Distribution and Characteristics of Escherichia coli Clonal Group A1

Among 1,102 recent Escherichia coli clinical isolates, clonal group A was identified in 17 of 20 (U.S. and non-U.S.) geographic locales, mainly among U.S. isolates (9% vs. 3%; p < 0.001) and those resistant to trimethoprim-sulfamethoxazole (10% vs. 1.7%; p < 0.001). The extensive antimicrobial resistance and virulence profiles of clonal group A may underlie its recent widespread emergence

Proportion of extended-spectrum ß-lactamase-producing Enterobacteriaceae in community setting in Ngaoundere, Cameroon

BACKGROUND: There is no information regarding the resistance mechanisms of extended-spectrum ß-lactamase (ESBL)-producing Enterobacteriaceae in community setting in Cameroon. The current study aimed to determine the proportion of ESBLs in Enterobacteriaceae isolated in the community and to analyse some risk factors associated with ESBL carriage. METHODS: Faecal samples were collected from 208 different outpatients and 150 healthy student volunteers between 3 January and 3 April 2009. Enterobacterial isolates resistant to third-generation cephalosporins were screened for ESBL production by the double-disk synergy test. Presumptive ESBL-producing isolates with positive synergy test were identified by Mass Spectrometry using the BioTyper MALDI-TOF. For such ESBL positive isolates, antibiotic susceptibility was determined by the Vitek 2 system. PCR and sequencing were performed for the detection of different types of ESBL genes in presumptive ESBL-producing isolates. Statistical methods were used for the univariate calculation of risk factors. RESULTS: During the study period, a total of 358 faecal samples were analysed; 58 of such samples (16%) showed an ESBL phenotype and were confirmed by PCR. The proportion of ESBL producers in faecal carriage was statistically different between outpatients and student volunteers (23.1% vs. 6.7%: p < 0.000). According to a univariate analysis, previous use of antibiotics (ciprofloxacin) appeared to be a risk factor for ESBL carriage (p < 0.05).Escherichia coli was the species most frequently isolated among the ESBL producers in outpatients (66.7%) and student volunteers (90%). Isolates showed additional resistance to gentamicin, ciprofloxacin and trimethoprim/sulfamethoxazole but none of them was resistant to temocillin, amikacin or meropenem. Most of the strains (97%) produced a CTX-M group 1 enzymes [CTX-M-15 (98%) or CTX-M-1 (2%)] and the remaining strains produced SHV-12 enzyme (3%). CONCLUSIONS: The use of drugs such as amoxicillin, ciprofloxacin and trimethoprim/sulfamethoxazole does not seem appropriate for empirical treatment because of emerging resistance. The implementation in Cameroon or in other African countries of methods of screening ESBL-producing organisms in routine laboratories is of great importance in order for us to offer patients appropriate treatment and for infection control efforts to succeed

Clinical profiles of patients colonized or infected with extended-spectrum beta-lactamase producing Enterobacteriaceae isolates: a 20 month retrospective study at a Belgian University Hospital

<p>Abstract</p> <p>Background</p> <p>Description of the clinical pictures of patients colonized or infected by ESBL-producing <it>Enterobacteriaceae </it>isolates and admitted to hospital are rather scarce in Europe. However, a better delineation of the clinical patterns associated with the carriage of ESBL-producing isolates may allow healthcare providers to identify more rapidly at risk patients. This matter is of particular concern because of the growing proportion of ESBL-producing <it>Enterobacteriaceae </it>species isolates worldwide.</p> <p>Methods</p> <p>We undertook a descriptive analysis of 114 consecutive patients in whom ESBL-producing <it>Enterobacteriaceae </it>isolates were collected from clinical specimens over a 20-month period. Clinical data were obtained through retrospective analysis of medical record charts. Microbiological cultures were carried out by standard laboratory methods.</p> <p>Results</p> <p>The proportion of ESBL-producing <it>Enterobacteriaceae </it>strains after exclusion of duplicate isolates was 4.5% and the incidence rate was 4.3 cases/1000 patients admitted. Healthcare-associated acquisition was important (n = 104) while community-acquisition was less frequently found (n = 10). Among the former group, two-thirds of the patients were aged over 65 years and 24% of these were living in nursing homes. Sixty-eight (65%) of the patients with healthcare-associated ESBL, were considered clinically infected. In this group, the number and severity of co-morbidities was high, particularly including diabetes mellitus and chronic renal insufficiency. Other known risk factors for ESBL colonization or infection such as prior antibiotic exposure, urinary catheter or previous hospitalisation were also often found. The four main diagnostic categories were: urinary tract infections, lower respiratory tract infections, septicaemia and intra-abdominal infections. For hospitalized patients, the median hospital length of stay was 23 days and the average mortality rate during hospitalization was 13% (Confidence Interval 95%: 7-19). <it>Escherichia coli</it>, by far, accounted as the most common ESBL-producing <it>Enterobacteriaceae </it>species (77/114; [68%]) while CTX-M-1 group was by far the most prevalent ESBL enzyme (n = 56).</p> <p>Conclusion</p> <p>In this retrospective study, the clinical profiles of patients carrying healthcare-associated ESBL-producing <it>Enterobacteriacae </it>is characterized by a high prevalence rate of several major co-morbidities and potential known risk factors. Both, the length of hospital stay and overall hospital mortality rates were particularly high. A prospective case-control matched study should be designed and performed in order to control for possible inclusion bias.</p

Insights on geochemical cycling of U, Re and Mo from seasonal sampling in Boston Harbor, Massachusetts, USA

Author Posting. © The Author(s), 2006. This is the author's version of the work. It is posted here by permission of Elsevier B.V. for personal use, not for redistribution. The definitive version was published in Geochimica et Cosmochimica Acta 71 (2007): 895-917, doi:10.1016/j.gca.2006.10.016.This study examined the removal of U, Mo, and Re from seawater by sedimentary processes at a shallow-water site with near-saturation bottom water O2 levels (240-380 μmol O2/L), very high organic matter oxidation rates (annually averaged rate is 870 μmol C/cm2/y), and shallow oxygen penetration depths (4 mm or less throughout the year). Under these conditions, U, Mo, and Re were removed rapidly to asymptotic pore water concentrations of 2.2–3.3 nmol/kg (U), 7–13 nmol/kg (Mo), and 11–14 pmol/kg (Re). The order in which the three metals were removed, determined by fitting a diffusion-reaction model to measured profiles, was Re < U < Mo. Model fits also suggest that the Mo profiles clearly showed the presence of a near-interface layer in which Mo was added to pore waters by remineralization of a solid phase. The importance of this solid phase source of pore water Mo increased from January to October as the organic matter oxidation rate increased, bottom water O2 decreased, and the O2 penetration depth decreased. Experiments with in situ benthic flux chambers generally showed fluxes of U and Mo into the sediments. However, when the overlying water O2 concentration in the chambers was allowed to drop to very low levels, Mn and Fe were released to the overlying water along with the simultaneous release of Mo and U. These experiments suggest that remineralization of Mn and/or Fe oxides may be a source of Mo and perhaps U to pore waters, and may complicate the accumulation of U and Mo in bioturbated sediments with high organic matter oxidation rates and shallow O2 penetration depths. Benthic chamber experiments including the nonreactive solute tracer, Br-, indicated that sediment irrigation was very important to solute exchange at the study site. The enhancement of sediment-seawater exchange due to irrigation was determined for the nonreactive tracer (Br-), TCO2, NH4 +, U and Mo. The comparisons between these solutes showed that reactions within and around the burrows were very important for modulating the Mo flux, but less important for U. The effect of these reactions on Mo exchange was highly variable, enhancing Mo (and, to a lesser extent, U) uptake at times of relatively modest irrigation, but inhibiting exchange when irrigation rates were faster. These results reinforce the observation that Mo can be released to and removed from pore waters via sedimentary reactions. The removal rate of U and Mo from seawater by sedimentary reactions was found to agree with the rate of accumulation of authigenic U and Mo in the solid phase. The fluxes of U and Mo determined by in situ benthic flux chamber measurements were the largest that have been measured to date. These results confirm that removal of redoxsensitive metals from continental margin sediments underlying oxic bottom water is important, and suggest that continental margin sediments play a key role in the marine budgets of these metals.We appreciate the financial support from the National Science Foundation (OCE-0220892). Funding for this work was also provided to JLM by the Postdoctoral Scholar Program at WHOI courtesy of the Cabot Marine Environmental Science Fund and the J. Seward Johnson Fund. Financial support to IMK was given by The Swedish Foundation for International Cooperation in Research and Higher Education

A model for uranium, rhenium, and molybdenum diagenesis in marine sediments based on results from coastal locations

Author Posting. © The Author(s), 2009. This is the author's version of the work. It is posted here by permission of Elsevier B.V. for personal use, not for redistribution. The definitive version was published in Geochimica et Cosmochimica Acta 73 (2009): 2938-2960, doi:10.1016/j.gca.2009.02.029.The purpose of this research is to characterize the mobilization and immobilization processes that control the authigenic accumulation of uranium (U), rhenium (Re) and molybdenum (Mo) in marine sediments. We analyzed these redox– sensitive metals (RSM) in benthic chamber, pore water and solid phase samples at a site in Buzzards Bay, Massachusetts, U.S.A., which has high bottom water oxygen concentrations (230–300 mol/L) and high organic matter oxidation rates (390 mol C/cm2/y). The oxygen penetration depth varies from 2–9 mm below the sediment–water interface, but pore water sulfide is below detection (< 2M). The RSM pore water profiles are modeled with a steady–state diagenetic model that includes irrigation, which extends 10–20 cm below the sediment–water interface. To present a consistent description of trace metal diagenesis in marine sediments, RSM results from sediments in Buzzards Bay are compared with previous research from sulfidic sediments (Morford et al., GCA 71). Release of RSM to pore waters during the remineralization of solid phases occurs near the sediment–water interface at depths above the zone of authigenic RSM formation. This release occurs consistently for Mo at both sites, but only in the winter for Re in Buzzards Bay and intermittently for U. At the Buzzards Bay site, Re removal to the solid phase extends to the bottom of the profile, while the zone of removal is restricted to ~2–9 cm for U and Mo. Authigenic Re formation is independent of the anoxic remineralization rate, which is consistent with an abiotic removal mechanism. The rate of authigenic U formation and its modeled removal rate constant increase with increasing anoxic remineralization rates, and is consistent with U reduction being microbially mediated. Authigenic Mo formation is related to the formation of sulfidic microenvironments. The depth and extent of Mo removal from pore water is closely associated with the balance between iron and sulfate reduction and the consumption of pore water sulfide via iron sulfide formation. Pore water RSM reach constant asymptotic concentrations in sulfidic sediments, but only pore water Re is constant at depth in Buzzards Bay. The increases in pore water U at the Buzzards Bay site are consistent with addition via irrigation and subsequent upward diffusion to the removal zone. Deep pore water Mo concentrations exceed its bottom water concentration due to irrigation–induced oxidation and remobilization from the solid phase. In sulfidic sediments, there is no evidence for higher pore water U or Mo concentrations at depth due to the absence of irrigation and/or the presence of more stable authigenic RSM phases. There are good correlations between benthic fluxes and authigenic accumulation rates for U and Mo in sulfidic sediments. However, results from Buzzards Bay suggest irrigation ultimately results in the partial loss of U and Mo from the solid phase, with accumulation rates that are 20–30% of the modeled flux. Irrigation can augment (Re, possibly U) or compromise (U, Mo) authigenic accumulation in sediments, and is important when determining burial rates in continental margin sediments.The authors also acknowledge financial support from the National Science Foundation (JLM, WRM: OCE–0220892), Research Corporation (JLM, CMC), Franklin & Marshall College, and the Hackman Summer Research Program at F&M

Targeted Ablation of Oligodendrocytes Triggers Axonal Damage

Glial dysfunction has been implicated in a number of neurodegenerative diseases. In this study we investigated the consequences of glial and oligodendrocyte ablation on neuronal integrity and survival in Drosophila and adult mice, respectively. Targeted genetic ablation of glia was achieved in the adult Drosophila nervous system using the GAL80-GAL4 system. In mice, oligodendrocytes were depleted by the injection of diphtheria toxin in MOGi-Cre/iDTR double transgenic animals. Acute depletion of oligodendrocytes induced axonal injury, but did not cause neuronal cell death in mice. Ablation of glia in adult flies triggered neuronal apoptosis and resulted in a marked reduction in motor performance and lifespan. Our study shows that the targeted depletion of glia triggers secondary neurotoxicity and underscores the central contribution of glia to neuronal homeostasis. The models used in this study provide valuable systems for the investigation of therapeutic strategies to prevent axonal or neuronal damage

Emergence of high drug resistant bacterial isolates from patients with health care associated infections at Jimma University medical center: a cross sectional study

Background: The rates of resistant microorganisms which complicate the management of healthcare associated infections (HAIs) are increasing worldwide and getting more serious in developing countries. The objective of this study was to describe microbiological features and resistance profiles of bacterial pathogens of HAIs in Jimma University Medical Center (JUMC) in Ethiopia.Methods: Institution based cross sectional study was carried out on hospitalized patients from May to September, 2016 in JUMC. Different clinical specimens were collected from patients who were suspected to hospital acquired infections. The specimens were processed to identify bacterial etiologies following standard microbiological methods. Antibacterial susceptibility was determined in vitro by Kirby-Bauer disk diffusion method following Clinical and Laboratory Standards Institute guidelines.Results: Overall, 126 bacterial etiologies were isolated from 118 patients who had HAIs. Of these, 100 (79.4%) were gram negative and the remaining were gram positive. The most common isolates were Escherichia coli 31(24.6%), Klebsiella species 30(23.8%) and Staphylococcus aureus 26 (20.6%). Of 126 bacterial isolates, 38 (30.2%), 52 (41.3%), and 24 (19%) were multidrug-resistant (MDR, resistant to at least one agent in three or more antimicrobial categories), extensively drug resistant (XDR, resistant to at least one agent in all but two or fewer antimicrobial categories (i.e. bacterial isolates remain susceptible to only one or two categories), pan-drug resistant (PDR, resistant to all antibiotic classes) respectively. More than half of isolated gram-negative rods (51%) were positive for extended spectrum beta-lactamase (ESBL) and/or AmpC; and 25% of gram negative isolates were also resistant to carbapenem antibiotics.Conclusions: The pattern of drug resistant bacteria in patients with healthcare associated infection at JUMC is alarming. This calls for coordinated efforts from all stakeholders to prevent HAIs and drug resistance in the study setting

Astrocytes: biology and pathology

Astrocytes are specialized glial cells that outnumber neurons by over fivefold. They contiguously tile the entire central nervous system (CNS) and exert many essential complex functions in the healthy CNS. Astrocytes respond to all forms of CNS insults through a process referred to as reactive astrogliosis, which has become a pathological hallmark of CNS structural lesions. Substantial progress has been made recently in determining functions and mechanisms of reactive astrogliosis and in identifying roles of astrocytes in CNS disorders and pathologies. A vast molecular arsenal at the disposal of reactive astrocytes is being defined. Transgenic mouse models are dissecting specific aspects of reactive astrocytosis and glial scar formation in vivo. Astrocyte involvement in specific clinicopathological entities is being defined. It is now clear that reactive astrogliosis is not a simple all-or-none phenomenon but is a finely gradated continuum of changes that occur in context-dependent manners regulated by specific signaling events. These changes range from reversible alterations in gene expression and cell hypertrophy with preservation of cellular domains and tissue structure, to long-lasting scar formation with rearrangement of tissue structure. Increasing evidence points towards the potential of reactive astrogliosis to play either primary or contributing roles in CNS disorders via loss of normal astrocyte functions or gain of abnormal effects. This article reviews (1) astrocyte functions in healthy CNS, (2) mechanisms and functions of reactive astrogliosis and glial scar formation, and (3) ways in which reactive astrocytes may cause or contribute to specific CNS disorders and lesions