VIM- and IMP-Type Metallo-ß-lactamase–Producing<i>Pseudomonas</i>spp. and<i>Acinetobacter</i>spp. in Korean Hospitals

Lee, Kyungwon; Lee, Wee Gyo; Uh, Young; Ha, Gyoung Yim; Cho, Ji-Hyun; Chong, Yunsop

doi:10.3201/eid09070.030012

Cited by 8 publications

(10 citation statements)

References 11 publications

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“…Of greater concern was the detection by PCR of a VIM-type MBL gene in isolates belonging to one of the three predominant molecular types encountered. Until recently, VIM enzymes have been identified very rarely in A. baumannii, being represented only by VIM-2 in isolates from South Korea [39,40], which is a country in which VIM enzymes are known to be widespread among members of the Enterobacteriaceae and Pseudomonas aeruginosa. However, unrelated strains of Acinetobacter spp.…”

Section: Discussionmentioning

confidence: 99%

Emergence and spread of carbapenem-resistant strains of Acinetobacter baumannii in a tertiary-care hospital in Poland

Wróblewska

Towner

Marchel

et al. 2007

Clinical Microbiology and Infection

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This study analysed the occurrence of carbapenem resistance among Acinetobacter baumannii isolates from a tertiary-care hospital in Poland, together with the molecular epidemiology of these isolates and the risk-factors for their acquisition and possible nosocomial spread. The medical charts of 21 patients with Acinetobacter infection or colonisation revealed that A. baumannii isolates were obtained most frequently from intensive care unit and surgical patients (particularly those receiving transplantation surgery). First isolation occurred, on average, on day 21 following admission (range 5-45 days). Infection with Acinetobacter contributed directly to the death of seven patients. Several patients were infected with more than one strain, and molecular typing revealed the co-circulation of three predominant clones, of which two belonged to the Acinetobacter lineages designated as European clones I and II. All three clones encoded an OXA-51-type carbapenemase, but were negative for carbapenemases belonging to the OXA-23, OXA-24 and OXA-58 families. The OXA-51 gene was found in both resistant and susceptible isolates, and was not associated directly with carbapenem resistance. Etests with imipenem and imipenem plus EDTA indicated production of a metallo-beta-lactamase (MBL) in carbapenem-resistant isolates. PCRs for IMP-type MBLs were negative, but PCR using consensus primers for VIM-type MBLs were positive for carbapenem-resistant isolates belonging to the European clone II lineage. The occurrence of a VIM-type MBL in association with one of the epidemic lineages of A. baumannii is a cause for concern. Further studies are needed to evaluate possible inter-hospital spread of resistant A. baumannii strains in Poland.

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Section: Discussionmentioning

confidence: 99%

Emergence and spread of carbapenem-resistant strains of Acinetobacter baumannii in a tertiary-care hospital in Poland

Wróblewska

Towner

Marchel

et al. 2007

Clinical Microbiology and Infection

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“…Generally, it shows resistance against the β-lactam antibiotics due to high production of cephalosporin AmpC with the mutation in OprD. P. aeruginosa producing the metallo-β-lactamase (MBL) was isolated from the breast cancer patient with VIM-7 gene (Lee et al, 2003;Poirel et al, 2011b;Tseng et al, 2013).…”

Section: Evaluation Of Antibiotic Resistance and Virulence Genes Among Clinical Isolates Of Pseudomonas Aeruginosa From Cancer Patientsmentioning

confidence: 99%

“…The clinically significant type of carbapenemases are VIM, IMP and SPM which are encoded by bla (VIM), bla (IMP) and bla (SPM) respectively. Fourteen types of VIMs and twenty three types of IMPs have been identified yet (Lee et al, 2003;Toval et al, 2015). The resistance against carbapenem was 60% in many hospitals and it was mainly due to the production of MBL (Tsakris et al, 2000;Wolter et al, 2008).…”

Section: Evaluation Of Antibiotic Resistance and Virulence Genes Among Clinical Isolates Of Pseudomonas Aeruginosa From Cancer Patientsmentioning

confidence: 99%

Evaluation of Antibiotic Resistance and Virulence Genes among Clinical Isolates of Pseudomonas aeruginosa from Cancer Patients

Ahmed

Ali

Riaz

et al. 2020

Asian Pac J Cancer Prev

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Objectives: The objectives of this study were to evaluate P. Aeruginosa isolates from cancer patients for the phenotypic pattern of antibiotic resistance and to detect the gene responsible for virulence as well as antibiotic resistance. Methods: A total of 227 P. aeruginosa isolates were studied and 11 antibiotics were applied for susceptibility testing. PCR detection of the genes BIC, TEM, IMP, SPM, AIM, KPC, NDM, GIM, VIM, OXA, toxA and oprI was done. Finally, the carbapenem resistant isolates were tested for phenotypic identification of carbapenemase enzyme by Modified Hodge test. Results: The results showed that the isolates were resistant to imipenem (95%), cefipime (93%), meropenem (90%), polymixin B (71%), gentamicin (65%), ciprofloxacin (48%), ceftazidime (40%), levofloxacin (39%), amikacin (32%), tobramycin (28%) and tazobactum (24%). The PCR detection of the carbapenem resistant genes showed 51% isolates were positive for IMP, GIM and VIM, 38% for AIM and SPM, 30% for BIC, 20% for TEM and NDM, 17% for KPC and 15% for OXA. However, toxA and oprI genes were not detected. 154 carbapenem resistant isolates were found positive phenotypically for carbapenemase enzyme identification by Modified Hodge test. Conclusion: The co-existence of multiple drug-resistant bodies and virulent genes has important implications for the treatment of patients. This study provides information about treating drug-resistant P. Aeruginosa and the relationship of virulent genes with phenotypic resistance patterns.

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“…There are marked geographical differences in the prevalence of the various mechanisms of carbapenem resistance in A. baumannii . Various different carbapenemases, for example OXA-58 oxacillinase in Turkey and VIM-2 in South Korea, have been described in Asia and Europe [4, 6, 7]. Here, we evaluated the epidemiology of carbapenem-resistant A. baumannii (CRAB) infections in a Korean hospital and investigated various mechanisms of carbapenem resistance in isolates and the effect of combinations of mechanisms on the degree of carbapenem resistance.…”

Section: Introductionmentioning

confidence: 99%

Carbapenem-resistantAcinetobacter baumannii: diversity of resistant mechanisms and risk factors for infection

Kim

et al. 2011

Epidemiol. Infect.

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Carbapenem-resistant Acinetobacter baumannii (CRAB) are an increasing infectious threat in hospitals. We investigated the clinical epidemiology of CRAB infections vs. colonization in patients, and examined the mechanisms of resistance associated with elevated minimum inhibitory concentrations (MICs) for carbapenems. From January to June 2009, 75 CRAB strains were collected. CRAB infection was significantly associated with malignancy and a high APACHE II score. The most dominant resistance mechanism was ISAba1 preceding OXA-51, producing strains with overexpression of efflux pump. Strains carrying blaOXA-23-like enzymes had higher carbapenem MICs than those carrying blaOXA-51-like enzymes; however, the presence of multiple mechanisms did not result in increased resistance to carbapenems. There was no difference in the resistance mechanisms in strains from infected and colonized patients. The majority of strains were genetically diverse by DNA macrorestriction although there was evidence of clonal spread of four clusters of strains in patients.

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VIM- and IMP-Type Metallo-ß-lactamase–ProducingPseudomonasspp. andAcinetobacterspp. in Korean Hospitals

Cited by 8 publications

References 11 publications

Emergence and spread of carbapenem-resistant strains of Acinetobacter baumannii in a tertiary-care hospital in Poland

Emergence and spread of carbapenem-resistant strains of Acinetobacter baumannii in a tertiary-care hospital in Poland

Evaluation of Antibiotic Resistance and Virulence Genes among Clinical Isolates of Pseudomonas aeruginosa from Cancer Patients

Carbapenem-resistantAcinetobacter baumannii: diversity of resistant mechanisms and risk factors for infection

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