a, b Pustules. c–i Conidiophores (Hairs visible in e). HDAC inhibitors list j Conidia. All from SNA. All from G.J.S. 00–72. Scale bars: a = 1 mm, b = 0.25 mm; c–e = 20 μm; f–i = 10 μm Fig. 10 Trichoderma gillesii, Hypocrea teleomorph. a, b Stroma morphology. c Stroma surface, macro view.

d Stroma surface, micro view. e–g Perithecia, median longitudinal sections showing surface region and internal tissue of stroma. h, i Asci. j Part-ascospores. Note the subglobose part-ascospores in Figs. i and j All from G.J.S. 00–72. Scale bars: a, b = 1 mm; c = 0.5 mm; d, g = 20 μm; e = 50 μm, f = 100 μm; h–j = 10 μm MycoBank MB 563905 Trichodermati sinensi Bissett, Kubicek et Szakacs simile sed ob conidia anguste ellipsoidea, 3.2–4.0 × 1.7–2.2 μm differt. Holotypus: BPI 882294. Teleomorph: Hypocrea sp. Optimum temperature for growth on PDA and SNA 25–35°C; after 72 h in darkness with intermittent light colony on PDA completely or nearly completely filling a 9-cm-diam Petri plate (slightly slower at 35°C); within 96 h in darkness with intermittent light colony radius on SNA 40–50 mm (slightly faster at 35°C). Conidia forming on PDA within 48–72 h at 25–35°C in darkness with intermittent light; after 1 week on SNA at 25°C under light. No diffusing pigment noted on PDA. Colonies grown on SNA for 1 week at 25°C under light slowly producing pustules. Pustules formed of intertwined hyphae, individual conidiophores not evident, slowly turning green. Conidiophores arising from hyphae of the pustule,

typically comprising a strongly developed main axis with fertile lateral branches and often terminating in a sterile terminal extension (‘hair’). Hairs conspicuous, short, stiff erect, https://www.selleckchem.com/products/c188-9.html sterile, blunt, septate. Fertile branches increasing in length from the tip of the conidiophore, often paired, rebranching to produce either solitary phialides or unicellular

secondary branches; secondary branches terminating in a whorl of 3–5 divergent phialides. Intercalary phialides not seen. Phialides lageniform, nearly obovoidal, typically widest below the middle, (4.0–)4.5–7.0(−9.5) μm long, (2.2–)2.5–3.0(−3.2) μm at the widest point, base (1.2–)1.5–2.0(−3.0) μm wide, L/W (1.4–)1.5–2.5(−3.5) μm, arising from a cell (1.7–)2.0–3.0(−3.7) μm wide. Conidia ellipsoidal, (3.0–)3.2–4.0(−4.5) × (1.5–)1.7–2.2(−2.5) μm, L/W (1.4–)1.5–2.2(−2.5), green, smooth. Chlamydospores not observed. Teleomorph: Stromata brown, discoidal, Urocanase margins slightly free, 3–4 mm diam, cespitose and covering an area ca. 15 mm diam, surface plane to undulate, conforming to the surface of the substratum and adjacent stromata, ostiolar openings appearing as minute black papillae, no reaction to 3% KOH, ostiolar area greenish in lactic acid. Cells of the stroma surface in face view pseudoparenchymatous, ca. 5.5 × 4.5 μm diam, slightly thick-walled. Perithecia elliptical in section, 220–250 μm high, 130–190 μm wide, ostiolar region formed of small cells and gradually merging with the cells of the surrounding stroma surface.

data). At present, we can only speculate about the mechanistic basis of the host influence on symbiont physiology. A plausible scenario, however, is that the amount, complexity, and reliability of nutrients provided to the symbionts can affect the symbionts’ evolutionary fate by relaxing or increasing selective pressures on maintaining metabolic versatility. Under

this scenario, a nutrient-rich and stable environment provided by the host sustains genome erosion in the symbiotic bacteria, leading SBI-0206965 ic50 to metabolic dependency and high host specificity (Figure 6). Despite the higher costs, providing a rich environment could be beneficial to the host by stimulating bacterial growth and increasing the number of bacterial cells applied onto the cocoon, which in turn leads to high antibiotic production and an effective symbiont-mediated host protection [35]. Simultaneously,

a rich environment could allow for selection of the best symbionts by ‘screening’ through increased competition, with the most competitive and best-defended strain winning out [36,37]. By contrast, a nutrient-poor environment (lower amount, diversity, and/or reliability of nutrients) would be less costly to the host and prevent genome erosion in the bacterial symbionts. The high metabolic versatility would enable the bacteria to persist as free-living forms and provide the opportunity Ferrostatin-1 mouse for host switching by horizontal transfer (Figure 6). Interestingly, different symbiont strains across individuals of the same host species have so far only been detected for North American Philanthus species ([28], this study: biovar ‘albopilosus’ strains alb539-2), suggesting that horizontal transfer of symbionts is indeed more common among these physiologically versatile strains than across species in the metabolically more restricted South American and Eurasian/African clades. Such horizontal transfer could occur in populations of sympatric host species through interspecific predation or by the acquisition of symbionts from the soil in reused or closely associated brood chambers (Figure 6). Figure 6 Scheme of

putative host-driven evolution within the monophyletic clade ‘ S. philanthi ’. Acquisition of Rucaparib symbionts occurs shortly before or during emergence of the adult female beewolf from the cocoon, and only few bacterial cells are taken up into the antennal gland reservoirs [26]. The strong bottleneck effect likely contributes to the low genetic diversity we observed within the antennae of individual beewolves, as well as across host individuals of the same species (see also [28]). While the genetic homogeneity of the symbionts reduces competition and conflict in the symbiosis, it also compromises the symbionts’ ability to adapt to changing environmental conditions [38]. Furthermore, the uptake of low numbers of symbiont cells from the cocoon surface may entail the risk of taking up non-symbiotic bacteria into the antennae.

94 × 10-1 K27 + 1.27 × 10-1 K51 + 6.24 × 10-1 K54 + 11.1 K1179 + 9.06 × 10-1 Transformants     K744-T + <1 × 10-4 K2480-T + <1 × 10-4 To

test for the presence of the ß-lactamase gene, blaZ was amplified by PCR using a primer set K shown in Table 3. N315 and FDA209P cells were used as positive and negative references, respectively. As seen in Figure 2, the PCR products amplified from N315 cells showed a large distinct band with nucleotide numbers corresponding to about 170 bp, FK228 in vivo which was the expected PCR product. The PCR product was undetectable when the FDA209P DNA was used as a template. Similarly, PCR was carried out using the template DNA from Mu3, K101, K638, K670, K744 and K2480 cells and no detectable band was found (Figure 2). The results suggested that these BIVR strains did not have the ß-lactamase gene, which was fully consistent with the finding of undetectable ß-lactamase activity. In contrast, PCR experiments

using the DNA template from non-BIVR strains showed clear bands corresponding to the expected blaZ product. These results Cell Cycle inhibitor were again consistent with that of the ß-lactamase assay and with the above explanation (i); whether or not BIVR cells possessed the gene encoding ß-lactamase, but did not give the answer to the above question (ii); whether the expression of the ß-lactamase gene in BIVR could be suppressed. Therefore, the following experiments were conducted. Table 3 Primer sets used Code Nucleotide sequence A (F) 5’-GGTTGCTGATAAAAGTGGTCAA-3’ (R) 5’-CTCGAAAATAATAAAGGGAAAATCA-3’ B (F) 5’-AAGAAATCGGTGGAATCAAAAA-3’ (R) 5’-GTTCAGATTGGCCCTTAGGA-3’ C (F) 5’-TTGCCTATGCTTCGACTTCA-3’ (R) 5’-GCAGCAGGCGTTGAAGTATC-3’ D (F) 5’-TCAAACAGTTCACATGCCAAA-3’

(R) 5’-TTTTTGATTCCACCGATTTCTT-3’ E (F) 5’-GCCATTTTGACACCTTCTTTC-3’ (R) 5’-CGAAGCATAGGCAAATCTCTT-3’ F (F) 5’-TGAGGCTTCAATGACATATAGTGATAA-3’ (R) 5’-GTTCAGATTGGCCCTTAGGA-3’ else G (F) 5’-TGTTTAATAATAAAAACGGAGACACTT-3’ (R) 5’-TCAACTTATCATTTGGCTTATCACTT-3’ H (F) 5’-AAGAAATCGGTGGAATCAAAAA-3’ (R) 5’-TTTAAAGTCTTGCCGAAAGCA-3’ I (F) 5’-AAGAAATCGGTGGAATCAAAAA-3’ (R) 5’-TCGAAAATAATAAAGGGAAAATCA-3’ J (F) 5’-GCCATTTTGACACCTTCTTTC-3’ (R) 5’-AGCAGCAGGCGTTGAAGTAT -3’ K* (F) 5’-ACTTCAACACCTGCTGCTTTC-3’ (R) 5’-TGACCACTTTTATCAGCAACC-3’ * Primer K was from reference [19]. F and R denote the forward and reverse sequences, respectively. Codes correspond with that in Figure 3. Figure 2 Agarose gel electrophoretograms of the PCR product. Primer K was used for the PCR of blaZ and the conditions for the thermal cycler setting are given in the text. A fixed agarose concentration (2%) was used. The gel was stained with GelRed and visualised under UV light. Marker, LowRange 100 bp DNA markers; FDA209P, negative control; N315, positive control; the MRSA class and strain number are shown in the figure.

However, this site overlaps the MEME predicted σ54 site, prompting the authors to screen for alternative σ54 binding regions. Subsequent analysis of the promoter using the PromScan algorithm, with a cut off

score of 0.70, identified a second σ54 consensus site at nucleotide Pitavastatin position 356. The proximal location of this site to the proposed GGAGG Shine Dalgarno ribosome binding sequence at nucleotide position 455 was more consistent with conventional σ54 promoter architecture, Figure 5(b). Primer extension analysis of RNA extracts from phenylacetic acid grown P. putida CA-3 confirmed the transcriptional start site at nucleotide 381, upon sequencing of the 5′ RACE PCR product, Figure 5(b) and 5(c). Figure 5 Analysis LCZ696 datasheet of the paaL promoter region. (a) Promoter structure of the archetypal σ54 factor dependent promoter employed by GenomeMatScan to predict the P. putida KT2440 sigmulon. The upstream activating sequence UAS is indicated, flanked by distal/proximal enhancer binding protein sites displaying diverse spatial positioning upstream of σ54-RNA polymerase promoter complex formation. Schematic originally proposed by Cases et al, [38]. (b) Annotated nucleotide sequence of the 456 bp intergenic region between the paaG stop codon, (X), and the paaL start codon (M) in P. putida CA-3. Nucleotide positions are indicated in italics. An imperfect integration host factor (IHF) binding site is highlighted in

bold italics with a tetrameric palindrome indicated by directional arrows. Both consensus GG-N10-GC σ54 factor binding sites are highlighted in grey, with the primer extension mapped transcriptional start site indicated numerically (+1). (c) RACE directed RT-PCR amplification of the paaL transcriptional start site. Lanes; 1 = 465 bp RACE product, 2 = negative control, (adapter ligated RNA), and M = Hyperladder II DNA marker (Bioline).

Relative sequence identities of paaL genes and promoters from diverse Pseudomonas species Clustal W analysis was performed with paaL genes and promoters from available PACoA catabolon host genomes, (P. entomophila Non-specific serine/threonine protein kinase L48, P. fluorescens Pf5, P. putida F1, P. putida KT2440, P. putida W619 and P. putida GB-1), and styrene degradation associated paaL genes from P. putida CA-3, Y2 and P. fluorescens ST, (Table 1). The analysis revealed greater diversity occurred in promoter sequences than in gene sequences. This is clearly demonstrated among the paaL genes from the styrene degraders P. fluorescens ST, P. putida CA-3 and Pseudomonas sp. Y2, which all share > 80% sequence identity with KT2440 paaL sequence, but less than 16% identity at the respective promoter level, Table 1. Among the three styrene degrading strains the authors note that the paaL promoters are 100% identical, while the catabolic genes share ~97% sequence identity, Table 1. Table 1 Clustal W alignment of microbial paaL genes and promoters. Percentage Sequence Identity – CA-3 F1 GB1 KT2440 L48 Pf5 ST W619 Y2 paaL Genes CA-3 – 81.

High rate of surgical site infection in the present study may be attributed selleck inhibitor to contamination of the laparotomy wound during the surgical procedure. Perforated peptic ulcer is a serious condition with an overall reported mortality of 5%-25%, rising to as high as 50%

with age [5–7, 9, 11, 44]. In this study mortality rate was high in patients who had age ≥ 40 years, delayed presentation (>24 hrs), shock at admission (systolic BP < 90 mmHg), HIV positivity, low CD4 count (< 200 cells/μl) and concomitant diseases. Also gastric ulcers were associated with an increased mortality risk. Boey's score, which is a score based on scoring factors as shock on admission, confounding medical illness, and prolonged perforation, has been found to be a useful tool in predicting outcome [11]. In this study, Boey score was a good predictor of both mortality and postoperative

complication and therefore should be used in our setting as a tool for predicting outcome in patients with perforated peptic ulcers. Since tests for detecting H. Pylori was not possible in our patients due to logistic problems, we did not take this into consideration in our discussion. However the use of the ‘triple regime’ produced excellent results in 82.6% of our patients which is comparable to the results from recent studies [3. 4, 21, 22, 45] which have successfully used simple closure AP26113 datasheet followed by eradication of H-Pylori as a treatment for perforated peptic ulcer. This is in contrast to the earlier studies [46, 47] which reported emergency definitive surgery as a means to prevent recurrence and re-operation rates. These findings are extremely important for developing countries like Tanzania where delay in presentation often prevents any attempt at definitive surgery. Before generalizing the results of our study several important issues need to be addressed. First, since all the subjects in the present study underwent pen repair, results from this study may not fully

represent those after laparoscopic repair. Second, we did not study the association of H. pylori with the postoperative outcomes because of lack of necessary facilities at the study center. Third, Gefitinib mouse data obtained retrospectively and failure to detect HIV infection during window period may have underestimated the prevalence of HIV infection. Fourth, since our duration of postoperative follow up was relatively short, we could not estimate the long term effect of Graham’s omental patch. Conclusion Perforation of peptic ulcer remains a frequent clinical problem in our environment predominantly affecting young males not known to suffer from PUD. Simple closure with omental patch followed by Helicobacter pylori eradication was effective with excellent results in majority of cases despite patients’ late presentation in our center.

J Gerontol A Biol Sci Med Sci 62:440–446PubMed 22. Mowe M, Haug E, Bohmer T (1999) Low serum calcidiol concentration in older adults with reduced muscular function. J Am Geriatr Soc 47:220–226PubMed 23. Plotnikoff GA, Quigley JM (2003) Prevalence of severe hypovitaminosis D in patients with persistent, nonspecific musculoskeletal pain. Mayo Clin Proc 78:1463–1470CrossRefPubMed 24. Kenny AM, Biskup B, Robbins B, Marcella G, Burleson JA (2003) Effects of vitamin D supplementation on strength, physical function, and health perception in older, community-dwelling men. J Am Geriatr Soc 51:1762–1767CrossRefPubMed 25. Verreault R, Semba RD, Volpato

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Popp-Snijders C, Pavel S, Schothorst AA, Meulemans CC, Lips P (1998) Ultraviolet irradiation corrects vitamin D deficiency and suppresses secondary hyperparathyroidism in the elderly. J Bone Miner Res 13:1238–1242CrossRefPubMed 32. Binkley N, Novotny R, Krueger D, Kawahara Y, Daida YG, Lensmeyer B, Hollis BW, Drezner MK (2007) Low vitamin D status despite abundant sun exposure. J Clin Endocrinol Metab 92:2130–2135CrossRefPubMed 33. Chel V, Wijnhoven HA, Smit JH, Ooms ME, Lips P (2008) Efficacy of different doses and time intervals of oral vitamin D supplementation without calcium in elderly nursing home residents. Osteoporosis Int 19:663–671CrossRef 34. Snijder MB, van Dam RM, Visser M, Deeg DJ, Dekker JM, Bouter LM, Seidell JC, Lips P (2005) Adiposity in relation to vitamin D status and parathyroid hormone levels: a population-based study in older men and women. J Clin Endocrinol Metab 90:4119–4123CrossRefPubMed 35. Greig CA, Young A, Skelton DA, Pippet E, Butler FM, Mahmud SM (1994) Exercise studies with elderly volunteers. Age Ageing 23:185–189CrossRefPubMed 36. Kallman DA, Plato CC, Tobin JD (1990) The role of muscle loss in the age-related decline of grip strength: cross-sectional and longitudinal perspectives. J Gerontol 45:M82–M88PubMed 37.

The size-dependent SHC of NPs has also been observed from previous studies [17, 18]. This increment of SHC with reducing particle size could be explained by the Debye model of heat capacity of solids, wherein the heat capacity increases

as the Debye temperature CH5183284 concentration reduces [18]. The Debye temperature decreases with reducing particle size [17], resulting in an increased SHC. Figure 4c shows the SHCs of solid salt and solid salt doped with 13-nm and 90-nm alumina NPs at 0.9, 2.7, and 4.6 vol.%, respectively (measured using model 7020 of EXSTAR). The effect of NP concentration on the SHC of the solid salt doped with NPs is not significant whereas the SHC decreases with increasing NP size. The NP-size-dependent SHC might be due to the fact that the larger NPs have a smaller SHC (see Figure 4b). Nevertheless, the effect of NP addition on the SHC of the

nanofluid is pronounced (see Figure 4a). The effects of size and concentration of the NPs on the SHCs of the nanofluids are illustrated in Figure 5. The temperature-averaged SHCs of nanofluids between 290°C and 335°C were taken to evaluate the effectiveness on the energy storage Ro 61-8048 of the nanofluids in the temperature range. The cross mark data at 0 vol.% in Figure 5 is the SHC of the molten salt without doping with NPs (measured using model Q20 of TA). The red solid squares and blue open squares are the experimental results of the temperature-averaged SHCs of the nanofluids having 13-nm and 90-nm alumina NPs at 0.9, 2.7, and 4.6 vol.%, respectively. A reduced SHC of the nanofluid as compared to that of the base fluid is observed, and the SHC Phosphoribosylglycinamide formyltransferase of the

nanofluid decreases with increasing NP concentration, which is similar to previous studies [6–10]. Furthermore, the SHC of the nanofluids is particle-size-dependent. The SHC decreases with reducing particle size, in contrast to the trend observed in the solid salt doped with NPs (see Figure 4c). The particle-size-dependent SHC in nanofluids had never been reported before and could not be explained by the size-dependent SHCs of alumina NPs since smaller NP has a larger SHC (see Figure 4b). Figure 5 Effects of NP size and concentration on the SHC of the nanofluid. The cross mark at 0 vol.% is the SHC of the molten salt without doping with NPs (measured using model Q20 of TA). The red dash and blue dash-dot lines show the model prediction using Equation 1 for 13- and 90-nm alumina NPs at various volume fractions. The red solid squares and blue open squares are the experimental results of the SHCs of the nanofluids having 13- and 90-nm alumina NPs at 0.9, 2.7, and 4.6 vol.%, respectively. The red solid line and blue dash line are the model predictions considering the nanolayer effect on the SHC of the nanofluid (Equation 5). The theoretical prediction using Equation 1 is also shown in Figure 5, where the values of c p,np are obtained from the temperature-averaged (290°C to 335°C) SHCs of the 13- and 90-nm alumina NPs shown in the Figure 4b (i.e., 1.30 and 1.

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Establishment of Biofilm Communities in a Two-Stage Continuous Culture System. Appl Environ Microbiol 2005, 71:7483–7492.PubMedCrossRef 38. Borja S, Saad N, Schmitter J-M, Bressollier P, Urdaci MC: Adhesive Properties, Non-specific serine/threonine protein kinase Extracellular Protein Production, and Metabolism in the Lactobacillus rhamnosus GG Strain when Grown in the Presence of Mucin. J Microbiol Biotechnol 2010, 20:978–984.CrossRef 39. Fakhry S, Manzo N, D’Apuzzo E, Pietrini L, Sorrentini I, Ricca E, De Felice M, Baccigalupi L: Characterization of intestinal bacteria tightly bound to the human ileal epithelium. Res Microbiol 2009, 160:817–823.PubMedCrossRef 40. Ruas-Madiedo P, Gueimonde M, Fernandez-Garcia M, de los Reyes-Gavilan C, Margolles A: Mucin degradation by Bifidobactrium strain isolated from human intestinal microbiota. Appl Environ Microbiol 2008, 74:1936–1940.PubMedCrossRef 41. Cantarel BL, Coutinho PM, Rancurel C, Bernard T, Lombard V, Henrissat B: The Carbohydrate-Active EnZymes database (CAZy): an expert resource for Glycogenomics.

Of note, SmaI-restricted S. lugdunensis in order to gain a band pattern is known to be more difficult compared to S. aureus due to methylation of SmaI sites [32]. These isolates were not typed due to the small sample size. However,

a cluster dendrogram find more and clinical analysis still provide epidemiological characteristics. The two isolates with a similarity of 96.0% were from a patient with a premature rupture of fetal membranes and a 14-day-old newborn. The isolate with a similarity of 87.3% or less with other isolates was from the outpatient clinic. The two isolates with a similarity of 96.6% were from the Department of Orthopedics, were both resistant to erythromycin, clindamycin, and penicillin and produce β-lactamase, suggesting that PFGE can provide epidemiological information for S. lugdunensis from different departments. Conclusions In summary, while the prevalence of S. lugdunensis in our study is low and warrants further investigations, it is of significant clinical concern that its rate of multi-drug resistance is so high. The diversity of S. lugdunensis by macrorestriction analysis with SmaI was limited for typing (due to sample

size) but sufficient to consider that PFGE with SmaI is suitable for epidemiological analyses. Further studies encompassing https://www.selleckchem.com/products/Y-27632.html detailed molecular methods similar to the current one will be required to characterize the nationwide prevalence and genetic diversity of the β-lactamase positive S. lugdunensis isolated in China. Methods Collection of bacterial isolates The Institutional Scientific and Ethics Committees of the General Hospital of the People’s Liberation Army approved the current

study. Between January and December of 2010, 670 non-replicate isolates of CoNS were collected from clinical specimens in our hospital, inclusive of blood (n = 74), sputa (n = 188), secretions (n = 84), synovial fluid (n = 17), semen (n = 19), drainage fluid (n = 52), Aspartate pus (n = 52), nose swabs (n = 20), throat swabs (n = 36), urine (n = 116), catheters (n = 13), and others (n = 36). All isolates were obtained after informed consent of the patients. The isolates were all stored at −86°C. DNA extraction Bacterial colonies cultured overnight on blood agar plates were suspended in 2 ml 0.85% NaCl solution to 5 McFarland units and centrifuged at 13,000 g for 1 min. The pellets were resuspended in 200 μL lysis buffer solution [1% Triton X-100, 10 mM Tris–HCl (pH 8.0), and 1 mM EDTA], boiled for 10 min, and centrifuged at 13,000 g for 2 min. Supernatants were collected and stored at −20°C. Identification of S. lugdunensis S. lugdunensis was isolated and identified from CoNS in three steps. First, the 670 isolates were screened successively with ornithine decarboxylase (ODC) and pyrrolidonyl arylamidase (PYR), and those that were positive for both (n = 8) were considered as suspected isolates of S. lugdunensis.

Appl Environ Microbiol 2004, 70:1442–1447.PubMedCentralPubMedCrossRef 33. Thakur S, Gebreyes WA: Prevalence and antimicrobial resistance of Campylobacter in antimicrobial-free and conventional pig production systems. J Food Prot 2005, 68:2402–2410.PubMed RG7112 solubility dmso 34. Norma PV, Friendship R, Dewey C: Prevalence of resistance to 11 antimicrobials among Campylobacter coli isolated from pigs on 80 grower-finisher farms

in Canada. Can J Vet Res 2007, 71:189–194. 35. Oosterom J, Dekker R, De Wilde GJA, van Kempen-de TF, Engels GB: Prevalence of Campylobacter jejuni and Salmonella during pig slaughtering. Vet Q 1985, 7:31–32.PubMedCrossRef 36. Nesbakken T, Eckner K, ROtterud OJ: The effect of blast chilling on occurance of human pathogenic Yersinia enterocolitica compared to Campylobacter

spp. and numbers of hygienic indicator on pig carcass. Int J Food Microbiol 2008,123(1–2):130–133.PubMedCrossRef 37. ICMSF: Micro-Organisms in Foods 6. Microbial Ecology selleck chemicals of Food Commodities. International Commission on Microbiological Specifications for Foods (ICMSF). London: Blackie Academic and Professional; 1998. Competing interests None of the authors have any competing interests. Authors’ contributions LG participated in study design, bacterial culture, data analysis and drafting manuscript, DKS participated in data analysis and bacterial culture identification, HBB participated in bacterial culture and identification, antibiogram and drafting manuscript, RKB conducted bacterial culture, antibiogram and assisted in

drafting manuscript, SD participated in data analysis and interpretation, survey of butchers and manuscript preparation and BS participated in bacterial culture, survey of butchers and drafting manuscript. All the authors read and approved the final manuscript.”
“Background Bacterial drug resistance is a growing global health challenge. Resistant infections are difficult to treat, tend to spread relatively rapidly and increase healthcare costs significantly Methane monooxygenase [1]. Empiric antibiotic therapy is commonly started before the results of antimicrobial susceptibility testing (AST) are available. This is mainly because the available AST methods are slow, typically requiring 24–72 hours, being primarily based on bacterial growth. Inappropriate empiric antibiotic regimens can be associated with treatment failures/prolonged illness [2, 3], and may also serve to promote resistant bacterial strains [4–7]. Pre-prescription AST, such as rapid point-of-care diagnostics, that can help identify the most effective antibiotic for bacterial infections would be advantageous, especially in the context of escalating resistance [8–10]. Bacterial antibiotic resistance can be due to a variety of mechanisms, including enzymatic inactivation of antibiotics, altered target sites, decreased uptake and/or increased efflux of the antimicrobial agents [11]. Multiple resistance factors can be present simultaneously [12, 13].