First report of colistin resistance among carbapenem-resistant Acinetobacter baumannii isolates recovered from hospitalized patients in Egypt

Abdulzahra, Amani T.; Khalil, Mahmoud A F; Elkhatib, Walid F.

doi:10.1016/j.nmni.2018.08.007

Cited by 43 publications

(36 citation statements)

References 39 publications

(45 reference statements)

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“…A. baumannii is now regarded as one of the most difficult nosocomial-acquired pathogens to treat and control, characterized by a worryingly increasing rate of colistin resistance, observed worldwide [7,23,24]. In our study, we propose that the incidence of MDR A. baumannii is very high in Egypt.…”

Section: Discussionmentioning

confidence: 76%

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Acquisition of Colistin Resistance Links Cell Membrane Thickness Alteration with a Point Mutation in the lpxD Gene in Acinetobacter baumannii

et al. 2020

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Acinetobacter baumannii is one of the most common causes of nosocomial infections in intensive care units. Its ability to acquire diverse mechanisms of resistance limits the therapeutic choices for its treatment. This especially concerns colistin, which has been reused recently as a last-resort drug against A. baumannii. Here, we explored the impact of gaining colistin resistance on the susceptibility of A. baumannii to other antibiotics and linked colistin resistance acquisition to a gene mutation in A. baumannii. The susceptibility of 95 A. baumannii isolates revealed that 89 isolates were multi-drug resistance (MDR), and nine isolates were resistant to colistin. Subsequently, three isolates, i.e., MS48, MS50, and MS64, exhibited different resistance patterns when colistin resistance was induced and gained resistance to almost all tested antibiotics. Upon TEM examination, morphological alterations were reported for all induced isolates and a colistin-resistant clinical isolate (MS34Col-R) compared to the parental sensitive strains. Finally, genetic alterations in PmrB and LpxACD were assessed, and a point mutation in LpxD was identified in the MS64Col-R and MS34Col-R mutants, corresponding to Lys117Glu substitution in the lipid-binding domain. Our findings shed light on the implications of using colistin in the treatment of A. baumannii, especially at sub-minimum inhibitory concentrations concentrations, since cross-resistance to other classes of antibiotics may emerge, beside the rapid acquisition of resistance against colistin itself due to distinct genetic events.

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Section: Discussionmentioning

confidence: 76%

“…In our study, we propose that the incidence of MDR A. baumannii is very high in Egypt. However, Abdulzahra and his colleagues demonstrated that only two A. baumannii isolates were colistin-resistant [24].…”

Section: Discussionmentioning

confidence: 99%

Acquisition of Colistin Resistance Links Cell Membrane Thickness Alteration with a Point Mutation in the lpxD Gene in Acinetobacter baumannii

et al. 2020

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“…In a burn ward in Iran, 96.92% of clinical isolates of A. baumannii were shown to be resistant to meropenem and imipenem, with CRAB isolates carrying the oxacillinase determinants of bla OXA-23 accounting for 74.6%, suggesting that high-level CRAB with bla OXA-23 in burn patients is a reason for A. baumannii resistance to carbapenems [ 33 ]. Abdulzahra revealed that 80% of A. baumannii isolates carry bla OXA-23 , which implies that it is a crucial healthcare concern in Egypt that necessitates strict interventions to eliminate such infections [ 34 ]. Lowo et al collected 141 A. baumannii strains from two tertiary academic hospitals (A and B) in South Africa; the results showed that these clinical isolates carried the bla OXA-23 gene at a rate of 96% (69/72) in hospital A versus 91% (63/69) in hospital B, implying that greater infection control and prevention strategies need to be developed [ 35 ].…”

Section: Discussionmentioning

confidence: 99%

Rapid and accurate detection of carbapenem-resistance gene by isothermal amplification in Acinetobacter baumannii

et al. 2020

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Background Acinetobacter baumannii (A. baumannii) is one of the pivotal pathogens responsible for nosocomial infections, especially in patients with low immune response, and infection with carbapenem-resistant A. baumannii has been increasing in recent years. Rapid and accurate detection of carbapenem-resistance genes in A. baumannii could be of immense help to clinical staff. Methods In this study, a 15-μL reaction system for recombinase polymerase amplification (RPA) was developed and tested. We collected 30 clinical isolates of A. baumannii from the Burn Institute of Southwest Hospital of Third Military Medical University (Army Medical University) for 6 months and tested antibiotic susceptibility using the VITEK 2 system. A. baumannii was detected based on the blaOXA-51 gene by PCR, qPCR and 15 μL-RPA, respectively. Sensitivity and specificity were evaluated. In addition, PCR and 15 μL-RPA data for detecting the carbapenem-resistance gene blaOXA-23 were comparatively assessed. Results The detection limit of the blaOXA-51 gene by 15 μL RPA was 2.86 CFU/ml, with sensitivity comparable to PCR and qPCR. No positive amplification signals were detected in non-Acinetobacter isolates, indicating high specificity. However, only 18 minutes were needed for the 15 μL RPA assay. Furthermore, an antibiotic susceptibility test showed that up to 90% of A. baumannii strains were resistant to meropenem and imipenem; 15 μL RPA data for detecting blaOXA-23 showed that only 10% (n = 3) of A. baumannii isolates did not show positive amplification signals, and the other 90% of (n = 27) isolates were positive, corroborating PCR results. Conclusion We demonstrated that the new 15 μL RPA assay for detecting blaOXA-23 in A. baumannii is faster and simpler than qPCR and PCR. It is a promising alternative molecular diagnostic tool for rapid and effective detection of A. baumannii and drug-resistance genes in the field and point-of-care testing.

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“…In the present MDR strains, tigecycline was an effective therapeutic agent with a susceptibility level of >95%, being considerably greater than that estimated in various local studies (20–70%) [ 2 , 3 ]. Although half of the isolates were resistant to aminoglycoside, studies in our region have reported different levels of gentamicin and amikacin resistance (25–96%) [ 4 ], while increased aminoglycoside resistance has been reported in studies in China and Egypt [ 17 , 18 ]. Furthermore, very high fluoroquinolone resistance levels were observed in our isolates, concurrent with previous reports from other GCC countries and Turkey [ 4 , 19 ].…”

Section: Discussionmentioning

confidence: 94%

Biofilm-Formation in Clonally Unrelated Multidrug-Resistant Acinetobacter baumannii Isolates

et al. 2020

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This study analyzed the genotype, antibiotic resistance, and biofilm formation of Acinetobacter baumannii strains and assessed the correlation between biofilm formation, antibiotic resistance, and biofilm-related risk factors. A total of 207 non-replicate multi-drug-resistant A. baumannii strains were prospectively isolated. Phenotypic identification and antimicrobial susceptibility testing were carried out. Isolate biofilm formation ability was evaluated using the tissue culture plate (TCP), Congo red agar, and tube methods. Clonal relatedness between the strains was assessed by enterobacterial repetitive intergenic consensus-PCR genotyping. Of the 207 isolates, 52.5% originated from an intensive care unit setting, and pan resistance was observed against ceftazidime and cefepime, with elevated resistance (99–94%) to piperacillin/tazobactam, imipenem, levofloxacin, and ciprofloxacin. alongside high susceptibility to tigecycline (97.8%). The Tissue culture plate, Tube method, and Congo red agar methods revealed that 53.6%, 20.8%, and 2.7% of the strains were strong biofilm producers, respectively, while a significant correlation was observed between biofilm formation and device-originating respiratory isolates (p = 0.0009) and between biofilm formation in colonized vs. true infection isolates (p = 0.0001). No correlation was detected between antibiotic resistance and biofilm formation capacity, and the majority of isolates were clonally unrelated. These findings highlight the urgent need for implementing strict infection control measures in clinical settings.

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First report of colistin resistance among carbapenem-resistant Acinetobacter baumannii isolates recovered from hospitalized patients in Egypt

Cited by 43 publications

References 39 publications

Acquisition of Colistin Resistance Links Cell Membrane Thickness Alteration with a Point Mutation in the lpxD Gene in Acinetobacter baumannii

Acquisition of Colistin Resistance Links Cell Membrane Thickness Alteration with a Point Mutation in the lpxD Gene in Acinetobacter baumannii

Rapid and accurate detection of carbapenem-resistance gene by isothermal amplification in Acinetobacter baumannii

Biofilm-Formation in Clonally Unrelated Multidrug-Resistant Acinetobacter baumannii Isolates

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