جستجوی مقالات مرتبط با کلیدواژه « efflux pump » در نشریات گروه « پزشکی »

Curcuma species have shown antibacterial activity against Pseudomonas aeruginosa. The current study was conducted to analyze the antibacterial activity of ethanol extracts of Curcuma species rhizomes, including Curcuma domestica, C. xanthorrhiza, C. mangga, C. zedoaria, and C. aeruginosa against multidrug-resistant Pseudomonas aeruginosa (MDR P. aeruginosa). Furthermore, the mechanism action of Curcuma species in combination with antibiotic against MDR P. aeruginosa and its chemical component were also investigated.

Determination of minimum inhibitory concentration (MIC) was carried out by the microdilution method. The synergistic effects of the extract and tetracycline were determined by the checkerboard method. The effect of the combination of Curcuma species and tetracycline to prevent bacterial resistance was investigated using inhibition of biofilm formation, permeability of bacterial cell membrane, and EtBr accumulation methods. Gas chromatography-mass spectrometry (GC-MS) analysis was also performed.

MIC of C. domestica, C. xanthorrhiza, and C. mangga against MDR P. aeruginosa were 125, 250, and 125 µg/mL, respectively. C. xanthorrhiza ethanol extract (7.8 µg/mL) in combination with tetracycline (1.9 µg/mL) revealed a synergistic activity with Fractional Inhibitory Concentration Index (FICI) value of 0.06. The combination of C. xanthorrhiza ethanol extract and tetracycline showed inhibitory effects on biofilm formation and efflux pump of MDR P. aeruginosa. This combination also had bacteriolytic activity. GC-MS analysis led to the identification of ar-turmerone (11.63%) and xanthorrhizol (11.36%) as the major compounds.

Combination of C. xanthorrhiza ethanol extract and tetracycline might be developed as an alternative treatment against MDR P. aeruginosa.

Acinetobacter baumannii is one of the most important known causes of hospital infections worldwide that is resistant to many common antibiotics. Efflux pumps are among the main reasons behind resistance in this bacterium.

This study was conducted to investigate the presence of efflux pump genes (adeI, adeJ) in clinical antibiotic-resistant isolates of A. baumannii in Tehran hospitals.

One hundred fifty clinical samples of wounds, urine, sputum, and blood were collected periodically (6 months) from Tehran hospitals. A. baumannii was identified using common biochemical methods. After conducting biochemical tests, the final confirmation of the samples was performed by examining the blaOXA-51-like gene by molecular polymerase chain reaction (PCR) method. The disk diffusion antimicrobial susceptibility testing was performed using Mueller Hinton agar growth medium according to Clinical and Laboratory Standards Institute (CLSI) guidelines on nine antibiotics. Then the samples were investigated for the presence of adeI and adeJ genes.

Examining the antibiotic resistance of the isolatesshowedthat the resistance level variedfrom48.1% to 98.2%, dependingon the antibiotic type. In this study, isolates showed the highest and lowest resistance to tetracycline and gentamicin, respectively. Also, positive isolates for the presence of adeI and adeJ genes showed the highest resistance to tetracycline, amikamycin, ceftazidime, and ceftriaxone. Isolates that were negative for the presence of these two genes showed the highest sensitivity to imipenem, gentamicin, and ciprofloxacin.

In this study, the correlation of antibiotic resistance test and PCR results showed that the presence of adeI and adeJ genes in the samples significantly increased the resistance to all investigated antibiotics. Therefore, evaluating efflux pumps proves to be useful in identifying antibiotic-resistant strains and appropriate drug treatment. Of course, the role of other factors in creating resistance should not be neglected.

Recently, ciprofloxacin resistance in Staphylococcus aureus strains, due to efflux pumps, has become a significant challenge. Therefore, this study was performed to evaluate the frequency of norA, norB, and norC efflux pump genes and their roles in resistance to ciprofloxacin in clinical isolates of S. aureus.

A total of one hundred clinical blood samples were collected from patient in Qom hospitals and S. aureus isolates were identified by standard microbiological tests. Antimicrobial susceptibility patterns were determined by the disk diffusion method using CLSI guidelines. Subsequently, the presence of norA, norB, and norC efflux pump genes in ciprofloxacin isolates was detected using the PCR method.

Among one hundred clinical samples, 36 S. aureus isolates were recovered and the results of antibiotic susceptibility tests showed that twenty of them were resistant to ciprofloxacin. 15 isolates were resistant to norfloxacin and one isolate was resistant to ofloxacin. Moreover, the norA, norB, and norC genes were found in 58%, 30%, and 41% of ciprofloxacin-resistant isolates, respectively.

Based on the results of this study, norA, norB, and norC efflux pumps may play a significant role in the development of resistance to ciprofloxacin in clinical isolates of S. aureus. Detecting these genes may prove useful in suggesting an effective treatment model for infections caused by S. aureus.

Acinetobacter baumannii is one of the most important causes of nosocomial infections. In this bacteria, several mechanisms contribute to resistance against antimicrobial agents. The present study investigated the prevalence of adeS and adeH genes and the role of efflux pumps in imipenem and colistin-resistant A. baumannii clinical isolates.

This study included 60 A. baumannii isolates collected from medical centers affiliated with the Shahid Beheshti University of Medical Science, Tehran, Iran. The antibiotic susceptibility pattern was examined using the broth microdilution MIC method according to Clinical and Laboratory Standards Institute (CLSI) guidelines. Also, the adeS and adeH genes were amplified by PCR.

The isolates were 100% imipenem-resistant and 86.7% colistin-resistant. All isolates were positive for the 51-blaOXA gene. The adeH and adeS genes were detected in 95% and 80% of the isolates.

The high frequency of adeS and adeH efflux pump genes and the high drug resistance in A. baumannii clinical isolates indicated that adeS and adeH efflux pump genes contribute to antibiotic resistance in this species. Therefore, our results provide essential information about high drug resistance in A. baumannii clinical isolates that can help limit the horizontal and vertical transmission of efflux pump genes in antibiotic-resistant A. baumannii isolates that causes nosocomial infections in susceptible strains.

The adeABC efflux pump has a crucial role in the resistance of Acinetobacter baumannii strains to antimicrobial agents; it is encoded by adeABC, adeR, adeS genes. We evaluated antibiotic resistance, efflux pump genes, clonal relationships, and analyzed a probable correlation that can exist between antibiotic resistance and the aforementioned genes.

We conducted this study on 27 food-originated and 50 human clinical Acinetobacter spp. in Southern Türkiye. MALDI-TOF system and disc diffusion/agar dilution (colistin) methods were used for the identification and antibiotic susceptibility. The efflux pump genes and genetic relatedness of the two groups were investigated by (PCR) and (PFGE) methods.

Foodborne A. dijkshoorniae strain was multidrug- resistant (MDR), and none of them resistant to colistin. Most of the clinical isolates (92%) were Extensive-Drug Resistant (XDR); highest resistant to ceftazidime, piperacillin-tazobactam, and imipenem (47, 94%), and were lowest to colistin (7, 14%), respectively. adeABC, and adeR, adeS genes were (23, 85.2%), (9, 33.3%), (27, 100%) and (10, 37.3%), (18, 66.7%) in foodborne strains respectively. These rates were (43, 86%), (48, 96%), (50, 100%), and (34, 68%), (48, 96.7%) in clinical strains respectively. A positive correlation existed between adeA gene positivity and piperacillin-tazobactam, ceftazidime, gentamycin, imipenem (P=0.048), amikacin (P=0.007) and trimethoprim-sulfamethoxazole (P=0.029) resistance in clinical strains. A positive correlation of trimethoprim-sulfamethoxazole resistance and adeS gene positivity was seen in foodborne strains (P=0.018).

Multiple-efflux pump genes rise in parallel to multidrug-resistance in clinical isolates, while susceptible to diverse antibiotics; food may be a potential provenance for the dissemination of adeABC, adeR and adeS genes.

Multidrug resistance Pseudomonas aeruginosa (MDRPA) is most important issue in healthcare setting. It can secrete many virulence effector proteins via its secretion system type (T1SS-T6SS). They are using them as conductor for delivering the effector proteins outside to begins harmful effect on host cell increasing pathogenicity, competition against other microorganism and nutrient acquisition. 

The study include investigation of 50 isolates of MDRPA for transport secretion system and resistance for antibiotics. Molecular diagnosis using P. aeruginosa specific primer pairs, investigation of AprF, HasF, XcpQ, HxcQ, PscC, CdrB, CupB3, and Hcp using specific primer pairs by PCR were also
performed.

The results revealed high resistance to beta lactam antibiotics (78% for ceftazidime, 78% for cefepime and 46% for piperacillin) can indicate possessing of isolates for beta lactamases and this confirmed by dropping resistance to piperacillin to 16% when combined with tazobactam. Also, the results shown the ability of MDRPA for pyocyanin biosynthesis using the system of genes.

The current study conclude that all isolates of P. aeruginosa were highly virulent due to their possessing of all transport secretion system to deliver different effector proteins with possible harmful effects of these proteins.

The increment in fungal infections, particularly due to Candida species, is alarming due to the emergence of multidrug resistance (MDR). Hence, the identification of novel drug targets to circumvent the problem of MDR requires immediate attention. The metabolic pathway, such as glyoxylate cycle (GC), which utilizes key enzymes (isocitrate lyase [ICL] and malate synthase [MLS]), enables C. albicans to adapt under glucose-deficient conditions. This study uncovers the effect of GC disruption on the major MDR mechanisms of C. albicans as a human pathogenic fungus.

For the purpose of the study, efflux pump activity was assessed by phenotypic susceptibilities in the presence of substrates rhodamine 6G (R6G) and Nile red, along with R6G extracellular concentration (527 nm). In addition, ergosterol content was estimated by the alcoholic potassium hydroxide hydrolysis method. The estimation of chitin was also accomplished by the absorbance (520 nm) of glucosamine released by acid hydrolysis.

The results revealed that the disruption of ICL enzyme gene (Δicl1) led to the impairment of the efflux activity of multidrug transporters belonging to the ATP-binding cassette superfamily. It was further shown that Δicl1 mutant exhibited diminished ergosterol and chitin contents. In addition, all abrogated phenotypes could be rescued in the reverting strain of Δicl1 mutant.

Based on the findings, the disruption of GC affected efflux activity and the synthesis of ergosterol and chitin. The present study for the first time revealed that metabolic fitness was associated with functional drug efflux, ergosterol and chitin biosynthesis and validated GC as an antifungal target. However, further studies are needed to comprehend and exploit this therapeutic opportunity.

Efflux pumps such as MexEF-OprN and mexXY-OprM play an important role in the resistance of Pseudomonas aeruginosa (P. aeruginosa) to antibiotics. The present study aimed to assess the reduced expression of efflux pump genes of P. aeruginosa with Satureja khuzistanica essential oil (SKEO). The present cross-sectional study was conducted in 2016 at the Microbiology Laboratory of Baqiyatallah University of Medical Sciences, Tehran, Iran. The disk diffusion method was used for susceptibility testing of gentamicin and norfloxacin. Minimum inhibitory concentration (MIC) was determined for gentamicin and norfloxacin. The antibacterial efficacy of SKEO was defined by determining the MIC values using the microdilution method. In vitro, the synergistic interaction of SKEO combined with gentamicin or norfloxacin was examined via checkerboard assay and defined as a fractional inhibitory concentration index. The reverse transcription-polymerase chain reaction technique was used to measure changes in the expression of the efflux pump genes. The data were analyzed using SPSS software version 16.0, and p The MIC values of SKEO were in the range of 6 to 12 µg/mL. In the presence of sub-inhibitory concentrations (1.16 to 2 MIC) of SKEO, synergistic effects were revealed using the checkerboard method. The effect of norfloxacin and gentamicin increased up to 8-fold. The expression of mexY and mexE was reduced after treatment with SKEO. SKEO reduced the expression of efflux pumps and the MIC values of norfloxacin and gentamicin in vitro.

Acinetobacter baumannii (A. baumannii) is one of the most important bacteria causing nosocomial infections worldwide. Over the past few years, several strains of A. baumannii have shown antibiotic resistance, which may be due to the activity of efflux pumps. This study was aimed to detect AdeFG efflux pump genes and their contribution to antibiotic resistance in A. baumannii clinical isolates.

A total of 200 A. baumannii clinical isolates were collected from clinical specimens of ulcers, pus, sputum, and blood. All isolates were identified using standard biochemical tests. After identifying and cleaving the genome by boiling, PCR was performed on samples using specific primers. The antimicrobial susceptibility patterns were determined by disk diffusion, with and without CCCP efflux pump inhibitor were determined according to CLSI guidelines.

We identified 60 clinical isolates of A. baumannii using biochemical differential tests. Identification of all A. baumannii isolates was confirmed by blaOXA-51-like PCR. According to the results of our study, 98.37% of A. baumannii isolates were resistant to ciprofloxacin, norfloxacin, and levofloxacin. PCR results indicated that all 60 A. baumannii isolates contained the AdeF and 76.66% contained AdeG.

the results of this study demonstrated that most of the A. baumannii isolates contained AdeF and AdeG efflux pump genes, and more than 98% of the isolates were resistant to ciprofloxacin, norfloxacin, and levofloxacin. This reflected the significant contribution of efflux pumps to the development of resistance to these antibiotics.

Efflux pump inhibitors (EPIs) can block efflux pumps and are helpful in potentiating the activity of aminoglycosides against Pseudomonas aeruginosa. The present study compared the effects of phenylalanine-arginine beta naphthylamide (PAβN) and curcumin on aminoglycoside minimum inhibitory concentration (MIC) on Pseudomonas aeruginosa clinical isolates.

For this descriptive-analytical study, 100 clinical isolates of Pseudomonas aeruginosa were collected and identified by differential diagnostic tests. The MICs of amikacin, gentamicin, and tobramycin were evaluated before and after adding EPIs using a micro-broth dilution test.

The bacteria were isolated from different types of samples, including urine (26 isolates), sputum (37 isolates), ulcers (20 isolates), catheters (eight isolates), blood (five isolates), feces (two isolates), and eyes (two isolates). Overall, 60% of the isolates were obtained from males (mean age = 47.85), and 40% from females (mean age = 44.76).
In the MIC test, 11 (25.5%), 15 (34.8%), and 18 (41.8%) isolates were resistant to amikacin, gentamicin, and tobramycin, respectively. Significant reductions in the MICs of amikacin, gentamicin, and tobramycin were observed after adding curcumin in 54-100% of aminoglycoside-resistant isolates, while fewer changes in the MICs of aminoglycosides were seen against these clinical isolates after adding PAβN (36-55%).

Curcumin and PAβN can potentiate the effect of aminoglycosides on clinical isolates of Pseudomonas aeruginosa and change their susceptibility pattern due to efflux pump inhibition. However, our outcomes detected that curcumin was more effective than the PAβN against the aminoglycoside-resistant isolates of P. aeruginosa.

Acinetobacter baumannii is one of the major bacteria causing nosocomial infections. The emergence of multidrug-resistant (MDR) isolates causes morbidity and mortality and lead to financial burdens for patients and public health systems.

Regarding the use of ciprofloxacin and increase of ciprofloxacin resistance, this study was aimed to investigate the role of the efflux pump and mutations in gyrA and parC genes as the mechanisms of ciprofloxacin-resistance.

This study was conducted on 55 strains of A. baumannii isolated from the patients hospitalized in Milad Hospital, Tehran. The isolates were identified by biochemical tests, and their antibiotic susceptibility was assessed by the disc diffusion method. To investigate the role of the efflux pump, minimum inhibitory concentration (MIC) of ciprofloxacin was determined in the presence and absence of the carbonyl cyanide m-chlorophenyl hydrazone (CCCP) inhibitor. The PCR was used for amplification of gyrA, and parC genes and sequencing of its products was carried out to track the mutations.

The highest and lowest antibiotic resistance were observed in ciprofloxacin (100%) and tobramycin (52.7%), respectively. Moreover, 96% of the A. baumannii isolates exhibited MDR. Five percent of strains showed 4-fold MIC reduction after the use of the inhibitor and were reported as the strains with high activity efflux pump. In 100% of the isolates, gyrA and parC genes were detected, and only one mutation was observed in parC and gyrA genes in the studied isolates that altered amino acid type.

Reduction in MIC in the presence of an efflux pump inhibitor confirmed its role in enhancing the resistance to ciprofloxacin in some isolates. The results of this study also revealed no significant relationship between the ciprofloxacin resistance of the studied isolates and mutation in the encoding region of parC and gyrA genes. Thus, the significance of other mechanisms, such as the expression of genes encoding efflux pump proteins, should not be neglected.

Activity of norA efflux pump is one of the antibiotic resistance mechanisms in ciprofloxacin resistant Staphylococcus aureus. In this study, the effect of Artemisia ciniformis extract on reducing the expression of norA efflux pumps gene in ciprofloxacin-resistant Staphylococcus aureus isolates was studied.

 Ciprofloxacin resistant S. aureus isolates, were treated by different concentration of A. ciniformis extract. After extracting RNA and synthesizing cDNA, norA efflux pump expression was evaluated by Real Time PCR. 

There was significant decrease of norA efflux pump expression in ciprofloxacin-resistant S. aureus isolates treated by A. ciniformis extract (P<0.05). Also, a different expression of norA efflux pump gene was reported.

 It seems A. ciniformis extract as a natural inhibitor, had potential for suppression of norA efflux pump activity.

Burn wound infections have emerged as an important cause of morbidity and mortality in patients due to prolonged hospital stay. Pseudomonas aeruginosa, is the second cause of bacterial burn wound infections. Resistance mechanisms among P. aeruginosa are intrinsic or acquired. Intrinsic resistance mechanisms among P. aeruginosa isolates are inducible AmpC cephalosporinase, decrease of specific porin OprD, and overexpression of RND efflux pump. The aim of this study was detection of mutations in nalC gene in carbapenem resistant P. aeruginosa isolated from burn wounds.

In this cross-sectional study, 180 burn-wound specimens were collected. Suspected lactose-negative colonies were identified by conventional biochemical methods. Kirby-Bauer and Etest methods were used for susceptibility testing. PCR and sequencing techniques were used for the detection of nalC mutation.

Out of 180 specimens received in the laboratory, 54 of isolates were isolated and identified as P. aeroginosa (30%). Of these isolates 20 (37%) were resistant to at least two carbapenems simultaneously. From these carbapenem resistant isolates, 19 (95%), 14 (70%), 14 (70%), 19 (95%) and 16 (80%) were resistant to imipenem, cefepime, piperacillin, ceftizoxime and gentamicin, respectively. Only 1 (2%) isolate was sensitive to all carbapenems and did not has mutation in nalC gene, 20 (37%) isolates were resistant to at least two carbapenems, and had mutations in nalC gene (Gly71►Glu and Ser209►Arg).

As the results showed, mutation in efflux pump was observed in carbapenem resistant isolate and this confirmed that the indiscriminate use of antibiotics for treatment or prophylaxis can increase mutation in efflux pump.

Salmonella enterica subsp. enterica serovar Enteritidis is a food-borne pathogenic bacterium that has recently become resistant to most quinolone antibiotics. The MarA efflux pump plays a significant role in the development of ciprofloxacin resistance in S. Enteritidis strains. The aim of this study was comparative evaluation of anti-efflux activity of Artemisia tournefortiana extract and commercial efflux inhibitor, carbonyl cyanide 3-chlorophenylhydrazone (CCCP) on marA efflux pump gene expression in S. Enteritidis clinical strains.  

In this experimental study, Artemisia tournefortiana extract was prepared using maceration method. Subsequently, MarA efflux pump was detected in 20 clinical strains of S. Enteritidis via cartwheel and PCR methods. Finally, after treatment of strains with subMIC concentration of extract and 20 µg/L and CCCP, their anti-efflux activity against MarA efflux pump was studied using Real Time PCR. 

The results of cartwheel and PCR methods indicated that all of ciprofloxacin resistant strains had MarA efflux pump. Subsequently, after treatment of strains with subMIC concentration of extract and CCCP, results show that both component have the ability to inhibit the MarA efflux pump, significantly. 

Considering the results of MarA efflux inhibition by A. tournefortiana and CCCP, it seems that this plant can be used as a potential source of drug use as a suppository pump inhibitor instead of CCCP.