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An ampC gene was cloned from a clinical isolate of Acinetobacter baumannii (strain RAN). DNA sequencing and primer extension studies showed that ampC is transcribed from a promoter contained within a putative insertion sequence element which has been found to abut several different genes in Acinetobacter spp.
Acinetobacter baumannii is an important nosocomial pathogen, especially in immunocomprimised patients and those hospitalized in intensive care units. After the first isolation of A. baumannii strains from the bronchial aspirates of two patients in the intensive care unit (ICU) of our hospital as a pure culture, screening studies were performed to define possible source(s). A. baumannii strains isolated from bronchial aspirates and blood cultures of the patients in ICU were collected as a possible part of the outbreak. A total of 23 screening samples collected from equipment (7), hands (4) and gloves (2) of the staff, and from ten different body regions of the patients in the ICU were cultured. Antimicrobial susceptibility test of the isolates was performed by the standardized disk-diffusion method. All isolates were subtyped by antibiogram, arbitrarily primed polymerase chain reaction (AP-PCR) and pulsed-field gel electrophoresis (PFGE) typing methods. A total of 26 A. baumannii strains including eight clinical and 18 screening isolates were identified. All isolates were susceptible only to meropenem, tobramycin, and imipenem. There was at least a 96% resistance rate to the other antibiotics tested. Antibiogram typing showed that 24 of the 26 isolates were epidemiologically related, two were unique. AP-PCR yielded two types, one of which had 21 isolates, the other had five. PFGE fingerprinting revealed that all isolates were clonally related, including four closely related and 22 indistinguishable strains. Based on the results of PFGE which has been accepted as a reference method it can be concluded that A. baumannii strains isolated from our intensive care unit originated from a single type of strain.
Twelve clonally related and multidrug-resistant Acinetobacter baumannii isolates were recovered during a 4-month period from 12 patients hospitalized at the Valenciennes Hospital in France. Antibiograms determined by the double-disk diffusion technique on cloxacillin-containing plates detected a clavulanic acid-inhibited extended-spectrum beta-lactamase (ESBL). PCR and sequencing identified the gene encoding the Ambler class A ESBL VEB-1. This gene was located on the chromosome and was part of a class 1 integron identical to that previously identified in Pseudomonas aeruginosa isolates from Thailand. Additionally, seven clonally related bla(VEB-1)-positive A. baumannii strains were identified in the immediate environment of the hospitalized patients. This is the first report of the ESBL VEB-1 in Acinetobacter spp. and the first description of VEB-1-producing strains as a source of an outbreak occurring outside Southeast Asia. This report underlines the difficulty of the identification of ESBLs in A. baumannii.
We investigated a multidrug-resistant Acinetobacter baumannii outbreak in the Intensive Care Unit (ICU) of a tertiary care hospital in Greece over a 3-month period. Molecular typing of the outbreak isolates from 31 patients revealed that two distinct genotypes were involved. Nine isolates, belonging to both genotypes, were resistant to carbapenems. Samples from the ICU environment and from the hands of personnel were collected to identify possible contamination. Class 1 integrons of 3.1, 2.5 and 2.2 kb were amplified from the clinical and environmental isolates. The 3.1 kb integron carrying five gene cassettes was found for the first time in A. baumannii. The outbreak ceased after implementation of hygienic measures in the ICU, including complete cleaning and disinfection.
The epidemiological characterization of multiply resistant Acinetobacter baumannii isolates from a six-bed Intensive Care Unit (ICU) is described. Investigations for A. baumannii were performed in three subsequent surveillance studies. In the first study, surveillance cultures were taken from patients, health care personnel and the environment; in the second study surveillance cultures were taken at 0, 4, and 7 days from all patients admitted consecutively to the ward; and in the third study surveillance cultures were taken from patients, health care personnel and the environment. During the first study all four hospitalized patients were found to harbour A. baumannii. Hand cultures did not grow any A. baumannii when staff entered the ward from home, but 7 positive health care workers were identified out of 25 samples taken during work, and two cultures of environmental specimens grew A. baumannii. During the second study, 4 of 86 (4.6%) patients resulted colonized with A. baumannii. In the third epidemiological study, no A. baumannii was cultured from either patients, health care personnel or the environment. All isolates recovered from various patients or sources produced conserved macrorestriction Pulsed-Field Gel Electrophoresis (PFGE) patterns and showed the same antibiotic resistance; therefore, they can be considered indistinguishable. The same antibiotic resistance and macrorestriction patterns were observed in previously isolated A. baumannii strains in the ward during May 1997, suggesting the persistence of a single A. baumannii in the ICU. The present study confirms that molecular typing is an essential tool in the epidemiology and control of nosocomial infections, showing here the persistence of a single A. baumannii clone in the ICU. The origin of this strain remains unknown but, when basic infection control measures were reinforced, emphasizing the importance of hand antisepsis and judicious use of gloves, control of A. baumannii spread in the ward was achieved.
INTRODUCTION: The increased incidence of nosocomial infections by multi-drug resistant Acinetobacter baumannii creates demand on the application of some combinations of older antimicrobials on that species. We conducted the present observational study to evaluate the efficacy of intravenous and aerosolized colistin combined with rifampicin in the treatment of critically patients with nosocomial infections caused by multiresistant A. baumannii. PATIENTS AND METHODS: Critically ill patients with nosocomial infections caused by A. baumannii resistant to all antibiotics except colistin in a medical intensive care unit. Diagnosis of infection was based on clinical data and isolation of bacteria. The bacterial susceptibilities to colistin were tested. Clinical response to colistin+rifampicin was evaluated. RESULTS: Twenty-six patients (43.58+/-18.29 years, Acute Physiology and Chronic Health Evaluation II Score (APACHE II): 6.35+/-2.99), of whom 16 cases of nosocomial pneumonia treated by aerosolized colistin (1x10(6) IU three times/day) associated with intravenous rifampicin (10 mg/kg every 12h), nine cases of bacteraemia treated by intravenous colistin (2x10(6)IU three times/day) associated with intravenous rifampicin (10 mg/kg every 12h) in which three cases associated with ventilator associated pneumonia and one case of nosocomial meningitis treated by intrathecal use of colistin associated with intravenous rifampicin. The clinical evolution was favourable for all ill patients. Concerning side effects, we have noticed a moderate hepatic cytolysis in three patients. CONCLUSION: This is the first clinical report of colistin combined with rifampicin for treatment of A. baumannii infection. Despite the lack of a control group and the limited number of patients, the results seem to be encouraging.
We describe an outbreak of Acinetobacter baumannii in a neonatal intensive care unit (NICU), and our investigation to determine the source and mode of transmission and identify the population at risk. A case (infected infant) was defined as a patient hospitalized in the NICU during the outbreak period, with clinical signs of sepsis and isolation of A. baumannii. In colonized infants, A. baumannii was isolated from body surfaces without signs of infection. Infected infants were separated and treated by a different medical team. Cultures were taken from working surfaces and along the infant's admission passage from the delivery room to the NICU. The outbreak strain was identified by pulsed-field gel electrophoresis (PFGE). Nine cases and eight colonized infants met the definition criteria. Cases were younger than colonized infants with regard to gestational age and age of diagnosis and had lower birthweights (P<0.01). The outbreak strain was only isolated from hygroscopic bandages used on skin under the ventilation tube and umbilical catheters. Discontinuing the use of the bandages put an end to the outbreak. We conclude that a rapid and thorough investigation of the environment during an outbreak of A. baumannii is essential to finding the source of the infection, and that hygroscopic bandages may be a source of such outbreaks.
A set of 103 epidemiologically well-defined Acinetobacter baumannii isolates obtained from nine hospital outbreaks and 21 unrelated strains were characterized by pulsed-field gel electrophoresis (PFGE) of total genomic DNA digested with ApaI. Among outbreak strains, eight different patterns and five possible variants were identified by PFGE. Results were compared with those from traditional typing methods such as plasmid profile analysis, antimicrobial susceptibility, and biotyping. Plasmid analysis revealed six different and two related patterns; one outbreak strain lacked plasmids. A total of 16 of the 21 unrelated strains harbored plasmids and exhibited unique patterns. Epidemiologically unrelated strains were placed into only two biotypes and had similar antimicrobial susceptibility patterns but were clearly distinguished by PFGE. PFGE of A. baumannii chromosomal DNA yielded reproducible and easily readable results and showed excellent discriminatory power. However, plasmid profile analysis may provide a cost-effective first step in epidemiological typing of A. baumannii isolates obtained from well-defined hospital outbreaks.
OBJECTIVES: Successful therapy of carbapenem-resistant Acinetobacter baumannii strains has been reported with colistin, but recently we argued against its use as monotherapy because of the poor results obtained in a mouse pneumonia model. Our aim was to identify antibiotic combinations that were valid therapeutic alternatives in the same model. METHODS: We used two carbapenem-resistant A. baumannii strains (D and E; MICs of imipenem, 8 and 512 mg/L, respectively). MICs of tobramycin, rifampicin and colistin for both strains were 8, 8 and 0.5 mg/L, respectively. RESULTS: In infections caused by strain D, lung bacterial counts (log(10) cfu/g, mean +/- s.d.) were: controls (10.86+/-0.25), imipenem (5.99+/-0.59, P < 0.05 versus controls), and colistin (10.43 +/- 1.09); imipenem + tobramycin was the most active combination (5.46+/-0.62, P < 0.05 versus controls). In infections caused by strain E, results were: controls (10.82+/-0.33), rifampicin (5.62+/-0.26, P < 0.05 versus controls), colistin (8.38+/-1.22, P < 0.05 versus controls), and imipenem (11.01+/-0.2); rifampicin + imipenem (3.79+/-0.99) and rifampicin + tobramycin (3.96+/-0.30) were the most active combinations (P < 0.05); results with rifampicin + colistin (5.59+/-1.17) were similar to those with rifampicin alone. CONCLUSIONS: Our data indicate that imipenem can still be the best alternative for carbapenem-resistant A. baumannii infections with moderate levels of imipenem resistance, preferably combined with aminoglycosides. For strains highly resistant to imipenem, a combination of rifampicin with imipenem, tobramycin or colistin may be useful, if resistance to rifampicin is only moderate.
Twenty-one patients with multidrug-resistant (MDR) Acinetobacter baumannii and Pseudomonas aeruginosa pneumonia were treated with nebulized polymyxin E (colistin). Overall clinical and microbiological response rates were 57.1% and 85.7%, respectively. Nebulized colistin may be reasonably efficacious and safe for treatment of MDR pneumonia. Its role in therapy warrants further investigation in comparative studies.
BACKGROUND: Acinetobacter baumannii has become an increasingly important nosocomial pathogen, particularly in intensive care units (ICUs). The aim of this investigation was to study the molecular epidemiology of A baumanii in a university hospital in Italy. METHODS: All A baumanii isolates were collected and typed with phenotypic and genotypic methods during a 7-month period. A 1-year prospective surveillance of ICU-acquired infections was performed by using the National Nosocomial Infections Surveillance methodology. RESULTS: A baumanni accounted for 28.4% of all infections and 46.7% of all pneumonia acquired in the ICU, with a nosocomial infection rate of 12.4% or 8 infections per 1000 patient-days. Risk factors for A baumannii acquisition in the ICU were mechanical ventilation and previous use of broad-spectrum antibiotics, whereas administration of carbapenems showed a significant protective effect. Pulsed-field gel electrophoresis of genomic Apa I digests identified at least 5 outbreaks in the ICU caused by 5 different clones, one replacing the other in a well-defined temporal order. CONCLUSIONS: Whereas the sequential temporal cluster of epidemic clones in the ICU is intriguing and requires further research, the clear evidence of cross-contamination of A baumannii isolates involved with infections in the ICU demands extensive preventive efforts.
The Acinetobacter baumannii type strain, ATCC 19606, secretes acinetobactin, a catechol siderophore highly related to the iron chelator anguibactin produced by the fish pathogen Vibrio anguillarum (Listonella anguillarum). This paper reports the initial characterization of the genes and gene products involved in the acinetobactin-mediated iron-acquisition process. Insertional mutagenesis resulted in the isolation of several derivatives whose ability to grow in medium containing the iron chelator 2,2'-dipyridyl was affected. One of the insertions disrupted a gene encoding a predicted outer-membrane protein, named BauA, highly similar to FatA, the receptor for ferric anguibactin. Immunological relatedness of BauA with FatA was confirmed by Western blot analysis. Another transposon insertion was mapped to a gene encoding a protein highly similar to FatD, the permease component of the anguibactin transport system. Further DNA sequencing and nucleotide sequence analysis revealed that these A. baumannii 19606 genes are part of a polycistronic locus that contains the bauDCEBA ORFs. While the translation products of bauD, -C, -B and -A are highly related to the V. anguillarum FatDCBA iron-transport proteins, the product of bauE is related to the ATPase component of Gram-positive ATP-binding cassette (ABC) transport systems. This entire locus is flanked by genes encoding predicted proteins related to AngU and AngN, V. anguillarum proteins required for the biosynthesis of anguibactin. These protein similarities, as well as the structural similarity of anguibactin and acinetobactin, suggested that these two siderophores could be utilized by both bacterial strains, a possibility that was confirmed by siderophore utilization bioassays. Taken together, these results demonstrate that these pathogens, which cause serious infections in unrelated hosts, express very similar siderophore-mediated iron-acquisition systems.
OBJECTIVE: To genetically analyze the epidemiology of the colistin-only-sensitive (COS) Acinetobacter baumannii (COS-AB) so as to provide experimental data for controlling COS-AB infection. METHODS: The drug resistance to 14 antibiotics of 136 COS-AB isolates collected in Ruijin Hospital from June 2004 to May 2005 were analyzed. 66 A. baumannii isolates were collected from May to December 2004, of which 33 strains were COS-AB and the other 33 non-COS-AB. Random amplified polymorphic DNA (RAPD) and pulsed-field gel electrophoresis (PFGE) were applied to analyze the homology of these strains. RESULTS: RAPD analysis (with the primers ERIC2 and 272) showed all COS-AB strains as identical, while PFGE analysis showed that these COS-AB were of two closely related genotypes distinctly different from that of the non-COS-AB. The COS-AB strains obtained from the Burns Ward were PFGE B type causing inter-ward outbreak of single clone. And the COS-AB strains obtained from another wards were PFGE BA type causing inter-departmental outbreak, mainly among the departments of surgical system. CONCLUSION: The cross-infection of COS-AB is severe. Strict disinfection and sterilization should be implemented. The epidemiology of COS-AB in environment and patients should be closely monitored. PFGE analysis is a more accurate method in typing A. baumannii.
Acinetobacter baumannii is an opportunist nosocomial pathogen of world-wide importance and produces severe infections in immunocompromised patients. However, the virulence factors contributing to its pathogenic properties are not well known. The effect of normal human serum against 18 clinical isolates of the most prevalent biotypes of A. baumannii in Chile was investigated. The effect of pre-treatment of the cells with ethylene diamine tetraacetic acid (EDTA) or bismuth subsalicylate (BSS), compounds known to decrease the amount of lipopolysaccharide (LPS) and bacterial capsular polysaccharide (CPS), respectively, in other gram-negative bacteria, was evaluated. Most isolates (16 of 18) showed resistance to normal human serum. Prior treatment with EDTA rendered nine of these isolates susceptible to serum, while seven isolates maintained their resistance. Pre-treatment with BSS did not modify the serum-resistant behaviour of the isolates. The results suggest that LPS might be involved in the resistance of A. baumannii to human serum whereas CPS does not seem to contribute to this property.
Acinetobacter baumannii is responsible for severe nosocomial pneumonia. To evaluate new therapeutic regimens for infections due to multiresistant strains and to study the pharmacodynamic properties of various antibiotics, we developed an experimental mouse model of acute A. baumannii pneumonia. C3H/HeN mice rendered transiently neutropenic were infected intratracheally with 5 x 10(6) CFU of A. baumannii. The mean log10 CFU/g of lung homogenate (+/- the standard deviation) were 9 +/- 0.9, 9.4 +/- 0.8, 8.6 +/- 1.2, and 7.7 +/- 1.4 on days 1, 2, 3, and 4 postinoculation. The lung pathology was characterized by pneumonitis with edema and a patchy distribution of hemorrhages in the peribronchovascular spaces of both lungs. Abscesses formed on days 3 and 4. Four days after inoculation, subacute pneumonitis characterized by alveolar macrophage proliferation and areas of fibrosis was observed. The cumulative mortality on day 4 was 85%. This new model was used to study the effects of 1, 2, or 3 50-mg/kg doses of imipenem. Imipenem concentrations in lungs were above the MIC for 2 h after the last dose. The in vivo postantibiotic effect (PAE) was determined during the 9-h period following the last dose; it decreased in duration with the number of doses: 9.6, 6.4, and 4 h after 1, 2, and 3 50-mg/kg doses, respectively. In contrast, no in vitro PAE was observed. This model offers a reproducible acute course of A. baumannii pneumonia. The presence of a prolonged in vivo PAE supports the currently recommended dosing intervals of imipenem for the treatment of human infections due to A. baumannii, i.e., 15 mg/kg three times a day.
While we were isolating Bartonella quintana from body lice, 40 Acinetobacter baumannii strains were also isolated and genotyped. One clone was unique and the other was ampicillin susceptible. A. baumannii DNA was later detected in 21% of 622 lice collected worldwide. These findings show an A. baumannii epidemic in human body lice.
Sixty nosocomial infections caused by Pseudomonas aeruginosa and Acinetobacter baumannii resistant to aminoglycosides, cephalosporins, quinolones, penicillins, monobactams, and imipenem were treated with colistin (one patient had two infections that are included as two different cases). The infections were pneumonia (33% of patients), urinary tract infection (20%), primary bloodstream infection (15%), central nervous system infection (8%), peritonitis (7%), catheter-related infection (7%), and otitis media (2%). A good outcome occurred for 35 patients (58%), and three patients died within the first 48 hours of treatment. The poorest results were observed in cases of pneumonia: only five (25%) of 20 had a good outcome. A good outcome occurred for four of five patients with central nervous system infections, although no intrathecal treatment was given. The main adverse effect of treatment was renal failure; 27% of patients with initially normal renal function had renal failure, and renal function worsened in 58% of patients with abnormal baseline creatinine levels. Colistin may be a good therapeutic option for the treatment of severe infections caused by multidrug-resistant P. aeruginosa and A. baumannii.
The AdeABC pump of Acinetobacter baumannii BM4454, which confers resistance to various antibiotic classes including aminoglycosides, is composed of the AdeA, AdeB, and AdeC proteins; AdeB is a member of the RND superfamily. The adeA, adeB, and adeC genes are contiguous and adjacent to adeS and adeR, which are transcribed in the opposite direction and which specify proteins homologous to sensors and regulators of two-component systems, respectively (S. Magnet, P. Courvalin, and T. Lambert, Antimicrob. Agents Chemother. 45:3375-3380, 2001). Analysis by Northern hybridization indicated that the three genes were cotranscribed, although mRNAs corresponding to adeAB and adeC were also present. Cotranscription of the two regulatory genes was demonstrated by reverse transcription-PCR. Inactivation of adeS led to aminoglycoside susceptibility. Transcripts corresponding to adeAB were not detected in susceptible A. baumannii CIP 70-10 but were present in spontaneous gentamicin-resistant mutants obtained in vitro. Analysis of these mutants revealed the substitutions Thr153-->Met in AdeS downstream from the putative His-149 site of autophosphorylation, which is presumably responsible for the loss of phosphorylase activity by the sensor, and Pro116-->Leu in AdeR at the first residue of the alpha(5) helix of the receiver domain, which is involved in interactions that control the output domain of response regulators. These mutations led to constitutive expression of the pump and, thus, to antibiotic resistance. These data indicate that the AdeABC pump is cryptic in wild A. baumannii due to stringent control by the AdeRS two-component system.