scholarly journals Antimicrobial Resistance Mechanisms amongCampylobacter

2013 ◽  
Vol 2013 ◽  
pp. 1-12 ◽  
Author(s):  
Kinga Wieczorek ◽  
Jacek Osek
Keyword(s):  
Antimicrobial Resistance ◽  
Antimicrobial Agents ◽  
Severe Disease ◽  
Resistance Mechanisms ◽  
Antimicrobial Treatment ◽  
Clear Correlation ◽  
Campylobacter Coli ◽  
Causative Agents ◽  
Contaminated Food ◽  
Alternative Choice

Campylobacter jejuniandCampylobacter coliare recognized as the most common causative agents of bacterial gastroenteritis in the world. Humans most often become infected by ingesting contaminated food, especially undercooked chicken, but also other sources of bacteria have been described. Campylobacteriosis is normally a self-limiting disease. Antimicrobial treatment is needed only in patients with more severe disease and in those who are immunologically compromised. The most common antimicrobial agents used in the treatment ofCampylobacterinfections are macrolides, such as erythromycin, and fluoroquinolones, such as ciprofloxacin. Tetracyclines have been suggested as an alternative choice in the treatment of clinical campylobacteriosis but in practice are not often used. However, during the past few decades an increasing number of resistantCampylobacterisolates have developed resistance to fluoroquinolones and other antimicrobials such as macrolides, aminoglycosides, and beta-lactams. Trends in antimicrobial resistance have shown a clear correlation between use of antibiotics in the veterinary medicine and animal production and resistant isolates ofCampylobacterin humans. In this review, the patterns of emerging resistance to the antimicrobial agents useful in treatment of the disease are presented and the mechanisms of resistance to these drugs inCampylobacterare discussed.

scholarly journals Antimicrobial Resistance in Campylobacter jejuni and Campylobacter coli Strains Isolated in 1991 and 2001-2002 from Poultry and Humans in Berlin, Germany

2003 ◽  
Vol 47 (12) ◽  
pp. 3825-3830 ◽  
Author(s):  
Petra Luber ◽  
Jutta Wagner ◽  
Helmut Hahn ◽  
Edda Bartelt
Keyword(s):  
Antimicrobial Resistance ◽  
Campylobacter Jejuni ◽  
Antimicrobial Agents ◽  
Antimicrobial Treatment ◽  
Campylobacter Coli ◽  
Retail Market ◽  
Poultry Products ◽  
Development Of Resistance ◽  
Resistance Rates ◽  
Sampling Times

ABSTRACT The susceptibilities of 430 Campylobacter jejuni strains and 79 C. coli strains to six antimicrobial agents were tested and analyzed. The two sets of strains originated from retail market chicken and turkey samples and from humans, respectively, in Berlin, Germany. Two groups of isolates, one dating from 1991 and the other dating from 2001-2002, were tested. Of the Campylobacter sp. isolates recovered from humans in 2001-2002, 45.1% were resistant to ciprofloxacin, 37.8% were resistant to tetracycline, 12.8% were resistant to ampicillin, and 50.0% were resistant to trimethoprim-sulfamethoxazole. All isolates were susceptible to gentamicin, while the overall rate of resistance to erythromycin was 6.1%. During the 10 years between the two sampling times, the rates of resistance to ciprofloxacin (P< 0.001), ampicillin (P = 0.035), and tetracycline (P = 0.01) increased significantly among strains isolated from humans. Furthermore, among human C. coli strains the rate of resistance to erythromycin rose from 7.1% in 1991 to 29.4% in 2001-2002. In comparison, Campylobacter sp. isolates from poultry already had high rates of resistance in 1991. Different rates of resistance to tetracycline among isolates from chickens and turkeys suggested the development of resistance during antimicrobial treatment in food animals. Thus, discrepancies in the antimicrobial resistance rates among Campylobacter isolates originating from poultry and humans support the hypothesis that at least some of the resistant Campylobacter strains causing infection in humans come from sources other than poultry products.

scholarly journals Bacterial Resistance to Antimicrobial Agents

Antibiotics ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 593
Author(s):  
Manuel F. Varela ◽  
Jerusha Stephen ◽  
Manjusha Lekshmi ◽  
Manisha Ojha ◽  
Nicholas Wenzel ◽  
...  
Keyword(s):  
Antimicrobial Resistance ◽  
Drug Targets ◽  
Bacterial Resistance ◽  
Antimicrobial Agents ◽  
Health Sector ◽  
Multidrug Resistant ◽  
Resistance Mechanisms ◽  
Resistant Bacteria ◽  
Cellular Mechanisms ◽  
Causative Agents

Bacterial pathogens as causative agents of infection constitute an alarming concern in the public health sector. In particular, bacteria with resistance to multiple antimicrobial agents can confound chemotherapeutic efficacy towards infectious diseases. Multidrug-resistant bacteria harbor various molecular and cellular mechanisms for antimicrobial resistance. These antimicrobial resistance mechanisms include active antimicrobial efflux, reduced drug entry into cells of pathogens, enzymatic metabolism of antimicrobial agents to inactive products, biofilm formation, altered drug targets, and protection of antimicrobial targets. These microbial systems represent suitable focuses for investigation to establish the means for their circumvention and to reestablish therapeutic effectiveness. This review briefly summarizes the various antimicrobial resistance mechanisms that are harbored within infectious bacteria.

scholarly journals Mechanisms of Antimicrobial Resistance in ESKAPE Pathogens

2016 ◽  
Vol 2016 ◽  
pp. 1-8 ◽  
Author(s):  
Sirijan Santajit ◽  
Nitaya Indrawattana
Keyword(s):  
Public Health ◽  
Antimicrobial Resistance ◽  
Antimicrobial Agents ◽  
Multidrug Resistant ◽  
Resistance Mechanisms ◽  
Global Public Health ◽  
Drug Usage ◽  
Inappropriate Use ◽  
Public Health Challenges ◽  
Eskape Pathogens

The ESKAPE pathogens (Enterococcus faecium,Staphylococcus aureus,Klebsiella pneumoniae,Acinetobacter baumannii,Pseudomonas aeruginosa, andEnterobacterspecies) are the leading cause of nosocomial infections throughout the world. Most of them are multidrug resistant isolates, which is one of the greatest challenges in clinical practice. Multidrug resistance is amongst the top three threats to global public health and is usually caused by excessive drug usage or prescription, inappropriate use of antimicrobials, and substandard pharmaceuticals. Understanding the resistance mechanisms of these bacteria is crucial for the development of novel antimicrobial agents or other alternative tools to combat these public health challenges. Greater mechanistic understanding would also aid in the prediction of underlying or even unknown mechanisms of resistance, which could be applied to other emerging multidrug resistant pathogens. In this review, we summarize the known antimicrobial resistance mechanisms of ESKAPE pathogens.

Antimicrobial Resistance and Association with Class 1 Integrons in Escherichia coli Isolated from Turkey Meat Products

2008 ◽  
Vol 71 (8) ◽  
pp. 1679-1684 ◽  
Author(s):  
M. L. KHAITSA ◽  
J. OLOYA ◽  
D. DOETKOTT ◽  
R. KEGODE
Keyword(s):  
Escherichia Coli ◽  
Antimicrobial Resistance ◽  
Antimicrobial Agents ◽  
Population Attributable Fraction ◽  
Meat Products ◽  
Resistance Mechanisms ◽  
E Coli ◽  
Class 1 Integrons ◽  
Turkey Meat ◽  
Class 1

The objective of this study was to quantify the role of class 1 integrons in antimicrobial resistance in Escherichia coli isolated from turkey meat products purchased from retail outlets in the Midwestern United States. Of 242 E. coli isolates, 41.3% (102 of 242) tested positive for class 1 integrons. A significant association was shown between presence of class 1 integrons in E. coli isolates and the resistance to tetracycline, ampicillin, streptomycin, gentamicin, sulfisoxazole, and trimethoprim-sulfamethoxazole. Attributable risk analysis revealed that for every 100 E. coli isolates carrying class 1 integrons, resistance was demonstrated for ampicillin (22%), gentamycin (48%), streptomycin (29%), sulfisoxazole (40%), trimethoprimsulfamethoxazole (7%), and tetracycline (26%). Non–integron-related antimicrobial resistance was demonstrated for ampicillin (65%), gentamycin (16.9%), streptomycin (42.1%), sulfisoxazole (35.8%), and tetracycline (49.7%). Population-attributable fraction analysis showed that class 1 integrons accounted for the following resistances: gentamycin, 71% (50 of 71), amoxicillin–clavulanic acid, 19.6% (6 of 33), nalidixic acid, 34% (7 of 21), streptomycin, 28% (30 of 107), sulfisoxazole, 38% (40 of 106), and tetracycline, 14%, (26 of 185). In conclusion, although class 1 integrons have been implicated in resistance to antimicrobial agents, other non–integron resistance mechanisms seem to play an important part.

scholarly journals Struggle To Survive: the Choir of Target Alteration, Hydrolyzing Enzyme, and Plasmid Expression as a Novel Aztreonam-Avibactam Resistance Mechanism

mSystems ◽  
2020 ◽  
Vol 5 (6) ◽  
Author(s):  
Ke Ma ◽  
Yu Feng ◽  
Alan McNally ◽  
Zhiyong Zong
Keyword(s):  
Antimicrobial Resistance ◽  
Antisense Rna ◽  
Antimicrobial Agents ◽  
Binding Protein ◽  
Resistance Mechanism ◽  
Resistance Mechanisms ◽  
Penicillin Binding Protein ◽  
Plasmid Copy ◽  
Copy Numbers

ABSTRACT Aztreonam-avibactam is a promising antimicrobial combination against multidrug-resistant organisms, such as carbapenemase-producing Enterobacterales. Resistance to aztreonam-avibactam has been found, but the resistance mechanism remains poorly studied. We recovered three Escherichia coli isolates of an almost identical genome but exhibiting varied aztreonam-avibactam resistance. The isolates carried a cephalosporinase gene, blaCMY-42, on IncIγ plasmids with a single-nucleotide variation in an antisense RNA-encoding gene, inc, of the replicon. The isolates also had four extra amino acids (YRIK) in penicillin-binding protein 3 (PBP3) due to a duplication of a 12-nucleotide (TATCGAATTAAC) stretch in pbp3. By cloning and plasmid-curing experiments, we found that elevated CMY-42 cephalosporinase production or amino acid insertions in PBP3 alone mediated slightly reduced susceptibility to aztreonam-avibactam, but their combination conferred aztreonam-avibactam resistance. We show that the elevated CMY-42 production results from increased plasmid copy numbers due to mutations in inc. We also verified the findings using in vitro mutation assays, in which aztreonam-avibactam-resistant mutants also had mutations in inc and elevated CMY-42 production compared with the parental strain. This choir of target modification, hydrolyzing enzyme, and plasmid expression represents a novel, coordinated, complex antimicrobial resistance mechanism and also reflects the struggle of bacteria to survive under selection pressure imposed by antimicrobial agents. IMPORTANCE Carbapenemase-producing Enterobacterales (CPE) is a serious global challenge with limited therapeutic options. Aztreonam-avibactam is a promising antimicrobial combination with activity against CPE producing serine-based carbapenemases and metallo-β-lactamases and has the potential to be a major option for combatting CPE. Aztreonam-avibactam resistance has been found, but resistance mechanisms remain largely unknown. Understanding resistance mechanisms is essential for optimizing treatment and developing alternative therapies. Here, we found that either penicillin-binding protein 3 modification or the elevated expression of cephalosporinase CMY-42 due to increased plasmid copy numbers does not confer resistance to aztreonam-avibactam, but their combination does. We demonstrate that increased plasmid copy numbers result from mutations in antisense RNA-encoding inc of the IncIγ replicon. The findings reveal that antimicrobial resistance may be due to concerted combinatorial effects of target alteration, hydrolyzing enzyme, and plasmid expression and also highlight that resistance to any antimicrobial combination will inevitably emerge.

scholarly journals Development and Persistence of Antimicrobial Resistance in Pseudomonas aeruginosa: a Longitudinal Observation in Mechanically Ventilated Patients

2007 ◽  
Vol 51 (4) ◽  
pp. 1341-1350 ◽  
Author(s):  
Anita Reinhardt ◽  
Thilo Köhler ◽  
Paul Wood ◽  
Peter Rohner ◽  
Jean-Luc Dumas ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Antimicrobial Resistance ◽  
Selective Pressure ◽  
Resistance Mechanism ◽  
Resistance Mechanisms ◽  
Antimicrobial Treatment ◽  
Aminoglycoside Resistance ◽  
Prolonged Intubation ◽  
Treatment Regimens ◽  
Underlying Mechanisms

ABSTRACT Intubated patients frequently become colonized by Pseudomonas aeruginosa, which is subsequently responsible for ventilator-associated pneumonia. This pathogen readily acquires resistance against available antimicrobials. Depending on the resistance mechanism selected for, resistance might either be lost or persist after removal of the selective pressure. We investigated the rapidity of selection, as well as the persistence, of antimicrobial resistance and determined the underlying mechanisms. We selected 109 prospectively collected P. aeruginosa tracheal isolates from two patients based on their prolonged intubation and colonization periods, during which they had received carbapenem, fluoroquinolone (FQ), or combined β-lactam-aminoglycoside therapies. We determined antimicrobial resistance phenotypes by susceptibility testing and used quantitative real-time PCR to measure the expression of resistance determinants. Within 10 days after the initiation of therapy, all treatment regimens selected resistant isolates. Resistance to β-lactam and FQ was correlated with ampC and mexC gene expression levels, respectively, whereas imipenem resistance was attributable to decreased oprD expression. Combined β-lactam-aminoglycoside resistance was associated with the appearance of small-colony variants. Imipenem and FQ resistance persisted for prolonged times once the selecting antimicrobial treatment had been discontinued. In contrast, resistance to β-lactams disappeared rapidly after removal of the selective pressure, to reappear promptly upon renewed exposure. Our results suggest that resistant P. aeruginosa is selected in less than 10 days independently of the antimicrobial class. Different resistance mechanisms lead to the loss or persistence of resistance after the removal of the selecting agent. Even if resistant isolates are not evident upon culture, they may persist in the lung and can be rapidly reselected.

scholarly journals Efflux Pump Mediated Antimicrobial Resistance by Staphylococci in Health-Related Environments: Challenges and the Quest for Inhibition

Antibiotics ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 1502
Author(s):  
Abolfazl Dashtbani-Roozbehani ◽  
Melissa H. Brown
Keyword(s):  
Antimicrobial Resistance ◽  
Antimicrobial Agents ◽  
Efflux Pump ◽  
Current Knowledge ◽  
Efflux Pumps ◽  
Multidrug Resistant ◽  
Resistance Mechanisms ◽  
Multidrug Efflux Pump ◽  
New Antibiotics ◽  
Efflux Pump Inhibitors

The increasing emergence of antimicrobial resistance in staphylococcal bacteria is a major health threat worldwide due to significant morbidity and mortality resulting from their associated hospital- or community-acquired infections. Dramatic decrease in the discovery of new antibiotics from the pharmaceutical industry coupled with increased use of sanitisers and disinfectants due to the ongoing COVID-19 pandemic can further aggravate the problem of antimicrobial resistance. Staphylococci utilise multiple mechanisms to circumvent the effects of antimicrobials. One of these resistance mechanisms is the export of antimicrobial agents through the activity of membrane-embedded multidrug efflux pump proteins. The use of efflux pump inhibitors in combination with currently approved antimicrobials is a promising strategy to potentiate their clinical efficacy against resistant strains of staphylococci, and simultaneously reduce the selection of resistant mutants. This review presents an overview of the current knowledge of staphylococcal efflux pumps, discusses their clinical impact, and summarises compounds found in the last decade from plant and synthetic origin that have the potential to be used as adjuvants to antibiotic therapy against multidrug resistant staphylococci. Critically, future high-resolution structures of staphylococcal efflux pumps could aid in design and development of safer, more target-specific and highly potent efflux pump inhibitors to progress into clinical use.

scholarly journals Molecular Characteristics and Antimicrobial Susceptibility Profile of Pseudomonas aeruginosa isolated from patients attending Healthcare Facilities in Mthatha, South Africa

2020 ◽  
Author(s):  
Mojisola C. Hosu ◽  
Sandeep D. Vasaikar ◽  
Grace E. Okuthe ◽  
teke apalata
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Antibiotic Resistance ◽  
Antimicrobial Resistance ◽  
Antimicrobial Agents ◽  
Resistance Mechanisms ◽  
High Rate ◽  
Infection Prevention And Control ◽  
Molecular Characteristics ◽  
Mortality And Morbidity ◽  
Resistance Patterns

Abstract Background: Pseudomonas aeruginosa is a common pathogen causing healthcare-associated infections most especially in critically ill and immunocompromised patients. This pathogen poses a public health threat due to its innate resistance to many antimicrobial agents and its ability to acquire new resistance mechanisms under pressure. Infections with Extended spectrum β-lactamases (ESBL)‑producing isolates result into outbreaks that lead to serious antibiotic management concerns with higher mortality and morbidity and significant economic causatives. In this study, we evaluated the antimicrobial resistance patterns and characterized genetically the ESBLs and Metallo- β-lactamases (MBL) produced by this pathogen. Methods: Isolates of P. aeruginosa cultured from patients who attended Nelson Mandela Academic Hospital and other clinics in the four district municipalities of the Eastern Cape between August 2017 and May 2019 were identified; and their antibiotic resistance patterns were tested against amikacin, aztreonam, cefepime, ceftazidime, ciprofloxacin, doripenem, gentamicin, imipenem, levofloxacin, meropenem, piperacillin, piperacillin/tazobactam and tobramycin using the bioMérieux VITEK® 2 and confirmed by Beckman autoSCAN-4 System. Real-time PCR was done using Roche Light Cycler 2.0 to detect the presence of ESBLs; blaSHV, blaTEM and blaCTX-M genes; and MBLs; blaIMP, blaVIM. Results: High antibiotic resistance in decreasing order was observed in piperacillin (64.2%), aztreonam (57.8%), cefepime (51.5%), ceftazidime (51.0%), piperacillin/tazobactam (50.5%), and imipenem (46.6%). A total of 75 (36.8%) multidrug resistant (MDR) isolates were observed of the total pool of isolates. The blaTEM, blaSHV and blaCTX-M was detected in 79.3%, 69.5% and 31.7% isolates (n=82), respectively. The blaIMP was detected in 1.25% while no blaVIM was detected in any of the isolates tested. Conclusions: The study showed a high rate of MDR P. aeruginosa in our setting. The vast majority of these resistant isolates carried blaTEM and blaSHV genes. Continuous monitoring of antimicrobial resistance and strict compliance towards infection prevention and control practices are the best defence against spread of MDR P. aeruginosa.

Prevalence and Antimicrobial Resistance in Campylobacter spp. Isolated from Retail Chicken in Two Health Units in Ontario

2010 ◽  
Vol 73 (7) ◽  
pp. 1317-1324 ◽  
Author(s):  
ANNE DECKERT ◽  
ALFONSO VALDIVIESO-GARCIA ◽  
RICHARD REID-SMITH ◽  
SUSAN TAMBLYN ◽  
PATRICK SELISKE ◽  
...  
Keyword(s):  
Antimicrobial Resistance ◽  
Campylobacter Jejuni ◽  
Antimicrobial Agents ◽  
Resistance Pattern ◽  
Campylobacter Coli ◽  
Multidisciplinary Study ◽  
Amoxicillin Clavulanic Acid ◽  
Campylobacter Lari ◽  
Human Campylobacteriosis ◽  
Campylobacter Spp

Campylobacter is an important enteric pathogen of humans and can cause diarrhea, fever, and abdominal pain. Campylobacter infections have frequently been associated with the handling and consumption of raw and undercooked poultry. Antimicrobial resistance among Campylobacter strains is of concern in the treatment of campylobacteriosis in vulnerable populations. A 2-year multidisciplinary study was conducted in the Perth and Wellington-Dufferin-Guelph public health units in Ontario, Canada, to investigate the prevalence and antimicrobial resistance of Campylobacter spp. in retail chicken. Retail chicken samples were collected from randomly selected stores in these health units. Resulting Campylobacter isolates were tested for susceptibility to amoxicillin–clavulanic acid (AMC), ampicillin (AMP), chloramphenicol (CHL), ciprofloxacin (CIP), clindamycin (CLI), erythromycin (ERY), gentamicin (GEN), nalidixic acid (NAL), tetracycline (TCY), and trimethoprimsulfamethoxazole (SXT) using the E test. The prevalence of Campylobacter in 1,256 retail chicken samples was 59.6%. Of these positive samples, 9% contained Campylobacter coli, 1% contained Campylobacter lari, and 90% contained Campylobacter jejuni. Of the chicken isolates that were resistant to one or more antimicrobial agents, 301 isolates (40%) were resistant to one agent, 374 (50%) were resistant to two, 39 (5%) were resistant to three, 20 (3%) were resistant to four, and 6 (1%) were resistant to five. Nine isolates (1%) were susceptible to all antimicrobial agents tested. All isolates were susceptible to AMC, CHL, and GEN. Less than 10% of isolates were resistant to NAL, CIP, CLI, ERY, and AMP. Resistance to TCY was common (56%). No isolates had a resistance pattern that included all three antimicrobials important in the treatment of human campylobacteriosis (CIP, ERY, and TCY); however, 24 isolates (3.2%) were resistant to at least two of these antimicrobials.

scholarly journals Relationship between the severity of acne vulgaris and antimicrobial resistance of bacteria isolated from acne lesions in a hospital in Japan

2014 ◽  
Vol 63 (5) ◽  
pp. 721-728 ◽  
Author(s):  
Keisuke Nakase ◽  
Hidemasa Nakaminami ◽  
Yuko Takenaka ◽  
Nobukazu Hayashi ◽  
Makoto Kawashima ◽  
...  
Keyword(s):  
Antimicrobial Resistance ◽  
Antimicrobial Agents ◽  
Acne Vulgaris ◽  
Normal Skin ◽  
Resistance Mechanisms ◽  
University Hospital ◽  
23S Rrna ◽  
Rrna Gene ◽  
Severe Acne ◽  
23S Rrna Gene

Propionibacterium acnes and Staphylococcus epidermidis are normal skin inhabitants that are frequently isolated from lesions caused by acne, and these micro-organisms are considered to contribute to the inflammation of acne. In the present study, we examined the antimicrobial susceptibilities and resistance mechanisms of P. acnes and S. epidermidis isolated from patients with acne vulgaris in a university hospital in Japan from 2009 to 2010. Additionally, we analysed the relationship between the antimicrobial resistance of P. acnes and the severity of acne vulgaris. Some P. acnes strains (18.8 %; 13/69) were resistant to clindamycin. All strains had a mutation in the 23S rRNA gene, except for one strain that expressed erm(X) encoding a 23S rRNA methylase. Tetracycline-resistant P. acnes strains were found to represent 4.3 % (3/69) of the strains, and this resistance was caused by a mutation in the 16S rRNA gene. Furthermore, three strains with reduced susceptibility to nadifloxacin (MIC = 16 µg ml−1) were detected. When analysing the correlation between the antimicrobial resistance of P. acnes and S. epidermidis, more than 80 % of the patients who carried clindamycin-resistant P. acnes also carried clindamycin-resistant S. epidermidis. However, no epidemic strain that exhibited antimicrobial resistance was detected in the P. acnes strains when analysed by PFGE. Therefore, our results suggest that the antimicrobial resistance of P. acnes is closely related to antimicrobial therapy. Additionally, those P. acnes strains tended to be frequently found in severe acne patients rather than in mild acne patients. Consequently, the data support a relationship between using antimicrobial agents and the emergence of antimicrobial resistance.

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