Our analysis shows that ART was found to be a greater risk factor among PLHIV compared with treatment-naïve patients and the increased risk was

particularly found for abacavir in the NRTI group among the ART classes. In contrast, a recent meta-analysis of RCT studies (published after our literature search) found that abacavir was not associated with a greater risk of MI or major CVD events, despite the significant impact of abacavir on the risk of CVD in some cohort studies [41]. This meta-analysis included HIV clinical trial data from studies that had a follow-up period of at least 24 weeks, with the selleck screening library majority of included studies having approximately 1 year of average follow-up. In contrast, a 96-week RCT follow-up study found that abacavir, compared with tenofovir, was associated with a greater risk for CVD, as discussed above. Of note, it may be that short-term use of abacavir has a low risk for CVD events among PLHIV. More specifically, we found that the annual RR associated with abacavir use was very low (RR 1.09; 95% CI 1.02, 1.16), learn more but that the risk increased with duration of ART. It is important to note that the majority of the cardiovascular events associated with the use of antiretroviral drugs were confined to patients who were already at increased absolute risk of CVD. Study type/design was not found to be a significant predictor of heterogeneity in our

estimates. A longer follow-up RCT measuring the use of abacavir and other antiretrovirals associated with CVD events would assist in ascertaining the role of abacavir among all patients as they continue to use ART long-term. We found that HIV, ART type and duration and CD4 cell count are associated with increased risk of CVD. The risk of CVD is greater in PLHIV than in people www.selleck.co.jp/products/cobimetinib-gdc-0973-rg7420.html not living with HIV, and higher again for people exposed to ART, and particularly PI-based regimens, and increases with the duration of treatment. Despite being a risk factor for CVD, ART use has increased the quality and

length of life of PLHIV by restoring immune function, reversing AIDS-defining events and reducing AIDS-related mortality rates. It is possible that the use of ART increases life expectancy and hence increases the average age of those taking ART in comparison to the reference group, which may lead to confounding of results. Although the health and survival of PLHIV have improved with effective ARTs, PLHIV are at substantially greater risk of developing other comorbidities, such as CVD, compared with uninfected people. Given that CVD is responsible for a large number of deaths world-wide, this is a significant issue for the population of PLHIV, particularly as they get older and become more treatment-experienced with second-line, third-line or more complex antiretroviral regimens. Increasingly, HIV-positive populations will require long-term clinical management of numerous conditions along with their HIV infection.

The NPS has developed seven competencies which describe essential activities aimed at ensuring that ‘prescribing is safe, judicious, appropriate, safe and effective’.[20] The information that this study provides on pharmacists’ perceived training

needs on therapeutic topics may assist tertiary institutions in meeting the competencies set, especially in relation to designing the content of courses aimed at pharmacists’ prescribing skills and knowledge. Apoptosis Compound Library Further research is needed to evaluate if this training should be provided at a tertiary level only and if so whether it should be incorporated in undergraduate or postgraduate pharmacy curricula. This may be dependent on the pharmacist prescribing model and whether this role is carried out as a specialist service or routinely Pifithrin-�� clinical trial by pharmacists. This study has found that the prescribing model preferred has no significant impact on pharmacists’ perceived need of additional training in order to assume expanded prescribing roles. This study would indicate that there is a perceived need in the areas of pathophysiology of diseases, principles of diagnosis, and patient assessment and monitoring. Training topic

preferences were influenced by the pharmacists’ years of registration and their current professional practice area. Supporters of an IPO model indicated a diminished perceived need for additional training in key therapeutic topics, which may reflect their confidence to prescribe for a limited number of conditions. These data provide current pharmacists’ perceptions relevant to the development

of courses many leading to the accreditation of pharmacists as prescribers. The Authors declare that they have no conflicts of interest to disclose. This research was entirely funded by the Curtin University, School of Pharmacy, Perth, Australia. The Authors wish to acknowledge the pharmacists that participated in this study and the statistical support provided Dr Richard Parsons and Jennifer Lalor at Curtin University. The Authors acknowledge the contribution of Teri Charrois of Curtin University in reviewing the paper. The Authors acknowledge that a part of the results in this study was presented at the 69th International Congress of the International Pharmaceutical Federation (FIP), 3–8 September 2009, Istanbul, Turkey. The study was designed by KH, JH and BS, and data were collected by KH, BS and JH. Analysis of the data was done by KH, and KH, BS and JH interpreted the data. Drafting of the paper was carried out by KH, and critical review was undertaken by JH, BS and KH. All Authors state that they had complete access to the study data that support the publication. “
“The aim of this article is to highlight the need for the development of pharmacy practice-based research networks (PBRNs).

With this in mind, we investigated whether changes in ADMA levels (Δ-ADMA) at an altitude of 4000 m can predict an individual’s susceptibility to AMS or HAPE. Twelve subjects spent two nights in a hypobaric chamber, the first night without exposure to altitude conditions and the second night at a simulated altitude of 4000 m. At identical

time points during both nights (after 2, 5, and 11 hours), we determined ADMA serum levels, PAP by Doppler echocardiography and estimated hypoxia www.selleckchem.com/products/ch5424802.html related symptoms by Lake Louise Score (LLS). Contrary to our initial hypothesis, subjects with a marked increase in ADMA at 4000 m showed PAP levels below the critical threshold for HAPE and were not affected by AMS. By contrast, subjects with a decrease in ADMA suffered from AMS and had PAP levels above 40 mmHg. After 2 hours of hypoxia we found a significant relationship between Δ-PAP t2 (Spearmans ρ = 0.30, p ≤ 0.05) respectively Δ-ADMA t2 (ρ = −0.92, p ≤ 0.05) and LLS. After 2 hours of hypoxia, the Δ-ADMA (positive or negative) can predict an LLS of >5 with a sensitivity of 80% and a specificity of 100% and can help assess

learn more the risk of an increase in PAP to more than 40 mmHg and thus the risk of HAPE (ϕ coefficient: 0.69; p ≤ 0.05). Worldwide, 40 million tourists are at risk of getting acute mountain sickness (AMS) each year, because they travel to altitudes of higher than 2500 m (AMS-incidence at altitudes of 2500–3000

m: 10–30%).[1-4] In general, the following conditions are distinguished: AMS, high-altitude cerebral edema (HACE), and high-altitude pulmonary edema (HAPE). An increase in pulmonary artery pressure (PAP), which is subject to individual differences, plays a crucial role in the development of HAPE.[5] The risk of developing HAPE increases massively when PAP exceeds 40 mmHg.[6] The measurement of PAP by Doppler echocardiography usually allows individuals at AMP deaminase risk of developing HAPE to be identified, especially in the setting of hypoxia.[7] For methodological reasons, however, Doppler echocardiography can be used only in individuals with (at least minor) tricuspid valve insufficiency. Although this insufficiency is often seen in association with an altitude-induced increase in PAP, high-altitude medical research has revealed the absence of tricuspid reflux in 5–30% of the subjects.[8] In addition, this method requires an experienced examiner and the availability of a suitable (mobile) system. This explains the need for simpler procedures. Against this background, the measurement of serum levels of asymmetric dimethylarginine (ADMA) may provide a new diagnostic approach. ADMA is a potent inhibitor of nitric oxide synthase (NOS). By increasing cyclic guanosine monophosphate (cGMP), nitric oxide (NO) causes smooth muscle relaxation and therefore induces rapid vasodilatation.

1 software package (Noldus Software, Wageningen, The Netherlands). The distance moved in a cage was calculated in 30-min time bins. Locomotor activity, the sleep–wake cycle and histamine release time series were

initially examined for the presence of statistically significant periods with lengths from 3 to 30 h by use of the Lomb–Scargle Vorinostat ic50 method (Ruf, 1999) implemented in lsp software (Refinetti et al., 2007). Identified periods were subjected to a multiple cosinor analysis (Bingham et al., 1982; Libre Office Calc, The Document Foundation) to obtain their mesor, orthophase and amplitude values. To verify the applicability of cosinor analysis, all of the time series were tested for zero amplitude and sinusoidality (whenever applicable). The parameters of periodicity in the population rhythm were separately estimated and tested for significance with the cosinor procedure. Cross-correlation Sirolimus analysis was performed with spss 15.0 (SPSS, Armonk, NY, USA). The correlation between histamine release and power spectrum frequencies was computed for individual mice with Spearman correlation coefficients. To obtain average correlation coefficients, the values were subjected to Fisher Z-transformation.

They were then averaged and reverse transformed. If no periodicity was detected, the data sets were compared by the use of two-way anova with time and strain as factor variables, and P ≤ 0.05 was considered to be significant. For the measurement of histamine and 1-methylhistamine concentrations and HDC and HNMT activities, samples were collected every 4 h for two consecutive days (as described above), and then approximated by use of a multiple cosinor procedure with a major period set to 24 h and a first harmonic of 12 h. When a period was considered to be non-significant, it was removed from the model, and the time series was further examined by use of a single cosinor model.

The significance levels Non-specific serine/threonine protein kinase were set to P ≤ 0.05 in all experiments, unless otherwise stated. The temporal pattern of hdc transcript expression in C57BL/6J mice was assessed with quantitative radioactive in situ hybridization. It was measured in E2/E3 and E4/E5 subpopulations of histaminergic neurons in the TMN region of the hypothalamus at 4-h intervals over a period of 24 h. No significant periodicity in mRNA expression was found in either group [E2/E3, F2,27 = 2.15 (P = 0.137); E4/E5, F2,27 = 0.96 (P = 0.38); Fig. 1]. The average expression levels [mean ± standard deviation (SD)] were 0.168 ± 0.028 μCi/g/pixel for the E2/E3 group, and 0.117 ± 0.017 μCi/g/pixel for the E4/E5 group. The activity of both enzymes was measured in hypothalamic, striatal and cortical samples of C57BL/6J mice. The enzymatic activity of HDC showed no 24-h periodicity in any structures analysed (Table 1), as estimated by multiple cosinor analysis. It was approximately three-fold higher in hypothalamic samples than in the other regions.

63%) were female and 66 (38.37%) were male. Most of the HIV-infected patients belonged to Trichostatin A concentration Centers for Disease Control and Prevention (CDC) categories B (43.02%) and C (30.23%). Most of the HIV-positive patients (68.60%) had CD4 counts<200 cells/μL (Table 2).

According to the CDC criteria [24], OIs were observed in 102 HIV-positive patients while 70 were asymptomatic. One hundred and two HIV-positive patients had experienced at least one AIDS event based on the occurrence of OIs (tuberculosis in 48 cases, pneumocystosis in 29 cases, toxoplasmosis in eight cases, cytomegalovirus infection in four cases, cryptococcosis in 17 cases, Kaposi sarcoma in 12 cases and prurigo in 22 cases). HIV-positive patients had significantly higher TG values (P<0.0001) and atherogenicity index (P<0.001) and significantly lower TC, HDLC and LDLC values (P=0.006, 0.0001 and 0.012, respectively) compared with controls (Table 3). HIV-positive patients had a significantly (P<0.0001) higher prevalence of hypertriglyceridaemia, TC hypocholesterolaemia, HDLC hypocholesterolaemia and LDLC hypocholesterolaemia compared with controls. The prevalence of hypotriglyceridaemia, TC hypercholesterolaemia, HDLC hypercholesterolaemia and LDLC hypercholesterolaemia was higher in HIV-positive patients compared with controls, but the difference was not significant (Table 4). Compared with the controls, TG was significantly

higher selleck screening library in patients in group 1 (P<0.0001), group 2 (P<0.001) and group 3 (P=0.003). The atherogenicity index was significantly higher in patients in groups 1, 3 and 4 (patients with CD4 counts>350 cells/μL) (P<0.0001), while TC was significantly lower in group 1 (P<0.0001) and group 2 (P<0.001). LDLC levels were significantly lower in patients in group 1 (P<0.0001) and HDLC levels were significantly

lower in all groups of patients (groups 1, 2, 3 and 4) (Table 5). Lipid and nutritional status results for 102 patients with active OIs or malignancies were compared with those for 70 patients with no OIs. Those with OIs had significantly lower TC (P=0.002) and HDLC (P=0.005) than those with no OIs, while their atherogenicity index was significantly higher. TG (227.86±36.25 mg/dL) and LDLC (99.98±62.32 mg/dL) were significantly higher (P<0.01) Rucaparib in patients with OIs than in patients without OIs (TG=205.81±23.54 mg/dL; LDLC=83.32±80.11 mg/dL). BMI was lower in patients with OIs (21.89±3.52 kg/m2) than in patients without OIs (23.62±4.32 kg/m2) but the difference was not significant (P=0.3) (Table 6). High TG values were associated or correlated with CD4 count<50 cells/μL (r=0.612, P=0.002) (group 1), with CD4 count between 50 and 200 cells/μL (r=0.601, P=0.002) (group 2) and with the occurrence of OIs (r=0.532, P=0.003). HDLC also correlated positively with CD4 count<50cells/μL (r=0.521, P=0.008), with CD4 count between 50 and 200 cells/μL (r=0.542; P=0.007) and with the occurrence of OIs (r=0.618, P=0.002).

The ISPC-6 (LC50 4.22 × 103 spores mL−1) and ISPC-5 (LC50 6.44 × 103 spores mL−1) strains exhibited comparatively lower larvicidal activity. Monnerat et al. (2004) have compared the larvicidal activity of different Brazilian B. sphaericus strains with standard 2362 and found that some of the strains exhibited higher toxicity towards C. quinquefasciatus. Similarly, four B. sphaericus isolates from China were also reported to be two to six

times more toxic than strain 1593 against C. quinquefasciatus (Sun et al., 1996). The virulence of entomopathogenic B. sphaericus isolates is related to the serotype and the phage group (Brownbridge & Margalit, 1987). Yousten (1984) has grouped virulent strains of B. sphaericus under serotype 5a5b and phage type III. In accordance with Alectinib supplier this, isolate ISPC-8 was also shown to be highly virulent against C. quinquefasciatus and grouped

under serotype 5a5b and phage type III (Table 1), whereas ISPC-5 and ISCP-6 belong to serotype 26a26b and phage type IV exhibiting lower toxicity; a similar observation was also reported by Yousten (1984). The varying levels of larvicidal activity of the ISPC-6 strain may be due to the loss of virulence during subculturing of the organism (Rao & Mahajan, 1990). As compared with other selleck screening library isolates, ISPC-8 was found to be highly toxic. Therefore, its spectrum of larvicidal activity was studied against different mosquito species. The DCLK1 results indicated that C. quinquefasciatus was most susceptible, followed by C. tritaeniorhynchus, A. albopictus and A. aegypti. The respective LC50 values

were 0.68 × 103, 2.01 × 103, 4.91 × 103 and 9.33 × 103 spores mL−1 (Table 2). Compared with Aedes sp., Culex sp. were found to be highly susceptible to ISPC-8. These observations are in line with earlier reports which showed that the B. sphaericus is more active against Culex sp., while B. thuringiensis ssp. israelensis is more active against Aedes sp. (Lacey & Undeen, 1986). Several authors have also observed a similar larvicidal profile for B. sphaericus 2362 and other strains (Sun et al., 1996; Monnerat et al., 2004). The target spectrum of B. sphaericus is limited to mosquitoes, primarily Culex and certain Anopheles sp. (Delécluse et al., 2000), while Aedes sp. required 100-fold higher doses of ISPC-8 as compared with Culex sp. Similarly, Sun et al. (1996) reported that A. aegypti larvae (LC50 43.7 ng mL−1) required higher doses of Chinese isolates of B. sphaericus than C. quinquefasciatus (LC50 1.41 ng mL−1). Some B. sphaericus spore/crystal preparations kill A. aegypti larvae at doses 100–1000-fold higher than that required for C. quinquefasciatus (Lacey & Undeen, 1986). An explanation for this pattern has been proposed by Davidson (1989), based on the affinity that a fluorescein isothiocyanate-labeled toxin binds to the larval midgut of these mosquito species. It was shown that the toxin does not bind to the midgut of A.

Cognitive interviews provided a valuable insight into how travelers used inferential and direct memory to recall travel events

and their confidence in the accuracy of these processes. Conclusions. The development and validation of questionnaires improve the accuracy of the data collected and should be considered an integral part of the methodology of travel-related studies. Epidemiological studies are used extensively in travel medicine for collecting information on travel-related exposures, outcomes, risk, and protective factors. Published studies are often based partly or completely on responses to questionnaires, but few have used existing validated instruments for data collection or attempted to validate newly developed questionnaires. Furthermore, it is difficult to view or obtain questionnaires used in previous studies and no archive of instruments used in published DNA Synthesis inhibitor travel medicine studies exists. To date, no multipurpose validated questionnaire that could be applied to several different studies of infections in travelers has been published. In designing studies that rely on self-reported data collected

via questionnaires, it is important to ensure that the questionnaires are clear, unambiguous, and permit respondents to provide accurate information. Information collected in studies of travelers is generally retrospective behavioral data: travelers are asked to report on events that have occurred Stem Cell Compound Library at some time during travel. This involves comprehension, recall using autobiographical

memory, and formulation of an appropriate response.1 Cognitive survey methodology uses a number of different techniques to reduce respondent error in health surveys and improve instruments used to collect autobiographical data, through specific attention to “cognition” (the mental process by which the mind becomes aware).2,3 The cognitive approach to questionnaire design is based on several information-processing models that have been proposed to account for how respondents answer questions about events.4 Each model includes at least four stages of information processing: Ureohydrolase (1) comprehension of question; (2) retrieval of information; (3) estimation/judgment; and (4) formulation of a response.5 We used nonexperimental cognitive methods to understand how travelers perceived questions, evaluated potential problems with selected items, and the cognitive tasks involved with responding to items. This article describes the development and validation of a travel questionnaire that was developed for use in a prospective cohort study of travelers, which aimed to estimate the risk of influenza, dengue fever, and Japanese encephalitis in Australian travelers to Asia.

More tourists presented for diarrhea than residents: 1,397 ZD1839 mouse (33%) versus 766 (16%) (relative risk 1.99; 95% CI 1.85–2.16, p < 0.001). In total, 390 cases and 185 controls

were enrolled with 381 cases and 176 controls eligible for analysis. Eighteen persons were excluded from the analysis due to incomplete information, wrong nationality, or inability to submit a stool sample. The mean age for cases was significantly younger than that for controls: 33.4 years (SD = 11.4, median = 30) versus 40.4 years (SD = 12.0, median = 39) (p < 0.001). There was no difference in gender with 203 (53%) female cases versus 101 (57%) female controls (p = 0.36). Most enrollees were from Europe (64% of cases vs 57% of controls), with the remainder from North America (25 and 32%, respectively), Australia/New Zealand (6 and 10%), and Japan (5 and 1%) (p = 0.02). More cases (56%) than controls (37%)

were tourists (p < 0.001). More cases had been in Nepal for <30 days than controls (p = 0.001). A significant portion of cases, n = 53 (14%), and just three controls selleck compound had taken an FQ prior to presentation. The likelihood of identifying a bacterial pathogen was less if the patient reported taking an FQ [odds ratio (OR) = 0.38, p = 0.003], whereas no significant association was observed if the patient reported taking an antimotility drug or other medication. The likelihood of identifying a bacterial pathogen was greater if the patient reported watery diarrhea (OR = 2.04, p = 0.022), fever (OR = 1.84, p = 0.004), and microscopic white blood cells (WBCs) and red blood cells (RBCs) when found in stool (OR = 3.35 and 4.24, respectively, p < 0.001). Seasonality did not affect finding of bacterial pathogens (Table 1). Reported use of an oxyclozanide antimotility drug was significantly associated for finding a viral pathogen (OR = 4.24, p = 0.001) and if the patient reported vomiting (OR = 2.99, p = 0.004). Viral pathogens were less likely to be found in the months of April to June (OR = 0.26, p = 0.037).

Cases in whom a protozoan pathogen was found were less likely to report sudden onset of diarrhea (OR = 0.27, p < 0.001) or abdominal pain (OR = 0.37, p = 0.001) and less likely that microscopic WBCs and RBCs were found in stool (OR = 0.42, p = 0.001 and OR = 0.31, p = 0.008, respectively). Interestingly, all pathogens, particularly protozoa, were more likely to be found in April to September, and Japanese were more likely than any other nationality to have protozoan pathogens (p = 0.009). At least one enteric pathogen was identified in 263 of 381 (69%) cases and 47 of 176 (27%) controls (p≤ 0.001; Table 2). Cases were 12 times more likely to have multiple pathogens detected than controls (p < 0.001). Among cases, multiple pathogens were more common among tourists (32%) than residents (18%) (p = 0.002). Campylobacter was the most prevalent pathogen isolated in cases (17%) and the second most common among controls (5%; p = 0.002).

The HIV viral Sirolimus research buy load response to therapy was similar, however, in patients with and without HCV. This deleterious effect is confirmed in some, but not all other studies [165–167]. 5.1.2.2 The influence of HIV on HCV infection. Only 20–30% of immunocompetent individuals with HCV will progress to cirrhosis over an average of 15–30 years. Evidence suggests

that in HIV-positive individuals progression is likely to occur more frequently and at a faster rate [31,168–171]. One study estimated the median time to cirrhosis as 32 years and 23 years from time of acquisition in HCV-infected and HCV/HIV-coinfected individuals, respectively [168]. This is now manifest as a proportional increase in deaths from ESLD throughout the HIV-infected population such that HCV infection is one of the major causes of death in people with HIV [31,168–173]. In selleck contrast, studies that have considered absolute numbers of deaths (rather than proportions of deaths from different causes) have often reported no increase in the number of deaths from liver failure [174], although one study in the HAART era which compensated for competing risks still showed a small increase in liver-related mortality [175]. It is therefore uncertain if there has

been a true increase in deaths from liver failure, or whether the apparent increase is simply a consequence of the longer survival times of individuals with HIV infection. It should also be noted that men with haemophilia and IDUs, in whom many of these studies have been carried out, have generally

ADP ribosylation factor been infected with HCV for some time before becoming infected with HIV. The impact of HCV seroconversion after HIV seroconversion is unclear. Coinfected patients have comparably higher levels of HCV viraemia and HCV in other body fluids [176] and these are inversely correlated with the CD4 cell count and degree of immunosuppression present. Several studies show that liver-related mortality rates are higher in those with a low CD4 cell count, irrespective of ART use [86,177]. Other variables that negatively influence HCV progression have been shown to be alcohol, increasing age at acquisition and the presence of HBV infection [170–178]. HCC is estimated to occur at a rate of 1–4% per annum in patients with HCV-related cirrhosis; in patients who also have HIV infection it tends to occur at a younger age and within a shorter time period [50]. The majority of individuals (75–85%) who become infected with HCV become chronic carriers with detectable HCV RNA in the blood indicating viraemia. The remainder (15–25%) clear virus spontaneously, usually within 6 months of becoming infected [179–182]. Diagnosis of chronic infection is usually made on the basis of a positive anti-HCV antibody test [enzyme-linked immunosorbent assay (ELISA) ± recombinant immunoblot assay (RIBA)], confirmed by a positive HCV RNA [reverse transcriptase–polymerase chain reaction (RT-PCR)] test.

RT-PCR was carried out using a SmartCycler®

II apparatus (Cepheid®, Sunnyvale); the results were analyzed using the rest 2009 software available at http://www1.qiagen.com/Products/REST2009Software.aspx#Tabs=t0 (Pfaffl et al., 2002). For comparative purposes, an SHV-1-producing K. pneumoniae strain I118 with a natural pattern of susceptibility to β-lactams (Table 1) (Livermore, 1995) from the collection of the hospital in Plzeň was used. The experiments were repeated three times. Six C-NS K. pneumoniae isolates from different patients were identified during the study period; from three of these patients, C-S isolates were also retained and were available for the analysis (Table 2). The investigation NVP-BKM120 solubility dmso of the clinical and microbiological data revealed that five of the six patients (patients P1–P5) had been colonized or infected with AmpC- or ESBL-producing C-S K. pneumoniae strains before the identification of the C-NS isolates (Table 2); however,

these C-S strains had not been stored. These five patients received long therapies with carbapenems, mostly with meropenem. Because of other infections, all of the patients were treated with a variety of antimicrobials overall. Regarding the C-NS K. pneumoniae, only patient P5 presented Alpelisib datasheet with symptoms of an infection caused by this organism (urinary tract infection), and was treated successfully with amikacin for this disease. The remaining patients were only colonized with the C-NS K. pneumoniae; therefore, they were not treated with antibiotics against these organisms. In all but one of these patients the C-NS isolates were not observed in further examinations performed 1–2 times weekly. The repeated C-NS isolates were only collected from the patient Racecadotril P4, who was severely ill with

a poor prognosis and eventually died because of organ failure in sepsis (not caused by K. pneumoniae). In three of the patients (patients P2, P3, and P6), the C-S K. pneumoniae isolates were identified within several weeks after the episodes with the C-NS isolates (Table 2), and these isolates were included in this study. The MICs are shown in Table 1. The MICs of carbapenems for the C-NS isolates varied from 2 to 32 μg mL−1, whereas the C-S isolates had MICs of ≤0.12 μg mL−1. Almost all of the isolates exhibited uniform resistance to other β-lactams tested, including penicillin–inhibitor combinations and expanded-spectrum cephalosporins. Two C-S isolates (P2/I177971 and P3/C154247) were susceptible to cefepime (MIC, 0.5 μg mL−1) and one of these (P3/C154247) had a low-level resistance to cefotaxime and ceftazidime (MICs, 2 and 8 μg mL−1, respectively). Except for ciprofloxacin, to which all of the isolates were resistant, the MICs of non-β-lactams varied; of note was the resistance to colistin in one C-NS isolate (P5/C163243; MIC, 16 μg mL−1).