Improvement of knowledge and practice behaviour among providers in pharmacies is needed. “
“It is with great pleasure that I introduce this SP600125 solubility dmso supplemental issue of the International Journal of Pharmacy Practice. In this supplement you will find abstracts of the pharmacy practice research papers and posters presented at the 2012 Royal Pharmaceutical Society Conference, held at the International Convention Centre, Birmingham. The theme of this year’s conference is “Enhancing patient care through innovation”. In common with previous years, this supplement

has been prepared in advance of the conference, to allow participants in the practice research sessions to read the abstracts prior to the sessions. One hundred and sixty seven abstracts were submitted for the Royal Pharmaceutical Society Conference 2012, and this year the Society’s Pharmacy Practice Research Panel accepted 106 for poster or oral presentation at the Conference. Please note that although the abstracts have already been examined by the Panel, they have not passed through the peer review process applied by the IJPP to all other contributions. The journal cannot therefore guarantee that they meet its usual stringent requirements. The abstracts have, however, been subjected to a full

editing process and, as far as possible, put into the normal IJPP editorial style. Authors were asked to limit the length of their contribution to allow each abstract to fit on to a single

page of this supplement. While most abstracts are classified as “Practice research”, authors can submit abstracts this website which describe “Quality Service Improvement”. Many of the abstracts contained in the supplement fall into this category. Spread over the two days of the conference there are six separate practice research sessions for oral presentation of accepted papers. These 30 abstracts are listed in this supplement in the order in which they appear in the programme. The remaining 76 abstracts RVX-208 are those presented as posters, beginning with “Practice research” posters (pages 36–106), followed by “Quality Service Improvement” posters (pages 36–106). This year’s prestigious Pharmacy Practice Research Award (sponsored by The Pharmacy Practice Research Trust) has been awarded to Dr Catriona Matheson, Senior Research Fellow at the University of Aberdeen. Her keynote lecture, entitled “Drug Misuse Treatment and Services: Pharmacy and Beyond”, will recognise how pharmacy as a profession has taken on this very difficult client group where other health professionals have been reluctant. I have witnessed, through my research, how community pharmacy has embraced this patient group and is now providing effective services that help drug users engage with treatment and as a consequence reduce the associated harm.

monocytogenes strains. The CPA assays were performed at a constant temperature 64 °C using seven specific primers and evaluated for specificity and sensitivity. The color change of positive amplification was directly observed by Loopamp® Fluorescent Detection Reagent (FD), and the DNA products were visualized as a ladder-like banding pattern on 2.5% gel electrophoresis. Moreover, the positive reactions were also detected by real-time measurement of turbidity. 50 L. monocytogenes and 46 non-L. monocytogenes strains were used for the method verification, and the specificity was 100%. The

limit of detection (LoD) of the S-CPA and D-CPA assays was 2.5 pg DNA per reaction and 10-fold more sensitive than PCR. A total of 60 pork samples were tested for L. monocytogenes using the S-CPA assay developed in the study, Neratinib and the accuracy of the S-CPA and the culture-biotechnical method was 100% identical. The results suggested that the S-CPA assay was a rapid, sensitive, and valuable tool for detection of Crizotinib ic50 L. monocytogenes in food products. “
“The optokinetic deficits in albinotic rats and ferrets are caused by the loss of direction selectivity in the accessory optic system (AOS). However,

the underlying mechanisms for this loss are still not clear. Here we tested the hypothesis that, in albino rats, the retinal input to the AOS lacks direction selectivity and, as a consequence, neurons in the AOS are direction non-selective. We investigated ON-center

direction-selective retinal ganglion cells, the major input to the AOS, in pigmented Long Evans and albino Wistar rats using extracellular in vitro patch-clamp techniques. To visualise putative AOS-projecting direction-selective ganglion cells, we retrogradely labeled them by injection of the infrared-sensitive dye indocyanine green Methocarbamol into the medial terminal nucleus of the AOS. The present study is the first to present physiological evidence for retinal ON-center direction-selective ganglion cells in rat. Our results show that, in albinotic and pigmented rats, ON-center retinal ganglion cells projecting to the AOS are similarly direction-selective, suggesting that the optokinetic deficit must be caused by the abolition of direction selectivity in the AOS itself. “
“We compared with a new psychophysical method whether flashes and averted eye-gazes of a cartoon face induce a ventriloquist illusion (an illusory shift of the apparent location of a sound by a visual distracter). With standard psychophysical procedures that measure a direct ventriloquist effect and a ventriloquist aftereffect, we found in human subjects that both types of stimuli induced an illusory shift of sound location. These traditional methods, though, are probably contaminated by response strategies.

The finding that the

PD group initiated voluntary saccades at abnormally long latencies in the baseline condition is consistent with many previous reports (Kennard & Lueck, 1989; Kitagawa et al., 1994; Amador et al., 2006). It is also consistent with the premise PLX3397 mouse that saccade initiation in PD is impaired due to over-activity of inhibitory outputs from the basal ganglia via the substantia nigra pars reticulata (SNr) projection to the SC (Albin et al., 1995; Mink, 1996; Hikosaka et al., 2000). The tonic inhibitory output to the SC must be selectively released to allow burst firing of saccade-triggering cells (Hikosaka & Wurtz, 1985). Nigral dopaminergic innervation of the striatum is crucially involved in generating the signal that suppresses the tonic inhibitory output from the SNr to the SC when a saccade is to be made (Hikosaka et al., 2000; Nakamura & Hikosaka,

2006). Thus, in PD, degeneration of nigral dopamine cells may result in over-activity of the inhibitory output from the SNr, thereby affecting the build-up of neural activity in the SC and delaying the triggering of saccades. In the PD group, latencies were abnormally reduced by (pre-saccadic) peripheral symbol changes when voluntary saccades were performed without the discrimination task. Olaparib This observation is consistent with other studies showing that exogenous stimuli can facilitate endogenous saccades (Shepherd et al., 1986). We suggest that peripheral visual events (i.e. the symbol changes in this paradigm) might 4-Aminobutyrate aminotransferase accelerate saccade initiation in PD by boosting the build-up of neural activity in saccade neurons. This exogenous boost might reduce the delay in the build-up of neural activity in the SC in PD. The PD group exhibited an abnormally large latency reduction when voluntary saccades were made in conjunction with the discrimination task. We suggest that the

intention to perform the discrimination task promotes the release and shift of attention away from the central fixation point, in preparation for the impending appearance of the discrimination symbol at the peripheral saccade target location. This effect supports and facilitates saccade planning and can thereby reduce saccade latencies (Montagnini & Chelazzi, 2005; Trottier & Pratt, 2005). Previously, we reported that the concurrent performance of a discrimination task abnormally reduced latencies of visually guided (or reflexive) saccades in the same PD group (van Stockum et al., 2011b). Especially in overlap trials, the continued presence of the fixation point apparently did not exert the same inhibitory effect in the PD group as in the control group. We proposed that the abnormal endogenous facilitation of visually guided saccades observed in PD may be associated with a decrease in the inhibition of saccade cells during fixation.

The AHL biosensor strain Agrobacterium tumefaciens NTL4[pZLR4] was grown in PF-02341066 order LB medium containing 30 μg mL−1 gentamicin (Luo et al., 2003). The method of Gantotti & Beer (1982) was used to generate a nonpigmented variant of P. vagans C9-1. An LB culture of C9-1 wild type was incubated at 38 °C for 24 h, and 10−5–10−6 dilutions were plated onto LB agar and incubated at 37 °C for 5 days. The nonpigmented variant C9-1W that was obtained was tested for the presence of the three C9-1 plasmids using PCR. Oligonucleotides (Supporting Information, Table S2)

were synthesized by Sigma-Genosys (Steinheim, Germany). The HotStarTaq Master Mix kit (Qiagen, Hilden, Germany) was used as described by the supplier. Chromosomal DNA was isolated using the Wizard Genomic DNA Purification Kit (Promega, Madison, WI). PCR was performed as described elsewhere (Innis et al., 1990). PCR products were visualized on 1.5% agarose gels (Sambrook et al., 1989). The metabolic profiles of P. vagans C9-1 and C9-1W were obtained using Biolog GN2 and AN plates (Hayward, CA). Precultures were grown in M9 medium with 5 mM glucose and allowed to grow to the late stationary phase to ensure complete substrate utilization. Cultures

were centrifuged at 4000 g and the cell pellets were washed once before resuspending in a fresh M9 medium. The attenuance at 600 nm (A600 nm) was set to 0.15 and each microtiter plate well was inoculated with 100 μL of this bacterial suspension. The plates were scored after 1, 2 and 5 days of incubation at 28 °C. For AHL bioassays, cell-free filtrates (150 μL) from Nutlin-3a cost stationary-phase cultures of P. vagans (16 h, 28 °C) were combined with 150 μL of a washed stationary-phase culture of A. tumefaciens NTL4[pZLR4] (Luo et al., 2003) (16 h, 28 °C) in a fresh LB medium containing 0.1% 5-bromo-4-chloro-3-indolyl β-galactoside (X-Gal). The production of AHL was determined qualitatively by observing a change to blue in the color of the microculture over the course of 3 days. The genome sequence

of plasmid pPag3 Bay 11-7085 from P. vagans C9-1 (Smits et al., 2009) was annotated using GenDB (Meyer et al., 2003) and was deposited at GenBank (Accession number CP001895). Sequence manipulations were performed using the Lasergene package (DNASTAR, Madison, WI). Additional blast searches (Altschul et al., 1990) were performed at NCBI (http://blast.ncbi.nlm.nih.gov/Blast.cgi). The genome sequence of P. vagans C9-1 (Smits et al., 2009) revealed a 530-kb plasmid, designated pPag3, encoding the carotenoid biosynthesis cluster crtEXYIBZ (Pvag_pPag30170–Pvag_pPag30175) as the most prominent feature. The encoded proteins share 91–97% sequence identity to the respective proteins of P. agglomerans pv. milletiae Wist 801 (GenBank: AB076662) and 70–89% to those of P. ananatis 20D3T (Misawa et al., 1990). The plasmid also carries four thiamine biosynthesis genes (thiOSGF; Pvag_pPag30158–Pvag_pPag30161) and a complete maltose metabolism gene cluster (Pvag_pPag30206–Pvag_pPag30215).

326) including 23 cases presented in children under 12. Immigrants (recently arrived and VFR) were younger than compound screening assay the other groups of travelers (p < 0.001). Epidemiological data in the different study groups are shown in Table 1. The most prevalent species was P. falciparum (143 cases, 84.1%), acquired mostly in Africa (97.9%); one case was acquired in India, one in Laos, and one in Ecuador. Plasmodium vivax was detected in 20 cases (11.8%), 6 of them acquired in Africa, 3 cases in Asia (India), and 3 cases in South America (1 in Ecuador, 1 in Brazil, and 1 in Peru). Infections produced by Plasmodium ovale (four cases, 2.4%) and Plasmodium malariae (two cases, 1.2%) were always acquired in sub-Saharan Africa.

One mixed infection due to P. falciparum and P. malariae was observed (0.6%). It was acquired in Equatorial Guinea. Parasitemia levels were studied in 144 cases: it was low (<1%) in 20.8%, moderate (1%–5%) in 58.3%, and high (>5%) in 20.8%. All cases with high parasitemia were caused by P. falciparum. Samples from five recent immigrants with negative microscopic examination were diagnosed with P. falciparum infection

using PCR assay. Molecular diagnosis contributed to identify Plasmodium species in another three patients with low parasitemia, infected with P. ovale (two) and P. vivax (one). Fever was the main symptom and was ABT-263 chemical structure present in 93.5% of the cases, but it was less frequent in recently arrived immigrants group (p < 0.001). In fact, four of these immigrants were apyretic during the whole episode, and consulting referring macroscopic hematuria, generalized edema

because of a nephrotic syndrome, parotid tumor and abdominal Lepirudin pain with splenomegaly, and asthenia linked to severe anemia (hemoglobin 5.7 g/dL). The most common laboratory abnormalities were thrombocytopenia (64.1%), presented more frequently in sailors than in the other groups, and anemia (34.9%), that was presented less frequently in tourists and business travelers. Clinical presentation and laboratory findings are summarized in Table 2. The most frequent regimens used were based on quinine, usually combined with doxycycline. Other combinations used, mainly in children, included: quinine + clindamicin, quinine + trimethoprim–sulfamethoxazole, and quinine + sulfadoxine–pyrimethamine. Treatment regimens used are summarized in Table 3. Almost 80% (77.6%) of patients were admitted to hospitals for treatment and control, and outpatients accounted for the 22.4%. However, oral administration was preferred in at least 87 (51.2%) patients. One strain of P. vivax imported from Asia presented tolerance to primaquine, and it was necessary to use higher doses of the drug in two different times for the patient treatment regimen. At least one indicator of severe malaria was present in 39 cases (22.9%), of those 19 (11.2%) required attention in critical care units. Renal failure (74.4%), followed by acute respiratory distress syndrome (33.3%) and disseminated intravascular coagulation (33.

For instance, in many HIV-infected cohorts, cigarette smoking, recreational drug use (including cocaine use), increased alcohol intake and reduced physical activity are highly prevalent [11]. These factors may also affect the risk of neurocognitive disorders (HIV-associated neurocognitive disease and dementia), non-AIDS-associated

malignancies, liver disease, diabetes, and renal and osteoporotic bone diseases. Some CHIR-99021 cohort studies have already suggested that modification of risk factors can decrease the incidence of non-AIDS-defining chronic conditions, including CVD [6]. Hence, it is important to screen and manage risk factors for long-term age-related diseases that increasingly affect the HIV-infected population. Most studies that have examined the contribution of HIV infection to mortality, including those discussed above, do not have an ideal control population. Hence, considerable caution needs to be exercised when attributing relative risk of mortality caused by HIV itself as opposed to unattributed associated confounding variables, particularly lifestyle factors. Even a supposedly ideal control population, such as individuals at high risk of HIV infection but who remain uninfected, might differ in terms of host

factors that govern both infectability and mortality. A study from Denmark that carefully matched cases and controls concluded that mortality in patients without risk factors on successful http://www.selleckchem.com/products/Fulvestrant.html HAART therapy is almost identical to that of the non-HIV-infected population [12]. It is important to further define the relationship between HIV infection and mortality, especially those factors that can be modified to attenuate any risk. Screening tools and risk calculators for the general population have been developed for some common noncommunicable chronic diseases, as best exemplified

by coronary heart disease (CHD), fragility fractures, diabetes and renal disease. Personalized risk prediction aims to estimate, communicate and monitor risk to motivate adherence to lifestyle change or therapies, and to allocate scarce prevention PJ34 HCl resources and strategies appropriately. The World Health Organization (WHO) has recently focused on noncommunicable diseases (NCDs), as they are the leading cause of death globally, killing more people each year than all other causes combined [13]. The WHO has recognized that, contrary to popular opinion, available data demonstrate that nearly 80% of NCD deaths occur in low- and middle-income countries [13]. CVD is one of the leading causes of death in the UK and is largely preventable [14]. In 2008, there were more than 191 000 deaths attributable to heart and circulatory disease in the UK, including 88 000 deaths from CHD and a further 43 000 from stroke.

, 1994). We cannot exclude that in contrast to pri2 in S. commune,

priB does play a role in mushroom formation in L. edodes. The monokaryotic Δjmj3 strain was also indistinguishable from the wild-type strain. However, the dikaryotic Δjmj3Δjmj3 strain grew somewhat slower than the wild type and formed a less dense mycelium. Yet, the mutant did form sporulating fruiting bodies (data not shown). Taken together, we have shown that the relative incidence of gene inactivation by homologous integration is drastically increased in a Δku80 strain when compared with the wild type. This strain will therefore be highly www.selleckchem.com/products/AZD2281(Olaparib).html instrumental in the functional analysis of genes in S. commune and, in this way, contribute towards our understanding of the biology of mushroom-forming basidiomycetes. This research was supported by the Dutch Technology Foundation STW, the Applied Science division of NWO and the Technology Program of the Ministry of Economic Affairs. “
“It is expected that Mannheimia hemolyticaA1 expresses a particular collection of genes during infection in the host. The bacterial gene products are produced in the in vivo environment to facilitate growth and survival. Here, we examined gene expression

by M. hemolyticaA1 in the bovine host after 6 days of infection. Total RNA from M. hemolyticaA1 recovered from pneumonic lungs of two animals was used to produce Quizartinib in vitro cDNA to screen a custom M. hemolyticaA1 microarray. The expression profile was compared to a RNA sample from an in vitro grown culture. The data showed that 44 genes were differentially expressed by more than eightfold when compared with the in vitro sample. Seventeen genes were found Erastin research buy to have higher expression in vivo and 27 genes had lower expression. Several virulence-associated genes including those encoding leukotoxin, a capsule biosynthetic enzyme and the serotype-specific antigen, Ssa, had reduced expression, suggesting that their products may not be important during the later stages of infection. Most of the genes up-regulated in vivo encoded hypothetical or conserved hypothetical

proteins. Three Mu-like bacteriophage-related genes were up-regulated in the in vivo sample, suggesting that the prophage may be transcriptionally active. The results provide a glimpse of gene expression by the bacterium in the host after pulmonary infection has been established. Bovine pneumonic pasteurellosis is the major cause of morbidity and mortality in beef cattle in North America and results in significant economic loss to the cattle industry (Griffin, 1997). The primary causative agent of pneumonic pasteurellosis is Mannheimia hemolytica A1, a Gram-negative, non-motile bacterium that is a part of the normal flora of the upper respiratory mucosa of cattle (Frank, 1988). To-date, there is no information pertaining to the global gene expression of M. hemolytica A1 within the bovine host during an infection. Roehrig et al. (2007) examined the transcriptome profile of M.

Cloning was performed using standard procedures, with plasmids transformed in E. coli strain DH5α or DH5αλpir, as described previously (Bose et al., 2008). Cloned PCR products were sequenced to ensure that unintended alterations were not incorporated. Sequencing was conducted at the University of Michigan DNA Sequencing Core Facility or at the University of Pifithrin-�� nmr Georgia Molecular Genetics Instrumentation Facility. Plasmids were mobilized into V. fischeri from E. coli by triparental mating using strain CC118λpir with pEVS104 as a helper (Stabb & Ruby, 2002), and mutations were placed on the chromosome by allelic exchange. Parent

strains and plasmids used for allelic exchange are listed in Table 1. Key plasmids and oligonucleotides are described in Table 1, and an overview of allele construction follows. To mutate fnr, an ∼3.3 kb region of the V. fischeri genome centered on fnr was PCR amplified with primers EVS97 and EVS98 using ES114

or MJ1 genomic DNA as a template, and the fragments were ultimately subcloned into pEVS136 and pJLB69, respectively (Table 1). We generated Δfnr∷tmpR alleles by replacing the ClaI to AvrII fragment of fnr with the trimethoprim-resistance gene (tmpR) from pJLB1 (Dunn et al., 2005) on a BstBI to AvrII fragment, resulting in tmpR replacing an selleckchem internal 255-bp fragment beginning in the middle of fnr, with tmpR in the same orientation as fnr. The ES114-derived Δfnr∷tmpR allele was placed in pJLB5 and pJLB70, and the MJ1-derived Δfnr∷tmpR allele was used in pCDW5. For complementation of E. coli with ES114 fnr, we ligated the fnr-containing BsrBI–PstI fragment from pEVS136 into SmaI- and PstI-digested pDMA5, generating pJLB6. To place lacZ under control of Fludarabine order the arcA promoter, we PCR amplified an ∼3.1-kb fragment containing an engineered lacZ (Tomich et al., 1988) using pVSV3 (Dunn et al., 2006) as a template and primers JBLACZ1

and JBLACZ2 (Table 1). We cloned this product into SmaI-digested pAJ4 and pJLB55 (Bose et al., 2007), which carry regions flanking arcA from ES114 and MJ1, respectively, with the sequence between the start and the stop codons of arcA replaced by a 6-bp SmaI recognition site. The ParcA-lacZ alleles contain the arcA start codon, followed by a 5′-CCC-3′ proline codon, and then the lacZ reporter (Tomich et al., 1988) from its second codon onward. These ES114- and MJ1-derived alleles were subcloned into pAS31 and pJLB139, respectively. Overnight cultures in LBS were diluted 1 : 1000 into SWTO and incubated at 24 °C with shaking (200 r.p.m.). Aerobic cultures contained 50 mL of SWTO in 250-mL flasks. For anaerobic cultures, aerobically grown overnight cultures were diluted 1 : 10 in LBS before inoculation of 0.2 mL into 20 mL SWTO in 165-mL sealed bottles with a headspace containing 5% CO2, 10% H2, and 85% N2.

We studied the roles of the PL, IL and dorsal peduncular PFC (DP) in the expression of context-induced reinstatement, reacquisition and extinction of alcoholic beer-seeking. In context-induced reinstatement (renewal), animals were trained to nosepoke

for alcoholic beer (context A), extinguished (context B) and then tested in context A and B. In reacquisition, animals received the same instrumental training and extinction without any contextual manipulation. On test, alcoholic beer was again available and responding was compared with naive controls. Just prior to the test, rats received bilateral infusion of baclofen/muscimol into the PL, IL or DP. Reversible inactivation of the PL attenuated ABA renewal but augmented reacquisition. Reversible inactivation of IL had no effect on the reinstatement or reacquisition of alcoholic beer-seeking and had no effect on extinction expression (ABB and AAA). Bortezomib concentration IL inactivation did, however, increase the latencies with which animals responded on test but only when animals were tested

in the extinction context. DP inactivation had no effect on reinstatement or reacquisition. These studies are inconsistent with the view that PL and IL exert opposing effects on drug-seeking. Rather, they support the view that PL is Selleck 3Methyladenine important for retrieval of drug-seeking contingency information and that the use of contextual information is enhanced with IL manipulation. “
“The neuron-specific potassium-chloride cotransporter 2 (KCC2) plays a crucial role in adjusting intracellular Cl− concentrations. The lack of KCC2 in the plasma membrane of the axon initial segment (AIS) of pyramidal cells contributes to variable reversal potentials for perisomatic γ-aminobutyric acid (GABA)A receptor-mediated postsynaptic potentials, but the distribution of KCC2 in pyramidal dendrites

remains to be established. We applied high-resolution pre-embedding immunolocalization to quantify KCC2 concentrations along dendritic, somatic and axonal regions of rat hippocampal principal cells. Confirming our results on neocortical pyramidal cells, membranes of AIS of CA1 pyramidal cells and dentate granule Abiraterone cells contained 6.4 ± 11.9% and 6.6 ± 14.1% of somatic KCC2 concentrations, respectively. Concentrations of KCC2 in basal dendritic shafts of stratum (str.) oriens were similar to somatic levels (109.2 ± 48.8%). Along apical dendritic shafts of CA1 pyramidal cells, the concentration of KCC2 showed a complex profile: normalized to somatic levels, the density of KCC2 was 124.5 ± 15.7%, 79 ± 12.4% and 98.2 ± 33.5% in the proximal and distal part of str. radiatum and in str. lacunosum moleculare, respectively. Dendritic spines of CA1 receiving excitatory inputs contained 39.9 ± 8.5% of KCC2 concentration measured in shafts of the same dendritic segments targeted by GABAergic inputs.

In this study, we investigated selleck chemical the presence of Tn6188 within the genus Listeria spp. Our screening indicates that the distribution of Tn6188 may be limited to L. monocytogenes.

We confirm that QacH is responsible for the observed increase in tolerance by complementation of a qacH deletion mutant and introducing qacH in a Tn6188 negative strain. We investigated the transporter’s substrate spectrum by determining minimal inhibitory concentrations (MICs) and showed that QacH also confers higher tolerance towards other QACs and ethidium bromide (EtBr). This result was supported by increased expression of qacH in the presence of the various substrates as determined by quantitative reverse transcriptase PCR (qRT-PCR). In addition, we detected expression of a Tn6188 transposase gene and circular forms selleckchem of Tn6188, suggesting activity and possible transfer of this transposon. “
“A 530-kb megaplasmid pPag3 contributing 10.8% of the total genome of Pantoea vagans biocontrol strain C9-1

was sequenced. A rare nonpigmented variant C9-1W was obtained and shown to have lost pPag3, but retained all other plasmids (pPag1, pPag2). Phenotypic characterization of the variant confirmed the function of several annotated genes that may influence ecological fitness and efficacy. Metabolic profiling revealed important plasmid-based carbon utilization phenotypes. Plasmid loss resulted in thiamine auxotrophy, absence of carotenoid pigmentation, desferrioxamine diffusible siderophore biosynthesis, inherent ampicillin resistance and expression of AI-1 quorum-sensing signaling. This confirmed the functional expression of the corresponding genes located on pPag3 in P. vagans. Pantoea is a diverse genus, with most species considered to be ubiquitous plant epiphytes and often isolated from a wide range Sclareol of other environmental habitats (e.g., soil, water,

insect/animal gut and clinical samples). Some plant isolates have demonstrated strong beneficial activity as biological control agents for pre- and postharvest fungal and bacterial diseases (Braun-Kiewnick et al., 2000; Bonaterra et al., 2005; Francés et al., 2006). The type species, Pantoea agglomerans, has undergone extensive taxonomic rearrangement emerging from the Enterobacter agglomerans–Erwinia herbicola complex (Ewing & Fife, 1972; Rezzonico et al., 2009). Recently, several closely related species, such as P. vagans, have been newly described based on molecular analysis (e.g., multilocus sequence analysis, DNA–DNA hybridization) (Brady et al., 2008, 2009; Rezzonico et al., 2009). Strain C9-1 is an important biocontrol agent (Ishimaru et al., 1988; Johnson & Stockwell, 1998) that is registered in the United States and Canada as Blight Ban C9-1 (NuFarms America).