Baumannii Nosocomial Infections Research Articles

Derivation and validation of a predictive mortality model of in-hospital patients with Acinetobacter baumannii nosocomial infection or colonization.

Acinetobacter baumannii (Ab) is a Gram-negative opportunistic bacterium responsible for nosocomial infections or colonizations. It is considered one of the most alarming pathogens due to its multi-drug resistance and due to its mortality rate, ranging from 34 to 44,5% of hospitalized patients. The aim of the work is to create a predictive mortality model for hospitalized patient with Ab infection or colonization. A cohort of 140 sequentially hospitalized patients were randomized into a training cohort (TC) (100 patients) and a validation cohort (VC) (40 patients). Statistical bivariate analysis was performed to identify variables discriminating surviving patients from deceased ones in the TC, considering both admission time (T0) and infection detection time (T1) parameters. A custom logistic regression model was created and compared with models obtained from the "status" variable alone (Ab colonization/infection), SAPS II, and APACHE II scores. ROC curves were built to identify the best cut-off for each model. Ab infection status, use of penicillin within 90 days prior to ward admission, acidosis, Glasgow Coma Scale, blood pressure, hemoglobin and use of NIV entered the logistic regression model. Our model was confirmed to have a better sensitivity (63%), specificity (85%) and accuracy (80%) than the other models. Our predictive mortality model demonstrated to be a reliable and feasible model to predict mortality in Ab infected/colonized hospitalized patients.

Risk Factors, Outcomes, and Predictions of Extensively Drug-Resistant Acinetobacter baumannii Nosocomial Infections in Patients with Nervous System Diseases.

Acinetobacter baumannii has evolved to become a major pathogen of nosocomial infections, resulting in increased morbidity and mortality. This study aimed to investigate the risk factors, outcomes, and predictions of extensively drug-resistant (XDR)-A. baumannii nosocomial infections in patients with nervous system diseases (NSDs). A retrospective study of patients infected with XDR-A. baumannii admitted to the Affiliated Hospital of Southwest Medical University (Luzhou, China) from January 2021 to December 2022 was conducted. Three multivariate regression models were used to assess the risk factors and predictive value for specific diagnostic and prognostic subgroups. A total of 190 patients were included, of which 84 were diagnosed with NSDs and 80% of those were due to stroke. The overall rates of all-cause mortality for XDR-A. baumannii nosocomial infections and those in NSDs were 38.9% and 40.5%, respectively. Firstly, hypertension, indwelling gastric tube, tracheotomy, deep puncture, bladder irrigation, and pulmonary infections were independent risk factors for XDR-A. baumannii nosocomial infections in patients with NSDs. Moreover, pulmonary infections, the aspartate aminotransferase (AST) to alanine aminotransferase (ALT) ratio, and the neutrophil-to-lymphocyte ratio (NLR) were significantly associated with increased mortality rates in patients with nosocomial infections caused by XDR-A. baumannii. Thirdly, NLR and cardiovascular diseases accounted for a high risk of mortality for XDR-A. baumannii nosocomial infections in patients with NSDs. The area under the curves of results from each multivariate regression model were 0.827, 0.811, and 0.853, respectively. This study reveals the risk factors of XDR-A. baumannii nosocomial infections in patients with NSDs, and proves their reliable predictive value. Early recognition of patients at high risk, sterilizing medical tools, and regular blood monitoring are all critical aspects for minimizing the nosocomial spread and mortality of A. baumannii infections.

Molecular Level Study and Characterization of Plasmid Deoxyribonucleic Acid Profile of Acinetobacter baumannii Isolated from Diabetic Foot Ulcers

The main objective is to study the genotypic and characterization of plasmid deoxyribonucleic acid content of resistant isolates in Erbil city. A total of 39 Acinetobacter baumannii were isolated from 102 diabetic foot ulcer patients, whose ages ranged from 37 to 88 y, attending various medical wards of hospitals in Erbil city, Iraq, between May 2020 and March 2021. Isolates were tested for the presence of extended-spectrum beta-lactamases and metallo beta-lactamases. The presence and prevalence of multidrug-resistant isolates namely blaOXA-51- like, blaOXA-23-like, ISAba1 and outer membrane protein A expression of oxacillinase carbapenemases gene and biofilm formation respectively were screened on the molecular level. Finally, plasmid deoxyribonucleic acid profile was determined and the biofilm-forming capacity was measured. Most isolates showed high resistance to different antimicrobial agents tested, the most effective agents were colistin and polymyxin B. 12 (30.76 %) isolates were tested positive for extended-spectrum beta-lactamases, while all 39 (100 %) were metallo beta-lactamase producers. 27 (69.23 %) of isolates were biofilm producers, while 12 (30.76 %) were nonbiofilm producers. The blaOXA-51-like, blaOXA-23-like, ISAba1 and outer membrane protein A genes were detected in all 39 (100 %) isolates. The genes encoding resistance to certain antibiotics, in addition to genes that coding for extended-spectrum beta-lactamase and biofilm formation were located on plasmids. Analysis of plasmid deoxyribonucleic acid content revealed that 25 (64.10 %) isolates harbored from one to several plasmid bands ranging from 1 kilo base pairs to more than 10 kilo base pairs. No thermo-sensitive plasmids were detected. Due to the emergence of multidrug-resistance, Acinetobacter baumannii is evolving into a global health threat. Carbapenems are effective therapeutic agents for Acinetobacter baumannii nosocomial infections. Before deciding the course of treatment, it is important to consider the aforementioned interaction since the presence of multiple species may worsen the infection.

Epidemiological study of Acinetobacter baumannii nosocomial infections

Introduction. Acinetobacter baumannii is a pathogen and a major cause of nosocomial infections in the current healthcare system worldwide due to its high resistance to antibiotics, including those considered as a last resort, thus posing threat to severe clinical forms, as well as exhibiting significant economic and clinical impact.
 Material and methods. A descriptive longitudinal and cross-sectional epidemiological study was carried out based on the model of multidisciplinary care hospitals.
 Results. The generalized clinical forms of Acinetobacter nosocomial infections predominate in 56.30%, including: pulmonary sepsis – 25.59%, abdominal sepsis – 11.81%, septicemia – 9.45%, wound sepsis– 6.30%, biliary sepsis – 1.97%, and urosepsis – 1.18% of cases. Local infections were found in 16.93% of wound infections and in 14.57% of pneumonia cases. A. baumanii was present in the etiological structure of 98.18% of cases, exhibiting an increased resistance to antibiotics, particularly to monobactams – 100.0%, macrolides – 98.82%, penicillins – 98.08%, cephalosporins – 97.65%, penicillins with beta-lactamase inhibitors – 93.20%, fluoroquinolones – 87.16%, and amphenicols – 84.17% of cases. A. baumanii strains isolated from patients with nosocomial infections were found to be multidrug resistant to antibiotics in 93.08% of cases. 
 Conclusions. Acinetobacter baumannii nosocomial infections represent a major public health issue that requires the implementation of strict surveillance and control strategies, including the rational use of antibiotics.

Carbapenemases: Transforming Acinetobacter baumannii into a Yet More Dangerous Menace.

Acinetobacter baumannii is a common cause of serious nosocomial infections. Although community-acquired infections are observed, the vast majority occur in people with preexisting comorbidities. A. baumannii emerged as a problematic pathogen in the 1980s when an increase in virulence, difficulty in treatment due to drug resistance, and opportunities for infection turned it into one of the most important threats to human health. Some of the clinical manifestations of A. baumannii nosocomial infection are pneumonia; bloodstream infections; lower respiratory tract, urinary tract, and wound infections; burn infections; skin and soft tissue infections (including necrotizing fasciitis); meningitis; osteomyelitis; and endocarditis. A. baumannii has an extraordinary genetic plasticity that results in a high capacity to acquire antimicrobial resistance traits. In particular, acquisition of resistance to carbapenems, which are among the antimicrobials of last resort for treatment of multidrug infections, is increasing among A. baumannii strains compounding the problem of nosocomial infections caused by this pathogen. It is not uncommon to find multidrug-resistant (MDR, resistance to at least three classes of antimicrobials), extensively drug-resistant (XDR, MDR plus resistance to carbapenems), and pan-drug-resistant (PDR, XDR plus resistance to polymyxins) nosocomial isolates that are hard to treat with the currently available drugs. In this article we review the acquired resistance to carbapenems by A. baumannii. We describe the enzymes within the OXA, NDM, VIM, IMP, and KPC groups of carbapenemases and the coding genes found in A. baumannii clinical isolates.

Drugs with new lease of life as quorum sensing inhibitors: for combating MDR Acinetobacter baumannii infections.

The emergence of multidrug-resistant (MDR) strains is a major health problem worldwide. There is an urgent need for novel strategies to combat bacterial infections caused by MDR strains like Pseudomonas aeruginosa and Acinetobacter baumannii. Quorum sensing (QS) is a critical communication system in bacterial community controlling survival and virulence. The awareness of the importance of QS in bacterial infections has stimulated research to identify QS inhibitors (QSIs) to defeat microbes. In this study, four FDA-approved drugs (besides azithromycin as positive QSI) were tested for potential QS inhibition against clinical A. baumannii isolates and P. aeruginosa (PAO1) standard strain. The inhibitory effect of these drugs on virulence factors of both microbes has been investigated. The studied virulence factors include biofilm formation, twitching and swarming motilities, proteolytic enzyme production, and resistance to oxidative stress. The four tested drugs (erythromycin, levamisole, chloroquine, and propranolol) inhibited QS in Chromobacterium violaceum by 84, 72, 55.1, and 37.3%, respectively. They also significantly inhibited virulence factors in both PAO1 and A. baumannii at sub-inhibitory concentrations. These findings were confirmed by qRT-PCR and mice mortality test, where tested drugs highly repressed the expression of abaI gene and showed significantly improved mice survival rates. In addition, molecular docking studies against AbaI and AbaR proteins of QS system in A. baumannii revealed the potential inhibition of QS by tested drugs. Beside their known activities, the tested drugs could be given new life as QSIs to combat A. baumannii nosocomial infections (alone or in combination with antimicrobials).Electronic supplementary materialThe online version of this article (10.1007/s10096-020-03882-z) contains supplementary material, which is available to authorized users.

Managing Acinetobacter baumannii infections.

We reviewed recent data about epidemiology of Acinetobacter baumannii, resistance mechanisms, and therapeutic options for severe infections caused by multidrug-resistant strains. A. baumannii is a major cause of nosocomial infections affecting mainly to debilitating patients in the ICU, although the spread to regular wards and to long-term care facilities is increasing. It is characterized by its great persistence in the environment and to have an extraordinary capability to develop resistance to all antimicrobials.Carbapenems may not be considered the treatment of choice in areas with high rates of carbapenem-resistant A. baumannii. Nowadays, polymyxins are the antimicrobials with the greatest level of in-vitro activity against A. baumannii. Colistin is the most widely used in clinical practice although polymyxin B seems to be associated with less renal toxicity. Colistin is administered intravenously as its inactive prodrug colistimethate. A loading dose of 9 million IU and subsequently high, extended-interval maintenance doses (4.5 million IU/12 h) are recommended. Combination therapy instead of monotherapy increases the rates of microbiological eradication although no clinical study has demonstrated a reduction in clinical outcomes (mortality or length of stay). The optimal treatment for multidrug-resistant A. baumannii nosocomial infections has not been established. There are no compelling data to recommend combination therapy for severe A. baumannii infections.

Incidence, risk factors and outcome of multi-drug resistant Acinetobacter baumannii nosocomial infections during an outbreak in a burn unit

BackgroundMultidrug-Resistant Acinetobacter baumannii (MR-AB) can cause outbreaks in burn units. We aimed to study the incidence, risk factors and outcome of MR-AB infections in a burn unit (BU). MethodsA prospective study was conducted from April to November, 2014 during an outbreak in a BU in Paris. Weekly surveillance cultures were performed to determine MR-AB colonization. MR-AB nosocomial infections, discharge or death without MR-AB infection were considered as competing events. To identify risk factors for MR-AB infection, baseline characteristics and time-dependent variables were investigated in univariate analyses using Cox models. ResultsEighty-six patients admissions were analyzed during the study period. Among them, 15 (17%) acquired MR-AB nosocomial infection. Median time to infection was 22days (interquartile range: 10–26 days). Cumulative incidence of MR-AB infections was 15% at 28days (95% CI=8–24). Risk factors for MR-AB infection in univariate analysis were SAPS II (Hazard Ratio (HR):1.08; 95% CI:1.05–1.12; P<0.0001) and ABSI (Abbreviated Burn Severity Index) scores (HR:1.32; 95% CI:1.12–1.56; P=0.001), MR-AB colonization (HR:10.2; 95%CI:2.05–50.3; P=0.004), invasive procedures (ventilation, arterial and/or venous catheter) (P=0.0001) and ≥2 skin grafts (HR:10.2; 95% CI:1.76–59.6; P=0.010). MR-AB infection was associated with an increased risk of death (HR: 7.11; 95%CI: 1.52–33.2; P=0.013) and longer hospital stay with a median estimated increase of 10days (IQR: 6; 14). ConclusionsIncidence of MR-AB nosocomial infection was high during this outbreak, and was associated with prolonged hospitalization and increased risk of death. High patient severity scores, prior MR-AB colonization, invasive procedures and repeated skin grafts were associated with an increased risk of nosocomial infection.

Risk factors associated with multi-drug-resistant Acinetobacter baumannii nosocomial infections at a tertiary care hospital in Makkah, Saudi Arabia - a matched case-control study.

ObjectiveTo determine risk factors for multi-drug-resistant Acinetobacter baumannii (MDR-AB) nosocomial infections in intensive care units in a tertiary care hospital, Makkah, Saudi Arabia.MethodsWe performed a hospital-based, matched case–control study in patients who were admitted to Al Noor Specialist Hospital between 1 January 2012 and 31 August 2012. The study included cases of A. baumannii nosocomial infection and controls without infection. Controls were matched to cases by age and ward of admission.ResultsThe most frequent site of infection was the respiratory tract (77.3%). Susceptibility to antimicrobial MDR-AB was 92.0% for ceftazidime and ciprofloxacin, while it was 83.3% for imipenem, 83.0% for trimethoprim, 79.0% for amikacin, and 72.7% for gentamicin. Multiple logistic regression of risk factors showed that immunosuppression (OR = 2.9; 95% CI 1.5–5.6; p = 0.002), clinical outcome (OR = 0.4; 95% CI 0.3–0.9; p = 0.01), invasive procedures (OR = 7.9; 95% CI 1.8–34.2; p = 0.002), a central venous catheter (OR = 2.9; 95% CI 1.5–5.6; p = 0.000), and an endotracheal tube (OR = 3.4; 95% CI 1.6–7.3; p = 0.001) were associated with MDR-AB.ConclusionsAcinetobacter nosocomial infections are associated with admission to the ICU (Intensive care unit) and exposure to invasive procedures.

Molecular characterization of oxacillinases among carbapenem-resistant Acinetobacter baumannii nosocomial isolates in a Saudi hospital.

Acinetobacter baumannii has successfully become a significant nosocomial pathogen because of its remarkable ability to acquire antibiotic resistance and to survive in nosocomial environments. This study aimed to determine the drug susceptibility patterns and the distribution of four subgroups of carbapenem-hydrolyzing class D β-lactamases (OXA-carbapenemases), as well as their insertion sequences (ISAba1), among A. baumannii nosocomial isolates from a Saudi tertiary care hospital. A total of 108 non-duplicate A. baumannii isolates were identified, and their susceptibilities to different antibiotics were determined using the breakpoint method. Isolates were then subjected to multiplex-PCR targeting blaOXA genes. More than 75% of the isolates showed resistance to different antibiotics. The rates of susceptibility to colistin, meropenem, imipenem and trimethoprim-sulfamethoxazole were 95.6, 50, 48.1 and 34.3%, respectively. All isolates possessed a blaOXA-51-like gene. Of the 56 carbapenem-resistant isolates, 48 isolates (85.7%) carried blaOXA-23-like, 3 isolates (5.4%) carried blaOXA-40-like and two isolates (3.6%) had blaOXA-58-like genes. The ISAba1 element was found upstream of the blaOXA-23 and blaOXA-24 genes in 40 (71.4%) and 3 (5.4%) isolates, respectively, while it was detected upstream of blaOXA-51 in only one (1.8%) isolate. Our findings further illustrate the challenge of increasing carbapenem-resistance in A. baumannii isolates in Saudi Arabia. The high distribution of class D carbapenemase-encoding genes, mainly ISAba1/OXA-23 and ISAba1/OXA-24 carbapenemases, is worrisome and presents an emerging threat in our hospital. Local molecular surveillance is essential to help control carbapenem-resistant A. baumannii nosocomial infections and to prevent DNA exchange among endemic nosocomial pathogens.

An outbreak of nosocomial infection with Acinetobacter baumannii in the neonatal intensive care unit of the Department of paediatrics, University Clinical Centre

Objective – Outbreaks of sepsis caused by multidrug-resistant Acinetobacter baumannii in neonatal intensive care units have been reported, but rarely from our country. We describe such an outbreak in the Department of Paediatrics of the University Clinical Centre Tuzla in 2012 to investigate risk factors, the mode of transmission and to assess control measures. Setting – An 18 bed, level 3 neonatal intensive care unit in a university affiliated teaching hospital. Patients and methods – Seventeen neonates who developed multidrug-resistant Acinetobacter baumannii nosocomial infection were matched to 17 neonates who were admitted to the same unit without infections, during the outbreak period. Cases and controls were compared for possible risk factors (birth weight, gender, intubation, antibiotic use, etc.). Surveillance cultures were collected from health care personnel and the environment. Results – Six out of the 17 neonates (35.3%) died. Surveillance cultures were negative. Seventeen isolates from newborns had the same patterns of resistance. Multidrug-resistant Acinetobacter baumannii was brought into the unit by an infected infant who was transferred from the neurosurgery hospital. Risk factors significantly associated with the infection were: incubator care (OR 6.66; p =0.034), exposure to a central venous catheter (OR 13.75; p=0.004), mechanical ventilation (OR 5.25;p =0.031) and exposure to a patient with Acinetobacter baumannii infection (OR 38.40; p =0.02). Conclusion – Surveillance cultures for all newborns transferred from other hospitals and isolation measures are important to prevent nosocomial infections and outbreak. Negative environmental and health care worker cultures have to be meticulously analyzed. Cohorting of affected newborns and nursing staff, contact isolation, and environmental cleaning are crucial to control the outbreak.

Emergence of oligoclonal Acinetobacter baumannii nosocomial infection in a Hospital in Nepal

The molecular epidemiology of fifteen clinical strains of Acinetobacter baumanniirecovered from various clinical specimens from different wards during January to June, 2010 from a hospital in Nepal was evaluated. Kirby-Bauer disk diffusion test was used for determining in-vitro activities of antibiotics. Molecular epidemiology was investigated by polymerase chain reaction-randomly amplified polymorphic DNA (PCR-RAPD) and plasmid profiling. A. baumannii recovered were multidrug resistant. Isolates represented three antibiotypes (a, b and c). Isolates in antibiotype c (n=12) were resistant to all antibiotics tested while isolates in antibiotype a (n=2) was susceptible to netilmicin and b (n=1) was susceptible to aminoglycosides and fluoroquinolones tested. Four plasmid profiles (i) 1 isolate; (ii) 1 isolate; (iii) 1 isolate; and (iv) 12 isolates and four PCR-RAPD types (I)1isolate; (II) 8 isolates; (III) 1 isolate; (IV) 5 isolates revealed oligoclonal population of A. baumannii. Antibiotypes, plasmid profiles and PCR-RAPD types showed no empirical association. A. baumannii isolates were oligoclonal and multi-drug resistant. The emergence of multi-drug resistant oligoclonal population of this pathogen in a hospital warrants for development of appropriate antibiotic policies and immediate implementation of infection prevention and control measures. Key words: Acinetobacter baumannii, multidrug-resistant, oligoclonal, Nepal.

Multiresistant Acinetobacter baumannii infections: epidemiology and management

We present recent data about epidemiology of Acinetobacter baumannii in the hospital setting, major resistance mechanisms, and therapeutic options for infections caused by multidrug-resistant strains. A. baumannii has emerged as a major cause of healthcare-associated infections. It commonly presents resistance to multiple antimicrobial agents, including carbapenems. These strains are now ussually resistant to the rest of antipseudomonal beta-lactams and sulbactam, a beta-lactamase inhibitor with bactericide activity against A. baumannii. Rifampicin has demonstrated its effectiveness in animal models but can never be used in monotherapy because of the rapid development of resistance. Colistin, an old antibiotic, has re-emerged as a valid alternative given its excellent in-vitro activity. Numerous studies have confirmed its efficacy in serious infections, including ventilator-associated pneumonia and nosocomial meningitis, with an acceptable safety profile. Tigecycline appears as a promising therapeutic option for multidrug resistant A. baumannii, althogh more clinical data about its efficacy especially in pulmonary infections are required. The role of combination therapy or the use or colistin in alternative routes (nebulized or intrathecally) has not been established. The optimal treatment for multidrug-resistant A. baumannii nosocomial infections has not been established. Carbapenems are the mainstay of treatment in susceptible isolates. Colistin and tigecycline retain good in-vitro activity and in many cases represent the only therapeutic options.

Treatment of Acinetobacter infections

Importance of the field: Acinetobacter baumannii has emerged as a major cause of healthcare-associated infections. It commonly presents resistance to multiple antimicrobial agents, occasionally including carbapenems and polymyxins, and hence, it is considered the paradigm of multidrug-resistant (MDR) or pandrug-resistant (PDR) bacterium. MDR A. baumannii is a rapidly emerging pathogen, especially in the intensive care setting, causing infections including bacteremia, pneumonia/ventilator-associated pneumonia (VAP), meningitis, urinary tract infection, central venous catheter-related infection, and wound infection.Areas covered in this review: All potential antimicrobial agents that are available for the treatment of Acinetobacter infections are presented. Emphasis was given to the management of nosocomial infections due to MDR A. baumannii and its close relatives, spp. 3 and 13TU. Areas covered include bloodstream infections, pneumonia or VAP, meningitis, urinary tract infection, skin and soft-tissue or wound infections due to Acinetobacter.What the reader will gain: The antibiotics that are usually effective against A. baumannii infections include carbapenems, polymyxins E and B, sulbactam, piperacillin/tazobactam, tigecycline and aminoglycosides. Carbapenems (imipenem, meropenem, doripenem) are the mainstay of treatment for A. baumannii, though carbapenem-resistant Acinetobacter strains have increasingly been reported worldwide in recent years. However, although well-designed trials of new therapeutic approaches are certainly required, the most important factor necessary to guide clinicians in their choice of empirical or targeted therapy should be knowledge of the susceptibility patterns of strains present in their own geographical area.Take home message: Pooled data suggest that infections caused by A. baumannii, especially those with inappropriate treatment, are associated with considerable attributable mortality. The optimal treatment for A. baumannii nosocomial infections has not been established, especially for MDR strains. Therefore, well-designed clinical studies are necessary to guide clinicians on decisions regarding the best therapeutic approach for patients with MDR A. baumannii infections. In addition, new experimental studies are warranted to evaluate the activity and safety of peptides and other novel antibacterial agents for A. baumannii infections.

First Report of Molecular Characterization of Carbapenem-Resistant Acinetobacter baumannii in Different Intensive Care Units in University Hospital Split, Croatia

Acinetobacter baumannii is an important cause of nosocomial infections such as pneumonia, septicaemia, urinary tract infections, and wound infections 1. It may become resistant to a wide range of antibiotics, thus complicating the treatment of nosocomial infections 1. The emergence of carbapenem resistance in Acinetobacter baumannii has become a global concern since these β -lactams are often the only effective treatment left against many multiresistant strains . According to a recent report, the overall resistance rate to imipenem in A. baumannii isolated from 17 representative laboratories in Croatia was 1 % (range 0%-8%) . However, molecular basis of carbapenem resistance was not investigated yet. We would like to report the molecular epidemiology of carbapenem resistant strains obtained from clinical samples of several patients hospitalised on different intensive care units inside University Hospital Split, Croatia. Eleven isolates of A. baumannii with an unusual resistance profile were isolated during 2003 and 2004, from patients hospitalised in three different intensive care units (two adults and one children ICU) on different locations inside UHS. Routine susceptibility testing was done by standard disc diffusion method according to the National Committee for Clinical Laboratory Standards guidelines. All collected isolates of A. baumannii displayed intermediate (MICs>8 mg/L) or resistant (MICs>16 mg/L) profile to imipenem and/or meropenem. Minimum inhibitory concentrations were also determined for ceftazidime, cefepime, ceftriaxone, amikacin, gentamicin, ciprofloxacin and piperacillin-tazobactam by broth microdilution method according to CLSI recommendation.. All isolates were multidrug-resistant exhibiting highly resistance to ceftazidime, cefepime, piperacillin/tazobactam, amikacin, gentamicin, netilmicin and ciprofloxacin. No resistance to ampicillin/sulbactam was observed which is not in use in our hospital. The isolates were genetically characterized with pulsed-field gel electrophoresis (PFGE). The preparation of genomic DNA of A. baumannii isolates was performed as previously described. Oxacillinases were detected by using a standard PCR technique with primers specific for blaOXA-23, blaOXA-40, blaOXA-58, and blaOXA-69 genes. Production of metallo-β -lactamases was screened by E test-MBL and PCR with primers specific for VIM and IMP β -lactamases. Β -lactamases were prepared from overnight broth cultures, released by sonication and cell debris was removed by centrifugation. PCRs were positive for the OXA-69 like enzyme in ten Acinetobacter strains belonging to unique PFGE profile characterised to pulsotype A, while strain characterised to pusotype B was the only strain isolated from children intensive care unit and carbapenemase gene was not found with tested primers. No significant hydrolysis of imipenem was detected. Acccording to the bibliographical data OXA-69 is a naturally occurring oxacillinase in A. baumannii and it does not confer on the producing isolates significant resistance to carbapenems, thus it can be concluded that resistance to imipenem and meropenem in our isolates is due to other mechanisms such as porin loss or efflux. Spread of the pulsotype A with OXA-69-type oxacillinases was due to clonal dissemination of multi-drug resistant A. baumannii between two different adult Intensive Care Units, probably by hospital staff during medical procedures. The infection control team of the hospital implemented restriction of carbapenem usage and strict antiseptic techniques, which included the rigorous use of alcohol-clorhexidine solutions before and between patient and equipment contact and before leaving the unit. To our knowledge, this is the first report on the molecular characterization carbapenem resistance in A. baumannii in Croatia. A similar finding underscores the progressive emergence of these determinants in different geographic areas. Consequently, incidence and spread of multidrug-resistant A. baumannii nosocomial infections suggest the necessity of a surveillance program and enforcing adequate control measures in different hospital settings

Alert surveillance of intensive care unit-acquired Acinetobacter infections in a Sicilian hospital

The epidemiological impact of Acinetobacter baumannii nosocomial infections in a Sicilian intensive care unit (ICU) was investigated to determine the Acinetobacter-specific infection rates, to estimate the preventable proportion of Acinetobacter infections, i.e., those resulting from cross-transmission, and to investigate the molecular epidemiology of antimicrobial resistance in Acinetobacter. The impact of Acinetobacter nosocomial infection in the ICU was determined to be 3.0 new cases per 100 admissions. Site-specific rates confirmed that ICU-acquired pneumonia was the most important infection type. The incidence rate, adjusted by the number of patient-days, was 3.3 infections/1000 patient-days. The estimated preventable proportion of A. baumannii nosocomial infections in the ICU was 66.7%. A class 1 integron, characterised by its gene cassette content, was present in all A. baumannii isolates of four different pulsed-field gel electrophoresis types, and was associated significantly with clones implicated in cross-transmission episodes. Furthermore, the same integron was detected in two genetically distinct isolates responsible for recurrent infection in the same patient, suggesting the occurrence of horizontal gene transfer in vivo. Even in an endemic setting with low infection rates, spread of A. baumannii was caused mainly by infection control shortcomings that require appropriate surveillance and control policies.

An outbreak of Acinetobacter baumannii septicemia in a neonatal intensive care unit of a university hospital in Brazil

We studied an outbreak of two multi-drug resistant clones of Acinetobacter baumannii in the Neonatal Intensive Care Unit of the Uberlândia Federal University Hospital in Minas Gerais state, Brazil, and we analyzed the contribution of cross-transmission in the rise in infection rates. Eleven neonates who developed multi-drug resistant A. baumannii nosocomial infection were matched to 22 neonates who were admitted to the same unit and did not develop an infection during the outbreak period, in order to identify risk factors for infection. Three out of the 11 neonates died. Epidemiological investigation included molecular typing, using pulsed field gel electrophoresis. Prior to the outbreak, from December 2001 to March 2002, no case of infection by this microorganism was diagnosed. Environmental and healthcare worker hand cultures were negative. Nine isolates had similar pulsed field gel electrophoresis patterns and two had another clone. The first clone was brought into the unit by an infected patient who was transferred from another hospital without a history of antibiotic use. The second clone did have its origin clearly defined. Both infected groups led us to conclude that several factors contributed to infection with A. baumannii. These factors were: exposure to antibiotics and invasive devices, birth weight < 1500 g, age < or = 7 days and duration of hospitalization > or = 7 days. Based on logistic regression, infected neonates were more exposed to carbapenem and mechanical ventilation than the control group. Cross transmission between infants contributed to the rise in the rates of multi-drug resistant A. baumannii infection.

An outbreak of Acinetobacter baumannii: the importance of cross-transmission.

To investigate an outbreak of nosocomial infections due to multidrug-resistant (MDR) Acinetobacter baumannii and to analyze the contribution of cross-transmission in the rise in infection rates. Epidemiological investigation; molecular typing using pulsed-field gel electrophoresis (PFGE); matched case-control study to identify risk factors for infection. A 34-bed surgical intensive care unit at a tertiary-care hospital. Eighteen patients who developed MDRA baumannii nosocomial infection were matched to 36 patients who were admitted to the same surgical intensive care unit (SICU) room and did not develop an infection during the outbreak period. Prior to the outbreak, the baseline attack rate of MDR A baumannii nosocomial infections was 3 per 100 patients per month. From February 1 through March 22, 1998, the attack rate rose to 16 per 100 patients per month, with a total of 18 infections. All isolates had indistinguishable PFGE patterns. Seventy environmental cultures were negative for MDR A baumannii. Following intense infection control education, the attack rate decreased to 4 per 100 patients per month. By conditional logistic regression, cases were exposed to a significantly higher number of patients with MDR A baumannii infections compared to controls (odds ratio, 1.1; 95% confidence interval, 1.01-1.2; P=.02), even after adjusting for length of SICU admission and exposure to antibiotics and invasive devices. Cross-transmission between patients contributed to the rise in rates of MDRA baumannii infections. A common environmental source was not detected.

PCR detection of aminoglycoside resistance genes: a rapid molecular typing method for Acinetobacter baumannii

Aminoglycoside resistance is common among strains of Acinetobacter baumannii responsible for nosocomial infections, and inactivation of these antibiotics by enzymatic modification is the main mechanism. Different types of aminoglycoside acetyltransferases (AAC), nucleotidyltransferases (ANT), and phosphotransferases (APH) are synthesized by clinical isolates, and several enzymes can be produced by a single strain. Using a multiplex PCR procedure carried out on bacterial thermolysates, we analyzed the aminoglycoside resistance gene content of strains belonging to eight clusters identified by pulsed-field gel electrophoresis. In a single reaction were combined three primer pairs in order to amplify the genes coding for AAC(6')-Ih, AAC(3)-I, and AAC(3)-II, three primer pairs for the genes coding for ANT(2'')-I, APH(3')-VI, and rRNA 16S as internal control, and finally two primer pairs for the genes coding for AAC(6')-Ib and APH(3')-I. According to the aminoglycoside resistance gene patterns, the strains of the eight clusters were distributed into seven classes. This simple and rapid (< 8 h) fingerprinting technique could be a useful tool for the epidemiological investigation of A. baumannii nosocomial infections.