protected time or job description requirements) for leaders of these committees to manage a program and conduct daily activities, and 55% of committees reported involvement with antibiotic stewardship programs. These data highlight opportunities, particularly in smaller hospitals, to improve the care and outcomes of patients with sepsis in the United States by ensuring that all hospitals have sepsis programs with protected time for program leaders, engagement of medical specialists, and integration with antimicrobial stewardship programs. CDC's Hospital Sepsis Program Core Elements provides a guide to assist hospitals in developing and implementing effective sepsis programs that complement and facilitate the implementation of existing clinical guidelines and improve patient care. Future NHSN annual surveys will monitor uptake of these sepsis core elements.
Subject(s)
Health Facilities , Sepsis , United States/epidemiology , Adult , Humans , Hospitals , Sepsis/epidemiology , Sepsis/therapy , Centers for Disease Control and Prevention, U.S. , Delivery of Health CareABSTRACT
Exposure to environmental contaminants, such as organochlorine insecticides during critical periods of neurodevelopment has been shown to be a major contributor to several neuropsychological deficits seen in children, adolescence, and adults. Although the neurobehavioral outcomes resulting from exposure to these compounds are known the neurotransmitter circuitry and molecular targets that mediate these endpoints have not been identified. Given the importance of the frontal cortex in facilitating numerous neuropsychological processes, our current study sought to investigate the effects of developmental exposure to the organochlorine insecticide, endosulfan, on the expression of specific proteins associated with neurotransmission in the frontal cortex. Utilizing in vitro models we were able to show endosulfan reduces cell viability in IMR-32 neuroblastoma cells in addition to reducing synaptic puncta and neurite outgrowth in primary cultured neurons isolated from the frontal cortex of mice. Elaborating these findings to an in vivo model we found that developmental exposure of female mice to endosulfan during gestation and lactation elicited significant alterations to the GABAergic (GAT1, vGAT, GABAA receptor), glutamatergic (vGlut and GluN2B receptor), and dopaminergic (DAT, TH, VMAT2, and D2 receptor) neurotransmitter systems in the frontal cortex of male offspring. These findings identify damage to critical neurotransmitter circuits and proteins in the frontal cortex, which may underlie the neurobehavioral deficits observed following developmental exposure to endosulfan and other organochlorine insecticides.
Subject(s)
Endosulfan/toxicity , Frontal Lobe/drug effects , Hydrocarbons, Chlorinated/toxicity , Insecticides/toxicity , Receptors, GABA-A/metabolism , Vesicular Inhibitory Amino Acid Transport Proteins/metabolism , Animals , Cell Line, Tumor , Cells, Cultured , Dopaminergic Neurons/drug effects , Dopaminergic Neurons/metabolism , Female , Frontal Lobe/cytology , Frontal Lobe/embryology , Frontal Lobe/growth & development , GABAergic Neurons/drug effects , GABAergic Neurons/metabolism , Humans , Male , Mice , Mice, Inbred C57BL , Pregnancy , Prenatal Exposure Delayed Effects , Receptors, GABA-A/genetics , Synaptic Transmission/drug effects , Vesicular Inhibitory Amino Acid Transport Proteins/geneticsABSTRACT
One in six nursing home residents and staff with positive SARS-CoV-2 tests ≥90 days after initial infection had specimen cycle thresholds (Ct) <30. Individuals with specimen Ct<30 were more likely to report symptoms but were not different from individuals with high Ct value specimens by other clinical and testing data.
Subject(s)
COVID-19 , Humans , SARS-CoV-2 , COVID-19 Testing , Skilled Nursing Facilities , Clinical Laboratory Techniques , Delivery of Health CareABSTRACT
INTRODUCTION: Hypertension is associated with adverse cardiovascular outcomes and is geographically concentrated in urban underserved neighborhoods. This study examines the temporal-spatial association between individual exposure to violent crime and blood pressure. METHODS: A retrospective observational cohort study analyzed 39,211 patients with 227,595 blood pressure measurements from 2014 to 2016 at 3 outpatient clinics at an academic medical center in Chicago. Patients were included in the study if they had documentation of blood pressure in the medical record and resided in census tracts with >1,000 observations. Geocoded violent crime events were obtained from the Chicago Police Department. Individual-level exposure was defined on the basis of spatial and temporal buffers around each patient's home. Spatial buffers included 100-, 250-, 500-, and 1,000-meter disc radii, and temporal buffers included 7, 30, and 60 days preceding each outpatient appointment. Systolic blood pressure measurements (mmHg) were abstracted from the electronic health record. Analysis was performed in 2019-2020. RESULTS: For each violent crime event within 100 meters from home, systolic blood pressure increased by 0.14 mmHg within 7 days of exposure compared with 0.08 mmHg at 30 days of exposure. In analyses stratified by neighborhood cluster, systolic blood pressure increased by 0.37 mmHg among patients in the suburban affluent cluster relative to that among those in an extreme poverty cluster for the same spatial and temporal buffer. CONCLUSIONS: Exposure to a violent crime event was associated with increased blood pressure, with gradient effects by both distance and time from exposure.
Subject(s)
Census Tract , Violence , Blood Pressure , Crime , Humans , Residence Characteristics , Retrospective Studies , Risk FactorsABSTRACT
Facility-wide testing performed at 4 outpatient hemodialysis facilities in the absence of an outbreak or escalating community incidence did not identify new SARS-CoV-2 infections and illustrated key logistical considerations essential to successful implementation of SARS-CoV-2 screening. Facilities could consider prioritizing facility-wide SARS-CoV-2 testing during suspicion of an outbreak in the facility or escalating community spread without robust infection control strategies in place. Being prepared to address operational considerations will enhance implementation of facility-wide testing in the outpatient dialysis setting.
Subject(s)
COVID-19 , Kidney Failure, Chronic , COVID-19 Testing , Humans , Outpatients , Renal Dialysis/adverse effects , SARS-CoV-2ABSTRACT
The contribution of environmental toxicants to the etiology and risk of Parkinson's disease (PD) has been clearly established, with organochlorine insecticides routinely shown to damage the nigrostriatal dopamine pathway. Although PD is generally considered an adult onset disease, it has been postulated that exposure to environmental contaminants or other factors early in life during critical periods of neurodevelopment could alter the dopaminergic circuit and predispose individuals to developing PD. Recent epidemiological evidence has found exposure to the organochlorine insecticide endosulfan to be a risk factor for PD. However, the specific dopaminergic targets or vulnerable developmental time points related to endosulfan exposure have not been investigated. Thus, we sought to investigate dopaminergic neurotoxicity following developmental exposure to endosulfan as well as following an additional challenge with MPTP. Our in vitro findings demonstrate a reduction in SK-N-SH cells and ventral mesencephalic primary cultures after endosulfan treatment. Using an in vivo developmental model, exposure to endosulfan during gestation and lactation caused a reduction in DAT and TH in the striatum of male offspring. These alterations were exacerbated following subsequent treatment with MPTP. In contrast, exposure of adult mice to endosulfan did not elicit dopaminergic damage and did not appear to increase the vulnerability of the dopamine neurons to MPTP. These findings suggest that development during gestation and lactation represents a critical window of susceptibility to endosulfan exposure and development of the nigrostriatal dopamine system. Furthermore, these exposures appear to sensitize the dopamine neurons to additional insults that may occur later in life.
Subject(s)
Corpus Striatum/drug effects , Dopaminergic Neurons/drug effects , Endosulfan/toxicity , Insecticides/toxicity , Substantia Nigra/drug effects , Animals , Cell Line, Tumor , Cell Survival/drug effects , Cells, Cultured , Corpus Striatum/metabolism , Dopaminergic Neurons/metabolism , Female , MPTP Poisoning , Male , Mice , Mice, Inbred C57BL , Neuroblastoma , Sex Factors , Substantia Nigra/metabolismABSTRACT
In the last several decades polybrominated diphenyl ethers (PBDEs) have replaced the previously banned polychlorinated biphenyls (PCBs) in multiple flame retardant utilities. As epidemiological and laboratory studies have suggested PCBs as a risk factor for Parkinson's disease (PD), the similarities between PBDEs and PCBs suggest that PBDEs have the potential to be neurotoxic to the dopamine system. The purpose of this study was to evaluate the neurotoxic effects of the PBDE mixture, DE-71, on the nigrostriatal dopamine system and address the role of altered dopamine handling in mediating this neurotoxicity. Using an in vitro model system we found DE-71 effectively caused cell death in a dopaminergic cell line as well as reducing the number of TH+ neurons isolated from VMAT2 WT and LO animals. Assessment of DE-71 neurotoxicity in vivo demonstrated significant deposition of PBDE congeners in the brains of mice, leading to reductions in striatal dopamine and dopamine handling, as well as reductions in the striatal dopamine transporter (DAT) and VMAT2. Additionally, DE-71 elicited a significant locomotor deficit in the VMAT2 WT and LO mice. However, no change was seen in TH expression in dopamine terminal or in the number of dopamine neurons in the substantia nigra pars compacta (SNpc). To date, these are the first data to demonstrate that exposure to PBDEs disrupts the nigrostriatal dopamine system. Given their similarities to PCBs, additional laboratory and epidemiological research should be considered to assess PBDEs as a potential risk factor for PD and other neurological disorders.