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PubMed2006

In vitro activity of tigecycline against quinolone-resistant Streptococcus pneumoniae, methicillin-resistant Staphylococcus aureus and vancomycin-resistant enterococci.

Tigecycline is a glycylcycline with promising broad-spectrum activity, including resistant Gram-positive organisms. This study characterizes in vitro activity of tigecycline against quinolone-resistant Streptococcus pneumoniae (QRSP), methicillin-resistant Staphylococcus aureus (MRSA) and vancomycin-resistant Enterococcus faecalis (VRE). An in vitro pharmacodynamic model generated specific bacterial kill profiles for tigecycline against clinical isolates of QRSP, MRSA and VRE. Tigecycline produced a 6.6 log total reduction and cleared QRSP from the pharmacodynamic model by 18 h. Tigecycline and vancomycin were unable to achieve 3-log reductions in the MRSA and VRE isolates; log reductions in MRSA and VRE were 1.5 and 1.2 logs for tigecycline and 2.8 and zero for vancomycin, respectively. Area under the concentration time curve to minimum inhibitory concentration (AUC/MIC) values for tigecycline ranged from 79 to 158 microg h/mL and tigecycline concentrations remained above the MIC (T>MIC) throughout the simulated dosing interval. Tigecycline showed in vitro activity against the QRSP, MRSA and VRE isolates studied. Low MIC values, prolonged elimination half-life and the associated post-antibiotic effect (PAE) observed with tigecycline are desirable attributes that make it a potentially attractive option for treating resistant Gram-positive organisms.

Anti-Bacterial Agents↗
PubMed1999

Near absence of vancomycin-resistant enterococci but high carriage rates of quinolone-resistant ampicillin-resistant enterococci among hospitalized patients and nonhospitalized individuals in Sweden.

Rates of colonization with enterococci with acquired resistance to vancomycin (vancomycin-resistant enterococci [VRE]) and ampicillin (ampicillin-resistant enterococci [ARE]) were determined by using fecal samples from 670 nonhospitalized individuals and 841 patients in 27 major hospitals. Of the hospitalized patients, 181 (21.5%) were carriers of ARE and 9 (1.1%) were carriers of VRE. In univariate analyses, length of hospital stay (odds ratio [OR], 4.6; 95% confidence interval [CI], 2.5 to 8.9) and antimicrobial therapy (OR, 4.7; 95% CI, 3.3 to 6.7) were associated with ARE colonization, as were prior treatment with penicillins (OR, 3.1; 95% CI, 1.8 to 5. 5), cephalosporins (OR, 2.9; 95% CI, 1.7 to 5.0), or quinolones (OR, 2.7; 95% CI, 1.5 to 4.7). In logistic regression analysis, antimicrobial therapy for at least 5 days was independently associated with ARE carriage (adjusted OR, 3.8; 95% CI, 2.6 to 5.4). Over 90% of the ARE isolates were fluoroquinolone resistant, whereas 14% of the ampicillin-susceptible Enterococcus faecium isolates were fluoroquinolone resistant. ARE carriage rates correlated with the use of fluoroquinolones (P = 0.04) but not with the use of ampicillin (P = 0.68) or cephalosporins (P = 0.40). All nine VRE isolates were E. faecium vanB and were found in one hospital. Seven of these isolates were related according to their types as determined by pulsed-field gel electrophoresis. Among the nonhospitalized individuals, the ARE carriage rate was lower (6%; P < 0.05), and only one person, who had recently returned from Africa, harbored VRE (E. faecium vanA). The absence of VRE colonization in nonhospitalized individuals reflects an epidemiological situation in Sweden radically different from that in countries in continental Europe where glycopeptides have been widely used for nonmedical purposes.

4-Quinolones↗
PubMed1994

Acquired Resistance in Barley (The Resistance Mechanism Induced by 2,6-Dichloroisonicotinic Acid Is a Phenocopy of a Genetically Based Mechanism Governing Race-Specific Powdery Mildew Resistance).

Treatment of susceptible barley (Hordeum vulgare) seedlings with 2,6-dichloroisonicotinic acid (DCINA) induces disease resistance against the powdery mildew fungus (Erysiphe graminis f. sp. hordei). A cytological analysis of the interaction reveals the hypersensitive cell collapse in attacked, short epidermal cells, along with the accumulation of fluorescent material in papillae, that appear at the time of fungal arrest. The cell-type-specific hypersensitive reaction occurs prior to formation of haustoria, reminiscent of the mechanism identified in genetically resistant barley plants containing the functionally active Mlg gene (R. Gorg, K. Hollricher, P. Schulze-Lefert [1993] Plant J 3: 857-866). This observation indicates that the mechanism of DCINA-induced resistance is a phenocopy of the mechanism governed by the Mlg locus. The onset of acquired resistance correlates with high-level transcript accumulation of barley defense-related genes encoding pathogenesis-related protein-1, peroxidase, and chitinase but not [beta]-1,3-glucanase. Subcellular localization of peroxidase activity shows an increase in enzyme activity in the epidermal cell layer and in the intercellular fluids of barley leaves. Four out of more than 10 identified extracellular isozymes are induced by DCINA. The epidermal cell layer contains a major constitutively formed isozyme, together with two isozymes specifically induced by DCINA. The data support the hypothesis that host cell death and high-level accumulation of defense-related gene transcripts are not only commonly controlled in certain types of race-specific resistance (A. Freialdenhoven, B. Scherag, K. Hollricher, D.B. Collinge, H. Thordal-Christensen, P. Schulze-Lefert [1994] Plant Cell 6: 983-994) but also in acquired resistance, which confers protection to a broad spectrum of different pathogens.

Journal Article↗
PubMed2003

Comparative analysis of multidrug-resistant, non-multidrug-resistant, and archaic methicillin-resistant Staphylococcus aureus isolates from Central Sydney, Australia.

In this study, the phenotypic and genotypic characteristics of 50 methicillin-resistant Staphylococcus aureus (MRSA) isolates (43 contemporary and 7 archaic strains from the mid-1960s) from four Sydney hospitals in the central Sydney area were compared. Phenotypic analysis based on antibiotic profiles and phage typing patterns categorized the MRSA isolates into three major groups: multidrug resistant (mMRSA), non-multidrug resistant (nmMRSA), and archaic. The nmMRSA isolates could be further subdivided into nmMRSA group 1, which was phage typeable and similar to the archaic group; nmMRSA group 2, which was non-phage typeable and only resistant to ciprofloxacin; and nmMRSA group 3, which was also nontypeable and generally resistant to other antibiotics. The characterization of all five phenotypic groups was then extended by genetic analysis. Restriction fragment length polymorphism (RFLP) analysis showed the 50 isolates could be sorted into 20 group-specific pulsotypes. mecI gene deletions and mutations at various percentages among the five MRSA groups were detected by sequencing. Several mec promoter mutations were also found. The overall findings indicated that nmMRSA strains may have independently acquired mec DNA and are more likely to be newly emergent strains than nmMRSA variants.

Anti-Bacterial Agents↗
PubMed1990

Differential sensitivity of multi-drug-resistant and -sensitive cells to resistance-modifying agents and the relation with reversal of anthracycline resistance.

Calcium channel blockers, calmodulin inhibitors, and some other classes of non-related compounds reverse multi-drug resistance. In the present study, we found that several resistance modifiers are more toxic for MDR cells than for the corresponding sensitive parent cells, whereas others show the opposite effect. Several calcium channel blockers including bepridil, diltiazem, nifedipine and verapamil, as well as the calmodulin inhibitor trifluoperazine, were more toxic for several MDR cell lines than for the parent cell lines. In contrast, cross-resistance for cyclosporin A and the verapamil analogue Ro II-2933/001 was observed in the MDR/sensitive cell couple CHRC5/AUXB1, probably due to a concentration-dependent stimulation of cell growth in the range of 0-4 microM cyclosporin A and of 1-4 microM Ro II-2933/001. In partially revertant CHRC5 cells, growth inhibition by Ro II-2933/001 at concentrations below I microM, as seen in CHRC5 cells, changed into growth stimulation, and the collateral sensitivity to verapamil and bepridil disappeared almost completely. In the MDR cells CHRC5, 2780AD and DC3F/DMXX, cross-resistance to another calcium channel blocking agent, Ro II-1781/001 (tiapamil), was observed as well. This compound showed exceptional behavior: it induced marked potentiation of Dx cytotoxicity as well as stimulation of Dx accumulation in AUXB1 cells, even at low tiapamil concentrations, but not in the CHRC5 cells, even at high concentrations. It is concluded that resistance modifiers can selectively influence growth of MDR cells via more than one process, and resulting in either strong growth inhibition in MDR cells relative to the effect on sensitive cells or in growth stimulation.

Animals↗
PubMed1987

Expressions of resistance and cross-resistance in teniposide-resistant L1210 cells.

Resistance to teniposide (VM-26) by VM-26 selected resistant L1210 cells in culture was attributed to alterations in the flux of VM-26 across the plasma membrane and to functions of homogeneously staining regions that appeared on one or more chromosomes. In the present study, electrophoresis of membrane-cytosol fractions of these resistant sublines demonstrated a protein band, Mr 22 kd, that was not evident in similar fractions of drug-sensitive L1210 cells or three revertant sublines. The distribution of this protein among various cellular fractions could be altered by manipulation of the concentration of calcium ions. A representative subline, LIa5 microM, was observed to have vesicles that reacted with Sudan black B stain, an indication of altered lipid metabolism. The LIa5 microM subline was cross-resistant to etoposide, vincristine, doxorubicin, amsacrine, and actinomycin D. Concentrations of VM-26 that inhibited cell division to the same extent caused an accumulation of fewer cells in the G2 stage of cell division in LIa5 microM cultures than in L1210 cultures. These observations indicate that the LIa5 microM subline expressed multiple drug resistance, as well as changes in the expression of cytotoxicity to VM-26.

Animals↗
PubMed2001

High-level chloroquine resistance in Sudanese isolates of Plasmodium falciparum is associated with mutations in the chloroquine resistance transporter gene pfcrt and the multidrug resistance Gene pfmdr1.

Polymorphisms were examined in 2 Plasmodium falciparum genes, as were chloroquine responses of clones and isolates from a village in eastern Sudan. There was a significant association between an allele of the P. falciparum chloroquine resistance transporter gene (pfcrt-T76) and both in vitro and in vivo resistance. There was a less significant association with the multidrug resistance gene pfmdr1-Y86 allele. A significant association between pfmdr1-Y86 and pfcrt-T76 was apparent among resistant isolates, which suggests a joint action of the 2 genes in high-level chloroquine resistance.

ATP-Binding Cassette Transporters↗
PubMed1990

[Studies on resistant mechanisms in the resistant bacteria to chlorhexidine. II. Chemical components of the cell membrane and the electron microscopical observation of cell surface structure of chlorhexidine-resistant bacteria].

The mechanisms of resistance of Serratia marcescens and Pseudomonas cepacia to chlorhexidine were studied. Leakage of the cellular component such as protein was observed in a chlorhexidine sensitive strain (S1) of S. marcescens when S1 was treated with chlorhexidine at 40 micrograms/ml concentration, while this phenomenon was not observed in a resistant strain (R1). The following observations were made concerning about cell surface structure in the chlorhexidine sensitive and resistant strains of S. marcescens by chemical analyses of membrane components and electron microscopical studies of the thin sections of the cells. (1) When the S1 strains was treated with chlorhexidine, the outer membrane of the cells formed a wrinkled surface with irregular blebs, and some of which broke out to form various sizes of granules. The R1 strain did not undergo such morphological changes under the same conditions used in the sensitive strain. (2) A prominent protein with apparent molecular weight of 45 K was found exclusively in the R1 strain of S. marcescens as major outer membrane protein, while it was not found in S1 strain. (3) There were no differences in the composition of phospholipids and the amount of 3-hydroxytetradecanoic acid between S1 and R1 strains of S. marcescens. In Pseudomonas cepacia PCJ1 which is resistant to chlorhexidine, 50 K protein was also observed as a major protein of outer membrane of the cells. In contrast to the strain, a mutant of the strain, #102 which was obtained from PCJ1 strain by the treatment with methanesulfonic acid ethylester, did not possess the 50 K protein in its outer membrane. These data suggested that outer membrane components of bacteria were related importantly in resistant mechanism.

Bacterial Proteins↗
PubMed2000

Genetic relatedness of multidrug-resistant, methicillin (oxacillin)-resistant Staphylococcus aureus bloodstream isolates from SENTRY Antimicrobial Resistance Surveillance Centers worldwide, 1998.

We reviewed Staphylococcus aureus bloodstream infection isolates from SENTRY centers worldwide during 1998 to evaluate the molecular epidemiology of multiply drug-resistant methicillin (oxacillin)-resistant S. aureus (MDR-MRSA). MDR-MRSA was defined as a S. aureus isolate with a MIC for oxacillin at >2 microg/ml and with four or more additional resistances. A total of 325 unique patient isolates of MDR-MRSA from five continents were analyzed using ribotyping and pulsed-field gel electrophoresis (PFGE). The frequency of MDR-MRSA among all S. aureus BSI isolates ranged from only 2.2% in Canada to 35.6% in the Asia-Pacific region. Forty-eight ribotypes (RT) were distinguished, but over 80% of the isolates were contained within the 10 most prevalent RTs. The most common RT, RT 184.5, which included 30% of all MDR-MRSA, was found on four of five continents. PFGE provided superior discrimination and identified numerous clusters of possible clonal dissemination of MDR-MRSA within individual medical centers and between institutions that are in geographic proximity. In four instances, strains with indistinguishable PFGE patterns were found on more than one continent. The predominant PFGE subtype in South America (RT 893.5/Ia) was isolated from patients at centers in Brazil, Argentina, and Portugal, and closely related subtypes were isolated in Chile and Italy. There is great geographic variation in rates of methicillin- and multidrug-resistance among S. aureus bloodstream isolates worldwide. Although many MDR-MRSA strains group geographically, a few closely related epidemic strains have wide regional and even global range.

Anti-Bacterial Agents↗
PubMed1998

Acquisition of methicillin resistance and progression of multiantibiotic resistance in methicillin-resistant Staphylococcus aureus.

Methicillin-resistant Staphylococcus aureus (MRSA) produces specific penicillin-binding protein, PBP2', which shows remarkably low affinities to most beta-lactam antibiotics except those such as penicillin G and ampicillin. The region surrounding mecA has been called additional DNA or mec and is thought to be of extraspecies origin. From the study of mec, we found that mec is a novel mobile genetic element and designated as staphylococcal cassette chromosome mec (SCCmec). There are three types of SCCmec. In the past decades, MRSA has become resistant to many antibiotics, such as carbapenems, new quinolones, and minocycline etc. It seems to be a characteristic of MRSA to acquire multi-resistance by accumulating multiple resistance genes around the mecA gene inside SCCmec.

Drug Resistance, Microbial↗
PubMed2006

Prognostic significance of multidrug resistance gene 1 (MDR1), multidrug resistance-related protein (MRP) and lung resistance protein (LRP) mRNA expression in acute leukemia.

The prognostic significance of multidrug resistance (MDR) gene expression is controversial. We investigated whether multidrug resistance gene 1 (MDR1), multidrug resistance-related protein (MRP) and lung resistance protein (LRP) mRNA expression are associated with outcomes in acute leukemia patients. At diagnosis we examined MDR1, MRP and LRP mRNA expression in bone marrow samples from 71 acute leukemia patients (39 myeloid, 32 lymphoblastic) using nested RT-PCR. The expression of each of these genes was then expressed as a ratio in relation to beta-actin gene expression, and the three genes were categorized as being either 0, 1+, 2+ or 3+. MDR1, MRP and LRP mRNA expression was detected in 23.9%, 83.1% and 45.1 %, respectively. LRP mRNA expression was significantly associated with resistance to induction chemotherapy in acute leukemia patients, and in the AML proportion (p=0.02 and p=0.03, respectively). MRP and high MDR1 mRNA expression was associated with poorer 2-yr survival (p=0.049 and p=0.04, respectively). Patients expressing both MRP and LRP mRNA had poorer outcomes and had worse 2-yr survival. The present data suggest that MDR expression affects complete remission and survival rates in acute leukemia patients. Thus, determination of MDR gene expression at diagnosis appears likely to provide useful prognostic information for acute leukemia patients.

Adolescent↗
PubMed1999

Histopathological assessment of multidrug resistance in gastric cancer: expression of P-glycoprotein, multidrug resistance-associated protein, and lung-resistance protein.

Because local recurrence is common after a curative resection for advanced gastric cancer, there has been significant interest in adjuvant chemotherapy. However, the overall effect of chemotherapy remains debatable regarding patients with advanced gastric adenocarcinoma. Multidrug resistance is thought to be a major cause of failure in cancer chemotherapy, and thus the expression of P-glycoprotein (P-Gp), multidrug resistance-associated protein (MRP), and lung-resistance protein (LRP) in tumor cells was evaluated by immunohistochemistry. In 20 gastric adenocarcinomas, 11 (55%), 2 (10%), and 0 (0%) were positive for MRP, LRP, and P-Gp. In malignant lymphomas, only 3 out of 10 cases were positive for MRP (30%). The positive rate of MRP staining was significantly higher in well and moderately differentiated adenocarcinomas (80%) than in poorly differentiated adenocarcinomas (20%). With regard to the degree of MRP expression and histological cell type, higher grades (grade 2-3) were observed only in well and moderately differentiated adenocarcinomas. In terms of the positive-stained cells and staining intensity, heterogeneity was observed in the staining profile of MRP. The proliferative cell nuclear antigen labeling index (PCNA LI) of MRP-positive and MRP-negative cases was 49.3% +/- 11.6% and 49.4 +/- 6.9%, respectively. No correlation was observed between the MRP expression and PCNA LI. In conclusion, the incidence of MRP expression in gastric cancer was the highest in three different multidrug resistance-related epitopes. An evaluation of the MRP expression thus seemed to be beneficial for determining the optimal strategy of chemotherapy.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed1997

High-level tetracycline-resistant Neisseria gonorrhoeae in Ontario, Canada--investigation of a cluster of isolates, showing chromosomally mediated resistance to penicillin combined with plasmid-mediated resistance to tetracycline.

Between 1991 and 1994, plasmid-mediated, tetracycline-resistant Neisseria gonorrhoeae (TRNG) increased from 61.8% to 85.96% of all resistant isolates in Ontario, Canada. Ninety-nine isolates with tetracycline MICs >32 mg/L were characterized by auxotype/serovar (A/S) class, plasmid profile, hybridization with eight tetracycline-resistant probes, and pulsed-field gel electrophoresis (PFGE) of genomic DNA after digestion with NheI and SpeI restriction endonucleases. A cluster of 82 isolates with penicillin MICs of 2-4 mg/L and tetracycline MICs of 128 mg/L (chromosomally mediated resistance) belonged to A/S class NR/IB-1 and had identical or closely related PFGE profiles. Seventeen isolates, TRNG (10) and penicillinase-producing TRNG (7), with tetracycline MICs of 64-256 mg/L, belonged to eight A/S classes and displayed 12 different PFGE profiles. The 99 isolates hybridized only with the TetM probe. Phenotypic and molecular characterization indicated a diverse population throughout the Province of Ontario.

Chromosomes, Bacterial↗
PubMed2005

Prevalence of resistance mechanisms against macrolides and lincosamides in methicillin-resistant coagulase-negative staphylococci in the Czech Republic and occurrence of an undefined mechanism of resistance to lincosamides.

High occurrence of the non-macrolide-lincosamide-streptogramin B resistance genes msrA (53%) and linA/linA' (30%) was found among 98 methicillin-resistant coagulase-negative staphylococci additionally resistant to macrolides and/or lincosamides. The gene msrA predominated in Staphylococcus haemolyticus (43 of 62 isolates). In Staphylococcus epidermidis, it was present in 7 of 27 isolates. A novel mechanism of resistance to lincosamides appears to be present in 10 genetically related isolates of S. haemolyticus in the absence of ermA, ermC, msrA, and linA/linA'.

Anti-Bacterial Agents↗
PubMed2005

Multidrug resistance markers P-glycoprotein, multidrug resistance protein 1, and lung resistance protein in non-small cell lung cancer: prognostic implications.

PURPOSE: The aim of this retrospective study was to comparatively investigate the expression of the three drug-resistance genes P-glycoprotein (P-gp), multidrug-resistance protein 1 (MRP1), and lung resistance protein (LRP), in non-small cell lung cancer (NSCLC) tissues, and to assess possible associations with clinicopathologic features. METHODS: Tumor specimens from 126 patients were analyzed by immunohistochemistry and, in selected cases, by reverse transcriptase polymerase chain reaction (RT-PCR), and data were statistically analyzed by SPSS. RESULTS: The mean expression levels of tumor tissues in the case of P-gp and LRP did not exceed the one of normal epithelia, while MRP1 was significantly enhanced in NSCLC. A weak association was observed between higher grading and P-glycoprotein expression (p <0.08) as well as lower grading and MRP1 expression in the case of adenocarcinoma (p <0.05). MRP1 levels were highest in TNM stage I and declined with advanced stage (p <0.03). A significant association was found between high MRP1 levels and longer overall survival (N =115, p <0.04), which was highly significant in the patient group never treated with chemotherapy (N =77; p <0.007). P-gp expression was enhanced in those patients who had received chemotherapy before surgery (p <0.05). CONCLUSIONS: Our data point towards a major role of MRP1 in the intrinsic treatment resistance of NSCLC and suggest, in addition, a significant activation of P-gp expression during chemotherapy.

ATP Binding Cassette Transporter, Subfamily B↗