[Effects of traditional Tibetan drug Liu Tea on proliferation and chemotherapeutic sensitivity of drug-resistant human gastric cancer cell BGC823/5-FU].

To investigate the effects of Liu Tea extracts(LTE) on proliferation, apoptosis and drug sensitivity of drug-resistant gastric cancer cell BGC823/5-FU. MTT assay was used to analyze effect of LTE on cell growth and sensitivity chemotherapeutic drugs, and synergistic effect of the combination of LTE with 5-FU on BGC823/5-FU cells. Combination index (CI) was calculated by CompuSyn. Cell apoptosis was measured by flow cytometry (FCM). Protein expressions of P-gp, Bcl-2, Bax and Caspase-3 (17KD) were detected by Western blot at different concentrations of LTE in BGC823/5-FU cells (100, 200, 400 mg•L⁻¹). The results showed that LTE had an inhibitory effect on growth of BGC823/5-FU cell in a dose-time-dependent manner and significantly reduced IC50 of 5-FU, CDDP, PTX and ADM to BGC823/5-FU cells(P<0.05), indicating it could reverse tolerance of drug resistant cells to chemotherapeutic drugs, with reversion multiples of 2.35, 1.68, 1.96, 0.52. The combination of LTE with 5-FU had positive synergistic effect on the BGC-823 cell line. FCM assay suggested that LTE could induce BGC823/5-FU apoptosis. The apoptosis rate was up to 46.2% when the cells were treated with 800 mg•L⁻¹ LTE after 24 h(P<0.01). According to the protein detection results, with the increase in concentration of LTE, the protein expression of Bcl-2 was gradually decreased(P<0.01), the expression of Bax and Caspase-3 were extremely increased(P<0.01), with statistical significance in difference(P<0.01) but no difference in the expression of P-gp between experiment group and control group. LTE can inhibit the growth of drug-resistant human gastric cancer cell BGC823/5-FU and reverse its chemotherapeutic tolerance to some extent. Inhibition of antiapoptotic proteins, activation of proapoptotic proteins and induction of apoptosis of resistant cells may be its main mechanisms.

High rates of multidrug resistance in Enterococcus faecalis and E. faecium isolated from inpatients and outpatients in Taiwan.

Longitudinal national data on resistance in Enterococcus faecalis and E. faecium from different sources in Taiwan are rare. The present study analyzed data from the Taiwan Surveillance of Antimicrobial Resistance program to address this issue. Between 2002 and 2010, a total of 1696 E. faecalis and 452 E. faecium isolates were studied. Although these 2 species together comprised similar percentages of all enterococci in each study year (94.1-97.2%, P = 0.19), the proportion of E. faecium increased from 12.4% in 2002 to 27.3% in 2010 (P < 0.001). The most noteworthy change in susceptibilities of these 2 species was vancomycin resistance in E. faecium (VREfm), which increased from 0.3% in 2004 to 24.9% in 2010 (P < 0.001). VREfm prevalence differed significantly between geographic regions, patient age groups, and locations. Multidrug resistance was very common in both species even in isolates from outpatients (82.7% for E. faecalis and 98.1% for E. faecium), at rates similar to those from intensive care unit (ICU) and non-ICU patients (80.5-80.9% in E. faecalis and 97.2-98.6% in E. faecium). Nonsusceptibility to linezolid was <0.5% in both species. All tested isolates were susceptible to daptomycin. Continuous surveillance of VRE prevalence and survey of community reservoirs of multidrug-resistant enterococci are warranted.

mecA-positive Staphylococcus aureus with low-level oxacillin MIC in Taiwan.

Although the presence of mecA is the genotypic determinant of methicillin-resistant Staphylococcus aureus (MRSA), certain MRSA strains, especially community-associated MRSA (C-MRSA), can display an oxacillin MIC in the Clinical and Laboratory Standards Institute susceptible breakpoint range (≤ 2 µg/ml). Among 91 and 180 isolates thought to be methicillin-susceptible S. aureus (MSSA) with oxacillin MICs of 2 and 1 µg/ml as determined by the Sensititre broth microdilution test initially, 52 (57.1%) and 6 (3.3%), respectively, were mecA positive. These mecA-positive low-oxacillin-MIC isolates belong to the dominant Taiwan C-MRSA clone (clonal complex [CC] 59), 56 of which carried SCCmec type V and were pvl positive, and 43 of which belonged to spa CC t437. All 271 isolates were retested by Sensititre, as well as by Vitek II and disk diffusion (DD). Based on the oxacillin results, the sensitivities of the Sensititre, Vitek II, and DD methods were 48.3% (28/58), 46.6% (27/58), and 89.6% (52/58), respectively. Although cefoxitin was better at detecting these isolates, 12.1, 10.4, and 5.2% of these isolates were still misidentified as MSSA by Sensititre, Vitek II, and DD, respectively. These results highlight the difficulty in the accurate identification of MRSA with borderline oxacillin MICs in the CC59:SCCmec V clone, which likely has contributed to its spread in the health care and community settings. Since this clone has now been detected in other countries, and since other C-MRSA lineages have also been found to have low-level ß-lactam resistance, the findings of the present study may be relevant to other regions. Further studies are warranted to determine the extent and clinical impact of such misidentification.

A multicenter surveillance of antimicrobial resistance on Stenotrophomonas maltophilia in Taiwan.

BACKGROUND: Stenotrophomonas maltophilia has emerged as an important opportunistic pathogen in debilitated hosts. Clinical management of S. maltophilia is challenging due to its intrinsic resistance to a variety of antibiotics. This study investigated the trend and prevalence of antimicrobial resistance in S. maltophilia from a nationwide surveillance study in Taiwan. METHODS: S. maltophilia isolates were collected biennially between 1998 and 2008 as part of the Taiwan Surveillance of Antimicrobial Resistance (TSAR) program from medical centers and regional hospitals throughout Taiwan. Minimal inhibitory concentrations (MIC) were determined using the Clinical and Laboratory Standards Institute reference broth microdilution method. RESULTS: A total of 377 non-duplicate S. maltophilia isolates were collected from 38 hospitals. The majority of the isolates were from the respiratory tract (256, 67.9%), followed by blood (48, 12.7%). Overall, 376 (99.7%) isolates were susceptible to minocycline, 362 (96%) to tigecycline, 311 (82.5%) to trimethoprim/sulfamethoxazole (TMP-SMX), 300 (79.6%) to levofloxacin, 92 (24.4%) to ceftazidime, and 70 (18.6%) to ticarcillin-clavulanic acid. The MIC(50)/MIC(90) of minocycline, tigecycline, TMP-SMX, levofloxacin, ceftazidime, and ticarcillin-clavulanic acid, were ≤0.5/1 µg/mL, 0.25/1 µg/mL, ≤0.25/8 µg/mL, 1/4 µg/mL, 32/128 µg/mL, and 64/128 µg/mL, respectively. A trend of increased non-susceptibility to levofloxacin (p=0.014) was observed over the 10-year study period. Compared to TMP-SMX-susceptible isolates, TMP-SMX-resistant isolates were less susceptible to levofloxacin (54.5% vs. 84.9%, p<0.001). CONCLUSION: In this 10-year study, minocycline and TMP-SMX remained the two antimicrobials with better in vitro activities against S. maltophilia than ceftazidime, levofloxacin, and ticarcillin-clavulanic acid. The activity of levofloxacin against S. maltophilia in Taiwan declined during the past 10 years.

Methicillin-resistant Staphylococcus aureus in Taiwan.

We found a virulent closely related clone (Panton-Valentine leukocidin-positive, SCCmec V:ST59) of methicillin-resistant Staphylococcus aureus in inpatients and outpatients in Taiwan. The isolates were found mostly in wounds but were also detected in blood, ear, respiratory, and other specimens; all were susceptible to ciprofloxacin, gentamicin, and trimethoprim-sulfamethoxazole.

Vancomycin-resistant enterococci from humans and retail chickens in Taiwan with unique VanB phenotype-vanA genotype incongruence.

Vancomycin resistant enterococci (VRE) with VanB phenotype-vanA genotype incongruence were found in all 39 VRE isolated from chicken carcasses and four human VRE isolates in Taiwan. Three identical mutations in the vanS gene were found in the VanB phenotype-vanA genotype VRE sequenced. This finding indicates possible transmission of glycopeptide resistance among different hosts.