Diversity of amino acid substitutions in PmrCAB associated with colistin resistance in clinical isolates of Acinetobacter baumannii

This study aimed to investigate the mechanisms of colistin resistance in 64 Acinetobacter baumannii isolates obtained from patients with ventilator-associated pneumonia hospitalised in Greece, Italy and Spain. In total, 31 A. baumannii isolates were colistin-resistant. Several novel amino acid substitutions in PmrCAB were found in 27 colistin-resistant A. baumannii. Most substitutions were detected in PmrB, indicating the importance of the histidine kinase for colistin resistance. In two colistin-resistant isolates, 93 amino acid changes were observed in PmrCAB compared with A. baumannii ACICU, and homologous recombination across different clonal lineages was suggested. Analysis of gene expression revealed increased pmrC expression in isolates harbouring pmrCAB mutations. Complementation of A. baumannii ATCC 19606 and ATCC 17978 with a pmrAB variant revealed increased pmrC expression but unchanged colistin MICs, indicating additional unknown factors associated with colistin resistance. Moreover, a combination of PmrB and PmrC alterations was associated with very high colistin MICs, suggesting accumulation of mutations as the mechanism for high-level resistance. The pmrC homologue eptA was detected in 29 colistin-susceptible and 26 colistin-resistant isolates. ISAba1 was found upstream of eptA in eight colistin-susceptible and one colistin-resistant isolate and eptA was disrupted by ISAba125 in two colistin-resistant isolates. Whilst in most isolates an association of eptA with colistin resistance was excluded, in one isolate an amino acid substitution in EptA (R127L) combined with a point mutation in ISAba1 upstream of eptA contributed to elevated colistin MICs. This study helps to gain an insight into the diversity and complexity of colistin resistance in A. baumannii.     

Colistin/daptomycin: an unconventional antimicrobial combination synergistic in vitro against multidrug-resistant Acinetobacter baumannii

The in vitro activity of the combination colistin/daptomycin was evaluated against multidrug-resistant Acinetobacter baumannii clinical isolates. Clonal relationships were assessed by pulsed-field gel electrophoresis. The following synergy studies were undertaken: (i) daptomycin MICs were determined by E-test on Mueller–Hinton agar plates supplemented with a subinhibitory concentration of colistin; and (ii) time–kill methodology using tubes containing an inoculum of 5 × 10⁵ CFU/mL and subinhibitory concentrations of each antibiotic alone or in combination subcultured at 0, 5 and 24 h for colony counting. Synergy was defined as ≥2 log₁₀ CFU/mL decrease of viable colonies compared with colistin alone. Ten colistin-susceptible and four colistin-resistant A. baumannii isolates were tested. Isolates were assigned to nine different clonal types. Enhanced in vitro activity of the combination was detected only against colistin-susceptible isolates; using plates supplemented with colistin, the daptomycin MIC was reduced by 4- to 128-fold. From a total of 30 isolate–concentration combinations in time–kill studies, a synergistic interaction was detected in 16 (53.3%). The combination exhibited synergy against 8 and 12 of these combinations at 5 h and 24 h, respectively. No antagonism was detected. Colistin alone was bactericidal against two colistin-susceptible isolates at 24 h, whereas the combination was bactericidal against 9 colistin-susceptible isolates at 24 h. Against all colistin-resistant isolates, the combination exhibited a static effect and indifference in time–kill studies. Potent in vitro synergistic interactions between colistin and daptomycin provide evidence that this unorthodox combination may be beneficial in the treatment of colistin-susceptible multidrug-resistant A. baumannii.     

Release of large amounts of lipopolysaccharides from Pseudomonas aeruginosa cells reduces their susceptibility to colistin

Pseudomonas aeruginosa is an important etiological agent of opportunistic infections. Injectable colistin is available as a last-line treatment option for multidrug-resistant P. aeruginosa infections. When cells were inoculated at a high number, colistin-susceptible P. aeruginosa grew on agar medium containing colistin at a concentration 10-fold higher than the minimum inhibitory concentration without acquiring colistin resistance. This study examined the responsible mechanism for growth in the presence of a high concentration of colistin. Cell wash fluid derived from P. aeruginosa efficiently reduced colistin antimicrobial activity. This reduction was mediated by lipopolysaccharide (LPS) in the wash fluid. Extracellular LPS inhibited colistin activity more effectively than cell-bound LPS in fixed cells. Cell wash fluids from Escherichia coli and Acinetobacter baumannii also reduced colistin activity; however, they were less potent than those from P. aeruginosa. The amount of LPS in cell wash fluid from P. aeruginosa was approximately 10-fold higher than that in fluid from E. coli or A. baumannii. In conclusion, cell-free LPS derived from bacterial cells inhibited the antimicrobial activity of colistin, and this effect was greatest for P. aeruginosa. Thus, large amounts of broken and dead cells of P. aeruginosa at infection foci will reduce the effectiveness of colistin, even against cells that have not yet acquired resistance.     

Multicentre study of risk factors for mortality in patients with Acinetobacter bacteraemia receiving colistin treatment

Colistin remains a last-line antibiotic for the treatment of infections by multidrug-resistant Acinetobacter species. However, mortality rates are high in patients with Acinetobacter infection receiving colistin treatment. This multicentre study evaluated whether colistin susceptibility, additional antimicrobial agents or other prognostic factors influenced the clinical outcomes of patients receiving colistin treatment for Acinetobacter bacteraemia. This retrospective study enrolled 122 adults receiving colistin for monomicrobial Acinetobacter bacteraemia at six medical centres in the ACTION Study Group over an 8-year period. Clinical information, antimicrobial susceptibility and colistin resistance determinants were analysed. The primary outcome measure was 14-day mortality. Among 122 patients, 18 and 104 were infected with colistin-resistant (ColR) isolates [minimum inhibitory concentration (MIC) ≥4 mg/L] and colistin-susceptible (ColS) isolates (MIC ≤2 mg/L), respectively. Patients infected with ColR and ColS isolates did not differ significantly with regard to Charlson comorbidity index, invasive procedures, sources of bacteraemia, disease severity and 14-day mortality rate (44.4% vs. 34.6%; P = 0.592). No specific additional antimicrobial agent was independently associated with higher or lower mortality. Coronary artery disease, higher Acute Physiology and Chronic Health Evaluation (APACHE) II score and bacteraemia caused Acinetobacter baumannii were independent risk factors associated with 14-day mortality. Mechanisms of colistin resistance were associated with amino acid variants in the pmrCAB operon. Finally, previously unreported Acinetobacter nosocomialis amino acid variants related to colistin resistance were identified. In conclusion, colistin susceptibility and colistin combination antimicrobial treatment were not associated with decreased 14-day mortality in patients with Acinetobacter bacteraemia receiving colistin treatment.     

2018—2019年西安交通大学第二附属医院鲍曼不动杆菌的分布及耐药性分析

目的 分析西安交通大学第二附属医院鲍曼不动杆菌的临床分布及耐药性,为临床医师选择合理的抗感染治疗方案提供参考依据。方法 以2018年1月-2019年12月西安交通大学第二附属医院住院的患者为研究对象,按照美国临床实验室标准化委员会（CLSI）推荐的方法进行鲍曼不动杆菌的初步筛选,用梅里埃VITEK 2 Compact全自动细菌鉴定及药敏分析系统进行细菌鉴定和药敏实验,用Excel进行数据统计分析。结果 2018-2019年本院住院患者中共分离出935株鲍曼不动杆菌,主要分布于急诊科,共181株;主要来源于痰液标本,共676株。感染人群主要为14岁以上的中青年及老年患者。药敏结果显示鲍曼不动杆菌对替卡西林/克拉维酸、多西环素、哌拉西林/他唑巴坦具有较高的耐药性,耐药率依次为87.43%、75.96%、64.98%;鲍曼不动杆菌对黏菌素、阿米卡星和替加环素具有良好的敏感性,敏感率依次为99.61%、85.02%、73.56%。结论 本院临床上鲍曼不动杆菌感染的高发人群为14岁以上的中青年及老年患者,鲍曼不动杆菌对多种抗生素都有很强的耐药性,应加强病原菌培养及耐药性监测,指导临床医师合理使用抗生素。     

Enhanced bacterial killing with colistin/sulbactam combination against carbapenem-resistant Acinetobacter baumannii

Aims: Polymyxin-based combination therapy is often used to treat carbapenem-resistant Acinetobacter baumannii (A. baumannii) infections. Although sulbactam is intrinsically active against A. baumannii, few studies have investigated colistin/sulbactam combinations against carbapenem-resistant A. baumannii.Methods: Whole genome sequencing was undertaken on eight carbapenem-resistant (colistin-susceptible) isolates of A. baumannii from Chinese patients. Bacterial killing of colistin and sulbactam, alone and in combination, was examined with checkerboard (all isolates) and static and dynamic time-kill studies (three isolates). In the dynamic studies, antibiotics were administered in various clinically-relevant dosing regimens that mimicked patient pharmacokinetics.Results: The eight isolates consisted of ST195, ST191 and ST208 belonging to clonal complex 208, which is the most epidemic clonal type of A. baumannii globally. All isolates possessed Acinetobacter-derived cephalosporinase (ADC-61 or ADC-78) and seven of eight isolates contained the carbapenem-resistance gene bla_OXA-23. The colistin/sulbactam combination was synergistic against two of eight isolates in checkerboard studies. In time-kill studies, rapid bacterial killing of ca. 3–6 log₁₀ CFU/mL was observed with colistin monotherapy, followed by steady regrowth. Sulbactam monotherapy was generally ineffective. Substantially enhanced bacterial killing was observed with colistin/sulbactam combinations in both static and dynamic models, especially with the higher sulbactam concentration (2 g) and/or longer sulbactam infusion time (2 hours) in the dynamic model.Conclusions: This study was the first to use a pharmacokinetics/pharmacodynamics model to investigate synergistic activity of colistin/sulbactam combinations against A. baumannii. It showed that clinically-relevant dosing regimens of colistin combined with sulbactam may substantially improve bacterial killing of multidrug-resistant and carbapenem-resistant A. baumannii.     

Correlation between overexpression and amino acid substitution of the PmrAB locus and colistin resistance in Acinetobacter baumannii

Relationships between the PmrAB two-component system and colistin resistance were investigated in Acinetobacter baumannii. The sequences of pmrA, pmrB and pmrC in 26 colistin-susceptible (ColS) and 7 colistin-resistant (ColR) A. baumannii isolates were determined. In addition, 30 ColR mutants (colistin minimum inhibitory concentration >64 mg/L) were selected in vitro from 10 ColS strains and the pmrA, pmrB and pmrC sequences of the in-vitro-selected ColR mutants were also determined. Expression of pmrA and pmrB was compared between the ColR mutants and their parent ColS strains using a quantitative real-time polymerase chain reaction method. Elevated expression of pmrA and pmrB genes was evident both in wild-type and in in-vitro-selected ColR strains. However, no amino acid differences in the pmrA, pmrB and pmrC genes were found between wild-type ColR and ColS isolates. Although six kinds of amino acid alterations in pmrB were identified in in-vitro-selected ColR mutants, no changes were found in some of the mutants. These findings indicate that increased expression of the PmrAB system is essential for colistin resistance in A. baumannii but that amino acid alterations might be only partially responsible for resistance.     

Silent transmission of an IS1294b-deactivated mcr-1 gene with inducible colistin resistance

Global dissemination of the mobile colistin resistance mcr-1 is of particular concern as colistin is one of the last-resort antibiotics for the treatment of severe infections caused by carbapenem-resistant Gram-negative bacteria. In this study, an inactive form of mcr-1 in a fluoroquinolone-resistant and colistin-susceptible uropathogenic Escherichia coli isolate (ECO3347) was characterised. The mcr-1 gene was deactivated by insertion of a 1.7-kb IS1294b element flanked by two tetramers (GTTC) and located on a 62-kb pHNSHP45-like plasmid (p3347-mcr-1). Single-step and multistep selections were used to induce colistin resistance in vitro in ECO3347. ECO3347 acquired colistin resistance (MIC?=?16–32?mg/L) only after a serial passage selection with increasing concentrations of colistin (2–8?mg/L). Deactivated mcr-1 was re-activated by loss of IS1294b without any remnants in most colistin-resistant mutants. In addition, a novel amino acid variant (Leu105Pro) in the CheY homologous receiver domain of PmrA was detected in one colistin-resistant mutant. Plasmid p3347-mcr-1⁺ carrying the re-activated mcr-1 gene is transferrable to E. coli J53 recipient with a high conjugation rate (ca. 10^–1 cells per recipient cell). Transconjugants showed an identical growth status to J53, suggesting lack of a fitness cost after acquiring p3347-mcr-1⁺. These results highlight that the disrupted mcr-1 gene has the potential for wide silent dissemination with the help of pHNSHP45-like epidemic plasmids. Inducible colistin resistance may likely compromise the success of clinical treatment and infection control. Continuous monitoring of mcr-1 is imperative for understanding and tackling its dissemination in different forms.     

Contributions of insertion sequences conferring colistin resistance in Klebsiella pneumoniae

BackgroundIncreasing colistin consumption is leading to expanding colistin resistance in Klebsiella pneumoniae worldwide, but particularly in Asia. Epidemiological studies indicate a link between specific insertion sequences (ISs) and colistin resistance; however, proof of a colistin-IS correlation is lacking.ObjectivesColistin-resistant mechanisms, and in vitro and in vivo efficacies of colistin against K. pneumoniae with ISs were investigated.MethodsColistin-resistant genes, including mcr-1 gene, were detected in 49 colistin- and carbapenem-resistant K. pneumoniae isolates. crrCAB genetic environments were analysed using whole-genome sequencing and polymerase chain reaction (PCR) mapping. Identified ISs were cloned into pRK415 vectors and investigated for potential contributions to colistin resistance. A Caenorhabditis elegans model was employed for in vivo analysis.ResultsmgrB gene alterations (32/49, 65.3%) were identified as the major colistin-resistant mechanism, followed by variations in crrB (57.1%), pmrB (32.7%), phoQ (20.9%), pmrA (16.3%) and phoP (8.2%) genes. Furthermore, 21 of the 49 tested isolates (42.9%) contained the IS elements, ISKpn26, ISEcp1, IS10R, IS903B or ISKpn14 in mgrB or in the surrounding region of crrCAB, indicating an association between these ISs and colistin resistance. The frequencies of colistin resistance significantly increased in colistin-susceptible K. pneumoniae laboratory strains, with plasmids carrying different ISs from clinical strains. In vivo analysis revealed that K. pneumoniae harboring ISKpn26 was associated with decreased lifespan during colistin treatment, leading to an increased risk for colistin treatment failure.ConclusionsThese findings indicate a correlation between diverse ISs and colistin resistance in K. pneumoniae and confirm a role for ISs in colistin treatment.     

Efficacy of six frog skin-derived antimicrobial peptides against colistin-resistant strains of the Acinetobacter baumannii group

The emergence of Acinetobacter sp. strains resistant to all antibacterial agents including colistin necessitates the development of new types of antimicrobial agents. Six cationic α-helical frog skin-derived peptides (CPF-AM1, PGLa-AM1, B2RP-ERa, [E4K]alyteserin-1c, [D4K]B2RP and [G4K]XT-7) were selected for this study on the basis of potent growth-inhibitory activity against Gram-negative bacteria and low haemolytic activity against human erythrocytes. All peptides were active against a range of colistin-susceptible [minimum inhibitory concentration (MIC)≤2 μg/mL] and colistin-resistant (MIC≥64 μg/mL) clinical isolates of multidrug-resistant strains of Acinetobacter baumannii and Acinetobacter nosocomialis. The most potent peptides against the colistin-resistant strains were [D4K]B2RP and [E4K]alyteserin-1c (MIC=4-16 μg/mL for both). The MIC values of these peptides against the colistin-susceptible strains were in the same range. The frog peptides show potential for development into drugs to treat infections caused by pandrug-resistant Gram-negative pathogens.     

2015—2020年兰州大学第一医院血流感染中鲍曼不动杆菌流行特征、耐药性及其感染危险因素分析

目的 分析2015—2020年兰州大学第一医院血流感染中鲍曼不动杆菌的临床分布特征、抗菌药物耐药性变迁及感染的危险因素,为医院感染的控制和临床合理治疗提供参考。方法 对2015—2020年兰州大学第一医院住院感染患者血培养阳性标本中分离出的鲍曼不动杆菌菌株的科室分布、抗菌药物耐药性特点及危险因素进行分析。结果 2015—2020年兰州大学第一医院住院感染患者血培养阳性标本中共分离到104株鲍曼不动杆菌,主要来源于重症监护病房（ICU）、老年病科、血液科。鲍曼不动杆菌对多种抗菌药物的耐药率超过90%以上。基础疾病、入住ICU、侵袭性操作及使用抗生素成为影响鲍曼不动杆菌血流感染的危险因素。结论 血流感染中分离的鲍曼不动杆菌对常见抗菌药物普遍耐药,应加强医院感染控制,防止耐药菌播散性。     

Characterisation of successive Acinetobacter baumannii isolates from a deceased haemophagocytic lymphohistiocytosis patient

In this study, 38 Acinetobacter baumannii isolates successively isolated from blood, skin swabs and tracheal aspirates from a single patient who died from haemophagocytic lymphohistiocytosis were investigated. The isolates were collected between March 2012 and August 2012. A. baumannii genotypes were determined by multilocus sequence typing (MLST) and pulsed-field gel electrophoresis (PFGE). In vitro antimicrobial susceptibility testing was performed and colistin heteroresistance and persistence were evaluated. The structure of AbaR resistance islands was explored, and serum sensitivity was determined. Based on MLST analysis, all 38 A. baumannii isolates showed the same sequence type (ST138). However, PFGE analysis showed that isolates from blood samples belonged to different genotypes depending on the isolation time: whilst blood isolates obtained at the early stages showed restriction patterns similar to those of isolates from other sources, isolates obtained at later stages exhibited a distinct pattern. All isolates were resistant to imipenem, cefepime, ciprofloxacin and piperacillin/tazobactam. Five isolates from tracheal aspirates and one from a skin swab were resistant to polymyxins, and two isolates from skin swabs and one from another source were non-susceptible to tigecycline. All colistin-susceptible isolates showed heteroresistance to colistin, and four were persisters. Isolates from blood showed higher survival rates against human serum than those from other sources. This study shows that the patient was infected with more than one A. baumannii strain. Heteroresistance, persistence or evasion of the innate immune response may explain the failure of antimicrobial treatments in this patient.     

In vitro pharmacokinetics/pharmacodynamics of continuous ceftazidime infusion alone and in combination with colistin against Pseudomonas aeruginosa biofilm

Objectives: The pharmacokinetics/pharmacodynamics of continuous infusion (CI) beta-lactams for Pseudomonas aeruginosa biofilm infections has not been defined. This study evaluated the efficacy of several dosage regimens of CI ceftazidime, with or without colistin, an antibiotic with a potential antibiofilm effect, against biofilm-embedded P. aeruginosa.Methods: Mature biofilms of the reference strain PAO1 and the clinical isolate HUB8 (both ceftazidime- and colistin-susceptible) were investigated over 54h using a dynamic CDC biofilm reactor. CI dosage regimens were ceftazidime monotherapy (4, 10, 20 and 40 mg/L), colistin monotherapy (3.50 mg/L), and combinations of colistin and ceftazidime (4 or 40 mg/L). Efficacy was evaluated by changes in log₁₀colony-forming units (cfu)/mL and confocal microscopy.Results: At 54 h, the antibiofilm activity of ceftazidime monotherapies was slightly higher for ceftazidime 20 mg/L (-2.84 log₁₀cfu/mL) and 40 mg/L (-3.05) against PAO1, but no differences were seen against HUB8. Ceftazidime-resistant colonies emerged with 4 mg/L regimens in both strains and with other regimens in PAO1. Colistin monotherapy had significant antibiofilm activity against HUB8 (-3.07), but lower activity against PAO1 (-1.12), and colistin-resistant strains emerged. Combinations of ceftazidime and colistin had higher antibiofilm activity at 54 h compared with each monotherapy, and prevented the emergence of resistance to both antibiotics; higher antibiofilm activity was observed with ceftazidime 40 mg/L plus colistin compared with ceftazidime 4 mg/L plus colistin (-4.19 vs. -3.10 PAO1; -4.71 vs. -3.44 HUB8).Conclusions: This study demonstrated that, with %T>MIC=100%, CI ceftazidime displayed concentration-dependent antibiofilm activity against P. aeruginosa biofilm, particularly in combination with colistin. These results support the use of high-dosage regimens of CI ceftazidime with colistin against biofilm-associated infections with ceftazidime-susceptible P. aeruginosa.     

Comprehensive proteomic and metabolomic profiling of mcr-1-mediated colistin resistance in Escherichia coli

Spread of the mcr-1 gene in human and veterinary medicine has jeopardised the use of polymyxins, last-resort antibiotics against life-threatening multidrug-resistant Gram-negative bacteria. As a lipid-modifying gene, whether mcr-1 causes proteomic and metabolomic changes in bacteria and affects the corresponding metabolic pathway is largely unknown. In this study, label-free quantitative proteomics and untargeted metabolomics were used to profile comprehensive proteome and metabolome characteristics of mcr-1-mediated colistin-resistant and -susceptible Escherichia coli in order to gain further insight into the colistin resistance mechanism. Large sets of differentially expressed proteins (DEPs) and metabolites were identified that contributed to mcr-1-mediated antimicrobial resistance, predominantly in different growth conditions with and without colistin. mcr-1 caused downregulated expression of most proteins in order to adapt to drug pressure. Pathway analysis showed that metabolic processes were significantly affected, mainly related to glycerophospholipid metabolism, thiamine metabolism and lipopolysaccharide (LPS) biosynthesis. The substrate phosphoethanolamine (PEA) for mcr-1 to mediate colistin resistance was accumulated in colistin-resistant E. coli. Notably, mcr-1 not only caused PEA modification of the bacterial cell membrane lipid A but also affected the biosynthesis and transport of lipoprotein in colistin resistance by disturbing the expression of efflux pump proteins involved in the cationic antimicrobial peptide (CAMP) resistance pathway. Overall, disturbed glycerophospholipid metabolism and LPS biosynthesis as well as accumulation of the substrate PEA was closely related with mcr-1-mediated colistin resistance. These findings could provide further valuable information to inhibit colistin resistance by blocking this metabolic process.     

Efficacy of ceftolozane/tazobactam,alone and in combination with colistin,against multidrug-resistant Pseudomonas aeruginosa in an in vitro biofilm pharmacodynamic model

Objectives

Ceftolozane/tazobactam is a potential tool for infections caused by multidrug-resistant (MDR) Pseudomonas aeruginosa (P. aeruginosa), but its efficacy against some difficult-to-treat infections has not been well defined.

Inactivation of mgrB gene regulator and resistance to colistin is becoming endemic in carbapenem-resistant Klebsiella pneumoniae in Greece: A nationwide study from 2014 to 2017

IntroductionIn Greece, the spread of carbapenem-resistant Enterobacteriaceae in humans has led to the reintroduction of colistin as a therapeutic agent. Unfortunately, colistin resistance with different mechanisms has emerged. The present work aims to determine the prevalence of carbapenem and colistin resistance and the corresponding mechanisms in Klebsiella pneumoniae clinical isolates from Greece.MethodsFrom 2014 to 2017, 288 carbapenem-resistant K. pneumoniae clinical strains were gathered from a collection of 973 isolates from eight different hospitals in Greece. Antibiotic susceptibility testing was performed using three different methods. Screening of carbapenem and colistin resistance genes was conducted using polymerase chain reaction (PCR) amplification and sequencing.ResultsAmong the 288 (29.6 %) carbapenem-resistant isolates, 213 (73.9%) were colistin-resistant (minimum inhibitory concentration [MIC] >2 mg/L). The KPC type was the most common carbapenemase gene (116; 40.3%), followed by VIM (41; 14.2%), NDM (33; 11.5%) and OXA-48 (22; 7.6%). Moreover, 44 (15.3%) strains co-produced two types of carbapenemases. No mcr genes were detected for colistin resistance but mutations in chromosomal genes were found. These included inactivation of the mgrB gene for 148 (69.5%) strains, including insertion sequences for 94 (44.1%), nonsense mutations for 4 (1.9%) and missense mutations for 24 (11.3%). Moreover, PCR amplification of mgrB gene was negative for 26 (12.2%) strains. Finally, 65 (30.5%) colistin-resistant strains exhibited a wild-type mgrB, the mechanisms of which remain to be elucidated.ConclusionThis study shows that K. pneumoniae clinical strains in Greece are resistant to both carbapenems and colistin and this is endemic and is likely chromosomally encoded.     

2009-2015年凉山州第二人民医院鲍曼不动杆菌的耐药性与抗菌药物用量的相关性分析

目的 对2009-2015年凉山州第二人民医院鲍曼不动杆菌的耐药性与抗菌药物用量的相关性进行分析,促进临床合理用药。方法 统计2009-2015年凉山州第二人民医院检验科鲍曼不动杆菌的分布及耐药性和抗菌药物的使用情况,并对鲍曼不动杆菌的耐药性与抗菌药物用量的相关性进行统计分析。结果 共分离出鲍曼不动杆菌2 719株,主要来源为痰液(75.62%),分离株数逐年增加。鲍曼不动杆菌对各类抗菌药物的耐药率均呈上升趋势,对左氧氟沙星耐药率的上升程度最大。对哌拉西林他唑巴坦、左氧氟沙星、替卡西林、头孢他啶、头孢吡肟的耐药率均接近50%。鲍曼不动杆菌对哌拉西林他唑巴坦、头孢他啶、头孢吡肟、左氧氟沙星和米诺环素的耐药率与左氧氟沙星的使用强度呈显著的正相关性。结论 合理使用抗菌药物对于降低鲍曼不动杆菌的耐药性具有重要意义,应根据药物半衰期和药敏试验制定恰当的给药方案。     

2012—2014年中山市陈星海医院鲍曼不动杆菌的分布及耐药性分析

目的研究中山市陈星海医院鲍曼不动杆菌的分布及耐药性,为合理用药提供参考。方法对2012—2014年中山市陈星海医院鲍曼不动杆菌的分布及耐药情况进行回顾性统计分析。结果共分离出461株鲍曼不动杆菌,其标本的主要来源为痰液,其次为分泌物和引流液。感染区分布主要为重症监护病房,其次为老年综合科和呼吸内科。鲍曼不动杆菌对头孢唑林、头孢替坦、磷霉素、厄他培南、美洛培南、氨苄西林、呋喃妥因、强力霉素的耐药性较强,对头孢哌酮/舒巴坦、阿米卡星和多黏菌素B的耐药性弱,而且鲍曼不动杆菌的耐药性逐年递增。结论鲍曼不动杆菌对多种抗菌药物具有较高的耐药性,应该加强其耐药性的监控,选择合适的药物进行治疗。对于感染的高危科室和高危部位,应重点防控。