Recently, Shewell et al. demonstrated that deletion of the glycosylated immunodominant C-terminus of AniA produced a truncated protein that elicited antibodies that inhibited nitrite reductase activity [69]. Vaccine-mediated inhibition of AniA function may be an effective approach because the capacity to grow anaerobically is likely an important adaptation during infection of the genital tract where oxygen tension is reduced. This hypothesis is supported by the detection of AniA-specific antibodies from women with lower or upper genital tract

infections and one patient with DGI [70]. AniA is also required for mature biofilm formation, which may protect against innate defenses Cilengitide in vivo [71]. The exciting development of group B meningococcal vaccines, which was a formidible challenge for many years, may provide a useful template for developing a gonorrhea vaccine [72], [73] and [74]. Some of these vaccines contain outer membrane vesicles (OMV) and some are genetically engineered to stabilize the expression

of phase variable antigens and increase the range of antigenic specificities. Detergent-treated OMVs or OMVs produced from LOS mutants have been used to diminish endotoxicity. Immunization and challenge studies with Gc OMV have not been reported; a Gc outer membrane protein preparation demonstrated protection in mice when delivered intranasally mTOR inhibitor with CT [54], but this approach was not successful in subsequent studies, possibly due to differences in the protein isolation methods used [35]. The Novartis 4CmenB vaccine consists of OMVs combined with the NadA protein and two fusion proteins, factor H-binding

protein (fHbp) and neisserial heparin binding antigen (NHBA) fused to two other conserved antigens [74]. None of the three proteins (fHBP, NHBA and NadA) in the 4CmenB vaccine [74] are predicted to be suitable vaccine targets for Gc [75]; however, gonorrhea research may benefit from the use of proteomics technology and, or genome mining, which have advanced medroxyprogesterone the development of vaccines for group B N. meningitidis. Immunization of the genital tract also challenges gonorrhea vaccine development, although we are encouraged by the success of the HPV vaccine. Most efforts to develop a vaccine against gonorrhea have focused on conventional parenteral immunization, which generates circulating, predominantly IgG antibodies, but is generally ineffective at inducing secretory (S) IgA at mucosal surfaces. However, the genital tract secretions of both males and females contain more IgG derived largely from the circulation than SIgA produced locally and transported through epithelial cells [57].

Other investigators, who remained blinded to treatment allocations, measured maximal inspiratory and expiratory pressures and the rapid shallow breathing

index twice a day until the end of the weaning period. The weaning period was defined as from the end of controlled ventilation (ie, the commencement of pressure-support ventilation) until extubation. A daily awakening trial with a minimum level of sedation identified which patients would be transitioned from controlled BEZ235 mechanical ventilation to pressure-support ventilation. The time of extubation was decided by the treating physicians, who were blinded to the treatment allocations. Patients were included in this study if they were aged 18 years or more, had undergone mechanical ventilation for more than 48 hours in a controlled mode, and were considered ready for weaning with pressure-support ventilation between 12 cmH2O and 15 cmH2O and positive end-expiratory pressure between 5 cmH2O and 7 cmH2O. They had to be haemodynamically stable without the aid of vasoactive drugs (dopamine, dobutamine or norepinephrine) or sedative agents. This study excluded patients with hypotension (systolic blood pressure < 100 mmHg or mean blood pressure < 70 mmHg), severe intracranial disease with inadequate consciousness level

(Glasgow Coma Scale ≤11), barotrauma, tracheostomy, or neuromuscular disease. In the experimental group, inspiratory muscle training began when the participants were changed from controlled to pressure-support ventilation. The patients were selleck screening library ventilated using one of three mechanical ventilatorsa. Before each training session, the patients were positioned in 45-deg Fowler’s position and cardiorespiratory variables (respiratory rate, heart rate, systolic and diastolic blood pressures, and oxyhaemoglobin saturation) were recorded to ensure that participants did not undertake training if they were haemodynamically unstable, defined as: respiratory Astemizole rate > 30 breaths/min, oxyhaemoglobin saturation < 90%, systolic blood pressure > 180 mmHg or < 90 mmHg, paradoxical breathing, agitation,

tachycardia, haemoptysis, arrhythmia, or diaphoresis (Caruso et al 2005). The pressure of the endotracheal tube cuff was maintained at 30 mmHg during the training session (Lewis et al 1978). The experimental group was trained using an inspiratory threshold deviceb with a load equal to 40% of the participant’s maximal inspiratory pressure. Each training session consisted of 5 sets with 10 breaths, twice a day, seven days a week. Supplementary oxygen was added if necessary during a training session (Martin et al 2002). The training session was interrupted in the presence of haemodynamic instability, as defined above. In the event of haemodynamic instability, the participant was returned to pressure-support ventilation.

Many physiotherapy interventions for AECOPD aim to restore or maintain function, such that patients can achieve a safe discharge and return to

an active lifestyle in the community. However, measuring the success of physiotherapy interventions for AECOPD is challenging. Patients may be severely dyspnoeic and unable to tolerate assessments that are commonly used in an outpatient setting, click here such as the 6-minute walk test. Dedicated testing space may not be available in a hospital ward environment. Length of hospital stay is often only a few days and assessment tools must therefore be responsive to changes occurring over a short period. Recently several simple tests of functional capacity have been examined in COPD and may

prove useful in this setting. These include the 4-metre gait speed test,83 a number of variants on sit-to-stand tests,84 and 85 and the Timed-Up-and-Go test.86 These tests are reliable, valid and responsive in stable COPD; however, their utility in AECOPD has not yet been examined. Whilst these tests may prove to be useful as global measures of function during and after an AECOPD, they provide little information about the impact of exercise on physiological parameters and will not be useful for exercise prescription. Further research is needed to identify an optimal assessment tool for physiotherapy interventions in the setting of AECOPD. In the clinical setting, physiotherapists have a strong and growing body of evidence to guide their practice when this website treating people with AECOPD (Figure 1). The evidence for important benefits Histamine H2 receptor of pulmonary rehabilitation after AECOPD is strong; referral to pulmonary rehabilitation at hospital discharge should be a priority for physiotherapy care. A clinical challenge that must be addressed is the articulation of inpatient physiotherapy management with outpatient pulmonary rehabilitation programs. Given the compelling benefits of rehabilitation after AECOPD for patients and the healthcare system, and the abysmal uptake of this treatment,63 more efforts must be made to provide flexible and

supportive pathways into pulmonary rehabilitation following hospital discharge. For patients whose attendance at an outpatient program is precluded by dyspnoea or frailty, this may require consideration of alternative rehabilitation models, such as well-resourced home-based programs.87 Finally, physiotherapists should take a more active role in prevention of future AECOPD. Using evidence-based treatments such as rehabilitation and self-management training, physiotherapists have the tools to make a long-term impact on the health, wellbeing and longevity of people with COPD. eAddenda: Figures 3, 5 and 7 can be found online at doi:10.1016/j.jphys.2014.08.018 Competing interests: Nil. Acknowledgements: Nil. Correspondence: Anne E Holland, La Trobe University, Alfred Health and Institute for Breathing and Sleep, Melbourne, Australia. Email: a.

NRG mice injected into the skin with SmyleDCs and SmartDCs and analyzed by non-invasive optical imaging analyses showed gradual disappearance of the iDCs within 1 month after administration. Mice maintained in observation for up to 100 selleck compound days post-injection showed no signs of disease. In summary, the results obtained with ID-LVs, were remarkably similar to previous observations using IC-LVs for genetically

programming iDCs [10]. Thus, as a logical progression, the two types of safety-enhanced ID-LVs were further compared regarding their capabilities to induce DCs with different immunologic properties (Table 1). The combination of recombinant click here GM-CSF/IFN-α has been extensively compared with GM-CSF/IL-4 for

generation of DCs [37], [38], [39] and [40]. In their work for the development of therapeutic DC vaccines against hepatitis C virus (HCV), Santini and collaborators proposed that IFN-α-DCs were “directly licensed” or more readily matured for cross-presenting low amounts of viral antigens by mechanisms likely involving the expression of IL-12 [39]. Our results comparing the autonomous ID-LV expression of GM-CSF/IFN-α with GM-CSF/IL-4 confirms some of the previous findings obtained with the recombinant cytokines, although in terms of expression of relevant immunologic markers and inflammatory cytokines the also two types of iDCs were remarkably similar (Table 1). Recent work in our laboratory analyzing the RNA expression pattern of conventional IL-4-DCs versus SmartDCs showed for the later up-regulation of several downstream genes involved with interferon regulatory circuits (Sundarasetty et al., in preparation), explaining the convergence of SmartDCs with SmyleDCs. The SmyleDC immunophenotypic characterization corroborated with previous findings that DCs grown in

the presence of IFN-α (instead of IL-4) lacked expression of CD209 (DC-SIGN). These results was expected, as DC-SIGN expression is dependent on the IL-4 cytokine but negatively regulated by IFN-α [41]. DC-SIGN is known to bind to several types of viruses and although its function might be related to T cell activation, pathogens seem to use this route to “hijack” DCs and modulate them [42]. Thus, since DC-SIGN is a potential target for the capture of DCs by pathogens, its down-regulation in a cell vaccine might be a positive hallmark enabling them to escape pathogen infection. It was previously reported that DCs generated in the presence of IFN-α displayed NK-like cytotoxicity and a mature immunephenotype [43]. SmyleDCs were not able to lyse K562 cells directly, but modestly stimulated NK cells in vitro ( Fig. S4a).

Therefore, in 2008, the International Federation of Pharmaceutical Manufacturers and Associations Influenza Vaccine Supply task force (IFPMA

IVS) developed a survey methodology to assess influenza vaccine dose distribution globally [7]. The survey requested information from its members on the supply of seasonal trivalent influenza vaccine doses to all WHO Member States. The supply period was defined by calendar year rather than influenza season to ensure that both Northern and Southern influenza seasons were captured. To ensure compliance with competition regulations, the survey results were collected and aggregated by an independent third-party legal counsel. Global distribution of vaccines can be used as a Anti-cancer Compound Library supplier proxy for vaccination coverage, survey results on dose distribution of influenza vaccines in 141 countries for 2004 to 2007 were reported in 2008 [7]. Updated and expanded results for 157 countries between 2004 and 2009 were reported in 2011 [8]. The aim of this paper is to update the results of the previous surveys and to show the evolution of the absolute number of influenza vaccine doses distributed between 2004 and 2011 inclusive, and the evolution in the per

capita doses distributed between 2008 and 2011. SAR405838 in vitro Member companies of the IFPMA IVS (Abbott Biologicals, Baxter, Biken, Crucell, bioCSL, Denka Seiken, GlaxoSmithKline Biologicals, Green Cross, Kaketsuken, Kitasato Institute, MedImmune, Novartis Vaccines, sanofi pasteur, Sanofi Pasteur MSD and Sinovac), which collectively

manufacture and supply the vast majority of the world’s seasonal and pandemic influenza vaccines, were requested to provide information on the supply of seasonal trivalent influenza vaccine doses to all WHO Member States during 2010 and 2011. To ensure compliance with anti-trust regulations, the survey results were confidentially collected and aggregated by the IFPMA Secretariat. The resulting anonymized database was then combined with the results Sitaxentan of the previous IFPMA IVS survey (2004–2009) [4], which had been compiled using a similar methodology. Doses distributed by country and by year were aggregated and then, to facilitate comparisons, were categorized by distribution to WHO region. To assess vaccine dose distribution in relation to each country’s population size, the study utilized population data from the United Nations’ (UN) statistics database [9]. Doses distributed to each country were expressed per 1000 population in 2008 and per 1000 population 2011 using the corresponding population figures from the United Nations’ (UN) statistics database. To facilitate comparisons, countries were then categorized by WHO region. T-test comparisons were performed between rates of dose distribution/1000 population in 2008 and 2011 by WHO region.

They should not offer treatment with either estramustine or sipuleucel-T to index 3 patients. Index patient 4 is symptomatic with evidence of metastases, poor performance status and has not received docetaxel. Clinicians may offer abiraterone plus prednisone in this setting.

They may offer ketoconazole plus steroid or radionuclide therapy to patients who are unable or unwilling to receive abiraterone plus prednisone. Clinicians may offer docetaxel or mitoxantrone chemotherapy in select cases, specifically when the poor performance status is directly related to cancer symptoms. However, based on FDA recommendations, patients should not be offered sipuleucel-T in this setting. Index case 5 is symptomatic with metastases, good performance status and has received docetaxel. Clinicians

should offer abiraterone plus prednisone, cabazitaxel or enzalutamide in this setting. If the patient received abiraterone Galunisertib plus prednisone before docetaxel chemotherapy, he should be offered cabazitaxel or enzalutamide. Clinicians may offer ketoconazole plus steroid if abiraterone plus prednisone, cabazitaxel or enzalutamide is unavailable. Clinicians may also offer re-treatment with docetaxel to select patients who were benefitting at the time of its discontinuation (due to reversible side effects). Index case 6 has symptomatic metastases, poor performance status and has received docetaxel. Clinicians should offer palliative care to these patients. Alternatively, for select patients, they may offer abiraterone plus prednisone, enzalutamide, ketoconazole Z-VAD-FMK in vivo plus steroid or radionuclide therapy. Clinicians should not offer systemic chemotherapy or immunotherapy to these patients. The guidelines also address bone health, and state that clinicians should offer all patients with CRPC preventive treatment to reduce the risk of fractures and skeletal related events.4 Clinicians may choose either denosumab or zoledronic acid for skeletal events related to bony metastases and mCRPC. Since publication of the CRPC guideline, radium-223 was approved by Oxymatrine the FDA after

demonstrating a survival advantage for patients with symptomatic bone metastases and no known visceral metastases regardless of prior exposure to docetaxel.5 This approval and that of additional agents, coupled with earlier indications (pre-chemotherapy enzalutamide) for existing agents, exemplify the rapidly changing CRPC landscape. Thus for urologists, in the expanding role as the primary caregivers of men with advanced prostate cancer, thorough knowledge of the various treatment options, clear understanding of risks/benefits of the various agents and enhanced collaboration with other specialists are required. For treatment of asymptomatic or minimally symptomatic CRPC, there is a paucity of Level 1 evidence to categorically recommend any one approved therapy over another.

4(a)). The reason for this is that if very old adults cannot be boosted then reduction in varicella incidence (reduced exposure to VZV) will have little effect on their risk of developing zoster. Thirdly, more effective vaccines (or effective programs) against varicella will produce the greatest increases in zoster cases (Fig. High Content Screening 4(b)). However, in the long-term the worst vaccines will produce a higher zoster incidence as more people will be infected with varicella

and therefore will have the possibility of reactivation (Fig. 4(b)). Finally, age-specific effective mixing can largely influence the impact of varicella on zoster. If older adults have very little contact with varicella cases (e.g. low contact rates with infected children) then reduction in varicella incidence following vaccination will only have a small impact on zoster (see England and Wales mixing scenario ( Fig. 4(c)). The expected increase in zoster predicted by the model is directly related to estimates of the force of infection in adults; the force

of infection in 25–44 years olds for the base case, find more England and Wales, Finland and Germany are 0.06, 0.03, 0.04 and 0.04 per person-year, respectively. Fig. 5 shows the impact of 2-dose varicella vaccination programs on varicella and zoster. The base model predicts that a 2-dose varicella vaccination program will significantly reduce varicella incidence under the three strategies investigated (Infant, Pre-school and Grade 4 ( Fig. 5)). Of note, our results suggest that giving the second isothipendyl dose in Grade 4 could help avoid the predicted epidemic of varicella 10 years into the 1-dose program by acting as: (1) catch-up vaccination in those yet to be immunised with a first dose and (2) a booster dose in vaccinees whose protection

will have waned. The main benefit of the second dose is its effectiveness at reducing breakthrough varicella (Fig. 5(b)). However, the short to medium term increase in zoster incidence (Fig. 5(c)) is predicted to be slightly higher under a 2-dose program (compared to 1-dose) because of its greater effectiveness at preventing varicella. Fig. 6 illustrates the incremental benefits of adding a second dose for different vaccine efficacy, mixing matrix and boosting assumptions. The base case model (range: min; max) predicts that adding a second dose will reduce varicella and zoster cases by an additional 22% (0%; 82%) and 6% (0%; 14%) over 80-years, respectively. Importantly, although the incremental benefit of adding the second dose is highly sensitive to assumptions regarding vaccine efficacy and mixing, the overall effectiveness of a 2-dose strategy at preventing varicella is not (Fig. 6). A 2-dose infant strategy (90% coverage) is predicted to reduce varicella cases by 72%–97%.

1H NMR (CDCl3) δ ppm; 9.35 (s, 1H, –NH), 3.85 (s, 3H, –OCH3), 4.76 (s, 2H, –CH2), 7.03–8.43 (m, 17H, Ar–H); 13C NMR (40 MHz, DMSO-d6): δ 38.15, 55.43, 107.42, 114.98, 115.24, 116.74, 118.21, 118.56, 119.84, 120.19, 121.84, 122.14, 123.98, 125.17, 126.32, 127.45, 128.15, 129.86, 130.21, 131.06, 136.22, 140.82, 156.83, 157.04, 159.49, 160.42, 164.53, 165.83, 168.86, 172.30, 174.39. Mass (m/z): 656. Anal. (%) for C32H24N5O2S, Calcd. C, 58.50; H, 3.66; N, 8.53; Found: C, 58.55; H, 3.64; N, 8.58. Yield 68%, mp. 177–180 °C, IR (KBr): 3176,

2986, 2922, 2842, 1697, 1665, 1612, 1538, 693. selleck products 1H NMR (CDCl3) δ ppm; 9.45 (s, 1H, NH), 3.70 (s, 3H, –OCH3), 4.75 (s, 2H, –CH2), 6.85–8.20 (m, 17H, Ar–H); 13C NMR (40 MHz, DMSO-d6): δ 24.06, 38.82, 55.87, 107.13, 110.61, 114.21, 115.83, 11602, 117.16, 117.53, 118.94, 119.28, 120.26, 123.75, 124.36, 126.81, 127.64, 128.01, 128.74, 130.76, 131.42, 131.22, 136.74, 137.08, 148.11, 157.32, 159.86, 160.54, 164.65, 165.32, 168.04, 168.42, 172.14, 174.72. Mass (m/z): 633.Anal. (%) for C34H27N5O4S2, Calcd. C, 64.43; H, 4.28; N, 11.04; Found: C, 64.40; H, 4.26; N, 11.02. Yield 79%, mp.128–130 °C, IR (KBr): 3170, 2914, 2840, 1694, 1602, 1532, 696. 1H NMR (CDCl3) δ ppm; 2.32 (s, 3H, –CH3),

9.26 (s, 1H, –NH), 3.76 (s, 3H, –OCH3), 4.62 (s, 2H, –CH2), 6.50–8.44 (m, 17H, Ar–H); out 13C NMR (40 MHz, DMSO-d6): δ 20.90, 38.75, 55.26, 107.42, 114.64, 115.46, 116.97, 117.42, 118.67, 119.55, 120.75, 121.13, 123.43, 124.08, 125.54, 126.53, 127.27, 128.28, 128.27, 130.71, 130.67, HDAC inhibitor 131.04, 134.76, 136.84, 150.53, 157.11, 159.64, 160.76, 164.97, 165.15, 168.02, 172.33, 174.64. Mass (m/z): 589. Anal. (%) for C33H26N4O3S2, Calcd. C, 67.08; H, 4.42; N, 9.46; Found: C, 67.04; H, 4.37; N, 9.42. Yield 70%, mp. 203–205 °C, IR (KBr): 3170, 2916, 2840, 1690, 1608, 1537, 695. 1H NMR (CDCl3) δ ppm; 9.36 (s, 1H, –NH), 3.82 (s, 3H,

–OCH3), 4.56 (s, 2H, –CH2), 7.15–8.51 (m, 18H, Ar–H); 13C NMR (40 MHz, DMSO-d6): δ 37.42, 55.43, 107.48, 114.04, 115.74, 116.13, 118.26, 118.32, 119.65, 120.29, 121.18, 123.42, 124.07, 125.37, 126.73, 127.19, 128.85, 128.29, 129.53, 130.30, 131.54, 132.64, 136.20, 153.17, 157.52, 159.67, 160.01, 164.32, 165.87, 168.42, 172.79, 174.02. Mass (m/z): 575. Anal. (%) for C32H24N4O3S2, Calcd. C, 66.64; H, 4.19; N, 9.71; Found: C, 66.64; H, 4.11; N, 9.76. Yield 82%, mp. 140–142 °C, IR (KBr): 3176, 2913, 2838, 1696, 1604, 1534, 692.

Other adaptive mutations have been found to increase replication of zoonotic influenza viruses with PB2 627E residue in mammalian cells, Ibrutinib mouse in association with increased pathogenicity in mice, providing additional pathways for adaptation to human or other mammalian hosts [120], [121], [122], [123], [124] and [125] (Table 2). Mutations in both PB1 and PB2 have been shown to enhance viral replication of a strain of HPAIV H5N1, yet the specific mutations

responsible for this effect have not been identified [126] and the role of many specific mutations in enhancing viral replication in mammalian cells remains largely unknown. Genomic analyses of avian and human influenza viruses have identified amino acids in all gene segments that characterize the host origin of the viruses, and may represent adaptive changes for better replication in human cells [127] and [128]. Many of these amino-acid signatures are present in the PB2, PA and NP proteins, and are associated with functional domains involved in protein interactions potentially essential

for viral replication. Following influenza virus transcription, viral proteins are synthesized and progeny virions are assembled and released from infected cells [53]. Influenza virus integral membrane proteins selleck (HA, NA and M2 proteins) are synthesized on membrane-bound ribosomes, translocated to the endoplasmic reticulum and Golgi apparatus, and transported to the apical membrane of polarized cells. vRNP formed in the nucleus associate with M1 and nuclear export proteins (NEP; formerly non-structural protein 2 NS2), and are exported into the cytoplasm.

NEP proteins have been shown to harbour nuclear export signals. Interactions between M1 and M2 proteins promote virus assembly and packaging of progeny viruses. The sialidase activity of the NA surface protein facilitates release of virions by cleaving attachment of HA proteins and sialic acids present on the cell membrane. Virus–host interaction barriers likely occur at the nuclear and cellular membranes upon nuclear Thymidine kinase export of vRNP and release of progeny viruses. Influenza virus NEP and NP proteins have been shown to interact with exportin protein 1 (hCRM1) [129] and [130]. However, it remains unknown whether species-specific differences in the use of various exportin proteins by these and the other proteins synthesized by avian and mammalian influenza viruses exist in a similar way to what has been described for their use of importin-α. Furthermore, mitogen-activated protein (MAP) kinases appear to control the active nuclear export of vRNP, yet the interactions of viral proteins with these enzymes have not been described [131]. Exportin proteins and MAP kinase pathways may provide ground for adaptive changes to optimize nuclear export of influenza virus vRNP in mammalian cells.

Standardized case information was abstracted from the hospital record. Sequelae were defined as complications attributable to IMD still present at discharge. The surveillance methodology has been detailed elsewhere [19] and [20]. Ethics approval was obtained at all participating hospitals. All IMPACT MenB cases with a viable isolate that occurred from 2006 to 2009 and were identified

as of August 2010 were included. NML determined serogroup, serotype, sub-serotype and PorA sequencing of case isolates. The clonal identity of isolates (defined by Multilocus Sequence Typing (MLST) [21]) and PorA variants were determined following the guidelines LY2157299 ic50 included in the Neisseria pubMLST website [22].

The classification of fHbp followed the scheme available in the public fHbp database which divides peptide subvariants among three major variants, 1, 2 and 3 [22]. This peptide ID is similar to the Novartis classification, although in the Novartis classification it is preceded by the major variant number. NHBA and NadA classification followed Lucidarme et al. [23] and Bambini et al. [24]. HPA studied the levels of expression and cross-reactivity of NadA, fHbp, and NHBA in the MenB isolates using the MATS ELISA relative potency (RP) [15]. The MATS method established a minimum level of RP, named the positive bactericidal learn more threshold (PBT) that predicts whether a given MenB isolate would be susceptible to killing in the human serum bactericidal antibody assay by antibodies induced by 4CMenB. Strain coverage was defined as the proportion of strains with RP above the PBT for at least one vaccine antigen in the MATS ELISA or matched to the PorA subtype P1.4 [15]. all To account for inter-laboratory differences

in the MATS, the 95% confidence intervals (CI) for vaccine strain coverage were calculated according to an inter-laboratory standardization study [25]. Chi-square and Fisher’s exact tests were used to test for significant difference between groups. SAS version 9.3 (SAS Institute, Cary NC) was used for all analyses. A total of 157/200 (78.5%) MenB cases were tested. A viable isolate was not available for 2 cases and 41 cases were confirmed solely by PCR. No significant differences in PCR confirmation rates were found by age or center (data not shown). The most frequent ccs among the 68 different STs identified were cc41/44 (n = 51), cc269 (n = 51), cc35 (n = 11), cc32 (n = 8) and cc60 (n = 6) cc213 (n = 2). Of the remaining 28 isolates, 21 were unassigned and 7 were singularly occurring ccs. Although cc41/44 and cc269 occurred with the same frequency, 25 different sequence types (ST) were identified among isolates in cc41/44 and only three of these contained multiple isolates (ST-154 (n = 15) and ST-571 (n = 11) and ST-340 (n = 3). In contrast, only 9 STs were found in cc269 and 90.