scholarly journals Prevalence of carbapenemase production in Pseudomonas aeruginosa isolates causing clinical infections in Lagos University Teaching Hospital, Nigeria

2021 ◽  
Vol 22 (4) ◽  
pp. 498-503
Author(s):  
A.O. Ettu ◽  
B.A. Oladapo ◽  
O.O. Oduyebo
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Teaching Hospital ◽  
Dipicolinic Acid ◽  
Phenylboronic Acid ◽  
Carbapenem Resistance ◽  
Clinical Isolates ◽  
University Teaching ◽  
Diffusion Method ◽  
Carbapenem Resistant ◽  
Mueller Hinton

Background: Pseudomonas aeruginosa has been highly associated with carbapenem resistance in which carbapenemases has been suggested to be a major contributory factor. Hence the objective of this study was to phenotypically detect KPC-type carbapenemase, metallo-β-lactamase and OXA-48 carbapenemase production in clinical isolates of P. aeruginosa in Lagos University Teaching Hospital (LUTH), NigeriaMethodology: One hundred and seventy-one P. aeruginosa isolates consecutively recovered from clinical specimens of patients with infections at the Medical Microbiology and Parasitology laboratory of the hospital were identified using MicrobactTM 24E kit. Preliminary screening for carbapenem resistance was determined by the disc diffusion method on Mueller-Hinton agar using single discs of meropenem and imipenem. Phenotypic detection of carbapenemase production among carbapenem-resistant isolates was performed by the combination disc test of meropenem-phenylboronic acid (MRPBO) and meropenem-dipicolinic acid (MRPDP) as recommended by EUCAST 2013 guideline. Results: Out of the 171 P. aeruginosa isolates, 35 (20.5%) were carbapenem non-susceptible (resistant) while carbapenemase production was detected in 27 (77.1%) of these carbapenem resistant isolates, and no enzyme was detected in 8 (22.9%). Of the 27 carbapenemase producing isolates, 22 (81.5%) produced MBL, 1 (3.7%) produced KPC, while 4 (14.8%) produced both KPC and MBL enzymes. Conclusion: This study revealed that carbapenem resistance among P. aeruginosa clinical isolates in our institution is gradually increasing. The mechanism for this rise is associated with carbapenemases, with MBL being the major carbapenemase involved. There is the need to ensure strict compliance with the LUTH infection control guidelines in order to check the rising incidence of infection caused by carbapenem resistant P. aeruginosa.   French title: Prévalence de la production de carbapénémases dans les isolats de Pseudomonas aeruginosa causant des infections cliniques à l'hôpital universitaire de Lagos, Nigéria   Contexte: Pseudomonas aeruginosa a été fortement associé à la résistance aux carbapénèmes dans laquelle les carbapénèmases ont été suggérées comme étant un facteur contributif majeur. Par conséquent, l'objectif de cette étude était de détecter phénotypiquement la production de carbapénémase de type KPC, de métallo-β-lactamase et de carbapénémase OXA-48 dans des isolats cliniques de P. aeruginosa au Lagos University Teaching Hospital (LUTH), Nigeria. Méthodologie: Cent soixante et onze isolats de P. aeruginosa récupérés consécutivement à partir d'échantillons cliniques de patients infectés au laboratoire de microbiologie médicale et de parasitologie de l'hôpital ont été identifiés à l'aide du kit MicrobactTM 24E. Le dépistage préliminaire de la résistance aux carbapénèmes a été déterminé par la méthode de diffusion sur disque sur gélose Mueller-Hinton en utilisant des disques uniques de méropénème et d'imipénème. La détection phénotypique de la production de carbapénèmes parmi les isolats résistants aux carbapénèmes a été réalisée par le test de disque combiné d'acide méropénème-phénylboronique (MRPBO) et d'acide méropénème-dipicolinique (MRPDP) tel que recommandé par la directive EUCAST 2013. Résultats: Sur les 171 isolats de P. aeruginosa, 35 (20,5%) étaient des carbapénèmes non sensibles (résistants) tandis que la production de carbapénèmes a été détectée dans 27 (77,1%) de ces isolats résistants aux carbapénèmes, et aucune enzyme n'a été détectée dans 8 (22,9%). Sur les 27 isolats producteurs de carbapénémases, 22 (81,5%) produisaient des MBL, 1 (3,7%) produisaient des KPC, tandis que 4 (14,8%) produisaient à la fois des enzymes KPC et MBL. Conclusion: Cette étude a révélé que la résistance aux carbapénèmes parmi les isolats cliniques de P. aeruginosa dans notre institution augmente progressivement. Le mécanisme de cette augmentation est associé aux carbapénémases, la MBL étant la principale carbapénémase impliquée. Il est nécessaire de garantir le strict respect des directives de contrôle des infections LUTH afin de contrôler l'incidence croissante des infections causées par P. aeruginosa résistant aux carbapénèmes.

scholarly journals New Delhi Metallo-β-lactamase (NDM)-mediated Carbapenem-Resistant Pseudomonas aeruginosa Clinical Isolates in Sudan

2018 ◽  
pp. 1-5
Author(s):  
Salma Elnour Rahma Mohamed ◽  
Alfadil Alobied ◽  
Mohamed Ibrahim Saeed ◽  
Wafa Mohamed Hussien
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Teaching Hospital ◽  
Carbapenem Resistance ◽  
Clinical Isolates ◽  
Diffusion Method ◽  
New Delhi ◽  
Army Hospital ◽  
Carbapenem Resistant ◽  
Wide Range ◽  
Data Documentation

Carbapenem resistance mediated by NDM is particularly gruesome as this carbapenemase can hydrolyze a wide range of β-lactam antibiotics. Aim: This study aims to detect NDM mediated carbapenem resistance in clinical isolates of Pseudomonas aeruginosa. Materials and Methods: 50 multi-drug resistant clinical urinary isolates of Pseudomonas aeruginosa from three major hospitals in Khartoum state Sudan; Khartoum Teaching Hospital, Medical Army Hospital and Omdurman teaching hospital, in period from July 2016 to September 2017, were investigated for carbapenem resistance using standard disc diffusion method and underwent real-time PCR to detect carbapenem resistance gene blaNDM. Data were analyzed using IBM SPSS. Results: 60% were positive for the blaNDM, 82% were resistant to Imipenem and 75% of the samples were resistant to Meropenem. Conclusion: The emergence of carbapenem resistance is a global problem that requires earnest attention. To make the suitable preventive measures, the emergence of these genes must be monitored closely. Our findings revealed that carbapenem-resistant due to the gene blaNDM is accounted for 60% of the cases, and due to lack of proper data documentation about the emergence of this gene in Sudan, these cases to the best of our knowledge are the first to be reported in Sudan.

scholarly journals oprD Genes Detected in Pseudomonas aeruginosa Isolates from a Teaching Hospital but Lost in a Carbapenem-Resistant Strain

2019 ◽  
pp. 1-8 ◽  
Author(s):  
Eucharia E. Nmema ◽  
Chioma S. Osuagwu ◽  
Eunice N. Anaele
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Teaching Hospital ◽  
Multiple Drug Resistance ◽  
Carbapenem Resistance ◽  
University Teaching ◽  
Diffusion Method ◽  
Multiple Drug ◽  
Disk Diffusion Method ◽  
Chain Reactions ◽  
Carbapenem Resistant

Aims: The aims of the study were to evaluate the multidrug resistance profile and mechanisms of carbapenem resistance in Pseudomonas aeruginosa clinical isolates using phenotypic and genotypic methods. Study Design: A descriptive laboratory based study. Place and Duration of Study: Microbiology Laboratory, Ondo State University of Science and Technology, Okitipupa, and Biotechnology Laboratory, Ladoke Akintola University of Technology, Osogbo, Nigeria, between June 2017 and November 2018. Methodology: Ten P. aeruginosa isolates were recovered from patients at Lagos University Teaching Hospital, and susceptibilities to imipenem (10 µg), meropenem (10 µg) and a panel of antibiotics were performed by the disk diffusion method. Genotypic methods including Polymerase Chain Reactions (PCR) and agarose gel electrophoresis were carried out according to established protocols. oprD and blaIMP gene primers were used for the PCR amplification. Results: Fifty percent (50%) of the isolates showed multiple drug resistance. Four isolates (40%) were carbapenem resistant (CR). oprD gene was detectedin 90% (9/10) of the isolates. 75% (3/4) of CR strains were among the strains showing oprD gene. 25% (1/4) CR strain (PA1421) was oprD negative. Loss or mutation of oprD gene seems to be the mechanism of carbapenem resistance in strain PA1421. Conclusion: Loss or mutation of oprD gene was identified in this study as a mechanism of carbapenem resistance. oprD gene encodes the outer membrane protein (OprD) porin in P. aeruginosa whose deficiency confers resistance to carbapenems, especially imipenem. Surveillance of the antimicrobial susceptibility patterns of P. aeruginosa is of critical importance in understanding new and emerging resistance trends, reviewing antibiotic policies and informing therapeutic options.

scholarly journals Molecular Detection of bla OXA-48 Gene Encoding Carbapenem Resistance Pseudomonas aeruginosa Clinical Isolates from Khartoum State Hospitals, Sudan

2020 ◽  
Author(s):  
Doha Omer Ali ◽  
Mohamed M.A. Nagla
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Teaching Hospital ◽  
Carbapenem Resistance ◽  
Clinical Isolates ◽  
Clinical Samples ◽  
P Value ◽  
Gene Encoding ◽  
State Hospitals ◽  
Carbapenem Resistant ◽  
Different Strains

AbatractCarbapenem resistance in Pseudomonas.aeruginosa is particularly worrisome because this class of β-lactam represents the last therapeutic resource for control of bacterial infection.So this study aimed to detect the frequency of bla OXA-48 resistance gene among Pseudomonas aeruginosa clinical isolates during the period from November 2018 to November 2019.Hundred Pseudomonas aeruginosa clinical isolates, 81 carbapenems (imipenem meropenem) resistant and 19 carbapenems sensitive were collected from Omdurman Teaching Hospital, Fedail Hospital and Soba Teaching Hospital in Khartoum State-Sudan. All isolates were re-identified using conventional bacteriological techniques, their susceptibility to carbapenems were tested using Kirby-Bauer method for confirmation and investigated for the presence of the bla OXA-48 gene using conventional PCR technique.60 (60.0%) out of 100 Pseudomonas aeruginosa clinical isolates were positive for blaOXA-48 gene. Out of 81 carbapenem resistant isolates 54(66.7%) were positive for bla OXA-48 gene, while among the (19) carbapenem sensitive isolates 6 (31.6%) were positive for blaOXA-48 gene. There was statistically significant association between carbapenem resistant isolates and the presence of blaOXA-48 gene (P-value = 0.006).Wound swabs were the predominant clinical samples detected harboring bla OXA-48 gene both among the sensitive 5 (83.3%) and carbapenem resistant isolates 29(53.7) (P.value> 0.05).Our findings revealed high frequency of bla OXA-48 among carbapenem resistant isolates so identification of bla OXA-48 producing strains and taking efforts to reduce the rate of transferring these gene between the different strains is essential for optimization of therapy and improves of patients outcomes.

scholarly journals Molecular characterization of resistance mechanisms in Pseudomonas aeruginosa isolates resistant to carbapenems

2018 ◽  
Vol 11 (12) ◽  
pp. 935-943 ◽  
Author(s):  
Mona Shaaban ◽  
Ahmed Al-Qahtani ◽  
Mohammed Al-Ahdal ◽  
Rasha Barwa
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Real Time ◽  
Real Time Pcr ◽  
Treatment Options ◽  
Carbapenem Resistance ◽  
Pulse Field ◽  
Diffusion Method ◽  
Clinical Samples ◽  
Pcr Analysis ◽  
Carbapenem Resistant

Introduction: Emergence of carbapenem resistance in Pseudomonas aeruginosa increases the therapeutic dilemma. In this study, we investigated various mechanisms involved in the resistance of P. aeruginosa clinical isolates to carbapenems. Methodology: P. aeruginosa isolates were isolated from different clinical samples. The antimicrobial susceptibility was evaluated by disc diffusion method. Carbapenemases were detected among carbapenem resistant isolates. Expression level of mexB and oprD was determined by real-time PCR. Molecular relatedness among isolates was detected based on pulse-field gel electrophoresis (PFGE). Results: Ninety P. aeruginosa isolates were purified from clinical specimens. High levels of resistance to imipenem and meropenem were detected in 16 isolates. PCR analysis of carbapenemases indicated the prevalence of Verona integron-encoded metallo-beta-lactamase (VIM); four isolates produced only VIM enzymes (VIM-1 or VIM-2), while the remaining twelve co-produced both VIM-1 or VIM-2 and NDM enzymes. Additionally, real-time PCR analysis elucidated high expression levels of mexB in seven of the carbapenem resistant isolates and low expression of oprD in seven isolates. The identified carbapenem-resistant isolates were clustered into eleven PFGE profiles where clusters E1 and E2 involved isolates exhibiting multiple carbapenemase genes (blaNDM-1, blaVIM-1 and blaVIM-2). Conclusion: Various mechanisms underlying carbapenem resistance have been detected in our P. aeruginosa cohort of isolates. Emergence of P. aeruginosa as a reservoir of multiple carbapenemases is increasing over time limiting the treatment options to this serious infection. This increases the urgency for infection control practices to reduce the incidence of this infection.

scholarly journals Relationship of Carbapenem Restriction in 22 University Teaching Hospitals to Carbapenem Use and Carbapenem-Resistant Pseudomonas aeruginosa

2009 ◽  
Vol 53 (5) ◽  
pp. 1983-1986 ◽  
Author(s):  
Amy L. Pakyz ◽  
Michael Oinonen ◽  
Ronald E. Polk
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Incidence Rate ◽  
Lower Incidence ◽  
Carbapenem Resistance ◽  
Incidence Rates ◽  
University Teaching ◽  
Teaching Hospitals ◽  
Carbapenem Resistant ◽  
Prior Approval ◽  
Days Of Therapy

ABSTRACT Many hospital antimicrobial stewardship programs restrict the availability of selected drugs by requiring prior approval. Carbapenems may be among the restricted drugs, but it is unclear if hospitals that restrict availability actually use fewer carbapenems than hospitals that do not restrict use. Nor is it clear if restriction is related to resistance. We evaluated the relationship between carbapenem restriction and the volume of carbapenem use and both the incidence rate and proportion of carbapenem-resistant Pseudomonas aeruginosa isolates from 2002 through 2006 in a retrospective, longitudinal, multicenter analysis among a consortium of academic health centers. Carbapenem use was measured from billing records as days of therapy per 1,000 patient days. Hospital antibiograms were used to determine both the incidence rate and proportion of carbapenem-resistant P. aeruginosa isolates. A survey inquired about restriction policies for antibiotics, including carbapenems. General linear mixed models were used to examine study outcomes. Among 22 hospitals with sufficient data for analysis, overall carbapenem use increased significantly over the 5 years of study (P < 0.0001), although overall carbapenem resistance in P. aeruginosa did not change. Hospitals that restricted carbapenems (n = 8; 36%) used significantly fewer carbapenems (P = 0.04) and reported lower incidence rates of carbapenem-resistant P. aeruginosa (P = 0.01) for all study years. Fluoroquinolone use was a potential confounder of these relationships, but hospitals that restricted carbapenems actually used fewer fluoroquinolones than those that did not. Restriction of carbapenems is associated with both lower use and lower incidence rates of carbapenem resistance in P. aeruginosa.

scholarly journals Phenotypic and genotypic study of carbapenem-resistant Pseudomonas aeruginosa strains isolated from hospitalized patients

2016 ◽  
Vol 24 (2) ◽  
pp. 201-211 ◽  
Author(s):  
Luminița Matroș ◽  
Tibor Ludovic Krausz ◽  
Stanca Lucia Pandrea ◽  
Monica Ioana Ciontea ◽  
Erica Chiorean ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Dipicolinic Acid ◽  
Screening Method ◽  
Carbapenem Resistance ◽  
Hospitalized Patients ◽  
Carbapenem Resistant ◽  
Genes Encoding ◽  
Immunosuppressed Patients ◽  
Phenotypic Methods ◽  
Encoding Genes

Abstract Introduction: Nosocomial infections caused by Pseudomonas aeruginosa producing carbapenemases represent an important cause of morbidity and mortality among immunosuppressed patients. The aim of our study was to detect the production of metallo-carbapenemases (MBLs) by phenotypic methods and to detect the presence of the MBLs encoding genes (blaIMP and blaVIM) by PCR in P. aeruginosa strains isolated from hospitalized patients to the Regional Institute of Gastroenterology and Hepatology, Cluj-Napoca. Material and methods: Between September 2014-February 2015, we tested thirty-eight P. aeruginosa strains resistant to carbapenems according to CLSI 2014 breakpoints, determined by Vitek®2(BioMérieux),isolated from various clinical specimens. Phenotypic detection of the MBLs production was performed using the KPC/MBL Confirmation kit (ROSCO®) and the MBL Etest® IP/IPI (BioMérieux). We used the PCR method for detecting MBLs encoding genes: blaIMP, blaVIM. Results: The strains were obtained from surgery (55.3%), ICU (15.8%) and gastroenterology wards (28.9%), isolated from pus (25.8%), tracheal secretion (22.7%), bile (13.6%), sputum (10.6%), blood (10.6%), other secretions (16.7%). These strains were resistant to multiple classes of antibiotics. By ROSCO® method 28/38 strains (73.7%) were positive with imipenem ± dipicolinic acid (DPA) and 22/38 (57.9%) with meropenem ± DPA. Etest® waspositive for the 28/38 strains (73.7%). 11 strains (28.9%) were positive for KPC with the screening method. We identified: 6 blaIMP+ (15.8%), 2 (5.3%) blaVIM+ and 4 blaIMP+/blaVIM+ strains (10.5%). Conclusion: Both genes encoding MBL were found, alone or in combination. The increasing level of carbapenem resistance of these strains impose their routine testing to detect MBL.

scholarly journals Carbapenem Resistance Mechanisms in Pseudomonas aeruginosa Clinical Isolates

2001 ◽  
Vol 45 (2) ◽  
pp. 480-484 ◽  
Author(s):  
Hyunjoo Pai ◽  
Jong-Won Kim ◽  
Jungmin Kim ◽  
Ji Hyang Lee ◽  
Kang Won Choe ◽  
...  
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Amino Acid ◽  
Amino Acid Substitution ◽  
Carbapenem Resistance ◽  
Resistance Mechanisms ◽  
Clinical Isolates ◽  
Efflux System ◽  
Clinical Strains ◽  
Carbapenem Resistant

ABSTRACT In order to define the contributions of the mechanisms for carbapenem resistance in clinical strains of Pseudomonas aeruginosa, we investigated the presence of OprD, the expressions of the MexAB-OprM and MexEF-OprN systems, and the production of the β-lactamases for 44 clinical strains. All of the carbapenem-resistant isolates showed the loss of or decreased levels of OprD. Three strains overexpressed the MexAB-OprM efflux system by carrying mutations inmexR. These three strains had the amino acid substitution in MexR protein, Arg (CGG) → Gln (CAG), at the position of amino acid 70. None of the isolates, however, expressed the MexEF-OprN efflux system. For the characterization of β-lactamases, at least 13 isolates were the depressed mutants, and 12 strains produced secondary β-lactamases. Based on the above resistance mechanisms, the MICs of carbapenem for the isolates were analyzed. The MICs of carbapenem were mostly determined by the expression of OprD. The MICs of meropenem were two- to four-fold increased for the isolates which overexpressed MexAB-OprM in the background of OprD loss. However, the elevated MICs of meropenem for some individual isolates could not be explained. These findings suggested that other resistance mechanisms would play a role in meropenem resistance in clinical isolates of P. aeruginosa.

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