The authors concluded that that the prognosis of HIV-related MCD remains poor even after the advent of cART. Unlike other lymphoproliferative disorders, cART did not impact on outcome of HIV-related MCD, suggesting that MCD can ‘escape’ immune reconstitution. A concomitant diagnosis of NHL and uncontrolled MCD seemed to be the main reason for an unfavourable outcome, particularly in the post-cART era. New therapeutic approaches, including rituximab, should therefore aim at avoiding NHL A-769662 mw transformation and controlling ‘MCD-related cytokine storm’. The risk of lymphoma in patients diagnosed with MCD is high (level of evidence 2C). cART

does not prevent MCD (level of evidence 2D). A rise in plasma HHV8 level can Mitomycin C cost predict relapse (level of evidence 2D). There are no definitive gold-standard treatments for MCD. Apart from a randomized controlled trial of valganciclovir treatment for suppression of HHV8 replication [36], the best evidence is derived from single-centre cohort studies. Follow-up is generally short. The effect of cART, chiefly in combination with cytotoxic chemotherapy, has been described in seven patients with MCD and HIV infection [37]. Six patients responded to chemotherapy, and immune reconstitution was described in five patients. However, patients

continued to require long-term maintenance chemotherapy to prevent recurrence. The median survival was 48 months, longer

than in the pre-cART era. Therefore, the principle that HIV should be fully controlled during and after treatment for MCD should be adhered to in order to try to prevent relapse of MCD and other HIV-related conditions. The use of an anti-CD20 monoclonal antibody, rituximab, routinely prescribed as therapy for B-cell lymphomas and autoimmune diseases, to target HHV8-infected plasmablasts in MCD is a novel and potentially beneficial approach to the treatment of this disease. It was initially the subject of several case reports. These patients were often pretreated with chemotherapy and follow-up was brief; nine of 11 experienced a complete response [38–44]. The efficacy and safety of rituximab in 21 consecutive patients with plasmablastic MCD have been Sclareol investigated [45]. These individuals received four infusions of rituximab 375 mg/m2 at weekly intervals and, of 20 evaluable patients, all achieved clinical remission with biochemical and haematological normalization, and 70% achieved a radiological response. The overall survival and disease-free survival at 2 years were 95% and 79%, respectively, and in three patients who relapsed, retreatment with rituximab was successful [46]. These data corroborate the benefit seen in the aforementioned case reports and demonstrate that rituximab therapy results in an impressive clinical, biochemical and radiological sustained response in HIV-related MCD.

The authors concluded that that the prognosis of HIV-related MCD remains poor even after the advent of cART. Unlike other lymphoproliferative disorders, cART did not impact on outcome of HIV-related MCD, suggesting that MCD can ‘escape’ immune reconstitution. A concomitant diagnosis of NHL and uncontrolled MCD seemed to be the main reason for an unfavourable outcome, particularly in the post-cART era. New therapeutic approaches, including rituximab, should therefore aim at avoiding NHL PD0325901 mw transformation and controlling ‘MCD-related cytokine storm’. The risk of lymphoma in patients diagnosed with MCD is high (level of evidence 2C). cART

does not prevent MCD (level of evidence 2D). A rise in plasma HHV8 level can EGFR tumor predict relapse (level of evidence 2D). There are no definitive gold-standard treatments for MCD. Apart from a randomized controlled trial of valganciclovir treatment for suppression of HHV8 replication [36], the best evidence is derived from single-centre cohort studies. Follow-up is generally short. The effect of cART, chiefly in combination with cytotoxic chemotherapy, has been described in seven patients with MCD and HIV infection [37]. Six patients responded to chemotherapy, and immune reconstitution was described in five patients. However, patients

continued to require long-term maintenance chemotherapy to prevent recurrence. The median survival was 48 months, longer

than in the pre-cART era. Therefore, the principle that HIV should be fully controlled during and after treatment for MCD should be adhered to in order to try to prevent relapse of MCD and other HIV-related conditions. The use of an anti-CD20 monoclonal antibody, rituximab, routinely prescribed as therapy for B-cell lymphomas and autoimmune diseases, to target HHV8-infected plasmablasts in MCD is a novel and potentially beneficial approach to the treatment of this disease. It was initially the subject of several case reports. These patients were often pretreated with chemotherapy and follow-up was brief; nine of 11 experienced a complete response [38–44]. The efficacy and safety of rituximab in 21 consecutive patients with plasmablastic MCD have been Methamphetamine investigated [45]. These individuals received four infusions of rituximab 375 mg/m2 at weekly intervals and, of 20 evaluable patients, all achieved clinical remission with biochemical and haematological normalization, and 70% achieved a radiological response. The overall survival and disease-free survival at 2 years were 95% and 79%, respectively, and in three patients who relapsed, retreatment with rituximab was successful [46]. These data corroborate the benefit seen in the aforementioned case reports and demonstrate that rituximab therapy results in an impressive clinical, biochemical and radiological sustained response in HIV-related MCD.

, 2006; Schlee et al., 2007). Moreover, an anomalous immune response against flagellin produced by the

commensal microbiota has recently been identified in certain cases of inflammatory bowel disease (Vijay-Kumar & Gewirtz, 2009a, b). In addition, preliminary results concerning the interaction of surface-associated protein extracts of the CH strain with peripheral blood mononuclear cells have suggested that the response driven by this flagellin may be different in terms of cytokine production, mainly by an increase of IL-6 and IL-1β (A. Suárez, pers. commun.). However, this statement deserves further experimentation. In this sense, it is known that Caco-2 cell monolayers have an atypical response to the flagellin from E. coli Nissle 1917, a probiotic strain, selleck chemical involving increases in the production of IL-8 (Schlee et al., 2007). In conclusion, we have characterized a recombinant L. lactis strain expressing the B. cereus CH flagellin gene. This strain was able to inhibit the adhesion of two enteropathogens selleck kinase inhibitor to mucin. Lactococcus lactis ssp. cremoris CH may be used as reference model for further studies

addressed to the study of the molecular mechanism of action of this probiotic flagellin. B.S. was the recipient of a Juan de la Cierva postdoctoral contract from the Spanish Ministerio de Ciencia e Innovación, and P.L. is the recipient of a postdoctoral contract from the project AGL2007-61805. Research in our group

is supported by grant AGL2007-61805 from the Spanish Ministerio de Ciencia e Innovación. “
“An isocitrate dehydrogenase from Zymomonas mobilis was overexpressed in Escherichia coli as a fused protein (ZmIDH). The molecular mass of recombinant ZmIDH, together with its 6× His partner, was estimated to be 74 kDa by gel filtration chromatography, suggesting a homodimeric structure. The purified recombinant ZmIDH displayed maximal activity at 55 °C, pH 8.0 with Mn2+ and pH 8.5 with Mg2+. Forskolin datasheet Heat inactivation studies showed that the recombinant ZmIDH was rapidly inactivated above 40 °C. In addition, the recombinant ZmIDH activity was completely dependent on the divalent cation and Mn2+ was the most effective cation. The recombinant ZmIDH displayed a 165-fold (kcat/Km) preference for NAD+ over NADP+ with Mg2+, and a 142-fold greater specificity for NAD+ than NADP+ with Mn2+. Therefore, the recombinant ZmIDH has remarkably high coenzyme preference for NAD+. The catalytic efficiency (kcat/Km) of the recombinant ZmIDH was found to be much lower than that of its NADP+-dependent counterparts. The poor performance of the recombinant ZmIDH in decarboxylating might be improved by protein engineering techniques, thus making ZmIDH a potential genetic modification target for the development of optimized Z. mobilis strains.

The higher response rate in the combined vaccine group may be due to the stronger priming effect of the primary vaccination course or the greater immunogenicity of the combined vaccine in equally primed subjects or a combination of both effects. As previously reported with the combined hepatitis A/B vaccine,7,9,10 vaccine response selleckchem was observed in subjects who had responded

to primary vaccination but had subsequently lost detectable antibodies, confirming the consideration that maintenance of anti-HBs antibody levels ≥10 mIU/mL is not essential for long-term protection against hepatitis B infection.11 In summary, the combined hepatitis A/B vaccine is immunogenic and well tolerated in adults aged >40 years, inducing higher and more persistent antibody levels (≥10 mIU/mL) against hepatitis B than corresponding monovalent vaccines. Use of a combined hepatitis A/B vaccine offers

a convenient approach to confer protection against these diseases in this population. The authors would like to thank LY2157299 datasheet all the subjects who participated in this study. We gratefully acknowledge the study nurses and other staff members for contributing in many ways to this study. We are indebted to Jennifer Coward for providing medical writing and editorial assistance in the preparation of this manuscript on behalf of GlaxoSmithKline Biologicals, Priya Diana Crasta for statistical support and Manjula K. for publication coordination (both employed by GSK). Twinrix, Engerix-B, and Havrix are trademarks of the GlaxoSmithKline group of companies; HBVAXPRO

is a trademark of Sanofi Pasteur MSD Ltd.; Vaqta is a trademark of Merck & Co. GlaxoSmithKline Biologicals was the funding source and was involved in all stages of the study conduct and analysis. GSK Biologicals also funded all costs associated with the development and the publishing of the present manuscript. Clinical Trial Registration Numbers: 111149 / NCT 00603252; 111572 / NCT00684671 R. C. declares to have board membership (GSK, MSD, CEVAG), received consultancy (GSK), payment for development of educational presentations including service on speakers’ bureaus (GSK, Pfizer, Sanofi Pasteur, Baxter), Resminostat and travel/accommodations expenses covered or reimbursed for attending medical conferences (GSK, Pfizer, Sanofi Pasteur) in the past 36 months. J. S. declares to have board membership with GSK on rotavirus vaccines, received payment for development of educational presentations including service on speakers’ bureaus (GSK, Baxter, Sanofi Pasteur) in the past 36 months. R. C. and J. S. declare that their institution “Vaccination Center” has obtained grants and support for travel to meetings for the study. F. V. S. declares to have served occasionally on an advisory board for GSK on flu vaccines. P. V. D.

, 2003). However, to our knowledge, a direct interaction with the pumps has not been demonstrated. To test whether thioridazine affects selected efflux pumps at the transcriptional level, we analyzed the expression of a putative efflux pump encoded by abcA, which has been associated with tolerance to β-lactam antibiotics, and of the major fluoroquinolone efflux pump encoded by norA, which is a known target of thioridazine (Couto et al., 2008). The level of abcA was for the most part unaffected by the addition of thioridazine and oxacillin alone or in combination (Fig. 4a), yet with a small reduction at 128 mg L−1 thioridazine. However, the norA levels were unaffected by

selleck products the drug additions (Fig. 4b). Despite a previous report showing that abcA was induced by methicillin (Schrader-Fischer & Berger-Bachi, 2001), we did not see any major effects of oxacillin, thioridazine, or the combination on the mRNA levels of abcA or norA. This indicates that the main effect of thioridazine on efflux pumps is at the protein level to inhibit efflux pump activity as was suggested previously (Kaatz et al., 2003). We have observed that thioridazine is able to resensitize MRSA to β-lactam antibiotics; however, the applicability of the drug combination for future treatment of infections depends

on whether the treatment has any undesirable effects on the bacteria. The expression of many toxins and other virulence factors are controlled by the agr locus. In our experiments, the P2 promoter of the agr locus was affected only by thioridazine, which selleck chemicals reduced RNAII levels at high concentrations of the drug (Fig. 5a). Similarly, the P3 RNAIII transcript was present at lower levels at high concentrations of thioridazine (Fig. 5b). When examining the expression level of spa and rot mRNA, we found that the transcription of these genes

were unaffected by the combinatorial treatment in accordance with our criteria for regulation (Fig. 5c and d). However, there were weak inductions with increasing concentrations of thioridazine, which may be explained by the coupled regulation of the two genes with RNAIII (Huntzinger et al., 2005; Geisinger et al., 2006). The cell-surface-associated virulence factors are involved Lenvatinib manufacturer in colonization and protection from the host immune system; yet the most extensive damage to host tissue is caused by secreted enzymes and toxins. Therefore, we speculate that treatment with thioridazine alone or in combination with oxacillin does not initiate processes in the bacteria that are harmful to the host, or that the treatment may even reduce the severity of the infection. We further analyzed the expression of the toxin genes hla (α-hemolysin), tst (toxic shock syndrome toxin-1), set6 (exotoxin 6), and SA1011 (exotoxin 3) and found that they were transcribed in a growth phase-dependent manner with the highest levels found in the postexponential growth phase.

5d,e). In case 2, fibrous tissues with hyalinization and hemosiderosis alone were found and no epithelial lining or reactive changes were observed (Fig. 5f, Table 3). In both cases, there was no significant infiltration of lymphocytes found histologically that suggested rejection. In case 1, menstruation resumed at 3 months after surgery. However, this was temporary and amenorrhea was subsequently observed. No response occurred in the uterus after administration of estrogen 5-Fluoracil price and progesterone, but no evidence of rejection was found in biopsy tissues of the cervical region. In echo findings obtained

6 months after surgery, the size of the uterus had not changed, but blood flow in the left uterine SCH727965 price artery could not be detected. Thus, surgery was performed 7 months after the first surgery to remove the uterus. The uterus was highly adhesive to the bladder and abdominal wall, and similar conditions were observed around the right adnexa (Fig. 6a). Although the size of the uterus was normal, the surface was whitish (Fig. 6b).

It was difficult to perform separate identification of the uterine artery due to adhesion. No visual or histopathological abnormalities were found in the removed right ovary and transplanted oviduct (Fig. 6c). In histopathological findings of the uterus, there was no endometrial tissue in the intrauterine cavity and the interstitium in almost all layers of the uterine wall showed hyaline degeneration, excluding the part close to the serous membrane, (Fig. 6d). No histopathological findings suggested a rejection response in the uterus, including in the transplanted oviduct. In case 2, menstruation did not resume and atrophy was found in ultrasonography at 3 months after surgery. Therefore, the uterus was removed after laparotomy. Severe adhesion was found in the pelvis

and the uterus was adhered with the rectum and the bladder, with atrophy in the funicular region. Severe adhesion was also found in the region crossing the ureter and uterine artery. Beating of the uterine artery was observed on the pelvic side of the adherent site, but not on the uterine side. Uterine stump diastasis was observed with complication of infection (Fig. 7a). Pathological findings of the resected uterus showed uterine atrophy, no epithelium (endometrium), and fibrosis with hemosiderosis and clonidine calcification (Fig. 7b). Immunostaining showed a non-specific inflammatory response with slight infiltration of CD8-positive and CD20-positive lymphocytes in the interstitium, and no rejection response. No marked thrombus was found in the uterine artery. The left ovary that was left in the pelvic cavity had follicles and corpora lutea and was normal. In this study, we conducted allogeneic UTx in cynomolgus monkeys. Allogeneic UTx in non-human primates has only been reported to date,[10] although similar procedures have been performed in several animals.

Rifaximin prophylaxis reduced risk of developing TD versus placebo (p < 0.0001). A smaller percentage of individuals who received rifaximin

versus placebo developed all-cause TD (20% vs 48%, respectively; p < 0.0001) or TD requiring antibiotic therapy (14% vs 32%, respectively; p = 0.003). More individuals in the rifaximin group (76%) completed treatment without developing TD versus those in the placebo group (51%; p = 0.0004). Rifaximin provided a 58% protection rate against TD and was associated with fewer adverse events than PF-562271 cost placebo. Conclusions. Prophylactic treatment with rifaximin 600 mg/d for 14 days safely and effectively reduced the risk of developing TD in US travelers to Mexico. Rifaximin chemoprevention should be considered

for TD in appropriate individuals traveling to high-risk regions. An estimated 40% of the 50 million individuals traveling from industrialized to developing countries each year develop travelers’ diarrhea (TD).1 This acute infectious 3-deazaneplanocin A solubility dmso illness is characterized by the passage of 7 to 13 watery stools over 2 days, accompanied by one or more additional enteric symptom.1,2 Based on microbiologic evaluation, enteric bacterial pathogens are thought to cause approximately 80% of TD cases, with strains of enterotoxigenic Escherichia coli (ETEC) and enteroaggregative E coli (EAEC) responsible for the majority of cases.3–5 Invasive bacterial pathogens including Shigella and Campylobacter contribute to approximately 4% to 20% of TD cases.5–7 Although TD is often self-limiting, lasting on average for 4 days, the negative consequences of acquiring this illness can be substantial, including disruption of travel plans and increased risk for development of postinfectious

complications,8 such as postinfectious irritable bowel syndrome (PI-IBS)9–14 and inflammatory bowel disease (IBD).15 Antibiotic chemoprophylaxis provides substantial protection from TD and prevents potentially severe complications.16 However, the guidelines recommended by the National Institutes of Health consensus panel in 1985 discouraged the routine administration of systemic antibiotics as ID-8 chemoprophylaxis for TD because of the potential adverse effects associated with administration and concern that overprescribing could contribute to the growing epidemic of antibiotic resistance.17 The ideal chemoprevention agent would achieve the efficacy of systemic antibiotics without the potential adverse effects and antibiotic resistance associated with these agents. Rifaximin (Xifaxan®; Salix Pharmaceuticals, Inc., Morrisville, NC, USA) is a gut-selective, nonsystemic antibiotic18 that has a low risk for development of clinically relevant antibiotic resistance.19 It is indicated for the treatment of TD caused by noninvasive strains of E coli2 and has demonstrated efficacy in treating TD in clinical studies.

, 2007; Belcheva & Golemi-Kotra, 2008; Eldholm et al., 2010; Belcheva et al., 2012). There is a wide variation in the fold-induction levels of different CWSS selleck chemicals llc genes, which is probably linked to the specificity of VraR-binding, although the exact VraR-binding consensus and the influence of specific nucleotide differences on expression and induction of different CWSS genes has not been thoroughly analysed (Martinez

et al., 2007; Belcheva & Golemi-Kotra, 2008; Belcheva et al., 2012). The magnitude of CWSS induction strongly depends on the class and concentration of cell wall antibiotics (Dengler et al., 2011). Disruption of wall teichoic acid (WTA) synthesis by targocil, which inhibits the WTA transporter TarG (TagG), was also shown to activate the CWSS (Campbell et al., 2012). WTA are anionic glycopolymers that are attached to the peptidoglycan www.selleckchem.com/products/PD-0325901.html of Gram-positive bacteria via a phosphodiester linkage, and they can constitute up to 60%

of the total cell wall biomass. WTA of B. subtilis are composed of poly(glycerol phosphate) and poly(ribitol phosphate), whereas S. aureus contains mainly poly(ribitol phosphate) WTA. The biosynthesis of WTA is catalysed by tag (teichoic acid glycerol) or tar (teichoic acid ribitol) genes in B. subtilis and S. aureus, respectively (reviewed in Swoboda et al., 2010). Besides the induction by cell wall active antibiotics, VraSR signal transduction is also triggered by internal disruption of cell wall synthesis caused by the depletion of essential Acyl CoA dehydrogenase cell wall biosynthesis enzymes such as MurA, MurZ, MurB (Blake et al., 2009), MurF (Sobral et al., 2007), PBP2 (Gardete et al., 2006) or depletion of enzymes involved in mevalonate biosynthesis, the direct precursor for undecaprenyl phosphate lipid carrier synthesis (Balibar et al., 2009). Induction of the CWSS enhances intrinsic resistance/tolerance to almost all cell wall damaging agents, regardless of their target or mode of action (Dengler et al., 2011; McCallum et al., 2011). Members of the CWSS directly linked to peptidoglycan

synthesis, such as PBP2, FmtA, MurZ and SgtB, are thought to contribute to the stress response by stimulating cell wall synthesis (Cui et al., 2009; Kato et al., 2010; Mehta et al., 2012). It is predicted that CWSS genes with unknown or poorly characterized functions are also likely to contribute to the stress response by directly or indirectly influencing cell wall synthesis. All three S. aureus LytR-CpsA-Psr (LCP) genes, msrR, sa0908 and sa2103, belong to the CWSS (Utaida et al., 2003; McAleese et al., 2006; Over et al., 2011). LCP proteins are unique to bacteria with Gram-positive cell walls (Hübscher et al., 2008; Kawai et al., 2011) and typically contain a short intracellular N-terminal region, a transmembrane domain and a large extracelluar region containing the LCP domain (Hübscher et al., 2008; Kawai et al., 2011). Deletion of LCP proteins in S. aureus alters cell surface properties and decreases virulence.

5% glucose and 12.5% fructose, resulting in 25% total sugar, with a total nitrogen concentration of 300 mg L−1 supplied as amino acids and ammonia, and was prepared as described previously (Bely et al., 1990). The fermentative potentials of wild-type strains and their transgenic derivatives were assessed in triplicate. Yeast precultures in YEPD were prepared and processed as described previously (Govender et al., 2008) and resuspended in MS300 medium. Small-scale aerobic shake-flask experiments of 100 mL MS300 medium contained in 250-mL Erlenmeyer flasks were performed by the inoculation of precultured cells at a density of 2 × 106 cells mL−1 and were performed at 27 °C.

The flocculation potential of wild type and their transgenic derivatives were FK506 clinical trial also assessed aerobically

in MS300 medium supplemented with one following red wine constituents: poly-d-galacturonic acid (pectin, 1 g L−1), potassium bitartrate (4 and 8 g L−1), diatomaceous earth (1 g L−1), gallic acid (20 mg L−1), caffeic acid (30 mg L−1) and catechin (50 mg L−1). To this end, MS300 medium was also supplemented with Biotan® (grape-derived tannin, Laffort, 400 mg L−1), Quertannin® (oak-derived tannin, Laffort, 200 mg L−1) and Tan’Cor® Tanespimycin cell line (oak- and grape-derived tannin mixture, Laffort, 300 mg L−1). Wine samples were routinely centrifuged and filtered (0.22 μm cellulose acetate) before

analysis. Oenological parameters including glucose, fructose, glycerol and ethanol were analysed via Fourier transform infrared (FT-IR) spectral measurements as described previously (Lilly et al., 2006) and the GC analysis of major volatile components in fermented Merlot wines was performed Olopatadine as described previously (Rossouw et al., 2008). The flocculation of yeast populations derived from the lees fraction of fermented wine samples were determined as described previously (D’Hautcourt & Smart, 1999; Govender et al., 2008). To assess sugar inhibition of flocculation phenotypes, either 1 M glucose or 1 M mannose was added to both the washing and suspension buffers of the modified Helm’s assay (D’Hautcourt & Smart, 1999). The sedimentation or Ca2+-independent flocculation ability of yeast cell populations that were harvested from the lees of red wines was assessed in 100 mM EDTA. Samples (1 × 108 cells) were dispensed into 1.5-mL microcentrifuge tubes and the cells were recovered by centrifugation at 10 600 g for 1 min. For the control assay (in five replicates), cells were resuspended in 1 mL 100 mM EDTA (pH 7), properly agitated by high-speed vortexing for 30 s and inverted five times in a period of 15 s. Immediately 10 μL aliquots were withdrawn from just below the meniscus and added to 990 μL 100 mM EDTA, pH 7 contained in a cuvette.

Data were gathered through semi-structured, face-to-face interviews with 21 patients. Severity of symptoms and insistence of family and friends were the main triggers to seek professional advice from GPs and NHS 24; no patients reported seeking community pharmacy advice. Several instances of delayed GP appointments were reported, possibly Alectinib mw resulting in later hospital admission. There was a lack of access to professional support available in community pharmacies. Self-care is a continuum of care from completely independent self-care with patients assuming total responsibility for their health to supported self-care, involving

the clinical judgement of health professionals.1 A number of United Kingdom government initiatives have promoted self-care and community pharmacy supported self-care to enhance access to treatment and advice, and reduce National Health Service direct and indirect costs. There is some evidence that patients inappropriately consult their general practitioners (GPs) rather than adopt self-care approaches or seek community pharmacy advice for colds and coughs.1 However, there is a lack of research on self-care

strategies adopted by those admitted to hospital with infective episodes. The aim of this study was to explore the patient pathway leading to hospital PS-341 order admission due to an infective episode, with focus on self-care strategies. Patients admitted to the infection or acute medicine admission units of a major Scottish teaching hospital, and commenced antibiotic therapy post-admission Sunitinib molecular weight were included. Exclusion criteria were: <16 years; no capacity to consent; and insufficient command of English. A draft semi-structured interview schedule was developed, reviewed, piloted in two patients and modified accordingly. The finalised schedule focused on: symptoms prior to admission; self-care strategies; triggers for seeking professional advice; and reflections on any professional advice prior to admission. Participants were identified by medical staff and informed consent obtained. Face-to-face interviews lasting around 15 minutes were audio-recorded and transcribed

verbatim. All transcripts were checked for accuracy prior to thematic analysis, with the coding frame constructed independently by two researchers and agreed by consensus. Data generation for 5 weeks took place during November – December 2012. The study was approved by the university and local NHS ethics committees. Twenty-one patients were invited to participate and all consented to interview. Eighteen transcripts were suitable for analysis (interview recording quality was poor for two patients, one patient was unfit for interview). Mean patient age was 56 years (standard deviation 20.9); eight were female; 11 were prescribed an antibiotic prior to admission; the most common diagnoses were skin and soft tissue infection (n = 9) and respiratory infections (n = 6). Severity of symptoms (e.