Detection of blaOXA-23 and blaNDM-1 carbapenemases in clinical isolates of Acinetobacter baumannii from Tabriz, northwest Iran (2023)


Acinetobacter baumannii(Acinetobacter baumannii) is an opportunistic pathogen that can cause a wide range of infections, including meningitis, bloodstream infections, ventilator-associated pneumonia, and urinary tract infections. In 1970, whenAcinetobacter baumanniiWhen the infection is first detected, most isolates are susceptible to most antibiotics. Currently, the emergence of multidrug-resistant bacteria (MDR)Acinetobacterstrains have become a serious threat to global health (Aliakbarzade et al., 2014; Azimi et al., 2015). Typically, MDR strains are resistant to 3 or more classes of antibiotics, including fluoroquinolones, third-generation cephalosporins, aminoglycosides, and carbapenems (Azizi et al., 2016; Kooti et al. , 2015). Reports over the past two years show a 74% increase in the prevalence of MDRAcinetobacter baumanniiInfection in Iran (Pourhajibagher et al., 2016). Recently, a new group of antibiotic resistanceAcinetobacterThere have been infections that are not treatable with carbapenems. Carbapenemase production is the most common mechanism of carbapenem resistanceAcinetobacter baumannii(Kuan et al., 2015). These enzymes are divided into nonmetal carbapenemases (classes A and D) and metallocarbapenems (class B). Of these, the carbapenem-hydrolyzing class D β-lactamases known as oxacillinases are by far the most prevalent type of carbapenem resistance.Acinetobacter baumannii(Evans and Amis, 2014). So far, six OXA carbapenemase families have been identified, including OXA-51-like, OXA-40/24-like, OXA-23-like, OXA-143-like, OXA-58-like and OXA-48-like (Nowak and Paluchowska, 2016; Van Bressem et al., 2001). Nevertheless, metallo-β-lactamases (MBLs) areAcinetobacter baumanniiIn contrast to OXA-type carbapenemases, these enzymes are able to hydrolyze almost all available β-lactam antibiotics. Four MBL types including SIM, VIM, IMP and most recently NDM are known so farAcinetobacter baumannii(Abbott et al., 2013). thisbraNDM-1The gene was first reported from India and then rapidly spread to other countries (Bedeni-ç et al., 2014; Poirel et al., 2011). According to research,AcinetobacterStrain carrybraNDM-1Genes confer resistance to almost all antibiotics (Muir and Weinbren, 2010). thisbraNDM-1The gene encodes the carbapenemase NDM-1, which hydrolyzes and inactivates all β-lactam antibiotics, including carbapenems except aztreonam (Yong et al., 2009).

It has been shown that the production of the NDM-1 enzyme depends on the presence of a strong promoter such as the ISAba125 gene (Poirel et al., 2011; Toleman et al., 2012). most,branoDM-1The gene is located between the two copies of ISAba125 as a Tn125 transposon (Poirel et al., 2012). Tn125 can be inserted at many gene locations as direct repeats on chromosomes or plasmids. According to previous research, inAcinetobacterisolated from Europe and North Africa,braNDM-1The gene is chromosomal, whereas in isolates from China and India it was mainly detected on plasmids (Hu et al., 2012; Jones et al., 2014; Wang et al., 2012; Zhou et al., 2011).

This study aimed to assess the frequency of carbapenem resistanceAcinetobacter baumanniiBy detecting the strainbraOXA-23andbraNDM-1drug resistance geneAcinetobacter baumanniiClinical isolates obtained from the Imam Reza Hospital in Tabriz, Northwest Iran.

partial fragment

Sampling and bacterial identification

In this cross-sectional study (from 2014 to 2015), clinical samples (blood, tracheal aspirates, bronchial washings, sputum, abscesses, wounds, catheters, ascites, and urine) were collected from referral to Iraqi patients. Tabriz Hospital Tabriz Hospital collected individuals from several wards in Mam Reza including Intensive Care Unit (ICU), Infectious Diseases, Traumatology, Neurology, Internal Medicine, Chest, General Surgery and Orthopedic wards. The patient's clinical data were recorded prior to sample collection.

The obtained samples were cultured in

Patient and Bacteria Isolation

A total of 100 clinical isolatesAcinetobacter baumanniiObtained from patients aged 10 to 80 years. Table 1 summarizes the demographics of the inpatients, including sex, age, sampled wards, and clinical specimen types.

Bacteria identification

thisAcinetobacter baumanniiClinical isolates were tested by standard microbiological and biochemical assays. Molecular detectionAcinetobacter baumanniiIsolates are made by amplifyingbraOXA-51like gene, shown as a 640bp band


Rising prevalence of nosocomial infections due to multidrug resistanceAcinetobacter baumanniiStrains have become a serious problem in clinical settings (Liu et al., 2014; Oh et al., 2013). According to recent studies, the rate of carbapenem resistance in Iran has increased from 51.1% in 2007 to 98% in 2017 (Bagheri Josheghani et al., 2015; Moradi et al., 2015). Therefore, continuous monitoring of antibiotic resistance patterns is critical in order to provide effective treatment policies.

Based on our

in conclusion

Our results show a high incidence ofbraOXA-23like genes and emergencebraNDM-1Gene as marker of resistance to nearly all antibioticsAcinetobacter baumanniistrains in the study area.


at the rate ofbraNDM1Resistance is recorded at 1%Acinetobacter baumanniiIsolated in the study area. Studies in larger populations may be necessary to determine the role of this important resistance mechanism inAcinetobacter baumanniiQuarantined in Iran.



    New Delhi - Metallo-beta-lactamases

    Acinetobacter baumannii

    Acinetobacter baumannii


    multidrug resistance

Ethics approval and consent to participate

The study was performed after obtaining ethical approval from the Ethics Committee of Tabriz Medical University, Tabriz, Iran (reference number: IR.TBZMED.REC.1396.811). Data and swab samples were collected after written consent and a brief explanation of the importance of the study to the participant.

Agree to publish

not applicable.


This study received no specific funding from a funding agency.

author's contribution

HKh designed the study and collected the samples. LR and SF drafted the work and wrote the manuscript. HF interprets the data. BN, AT participated in the research analysis. Final manuscript read and approved by all authors.

Availability of data and materials

All data generated or analyzed in this study are included in this published article.

Statement of Competing Interests

The authors have no conflicts of interest.

thank you

This study was supported by a grant from the Biotechnology Research Center (No. 64354),tabriz medical university, Tabriz, Iran.

Quoted by (9)

  • Produced bla isolated from clinical samples around the worldNDMPrevalence of Acinetobacter baumannii strains; systematic review

    2023, Gene Reports

    Citation excerpt:

    A discussion was held to resolve disagreements among the reviewers. Initial searches identified 3583 articles in electronic databases, of which, based on the screening process shown in Figures 1 and 2. 1, 67 articles (Table 1) were eligible for final analysis (Dally et al., 2013; Hasan et al., 2014; Islam et al., 2012; Chen et al., 2011; Tran et al., 2017; Saranathan et al. Solanki et al., 2013; Bernabeu et al., 2017; Mathlouthi et al., 2016; Shamsuzzaman, 2017; Leungtongkam et al., 2018; Bakour et al., 2014; Rafei et al., 2014; Rocha et al., 2019a; Pritsch et al., 2017; Kim et al., 2016; Yagoubat et al., 2017; Sjölander et al., 2014; Mishra et al., 2013; Salloum et al., 2018 ; Banerjee et al., 2018; Gomaa et al., 2017; Chatterjee et al., 2016; Khorsi et al., 2015; Ghebremedhin et al., 2016; Kleinkauf et al., 2014; Memish et al., 2015; Wassef et al., 2016; Jose et al., 2017; Ramoul et al., 2016; Hadjadj et al., 2018; Kumar and VinodKumar, 2017; Srirattakarn et al., 2017; Uwingabiye et al., 2017; et al., 2017; Solanki et al., 2014; Shenoy et al., 2014; Rahman et al., 2018; Jaidane et al., 2018; Patil et al., 2019; Tada et al., 2019; Ogbolu et al., 2020; Rao et al., 2020; Rahbarnia et al., 2020; Sharma et al., 2020; Fernandez-Cuenca et al., 2020; Kongthai et al., 2021; Vijayakumar et al. , 2020; Gomez-Gamboa et al., 2019; Al-Hassan and Al-Madboly, 2020; Li et al., 2019; Callad et al., 2020; Kalal et al., 2020; Al-Hamad et al., 2020; Anane et al., 2020; Kumar et al., 2019; Tada et al., 2020; Wang et al., 2019; Eslami et al., 2019; Al-Hassan et al., 2019; Villacís et al., 2019; Rossi et al., 2021; Abouelfetouh et al., 2019; Benmahmod et al., 2019; Lukovic et al., 2020; López-Leal et al., 2019; Jain et al., 2019). The reasons for excluding studies based on title, abstract and full text are shown in Figure 1.

    An increasing number of nosocomial infections are associated withAcinetobacter baumannii(Acinetobacter baumannii) lead to this bacterium becoming a more clinically significant organism. Emergence of NDM-type carbapenemases has aroused great concern in the medical communityAcinetobacter baumanniiStrains that hinder the effectiveness of nearly all antimicrobials. This systematic review aimed to assess the global prevalence of carbapenem-resistant NDM variantsAcinetobacter baumanniistrain.

    Using PubMed, Web of Science, and Embase databases, we identified all studies addressing the prevalence and variation of NDMAcinetobacter baumanniiisolation. The publications selected for this review were published between 2000 and 2020.

    After screening and reviewing the journals, 67 articles finally met the review criteria. The results showed that NDM variants exhibited the greatest diversity in Europe. The prevalence of NDM-1 in Asia, Africa and Europe was 64.02%, 28.05% and 5.56%, respectively. Studies examining genotypes producing NDMAcinetobacter baumanniiMost commonly used strains for PCR.

    We've seen an increase in reports of strainsAcinetobacter baumanniiNDMs have been produced on all continents over the past few years, so healthcare providers and physicians as well as microbiologists must pay more attention to preventing the spread of these strains.

  • SARS-CoV-2 and HIV coinfection; clinical features, diagnosis, and treatment strategies: a systematic review and meta-analysis

    2022, Gene Reports

    Coronavirus disease 2019 (COVID-19) may be associated with a greater risk of serious complications in immunocompromised human immunodeficiency virus (HIV)-infected individuals. To date, no comprehensive studies have been conducted to assess HIV infection in patients with COVID-19. In this study, we assessed the status of patients coinfected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and HIV through a systematic review and meta-analysis.

    A systematic literature search strategy was performed by reviewing original research articles published in Medline, Web of Science and Embase databases in 2019 and 2020. Statistical analyzes reporting HIV prevalence among COVID-19 patients were performed using STATA software version 14.0 (Stata Corporation, College Station, Texas, USA). Case reports/case series were also assessed as systematic reviews.

    Our study included 63 studies (53 case reports/case series and 10 prevalence studies). A meta-analysis of prevalence studies showed that six countries (Uganda, China, Iran, USA, Italy, and Spain) reported HIV infection among patients with COVID-19, with an overall frequency of 1.2% [(95% CI) 0.8–1.7] in of 14,424 COVID-19 patients. Based on case reports and case series, among 113 patients with COVID-19 from 19 countries, 111 patients with HIV were reported. Most cases have occurred in the United States, China, Italy and Spain.

    The small number of patients with SARS-CoV-2-HIV co-infection reported in the literature makes it difficult to draw precise conclusions. However, because HIV-infected individuals are more likely to develop more severe COVID-19 complications, targeted policies should be considered to address this increased risk in the current pandemic. Our findings highlight the importance of identifying underlying conditions, co-infections, comorbidities, laboratory findings, and beneficial treatment strategies for HIV patients during the COVID-19 pandemic.

  • Molecular characterization and genetic diversity of clinical isolates of multidrug and extensively drug-resistant Acinetobacter baumannii

    2022, Gene Reports

    Citation excerpt:

    Acinetobacter baumannii (A. baumannii) is an opportunistic pathogen that is a major cause of several infections, including pneumonia, meningitis, blood, wound and urinary tract infections, especially in intensive care units (Zarrilli et al. , 2004; Pogue et al., 2013). The overuse of antibiotics in healthcare settings has led to the expansion of antibiotic resistance and the emergence of multidrug-resistant (MDR), extensively drug-resistant (XDR) and even pan-drug-resistant (PDR) strains (Ghavghani et al., 2019); Rahbarnia et al., 2020; Bahadori et al., 2021). According to a meta-analysis study, the prevalence of MDR in Iran averaged 71%, higher than in other countries, highlighting the urgent need for strict standards to keep the spread of these strains to a minimum (Bialvaei et al., 2017 ).

    The increasing prevalence of multidrug-resistant (MDR) strains is now a serious threat to public health. The aim of the study was to investigate the relationship between carbapenemase variants and the spectrum of antibiotic resistanceAcinetobacter baumanniiA strain isolated from Tabriz in northwestern Iran.

    127 totalAcinetobacter baumanniiIsolates were obtained from two teaching hospitals in Tabriz, northwest Iran. Multiplex PCR was performed to detect the carbapenemase-encoding gene. In addition, the genetic relationship of the isolates was investigated by Enterobacteriaceae intragenic repeat sequence (ERIC)-PCR technique.

    All isolates were resistant to carbapenems based on resistance to meropenem and imipenem. The frequencies of multidrug resistance (MDR) and extensive drug resistance (XDR) were 74.80% and 33.07%, respectively. The most prevalent MDR and XDR were associated with patients younger than 50 years (p<0.05). thisbraOXA-23 sampleGenes were most dominant in 82 (64.5%) of the isolates tested, followed bybraOXA-143 class, 54 (42.51%);braOXA-72, 39 (30.7%). None of the isolates were positivebraOXA-58 classGene. There is a significant relationship between the existence ofbraOXA-23frequency of genes and XDR strains (p<0.01). Based on ERIC-PCR, 88 isolates were clustered into 7 groups, while the remaining 21 were single isolates. Most MDR isolates were associated with clusters B and C (p<0.05). The frequency of OXA-143and OXA-72Significantly higher in A and B clusters (p<0.05). This is the first report of a high incidencebraOXA-143andbraOXA-72positiveAcinetobacter baumanniiIranian pressure. genetic relatednessAcinetobacter baumanniiThe isolates were high, suggesting cross-transmission among hospitalized patients.

    High prevalence of MDR and XDRAcinetobacter baumanniiStrains with novel resistance mechanisms have been observed in our region. The incidence of OXA-type carbapenemases varied among clusters classified by ERIC-PCR typing.

  • Prevalence of biofilm-encoding genes among multidrug-resistant Acinetobacter baumannii isolates

    2021, Gene Reports

    Citation excerpt:

    Furthermore, the isolate was further confirmed by detecting the intrinsic blaOXA-51 gene using specific primers (forward: 5′-ACAAGCGCTATTTTTATTCAG-3′, reverse: 5′-CCCATCCCCAACCACTTTT-3′) (Brossard and Campagnari, 2012). Antibiotic resistance profiles of Acinetobacter baumannii isolates were examined by the Kirby Bauer disk diffusion method according to Clinical Laboratory Standards Institute (CLSI) guidelines (Hudzicki, 2009; Rahbarnia et al., 2020). Antibiotic tablets used were as follows: trimethoprim-sulfamethoxazole (co-trimoxazole) (25 μg), gentamicin (10 μg), ceftazidime (30 μg), amikacin (30 μg) , piperacillin-tazobactam (110 μg), ciprofloxacin (5 μg), lomefloxacin (5 μg), cefotaxime (30 μg), imipenem (10 μg), ceftizole Oxime (30 μg), tigecycline (15 μg) and meropenem (10 μg) antibiotic tablets (MAST, Merseyside, UK).

    Increased prevalence of multidrug resistance (MDR)Acinetobacter baumannii isolates coupled with the ability to survive under adverse conditions make this pathogen a serious threat to global health. A cross-sectional study was performed to examine biofilm-forming genes and antibiotic resistance profilesAcinetobacter baumanniiClinical isolates from Tabriz, NW Iran.

    Total 100Acinetobacter baumanniiThe strain was isolated from hospitalized patients in the city of Tabriz in northwestern Iran. These isolates were detected by standard microbiological and biochemical testing,braOXA-51detection. After examining the antibiotic resistance profile, the biofilm forming ability was studied by microtiter plate assay. The presencebapandOPGenes related to biofilm formation were detected by PCR reaction.

    The highest resistance rates were for meropenem (100%), tigecycline (100%), and ceftizoxime (99%), respectively. Resistance analysis of different antibiotic classes showed that 100% of the isolates were multidrug resistant (MDR) and 79% of them were extensively resistant (XDR). Overall, 84% of the isolates were able to produce biofilms, and 3.57% (3/84) of the isolates had a strong ability to form biofilms. All powerful biofilm formationAcinetobacter baumanniiThe isolate was found to be XDR. Furthermore, 100% of the isolates hadOPOne gene, 89% of which are positivebapGene.

    Our findings reveal high prevalence of biofilm formation and biofilm-associated genesbapandOPA multidrug resistanceAcinetobacter baumanniistrains in the study area. According to our results, there is a correlationbapGenes and biofilm formation.

View all citing articles on Scopus

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What is the detection method for Acinetobacter baumannii? ›

Acinetobacter baumannii is a frequent cause of the nosocomial infections. Herein, a novel isothermal amplification technique, multiple cross displacement amplification (MCDA) is employed for detecting all A. baumannii strains and identifying the strains harboring blaOXA-23-like gene.

What are the symptoms of carbapenem-resistant Acinetobacter? ›

Carbapenem-resistant Acinetobacter cause pneumonia and wound, bloodstream, and urinary tract infections. These infections tend to occur in patients in intensive care units. Carbapenem-resistant Acinetobacter can carry mobile genetic elements that are easily shared between bacteria.

What infections are caused by carbapenem-resistant Acinetobacter baumannii? ›

Carbapenem-resistant Acinetobacter baumannii (CRAB) is a type of bacteria commonly found in the environment, especially in soil and water. CRAB can cause human infections of the blood, urinary tract, lungs, wounds, and other body sites. The bacteria are multidrug-resistant, making infections very difficult to treat.

Is Acinetobacter baumannii in urinary infection? ›

Acinetobacter baumannii can cause infections in the blood, urinary tract, and lungs (pneumonia), or in wounds in other parts of the body. It can also “colonize” or live in a patient without causing infections or symptoms, especially in respiratory secretions (sputum) or open wounds.

How to test for carbapenem resistant Acinetobacter baumannii? ›

Screening by rectal swab or stool specimen has 61%–99% sensitivity to detect VRE,8 and 76%–100% sensitivity to detect CRE. An important issue to consider before implementing a screening policy is the pretest probability of screening positive.

Where is Acinetobacter baumannii most commonly found? ›

Acinetobacter baumannii is a nosocomial pathogen, with cases of infection with the organism being found almost exclusively in hospital patients. Unlike the ubiquitous Acinetobacter spp., A. baumannii rarely has been found on human skin.

How serious is Acinetobacter? ›

Acinetobacter can live on or in a patient without causing infection or symptoms, but can also potentially cause a variety of diseases, including lung infections (“pneumonia”) and blood, wound, or urinary tract infections. Typical symptoms of pneumonia could include fever, chills, or cough.

Can Acinetobacter be cured? ›

The clinical cure rates with imipenem for ventilator-associated pneumonia due to Acinetobacter range from 57 to 83 percent in small series [46-48,60]. For bacteremia, one small case series reported successful clinical outcome in 56 percent of individuals treated with imipenem [55].

How do you treat carbapenem-resistant Acinetobacter? ›

Ampicillin-sulbactam has been used successfully to treat invasive infections caused by A. baumannii strains [28], with sulbactam being the active component of this combination against some carbapenem-resistant strains [29].

What are the signs and symptoms of Acinetobacter baumannii? ›

What are the signs and symptoms of an Acinetobacter baumannii infection?
  • Fever.
  • Red, swollen, warm, or painful skin areas or wounds.
  • An area of orange, bumpy skin with blisters.
  • Cough, chest pain, or trouble breathing.
  • Burning feeling while you urinate.
  • Sleepiness, headaches, or a stiff neck.
Mar 2, 2022

What is the survival rate of Acinetobacter baumannii? ›

Acinetobacter baumannii, primarily a nosocomial pathogen, is one of the most antibiotic resistant pathogens in clinical medicine (1). Estimates of mortality rates among patients with A. baumannii infections have ranged from 26.0% to 55.7%, with estimated attributable mortality rates between 8.4% and 36.5% (2).

Is carbapenem resistant Acinetobacter contagious? ›

CRAB is most often spread person-to-person in health care through direct contact with infected or colonized residents, via health care workers' hands following care of those residents, or from the bacteria's persistence in the resident's environment.

How do you treat Acinetobacter baumannii infection? ›

Owing to the propensity of Acinetobacter to develop resistance to antibiotics, current treatment strategies remain limited. Beta-lactam antibiotics are the preferred antibacterial choices for susceptible A baumannii infections.

How long is treatment for Acinetobacter UTI? ›

But, there have been more recent outbreaks with extensively drug-resistant Acinetobacter which makes the management of these infections much more complicated. [20] The duration of therapy is from 7 to 10 days, depending on the patient illness.

Can Acinetobacter baumannii cause sepsis? ›

baumannii isolates (4,–7) whose resistance allows them to disseminate, giving rise to septic shock and disseminated intravascular coagulation (DIC). Consequently, mortality rates range from 30 to 75% depending on the route of infection (8).

What is the best antibiotic for Acinetobacter baumannii? ›

In 2019, Assimakopoulos et al. reported positive results in treating 10 ICU patients with VAP from Pan Drug-Resistant Acinetobacter baumannii with a combination of antibiotics, which consisted of a high dose of tigecycline and ampicillin/sulbactam, and colistin, given both by inhalation and intravenously (22).

What does Acinetobacter baumannii UTI cause? ›

baumannii causes infections of the urinary tract, usually associated with the presence of percutaneous nephrostomy tubes or urinary catheters. These pathogenic strains are also responsible for meningitis, osteomyelitis, endocarditis and wound infections.

Which is the most recommended test for detection of carbapenemase production? ›

Modified Hodge test

Carbapenemase producing isolate is detected by the MHT when the test isolate produces the enzyme and allows the growth of the carbapenem susceptible E. coli ATCC 25922 strain towards the disk.

What conditions does Acinetobacter grow in? ›

Strictly aerobic, Acinetobacter spp. grow on most routinely used media at temperatures of 20–44 °C (68–111 °F). Acinetobacter spp. isolated from human specimens grow readily at 37 °C (99 °F).

What food sources does Acinetobacter come from? ›

Acinetobacter baumannii has been isolated from soil, water and foods including meat, fish, fruits and vegetables, raising concerns food could be a potential source of infection to humans, particularly in healthcare settings. Acinetobacter includes a group of bacteria commonly found in soil and water.

Is Acinetobacter baumannii a superbug? ›

The superbug in question is Acinetobacter baumannii, which the World Health Organization has classified as a “critical” threat among its “priority pathogens” – a group of bacteria families that pose the “greatest threat” to human health.

How long does Acinetobacter live? ›

baumannii can survive for 6 days on dry filter paper (1), 13 days on formica (12, 19), more than 7 days on glass (16), and more than 25 days on cotton (16).

What is the survival time on surfaces of Acinetobacter? ›

The mean survival times of the various A. baumannii isolates tested are shown in Tables ​1 and ​ 2. The mean survival time for sporadic strains was 27.29 days (range, 21 to 32 days), while the mean survival time for outbreak strains was 26.55 days (range, 21 to 33 days).

Is Acinetobacter normal? ›

Acinetobacter baumannii is not part of the normal human skin or gut flora and is usually not carried by a previously healthy individual.

Is Acinetobacter airborne? ›

Infected patients spreads Acinetobacter to the air of intensive care unit (ICU). These strains can remain in ICU air about four weeks.

Why is Acinetobacter important? ›

The ability of Acinetobacter strains to adhere to surfaces is an important mechanism in the pathogenicity. It frequently causes infections associated with medical devices, e.g., vascular catheters, cerebrospinal fluid shunts or Foley catheters. Biofilm formation is a well-known pathogenic mechanism in such infections.

What is the isolation for Acinetobacter? ›

Isolation of Acinetobacter from colonized patients requires no specific therapy. Acinetobacter isolates demonstrate increasing resistance to commonly prescribed antimicrobials.

What is the mortality rate of carbapenem resistant Acinetobacter? ›

Among patients with CR A. baumannii infections, the highest mortality rate was observed for bloodstream infections (40.9%; Table 3) followed by respiratory tract infections (21.9%), while mortality was 9.3% for patients with urinary tract infections and 6.6% for those with wound infections (Table 3).

Why is A. baumannii difficult to treat? ›

Mechanisms of Resistance. The management of AB infections is particularly complicated due to this pathogen's multiple intrinsic and acquired mechanisms of resistance including β-lactamases, aminoglycoside-modifying enzymes, efflux pumps, permeability defects, and target site modifications.

How do you get carbapenem resistant organism? ›

Typically patients with CRE infections have a history of long term exposure to health care facilities usually due to unrelated comorbidity. This exposure usually coincides with long term and varied antibiotic use leading to the gradual development of more and more resistant bacterial infections.

What is the difference between a penicillin and a carbapenem? ›

Carbapenem has a five-membered ring, as does penicillin, but it has a carbon at C-1 instead of sulfur.

What kills Acinetobacter? ›

Highly antibiotic-resistant Acinetobacter baumannii clinical isolates are killed by the green tea polyphenol (–)-epigallocatechin-3-gallate (EGCG)

Does Acinetobacter cause endocarditis? ›

Infective endocarditis caused by Acinetobacter (A.) baumannii is a rare but severe complication that affects seriously ill, hospitalized patients undergoing invasive procedures.

Which media is used for Acinetobacter baumannii? ›

MacConkey agar was 89% sensitive for Acinetobacter species and 91% sensitive for MDR-A. baumannii when compared to sheep blood agar.

What are the identifying characteristics of Acinetobacter species? ›

Characteristics. Acinetobacters are short, plump rods, typically measuring 1.0–1.5 × 1.5–2.5 μm when in the logarithmic phase of growth, but they often become more coccoid in the stationary phase. They are Gram-negative but may appear Gram variable, as is typical of members of the Moraxellaceae generally.

How do you determine antibacterial susceptibility test? ›

The Kirby-Bauer agar diffusion method is well documented and is the standardized method for determining antimicrobial susceptibility. White filter paper disks (6 mm in diameter) are impregnated with known amounts of antimicrobial agents. Each disk is coded with the name and concentration of the agent.

What are the distinguishing characteristics of Acinetobacter baumannii? ›

baumannii is one of the most challenging bacterial pathogens because of its unique antibiotic resistance characteristics. The genus Acinetobacter includes non-lactose-fermenting, catalase-positive, non-motile, non-fastidious, oxidase-negative, and aerobic Gram-negative coccobacilli.

How do you treat Acinetobacter baumannii skin infection? ›

First-line antibiotics — Infections caused by antibiotic-susceptible Acinetobacter isolates may have several first-line therapeutic options, including broad-spectrum cephalosporins (ceftazidime or cefepime), piperacillin-tazobactam, ampicillin-sulbactam, carbapenems (eg, meropenem or imipenem-cilastatin), and ...

Is Acinetobacter baumannii positive or negative? ›

Acinetobacter baumannii is a Gram-negative bacillus that is aerobic, pleomorphic and non-motile. An opportunistic pathogen, A. baumannii has a high incidence among immunocompromised individuals, particularly those who have experienced a prolonged (> 90 d) hospital stay.

What are the signs and symptoms of Acinetobacter infection? ›

Symptoms of a bloodstream infection might include fever, chills, vomiting, and confusion. A wound infection might cause fever and redness, increasing pain, and pus around the wound.

What type of isolation is required for Acinetobacter? ›

Isolation of Acinetobacter from colonized patients requires no specific therapy. Acinetobacter isolates demonstrate increasing resistance to commonly prescribed antimicrobials. Resistance has been tracked to plasmids, transposons and chromosomes.

What is the confirmation test for Acinetobacter? ›

The negative oxidase test is important for rapid presumptive identification to differentiate the genus Acinetobacter from other similar non-fermentative organisms (Joshi and Litake, 2013). ...

What is the strongest antibiotic for bacterial infection? ›

Vancomycin 3.0 is one of the most potent antibiotics ever created.

What do susceptibility test results mean? ›

A “susceptible” result indicates that the patient's organism should respond to therapy with that antibiotic using the dosage recommended normally for that type of infection and species [13, 20].

How do you treat antibiotic resistant bacteria? ›

Sometimes doctors prescribe a combination of medications. Treatment of a MRSA infection at home often involves a 7- to 10-day course of an antibiotic such as clindamycin, doxycycline, or a combination of sulfamethoxazole–trimethoprim and linezolid.

What are two Acinetobacter species of clinical importance? ›

Clinically relevant species are mostly confined to the Acinetobacter calcoaceticus/Acinetobacter baumannii (ACB) complex, namely, A. baumannii, A. calcoaceticus, Acinetobacter pittii, Acinetobacter nosocomialis, and the recently added numerous other species [3,4,5,6]. However, among the ACB complex, A.

What is the difference between Acinetobacter baumannii colonization and infection? ›

baumannii colonization means sputum culture from lower respiratory tract is positive without infection signs. And A. baumannii infection means sputum culture from lower respiratory tract is positive with infection signs.


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