Clonal spread of multidrug-resistant Acinetobacter baumannii in eastern Taiwan

Chang, Kai‐Chih; Lin, Ming-Chyuan; Lin, Ning; Wu, Wen-Jui; Kuo, Han-Yueh; Lin, Teng-Yi; Yang, Tsai-Lian; Chen, Yu-Chuan; Liou, Ming-Li

doi:10.1016/j.jmii.2011.09.019

Cited by 41 publications

(21 citation statements)

References 27 publications

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“…Colistin is a key component of combination therapies used to treat MDR A. baumannii infections (Cai et al, 2012). The rate of colistin resistance (10.4%) in MDR A. baumannii isolates is lower than that of rifampicin (47.8%) or tigecycline (45.5%) resistance (Chang et al, 2012). Similar results were reported in another study (Muthusamy et al, 2016).…”

Section: Prospective Treatment Optionsmentioning

confidence: 99%

Biology of Acinetobacter baumannii: Pathogenesis, Antibiotic Resistance Mechanisms, and Prospective Treatment Options

Lee

Park

et al. 2017

Front. Cell. Infect. Microbiol.

755

585

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Acinetobacter baumannii is undoubtedly one of the most successful pathogens responsible for hospital-acquired nosocomial infections in the modern healthcare system. Due to the prevalence of infections and outbreaks caused by multi-drug resistant A. baumannii, few antibiotics are effective for treating infections caused by this pathogen. To overcome this problem, knowledge of the pathogenesis and antibiotic resistance mechanisms of A. baumannii is important. In this review, we summarize current studies on the virulence factors that contribute to A. baumannii pathogenesis, including porins, capsular polysaccharides, lipopolysaccharides, phospholipases, outer membrane vesicles, metal acquisition systems, and protein secretion systems. Mechanisms of antibiotic resistance of this organism, including acquirement of β-lactamases, up-regulation of multidrug efflux pumps, modification of aminoglycosides, permeability defects, and alteration of target sites, are also discussed. Lastly, novel prospective treatment options for infections caused by multi-drug resistant A. baumannii are summarized.

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Section: Prospective Treatment Optionsmentioning

confidence: 99%

Biology of Acinetobacter baumannii: Pathogenesis, Antibiotic Resistance Mechanisms, and Prospective Treatment Options

Lee

Park

et al. 2017

Front. Cell. Infect. Microbiol.

755

585

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“…Similar to tetracyclines, tigecycline can reversibly bind to the 30 S subunit of the bacterial ribosome to prevent amino acid synthesis [8]. However, with the increasing application of tigecycline, resistant isolates have constantly been reported [9][10][11]. Currently, the resistance-nodulation-cell division (RND) family of efflux pumps, such as AdeABC, AdeFGH, and AdeIJK, are considered to be the primary tigecycline resistance mechanism in A. baumannii [12,13].…”

Section: Introductionmentioning

confidence: 99%

Tigecycline resistance in Acinetobacter baumannii mediated by frameshift mutation in plsC, encoding 1-acyl-sn-glycerol-3-phosphate acyltransferase

Liu

et al. 2014

Eur J Clin Microbiol Infect Dis

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Acinetobacter baumannii is an important pathogen of healthcare-associated infections and shows multidrug resistance. With the increasing application of tigecycline, isolates resistant to this antibiotic are of growing concern clinically. However, the definitive mechanism of tigecycline resistance remains unclear. To explore the mechanism of tigecycline resistance in A. baumannii, a tigecycline-resistant strain was obtained by increasing the concentration of the antimicrobial in liquid culture. Three mutations were identified by the whole genome comparison, including one synonymous substitution in a hypothetical protein and a frameshift mutation in plsC and omp38. The plsC gene was confirmed to cause decreased susceptibility to tigecycline by a complementation experiment and cellular membrane change was detected by flow cytometry. By measuring the relative growth rate, the fitness cost of plsC was estimated to be approximately 8 %. In conclusion, plsC was found to play an important role in tigecycline resistance in A. baumannii. The minor fitness cost of plsC indicates a high risk of the emergence and development of tigecycline resistance in A. baumannii.

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“…In Kuwait, colistin resistance was found to be 12% (Al-Sweih et al, 2011). In a study done by Chang et al (2012) 10.4% colistin resistance was found. In another study colistin resistance was found to be 7.1% (Rodriguez et al, 2010).…”

Section: Discussionmentioning

confidence: 96%

In-vitro efficacy of polymyxin B with rifampin, colistin and doxycycline against extensively drug resistant Acinetobacter baumannii

Hannan¹,

Muhammad²

2014

Afr. J. Microbiol. Res.

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Acinetobacter baumannii is an opportunistic Gram negative coccobacillus that can grow easily in moist as well as dry conditions. During the last decade, A. baumannii emerged as one of the most resistant opportunistic pathogens responsible for nosocomial infections including ventilator associated pneumonia. The bug remains an important and difficult to treat pathogen whose pan-drug resistant nature has created a serious challenge. This has restricted the choice of treatment modalities. Currently, it appears as if all the available antibiotics are failing against this pathogen while single antibiotic therapy is certainly not working anymore. Thus, there is a strong need, thus, to explore new regimens to combat this resistant organism. A wide range of various combinations of drugs should therefore be tested for their synergistic activity against this pathogen. This study was aimed to find some effective combinations against extensively drug resistant (XDR) A. baumannii by combining various antibacterials. The microdilution checkerboard titration method was used for this purpose and fractional inhibitory concentrations (FICs) were calculated. In-vitro synergy was found in polymyxin Bcolistin (n = 3; 15%) and polymyxin B-rifampin (n = 3; 15%) combinations. Only additive effect was noted with polymyxin B-doxycycline (n = 12; 60%), polymyxin B-rifampin (n = 11; 55%), and polymyxin Bcolistin (n = 13; 65%). However, antagonism was detected in the polymyxin B-rifampin combination in one of the 20 strains evaluated for the purpose. Polymyxin B in combination with rifampin and colistin may be exploited against XDR A. baumannii. Synergy between polymyxin B and colistin have been demonstrated in only 15% of strains, this fully warrants the testing of more combinations.

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Clonal spread of multidrug-resistant Acinetobacter baumannii in eastern Taiwan

Abstract: This study confirms the high prevalence of resistance to rifampicin and tigecycline in MDR A baumannii in the three hospitals that were studied, and the high proportion of identical strains that exist in eastern Taiwan.

Cited by 41 publications

References 27 publications

Biology of Acinetobacter baumannii: Pathogenesis, Antibiotic Resistance Mechanisms, and Prospective Treatment Options

Biology of Acinetobacter baumannii: Pathogenesis, Antibiotic Resistance Mechanisms, and Prospective Treatment Options

Tigecycline resistance in Acinetobacter baumannii mediated by frameshift mutation in plsC, encoding 1-acyl-sn-glycerol-3-phosphate acyltransferase

In-vitro efficacy of polymyxin B with rifampin, colistin and doxycycline against extensively drug resistant Acinetobacter baumannii

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