Carbapenemase-producing Enterobacteria (CPE) is nowadays a major

Carbapenemase-producing Enterobacteria (CPE) is nowadays a major public health concern worldwide.[1] The link between international spread of antibiotic resistance and travels is well known.[2-4] Carriage

of CPE has been identified in Great Britain in travelers having been hospitalized in Pakistan or India.[5] In France, resistance of Enterobacteria to carbapenems remains uncommon but involves most often patients with a history of hospitalization abroad.[6] The first outbreak of CPE in France, that occurred in 2004 in a hospital of Assistance Publique-Hôpitaux find more de Paris (AP-HP), followed the transfer of a patient from a Greek hospital.[7] Following this outbreak, AP-HP launched a long-term program to survey and

control CPE, particularly in patients previously hospitalized in foreign countries. We describe here the emergence of CPE in AP-HP hospitals from 2004 to December 2011 and the link with cross-border exchanges. AP-HP is a public health institution administering 38 teaching hospitals (23 acute care and 15 rehabilitation/long-term care hospitals, spread over Paris, suburbs, and surrounding counties), with a total of 23,000 beds (10% of all public hospital beds in France) and serving 11.6 million inhabitants. AP-HP admits approximately selleck 1 million inpatients per year, employs 19,000 physicians, 18,500 nurses, and 29,800 assistant nurses. Local administrators and medical committees manage AP-HP hospitals, but decisions on large investments and medical developments are taken by the central administration. A local infection control team (LICT) is in charge of prevention and surveillance of hospital-acquired infections in each hospital, but actions of foremost importance for the whole institution, eg, multidrug-resistance (MDR) control program, are coordinated centrally by a multidisciplinary infection control team (head of the infection control team

[CICT], infectious disease physician, bacteriologist, epidemiologist, and nurse).[8] One second case was defined as any infected or colonized patient with CPE species. An event was defined as one index case with or without secondary cases. An outbreak was defined as at least two CPE cases (ie, one index case and at least one secondary case) occurring in a given hospital, with a clear epidemiological link (stay during the same period of time in the same unit). In 2004, following the first CPE outbreak in a hospital of AP-HP, every LICT was asked to report quickly every new CPE case to the AP-HP CICT. In 2008, based on the analysis of the CPE events identified during the first 3 years of the survey, LICTs were advised to screen for CPE every patient transferred from a foreign hospital.

We investigated whether orientation learning in this condition wa

We investigated whether orientation learning in this condition was still restricted to the relative locations of the two stimuli in the spatiotopic reference frame. Nine naive subjects were trained at 55° orientation in the congruent condition (left panels in Fig. 3A). After the training, their thresholds significantly decreased (pre-training threshold 6.68° ± 0.63° vs. post-training threshold 3.40° ± 0.42°, Alectinib t = 9.13, P = 1.7 × 10−6, paired t-test). As in Experiment I, a mere change in the spatiotopic stimulus relation from trained to untrained significantly increased the threshold at the trained 55°

orientation (t = 4.89, P = 0.0012; left two bars in Fig. 3B; for data from individual subjects, see Fig. 3C; five of the nine subjects showed a significant spatiotopic preference in the post-training test; bootstrapping, P < 0.05). The mean thresholds at the untrained 140° orientation were indistinguishable between the trained and untrained stimulus relations (t = 0.44, P = 0.67; right two bars MAPK inhibitor in Fig. 3B). These results were similar to those in Experiment I, even though the first stimulus here was irrelevant to orientation discrimination. It is possible that the first stimulus could serve as an anchor for deploying

initial attention and for subsequent remapping of attention to the location of the second stimulus, and that training could improve the predictive remapping of attention. If this hypothesis holds, the onset of a behavior-irrelevant stimulus that reflexively captures involuntary attention could also act as an anchor for subsequent attentional remapping. We tested this speculation in Experiment IV by slightly modifying the design of Experiment III. All random lines in the first stimulus were made iso-luminant, and 13 naive subjects were simply instructed to perform orientation discrimination on the

second stimulus while ignoring the first (Fig. 4A). Even though the first stimulus was entirely behavior-irrelevant and was not required to be voluntarily attended, we still observed a certain degree of spatiotopic learning (compare Fig. 4 with Fig. 3). Specifically, the subjects’ thresholds significantly decreased with training (pre-training 7.53° ± 0.40° vs. post-training 3.57° ± 0.22°, t = 12.74, P = 2.5 × 10−8, Galeterone paired t-test). When the spatiotopic stimulus relation was changed to the untrained condition, there was a significant increase in threshold at the trained 55° orientation (t = 2.51, P = 0.027; left two bars in Fig. 4B; data from individual subjects are shown in Fig. 4C; six of 13 subjects showed a significant spatiotopic preference in the post-training test; bootstrapping, P < 0.05). The mean thresholds at the untrained 140° orientation were not significantly different between the trained and untrained stimulus relations (t = 0.20, P = 0.84; right two bars in Fig. 4B).

MICs were determined as described previously (Sim et al, 2010)

MICs were determined as described previously (Sim et al., 2010). Western blot analysis of the chloramphenicol acetyl transferase (CAT) protein was performed as described previously (Kim et al., 2009). To measure steady-state levels of mutant bdm′-′cat mRNA, cDNA was synthesized using a Prime Script first-strand Tofacitinib cDNA synthesis kit (Takara) using 1 μg of total RNA isolated from E. coli cells expressing mutant bdm′-′cat mRNA as a template. Then, real-time PCR was performed in a C1000 Thermal Cycler (BioRad) using SYBR Premix Ex Taq (Takara) with the synthesized

cDNA as a template. The primers used were: 5′-ATGTTTACTTATTATCAGGCAG and 5′-TTAAAGCGTAGGGTGCTGGCCAC for bdm, 5′-TGACGAAGTTGACGTTGCTC and 5′-CTTCCAGGTGCAGAGTGTCA for rpsA. Both a primer extension analysis and an in vitro RNA cleavage assay were performed as described previously (Sim et al., 2010). In this study,

selleck chemicals bdm loop RNA transcripts were synthesized using PCR DNA as a template. PCR DNA was synthesized using two primers, T7 bdm loop F (5′-TAATACGACTCACTATAGGGGCATGGTGTTGTCACTG) and bdm +175R (5′-TTGCTGGTAGATATCAC), and the template DNA was pBRS1 or pBRS1, which contained mutations at the RNase III cleavage sites. Synthesized bdm loop RNA transcripts were either 5′-end labeled with [γ-32P]ATP (3000 mCi mmol−1) and T4 polynucleotide kinase (Takara) or 3′-end labeled with [5′-32P]pCp (3000 mCi mmol−1) and T4 RNA ligase (New England Biolab), separated in 4% polyacrylamide

gels containing 8 M urea. The transcripts were eluted from the gel via mixing in a buffer containing 30 mM Tris-HCl, pH 7.9, 10 mM NaCl, 0.1% sodium dodecyl sulfate, and 0.1 mM EDTA, pH 8.0, for 16 h and were Oxalosuccinic acid purified using phenol–chloroform extraction and ethanol precipitation. His-tagged RNase III purification and cleavage assays were performed as described previously (Amarasinghe et al., 2001). Briefly, 1 pmol of labeled RNA was incubated with 0.5 μg of purified RNase III in the presence of 0.25 μg mL−1 of yeast tRNA (Ambion) and 20 U of RNaseOUT™ (Takara) in cleavage buffer (30 mM Tris-HCl, pH 7.9, 160 mM NaCl, 0.1 mM dithiothreitol, 0.1 mM EDTA, pH 8.0). Cleavage reactions were initiated by adding 10 mM MgCl2 after 5 min of incubation at 37 °C. Samples were removed at the designated time intervals, mixed with an equal volume of Gel Loading Buffer II (Ambion), denatured at 65 °C for 10 min, and separated on an 8% polyacrylamide gel containing 8 M urea. EMSAs were performed as described previously (Pertzev & Nicholson, 2006). In these assays, Mg2+ was replaced by Ca2+, promoting substrate binding to RNase III while preventing substrate cleavage. Briefly, 5′-end-labeled RNA was incubated at 37 °C for 10 min with RNase III in a buffer containing 30 mM Tris-HCl, pH 8.0, 160 mM NaCl, 10 mM CaCl2, 0.1 mM EDTA, 0.1 mM dithiothreitol, 5% glycerol, and yeast tRNA (5 μg mL−1).

The data showed that deferring HAART until after TB treatment was

The data showed that deferring HAART until after TB treatment was completed was associated with a significant increase in mortality, even in patients with CD4 counts of >200 cells/μL, although there were few clinical events. We do not know if the six patients in this SAPIT study who died, out of the 86 who had TB, still had CD4 counts >200 cells/μL at the time of death. A recent study from Cambodia suggested that treatment with HAART Staurosporine in the first 2 weeks of TB treatment resulted in a lower mortality

rate than in the group delaying HAART to 8 weeks. The majority of these patients had a CD4 count of <100 cells/μL at enrolment [146]. The STRIDE (ACTG 5221) Study [147] also showed that starting HAART within 2 weeks resulted in a lower mortality rate than in the group delaying HAART until 8–12 weeks in patients who had

a blood CD4 count of <50 cells/μL at enrolment [146]. In these trials the disadvantage of starting early was an increased risk of IRIS. Until we have further analyses of all data, we believe it is safer and more practicable to set a blood CD4 count of <100 cells/μL as the point below which HAART should be started within 2 weeks of commencing TB treatment. Other data sets suggest that starting HAART early, independent of CD4 cell count, improves long-term outcome [148,149]. Some physicians believe that starting HAART irrespective of CD4 cell count, including >350 cells/μL, is beneficial in patients with active TB. Although the SAPIT study suggested HAART started during the course of TB therapy, even in those with CD4 counts >350 cells/μL, was beneficial, almost all Edoxaban the patients within this arm had a CD4 count below that threshold. A study of the risks and benefits of starting HAART early vs. late in patients with HIV-associated TB meningitis in the developing world, where 90% of patients were male, the majority

were drug users, many had advanced disease and the diagnosis was made clinically in 40% of patients, showed no difference in mortality if HAART were started early, although there was a greater incidence of severe adverse events in the early arm [150]. How this translates to UK clinical practice remains unclear. Taking into account all the limited data available, we recommend: CD4 count (cells/μL) When to start HAART <100 As soon as practicable 100–350 As soon as practicable, but can wait until after completing 2 months of TB treatment, especially when there are difficulties with drug interactions, adherence and toxicities >350 At physician’s discretion After starting anti-tuberculosis treatment, some patients develop an exacerbation of symptoms, signs or radiological manifestations of TB. This has been well described in patients without HIV infection, but appears to occur more commonly in HIV-positive patients [151–169]. The phenomenon is known as IRIS, IRD or paradoxical reaction.

We therefore used the following method to determine the coordinat

We therefore used the following method to determine the coordinate for fixation. If, within one set of eight blocks with the same calibration, the difference between median eye position in the different blocks was < 1°, we used the median x-values and y-values Trichostatin A research buy across all blocks as the fixation point coordinates. Otherwise, the eye-tracking data were analysed without this correction. On this filtered data, we removed all trials in which the subjects’ eyes moved by more than 1.75° from the fixation point. Two participants were excluded

because of excessive eye movements. All EEG data analyses were performed in matlab with the fieldtrip toolbox (Oostenveld et al., 2011) as well as custom scripts. The EEG recording was high-pass-filtered with a low cut-off of 0.5 Hz, by the use of fourth-order Chebyshev filters with zero phase-shift. This filter has the advantage BMS 354825 of very high attenuation in the stop band with minimal attenuation in the pass-band (< 0.1 dB). After filtering, bad channels were determined from the statistics of neighboring channels, and interpolated by the use of linear, distance-weighted interpolation. The EEG data were

then referenced to the average. In addition to the deletion of trials on the basis of eye movements, there was also an EEG threshold of ±125 μV. If more than six channels or any of the occipital electrodes of interest exceeded this threshold, the trial was discarded. Otherwise, high-amplitude channels were interpolated by the use of linear, distance-weighted interpolation. Three participants were excluded because of large numbers of trials with EEG artefacts, bringing the total number of participants used in further analysis see more to 14. After removal of artefact trials, an average of 117 trials per condition and participant

remained. Temporal second-order kernels (e.g. Sutter, 2000) representing evoked cortical responses were extracted for each electrode and each of the four stimulus locations, by reverse-correlating the EEG response with the known sequence of pattern reversals. The second-order response takes into account the history of visual stimulation, i.e. whether the current pattern is the same as the one presented one monitor refresh before. Given the findings of previous studies on spatial attention (e.g. Lalor et al., 2007; Kelly et al., 2008; Frey et al., 2010), we expect attentional modulation of the evoked responses during early cortical processing, as represented by responses in the C1 and P1 time-frame. As evoked response kernels represent activity in the early retinotopic cortex, which is very variable across participants (Ales et al., 2010a), the topographical distribution of peak activity was inconsistent across participants. For each stimulus location, we therefore selected two electrodes for each participant by determining mean activity across all four experimental conditions and selecting the two electrodes on the peak of the C1 and P1 topography, respectively.

Higher rates of negative HBsAg or anti-HCV EIA results in viraemi

Higher rates of negative HBsAg or anti-HCV EIA results in viraemic samples have been observed in immunocompromised HIV-infected patients [2,7]. In addition, the exclusion of patients presenting with serum liver enzyme levels higher than three or five times the ULN values (depending on the initial study) could have led to an underestimation of the prevalence. The comparison of our HBV and HCV estimates to those reported by the few other African studies in patients initiating antiretroviral therapy should be viewed as indicative only because of the

methodological differences. In South Africa, HBV DNA was detected in 40.6% of 192 patients Cabozantinib price (100% of 44 HBsAg-positive patients and 23.0% of 148 HBsAg-negative patients) [3]. In Cameroon’s neighbour Nigeria, 8.2% of 146 patients were found with HCV RNA (all patients were tested for HCV viraemia) [4]. The prevalence of co-infections in other HIV-infected populations are much lower. For instance, HBV DNA was detected in 2.4% of pregnant women in both

Côte d’Ivoire and South Africa [8,9]. The prevalence of HCV RNA was 0% in blood donors in Tanzania and 1.0% in pregnant women in Côte d’Ivoire [8,10]. Frequent co-infections are also found in Europe and the USA, where the prevalence of HIV, HBV and HCV in the general population is lower than in Africa. However, the predominant modes of transmission of all three infections are similar in Western countries (intravenous drug use and sexual contact) [11,12] whereas they appear very dissimilar in Africa (for HIV, the heterosexual route; for HBV, close contact within households during early childhood and, to a lesser extent, RAD001 order vertical transmission; and for HCV, unclear routes of transmission) [1,2]. Undetected HBV or HCV co-infections had clinical implications for antiretroviral therapy in our patients. All HBV co-infected patients

received anti-HBV lamivudine monotherapy, which has been shown to lead to frequent emergence of drug resistance [13] and, consequently, to possible acute hepatitis, fulminant hepatic failure and death [2]. The World Health Organization Histamine H2 receptor now recommends the use of tenofovir plus either lamivudine or emtricitabine as the nucleoside reverse transcriptase inhibitor (NRTI) backbone of antiretroviral therapy in HBV co-infected patients whenever possible (tenofovir has been available in Cameroon since 2007) [14]. Also, 46 and 55% of HBV and HCV co-infected patients, respectively, received nevirapine despite moderate liver enzyme elevations. In these patients, efavirenz or a third NRTI is preferred [14]. Two strategies should be considered for the management of HIV-infected patients needing treatment in Africa. Where possible, testing for HBsAg and anti-HCV should be performed systematically in addition to serum liver enzymes before initiating antiretroviral therapy in order to avoid nevirapine and anti-HBV lamivudine monotherapy when necessary.

Forty-two (778%)

of 54 patients with AHC who received th

Forty-two (77.8%)

of 54 patients with AHC who received therapy started it before week 12. Further characteristics of both populations are listed buy SRT1720 in Table 1. The IL-28B genotypes were in Hardy–Weinberg equilibrium (P=0.791 for AHC and 0.821 for CHC). The prevalence of the rs12979860 CC genotype was 47.5% among patients with AHC and 45.8% in those with CHC (P=0.778) (Table 1). In the group of individuals with AHC, 31 subjects with genotype CC (81.6%) were infected with HCV genotype 1 or 4 and 7 (18.4%) with genotype 2 or 3. Among CT/TT patients with AHC, 32 (76.2%) were infected with genotype 1 or 4 and 10 (23.8%) with genotype 2 or 3, respectively (P=0.948). In the group of patients with CHC, 119 (54.6%) of those with rs12979860 genotype CC were carriers of HCV genotype 1 or 4, while

99 (45.4%) were infected with HCV genotype 2 or 3. Of those harbouring rs12979860 genotype CT/TT, 200 (77.5%) bore HCV genotype 1 or 4 and 58 (22.5%) genotype 2 or 3 (P<0.001). A more detailed genotype distribution is shown in Table 2. In the subpopulation of patients with CHC enrolled in the German cohort, the distribution of HCV Cabozantinib genotypes was also significantly different from that found in patients with AHC. Specifically, 41 (53.9%) German patients with CHC and rs12979860 CC harboured HCV 1 or 4 vs. 65 (75.6%) of those bearing CT/TT (P=0.034). There were no significant differences in HCV plasma load among patients with different IL-28B genotypes in the overall population. Thus, the median (Q1–Q3) HCV-RNA level was 6.36 (5.68–6.88) log10 IU/mL in carriers of rs12979860 CC and 6.27 (5.59–6.79) log10 IU/mL in those harbouring CT or TT (P=0.458). However, HCV-RNA load was significantly higher in patients with AHC and the CC genotype than Org 27569 in those with AHC and rs12979860 CT/TT (Table 3). ALT levels in the entire population were higher in patients with the CC genotype [83 (58–165) in CC carriers vs. 74 (45–126) in CT/TT carriers; P=0.022]. The relationships between the IL-28B genotype and several parameters in the AHC and CHC groups are listed

in Table 3. Spontaneous clearance of HCV, as defined in this study, was documented in eight (10.1%) of the 79 patients in whom this information was available. There was no relationship between spontaneous clearance of the virus and HCV genotype. Thus, the numbers of patients who cleared HCV were as follows: six (11.3%) with genotype 1, one (12.5%) with genotype 2, one (10%) with genotype 3 and none with genotype 4 (P=0.746). The association between IL-28B genotype and spontaneous clearance did not reach statistical significance. Five (13.5%) of the patients with rs12979860 genotype CC and three (7.1%) of the patients with genotype CT or TT (P=0.349) showed spontaneous HCV clearance. The associations between IL-28B genotype and other factors are displayed in Table 3.

Earlier pharmacological and POMC gene transfer studies demonstrat

Earlier pharmacological and POMC gene transfer studies demonstrate that melanocortin activation in either site alone improves insulin sensitivity and reduces obesity. The present study, for the first time, investigated the long-term

efficacy of POMC gene transfer concurrently into both sites in the regulation of energy metabolism in aged F344xBN rats bearing adult-onset obesity. Pair feeding was included to reveal check details food-independent POMC impact on energy expenditure. We introduced adeno-associated virus encoding either POMC or green fluorescence protein to the two brain areas in 22-month-old rats, then recorded food intake and body weight, assessed oxygen consumption, serum leptin, insulin and glucose, tested voluntary wheel running, analysed POMC expression, and examined fat metabolism in brown and white adipose tissues.

POMC mRNA was significantly increased in both the hypothalamus and NTS region at termination. Relative to pair feeding, POMC caused sustained weight reduction and additional fat loss, lowered fasting insulin and glucose, and augmented white fat hormone-sensitive lipase activity and brown fat uncoupling protein 1 level. By wheel running assessment, the POMC animals ran twice the distance as the Control or pair-fed rats. Thus, the dual-site POMC treatment ameliorated adult-onset obesity effectively, compound screening assay involving a moderate hypophagia lasting ∼60 days, enhanced lipolysis and thermogenesis, and increased physical activity in the form of voluntary wheel running. The latter finding provides a clue for countering age-related decline in physical activity. “
“Sympathetic preganglionic neurons (SPNs) are located in the intermediolateral column

(IMLC) of the spinal Carnitine palmitoyltransferase II cord. This specific localization results from primary and secondary migratory processes during spinal cord development. Thus, following neurogenesis in the neuroepithelium, SPNs migrate first in a ventrolateral direction and then, in a secondary step, dorsolaterally to reach the IMLC. These migratory processes are controlled, at least in part, by the glycoprotein Reelin, which is known to be important for the development of laminated brain structures. In reeler mutants deficient in Reelin, SPNs initially migrate ventrolaterally as normal. However, most of them then migrate medially to become eventually located near the central canal. Here, we provide evidence that in wild-type animals this aberrant medial migration towards the central canal is prevented by Reelin-induced cytoskeletal stabilization, brought about by phosphorylation of cofilin. Cofilin plays an important role in actin depolymerization, a process required for the changes in cell shape during migration. Phosphorylation of cofilin renders it unable to depolymerize F-actin, thereby stabilizing the cytoskeleton.

Following 1 and 2 h of co-incubation, the ∆TTSS-2 strain displaye

Following 1 and 2 h of co-incubation, the ∆TTSS-2 strain displayed a 2.6- and 1.6-fold decrease in translocation, respectively, compared to wt, although these decreases were not statistically significant (Fig. 3). These data demonstrate that the TTSS do not inhibit V. parahaemolyticus translocation. Instead the bacteria are transported across the M cell-like co-culture model independently

of TTSS-1, while TTSS-2 has a modest enhancing effect on translocation at early stages of infection. To investigate whether V. parahaemolyticus translocates across the M cell-like co-culture model by disrupting the epithelial monolayer, the TER was measured in response to infection with wt, ∆TTSS-1 or ∆TTSS-2 bacteria. Measurement of the TER is one of the main ways to examine epithelial integrity see more 17-AAG supplier in vitro (Terres et al., 1998) as it represents the resistance to ion flow across the epithelial monolayer. Infection of the co-culture model with the wt bacteria resulted in a sharp decrease in TER 1 h postinfection with a further decrease observed 2 h postinfection (Fig. 4a). Similar decreases were detected for the ∆TTSS-1 and ∆TTSS-2 bacteria. Consequently, examination of the effects of V. parahaemolyticus on the TER of the M cell-like co-culture model indicates

that the disruption occurs independently of either TTSS-1 or TTSS-2. Infection of the Caco-2 monolayer with wt bacteria also resulted in a decrease in TER (Fig. 4b). Comparison of these data indicates that V. parahaemolyticus infection results in an increase in TER disruption in co-culture models when compared to Caco-2 monolayers. Although RAS p21 protein activator 1 not statistically significant, the difference

in TER decrease between Caco-2 and co-cultures was detected consistently. To determine whether MAPK activation has a role in the effects elicited by the bacteria on the co-culture, disruption of the TER in response to wt infection in the presence of MAPK inhibitors was examined. There was minimal difference between untreated co-cultures and co-cultures treated with the MAPK inhibitors (Fig. 4c). These nominal differences demonstrate that MAPK activation is not necessary for the disruption of the co-culture model in response to V. parahaemolyticus infection. Comparison of Caco-2 monolayers with a co-culture M cell model in this study indicates that V. parahaemolyticus is translocated in increased numbers (threefold increase) across the co-culture model. In the intestine, Peyer’s patch M cells actively endocytose bacteria and other foreign material for delivery to underlying lymphocytes, and this intracellular translocation would be the principal explanation for the observed increases (Neutra et al., 1996; Siebers & Finlay, 1996; Wong et al., 2003; Jang et al., 2004; Brayden et al., 2005). Enhanced transport of other M cell tropic bacteria such as Salmonella across an in vitro co-culture model (Martinez-Argudo & Jepson, 2008) and invasion through murine Peyer’s patches (Jones et al.

Our study aimed to identify the (1) prevalence of mobile device a

Our study aimed to identify the (1) prevalence of mobile device and antimicrobial resource use by GPs, (2) factors that may influence

use of an antimicrobial guidance app, and (3) antimicrobial-related app features that GPs would find useful. A 22-item online questionnaire was constructed following critical review of the literature and iteratively developed following piloting on a limited number of clinicians. A sample size calculation identified that 260 responses were needed and the questionnaire was distributed in November 2013 through a national internet-based network which included approximately 56,800 clinicians (89% of all UK registered GPs) to maximise recruitment diversity. Participants were stratified to be representative in number across England, Scotland, Wales and Northern Ireland. Data were analysed using descriptive statistics. Logistic regression was used to assess the relationship between GP variables and their intention to use an app for national antimicrobial guidance. selleck chemicals llc Ethical review was not required as the research involved healthcare staff recruited as research participants by virtue of their professional role. We capped the survey at 264 responses which were

received by 27 November: 58% were GP principals, 31% salaried GPs, 11% locum GPs and 1 GP registrar. Median age of GPs was 41 years (IQR 37–49) and 57% were male. The majority (92%) owned at least one mobile device, of these, the three most common were: iPad® (53%), iPhone®

(51%) and Android™ smartphone (33%). The paper British National Formulary (BNF®) and BNF for Children (BNFC®) were more widely used (74% and 68% of 264 GPs, respectively used these at least monthly) for antimicrobial information than the Pyruvate dehydrogenase BNF® website (32%), BNFC® website (20%), ‘MIMS™’ (paper 27%, website 4%), local guidance (paper 39%, electronic 44%) or national guidance (paper 14%, website 28%). Furthermore, 14% used the BNF® app, 8% BNFC® app and 5% local guidance app. Four in five GPs would use an app to access their local (80%) and national (78%) antimicrobial guidance if it was available. Compared to GPs aged 29–39 years, those aged 40–49 years and 50–65 years were less likely to use an app for national antimicrobial guidance (40–49 years: OR 0.57, 95% CI 0.25–1.31; 50–59 years: OR 0.18, 95% CI 0.08–0.43). GPs wanted an antimicrobial app that provides links to: paediatric doses (72%), advice in pregnancy (72%), local microbiological susceptibility patterns (61%), and hospital antimicrobial prescribing guidance (52%). The majority (61%) of GPs would access medical information from a mobile device in front of a patient but half (53%) believed patients’ acceptance of this practise was situation dependent. Our study has quantified the use of antimicrobial resources by GPs, identified that mobile device ownership is high, and that GPs (particularly younger GPs) would use an antimicrobial app.