Ied in community-acquired KP infection and is not associated with primary

Ied in community-acquired KP infection and is not Pemafibrate site associated with primary KP liver abscess.11 In addition, Lee et al. reported a negative association of the HV phenotype with ESBL-KP Oxaliplatin manufacturer isolates (OR 0.042, p D 0.003).8 In China, Li et al. found a significantly lower proportion of ESBLKP in the HV-positive isolates than in the HV-negative isolates (17 vs. 56 , P D 0.0006). Li et al noticed an increasing trend of ESBL-KP among the hypermucoviscous isolates over time.12 In a small series from Algiers, the virulence profiles of 54 KP isolates have been well elucidated.13 The study comprised 74.1 isolates with multiresistance particularly to extended-spectrum cephalosporins, which can be due to ESBL production. Overall, 5 (9.2 ) and 2 (3.7 ) isolates had HV and rmpA, respectively. One rmpA-positive isolate did not have HV phenotype. From the above-mentioned studies, it remains unknown why the ESBL-KP isolates rarely exhibit the HV phenotype. The goals of the study were to explain the difference in the prevalence of the HV-related virulence determinants between the KP isolates with and without the ESBL production and to explore the reason why some rmpA-positive KP strains were HVnegative. We hypothesized that low prevalence of rmpA and/or rmpA2 in ESBL-KP isolates contributed to their rare HV phenotype. Our additional hypothesis was that genetic mutation of rmpA and/or rmpA2 was associated with the negative HV phenotype in the rmpA- and/or rmpA2-positive KP isolates.isolates (204?005) was more common than non-blood isolates within ESBL-KP group (p D 0.033), but was not significantly different to non-ESBL blood isolates, albeit with a lower trend (30 vs 55 , p D 0.171). To reduce the selection bias from the small sample size of the ESBL-KP blood isolates (2004?005, n D 10), therefore, we further collected 166 ESBL-KP blood isolates (2007?010) and 48 non-ESBL KP blood isolates (2010). The difference in HV prevalence of the ESBL-KP blood isolates between 2 periods (2004?005 vs 2007?010) was not statistically significant. Again, the HV phenotype of ESBL-KP blood isolates (2007?010) was more common than ESBL-KP nonblood isolates (2004?005), but became significantly less common than non-ESBL KP blood isolates (2004?005 and 2010, respectively,Table 1). Moreover, 105 community-acquired blood KP isolates extracted from our previous study during 2003?004,1 which were almost non-ESBL isolates, showed similar prevalence of HV phenotype to 2004?005 non-ESBL KP blood isolates (48.6 vs. 55 , p D 0.403), but were more HV-positive than journal.pone.0158910 ESBL-KP blood isolates obtained from 2007?010 (48.6 vs. 22.3 , p < 0.0001,Table 1). The prevalence of rmpA and rmpA2 genes among isolates The rmpA was significantly lower in ESBL-KP isolates than that in non-ESBL KP isolates (21.1 vs. 58.6 . p < 0.0001, Table 2). Specifically, the rmpA-positive sputum isolates were more common in non-ESBL than ESBL group (p D 0.001). Similar to HV phenotype, the rmpA prevalence of ESBL-KP blood isolates (2007?010) was significantly lower than the non-ESBL blood isolates (2004?005 and 2010, respectively). Different to higher HV phenotype of blood isolates in ESBL group and rarer HV phenotype of urine isolates in non-ESBL group (Table 1), however, rmpA prevalence was j.neuron.2016.04.018 not statistically different among various isolates within each group (Table 2). For further external validation, the rmpA prevalence of the community-acquired KP blood isolates (2003?004)1 was similar to non-ESBL blood isolates (2.Ied in community-acquired KP infection and is not associated with primary KP liver abscess.11 In addition, Lee et al. reported a negative association of the HV phenotype with ESBL-KP isolates (OR 0.042, p D 0.003).8 In China, Li et al. found a significantly lower proportion of ESBLKP in the HV-positive isolates than in the HV-negative isolates (17 vs. 56 , P D 0.0006). Li et al noticed an increasing trend of ESBL-KP among the hypermucoviscous isolates over time.12 In a small series from Algiers, the virulence profiles of 54 KP isolates have been well elucidated.13 The study comprised 74.1 isolates with multiresistance particularly to extended-spectrum cephalosporins, which can be due to ESBL production. Overall, 5 (9.2 ) and 2 (3.7 ) isolates had HV and rmpA, respectively. One rmpA-positive isolate did not have HV phenotype. From the above-mentioned studies, it remains unknown why the ESBL-KP isolates rarely exhibit the HV phenotype. The goals of the study were to explain the difference in the prevalence of the HV-related virulence determinants between the KP isolates with and without the ESBL production and to explore the reason why some rmpA-positive KP strains were HVnegative. We hypothesized that low prevalence of rmpA and/or rmpA2 in ESBL-KP isolates contributed to their rare HV phenotype. Our additional hypothesis was that genetic mutation of rmpA and/or rmpA2 was associated with the negative HV phenotype in the rmpA- and/or rmpA2-positive KP isolates.isolates (204?005) was more common than non-blood isolates within ESBL-KP group (p D 0.033), but was not significantly different to non-ESBL blood isolates, albeit with a lower trend (30 vs 55 , p D 0.171). To reduce the selection bias from the small sample size of the ESBL-KP blood isolates (2004?005, n D 10), therefore, we further collected 166 ESBL-KP blood isolates (2007?010) and 48 non-ESBL KP blood isolates (2010). The difference in HV prevalence of the ESBL-KP blood isolates between 2 periods (2004?005 vs 2007?010) was not statistically significant. Again, the HV phenotype of ESBL-KP blood isolates (2007?010) was more common than ESBL-KP nonblood isolates (2004?005), but became significantly less common than non-ESBL KP blood isolates (2004?005 and 2010, respectively,Table 1). Moreover, 105 community-acquired blood KP isolates extracted from our previous study during 2003?004,1 which were almost non-ESBL isolates, showed similar prevalence of HV phenotype to 2004?005 non-ESBL KP blood isolates (48.6 vs. 55 , p D 0.403), but were more HV-positive than journal.pone.0158910 ESBL-KP blood isolates obtained from 2007?010 (48.6 vs. 22.3 , p < 0.0001,Table 1). The prevalence of rmpA and rmpA2 genes among isolates The rmpA was significantly lower in ESBL-KP isolates than that in non-ESBL KP isolates (21.1 vs. 58.6 . p < 0.0001, Table 2). Specifically, the rmpA-positive sputum isolates were more common in non-ESBL than ESBL group (p D 0.001). Similar to HV phenotype, the rmpA prevalence of ESBL-KP blood isolates (2007?010) was significantly lower than the non-ESBL blood isolates (2004?005 and 2010, respectively). Different to higher HV phenotype of blood isolates in ESBL group and rarer HV phenotype of urine isolates in non-ESBL group (Table 1), however, rmpA prevalence was j.neuron.2016.04.018 not statistically different among various isolates within each group (Table 2). For further external validation, the rmpA prevalence of the community-acquired KP blood isolates (2003?004)1 was similar to non-ESBL blood isolates (2.