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PubMed1989

Control of an epidemic spread of a multi-resistant strain of Acinetobacter calcoaceticus in a hospital.

The spread of a multi-resistant glucose-acidifying Acinetobacter calcoaceticus strain in a community hospital was studied. After admission of a colonized patient to the hospital the strain was found in clinical specimens from ICU patients and subsequently from several of these patients after transfer to medical wards. Environmental specimens from the ICU and medical wards were analysed in order to investigate the mode of spread of the strain. Isolates of A. calcoaceticus were screened by their antibiotic resistance pattern. In addition, the cell envelope protein electrophoretic profiles were used as epidemiological markers. The multi-resistant acinetobacters all had the same protein profile. To prevent spread of the epidemic strain strict hygienic measures were enforced, e.g. scrupulous cleaning of the room after discharge of any colonized patient and increased attention to the hand hygiene of the medical and nursing staff. Furthermore, the use of antibiotics was restricted. Although this strain was only eradicated with difficulty in the affected patients, it did not spread throughout the hospital. Colonization of patients with the multi-resistant micro-organism was predominantly localized to the ICU.

Acinetobacter↗
PubMed1995

Acinetobacter baumannii outbreak isolates characterized by three typing methods.

Forty-two strains of Acinetobacter baumannii were isolated from 15 patients hospitalized in a French intensive care unit. An epidemiological study based on the typing of these isolates was carried out using biotyping, antibiotyping, and ribotyping to recognize the transmission of multiresistant strains by transfer of a patient from one hospital to another. Fifteen strains from the outbreak (1 strain for each patient), five Acinetobacter baumannii strains isolated before the outbreak in Bellevue Hospital (St. Etienne), and five strains isolated in Cochin Hospital (Paris) were included. The three methods gave a good correlation: the epidemic strains had the same antibiotic resistance pattern, the same biotype, and the same ribotypes obtained with three different endonucleases.

Acinetobacter↗
PubMed1998

Carbapenem resistance mediated by beta-lactamases in clinical isolates of Acinetobacter baumannii in Spain.

Four patients colonized/infected with carbapenem-resistant strains of Acinetobacter baumannii are described. The first patient had a decubitus ulcer infection and had been on intravenous imipenem for 50 days. Two other patients, from whom Acinetobacter baumannii was isolated from urine, were hospitalized in the same ward as the first patient. The fourth patient had been mechanically ventilated in the intensive care unit for 4 month and had nosocomial pneumonia. He had been on intravenous meropenem for 1 month. Minimum inhibitory concentrations (MICs) of imipenem (128 mg/l) and meropenem (> 128 mg/l) were the same for the isolates from the first three patients, and all of these isolates had the same repetitive extragenic palindromic polymerase chain reaction (rep-PCR) pattern. The MICs of carbapenems were lower for patient 4's isolate, which also had a different rep-PCR pattern. Beta-lactamases that hydrolyzed imipenem were detected in all four isolates; isoelectric points were 8.6-7.7 in the first three isolates and 6.8-7 in the fourth isolate.

Acinetobacter↗
PubMed1997

Risk factors, clinical features and outcome of Acinetobacter bacteremia in adults.

The medical records of 39 patients with Acinetobacter bacteremia identified in the period between 1985 and 1995 were reviewed. In 24 cases (62%) the bacteremia was considered to have been clinically significant. Most of the infections (79%) were nosocomial, and the majority of these were acquired in an intensive care unit. Ten (42%) patients developed septic shock complicating the bacteremia and 13 (54%) died. In most of these cases (85%), Acinetobacter bacteremia was thought to have caused or contributed to death. The following variables were associated with a greater risk of mortality: age > 65 years (OR = 16; p = 0.01); development of septic shock (OR = 22; p = 0.004); and the presence of coagulopathy (OR = 20; p = 0.03).

Acinetobacter↗
PubMed1997

Molecular typing of Acinetobacter baumannii from ten different intensive care units of a university hospital.

Thirty-one isolates of Acinetobacter baumannii were collected from ten intensive care units of an Austrian university hospital. All isolates were typed by enterobacterial repetitive intergenic consensus polymerase chain reaction (ERIC-PCR). Two strains colonizing 13 infants in the neonatal intensive care unit were identified by ERIC-PCR. All other Acinetobacter baumannii isolates had highly divergent ERIC-PCR patterns, despite having the same antibiogram. Thus, a hospital-wide clonal distribution, as suggested by identical antibiogram patterns, was excluded by ERIC-PCR.

Acinetobacter↗
PubMed1992

Identification of an epidemic strain of Acinetobacter baumannii using electrophoretic typing methods.

Nosocomial infections due to Acinetobacter baumannii dramatically increased in a Lebanese medical center following an outbreak of hostilities in Lebanon in 1984. The incidence of infection caused by this organism has remained high in this institution, thus requiring the implementation of a strain typing system to aid in infection control. Three methods were investigated for their utility in differentiating among a representative group of 36 nosocomial Acinetobacter baumannii isolates obtained over a 10 month period from specimens of hospitalized patients. Isolates were typed by antibiogram analyses, plasmid fingerprinting, and total cell protein profiles. Only three distinct total cell protein profiles were detected, with one pattern accounting for 26 (72.2%) of the isolates. However, eight different plasmid profiles were observed, with 20 (55.5%) isolates having the same profile. Eleven distinct antibiograms were seen with the most prevalent pattern occurring in 21 isolates. Twenty of the 21 (95%) isolates with the common antibiogram also had the same plasmid profile and total protein profile (44.4% of total isolates). The combination of these three typing methods was useful in tracing the spread of these organisms in the medical center. The data obtained suggest the distribution of a common strain among at least six wards of this hospital.

Acinetobacter↗
PubMed1999

Evolution of resistance among clinical isolates of Acinetobacter over a 6-year period.

The aim of this report was to study the evolution of susceptibilities of 1532 clinical isolates of Acinetobacter recovered over a period of 6 years. The minimal inhibitory concentrations (MICs) of 15 antimicrobial agents were determined for all the isolates. The respective percentages of resistant strains in the years 1991 and 1996 were as follows: ciprofloxacin, 54.4% and 90.4%; tobramycin, 33% and 71.8%; amikacin, 21% and 83.7%; ampicillin plus sulbactam, 65.7% and 84.1%; ceftazidime, 57.4% and 86.8%; ticarcillin, 70% and 89.4%; trimethoprim plus sulfamethoxazole, 41.1% and 88.9%; and imipenem, 1.3% and 80%. The MIC90s of ciprofloxacin, sparfloxacin, biapenem, meropenem, imipenem, cefepime, cefpirome, and rifampicin against 250 imipenem-resistant Acinetobacter strains were >32, >32, 128, >256, 256, >256, 256, and 16 mg/l, respectively. With serious infections, it was necessary to resort to the use of colistin, the only antibiotic active in vitro.

Acinetobacter↗
PubMed1987

Hospital outbreak of multi-resistant Acinetobacter anitratus: an airborne mode of spread?

During a 10-month period, from October 1984 to July 1985, a multi-resistant strain of Acinetobacter anitratus was isolated from 36 patients in three neurosurgical wards, one medical ward and the intensive care unit of a district general hospital, and from two patients in the intensive care unit of a hospital in another district. Fourteen patients developed significant infection including pneumonia (10), meningitis (2), septicaemia (2) and wound infection (4). The majority of cases (28) involved the respiratory tract of ventilated patients, although respiratory equipment was not implicated as a source of the infection. The epidemic strain was recovered from the skin, nose, mouth and rectum of colonized patients and from the hands of personnel. However, extensive air and environmental contamination in the vicinity of colonized patients was also demonstrated. This is the first outbreak of infection with Acinetobacter, of which we are aware, where airborne spread has been observed.

Acinetobacter↗
PubMed1989

Acinetobacter calcoaceticus biovar anitratus septicaemia in a neonatal intensive care unit: epidemiology and control.

Nineteen neonates with septicaemia caused by Acinetobacter calcoaceticus biovar anitratus were treated in a neonatal intensive care unit between October, 1983 and March, 1986. The ages of the patients at the onset of septicaemia ranged from 4 to 22 days (mean 9.7 days). Their birth weights ranged from 1000 g to 3350 g (mean 1790 g) and were less than 2000 g in 14 patients. Antibiotics had been administered to 17 of the 19 neonates before the onset of septicaemia, and all mature infants had received prior antibiotic therapy, intubation or had suffered from a convulsion. Acinetobacter anitratus strains were isolated from pharyngeal swabs and/or faeces from 35 (79.5%) out of 44 infants of less than 2000 g. These strains were also isolated from the hands of staff members, and from equipment such as sinks and baths in the unit. It was likely that nosocomial infection via the hands of the staff occurred. Encouraging frequent hand-washing, strict antibiotic use, and cohorting of colonized infants resulted in a reduction of colonization and no further cases of septicaemia were reported.

Acinetobacter↗
PubMed1990

The survival of Acinetobacter calcoaceticus inoculated on fingertips and on formica.

When inoculated on the fingers of three volunteers, strains of Acinetobacter calcoaceticus var. anitratus survived better than strains of var. lwoffii; 60 min after an inoculum of 10(4) cfu/finger, washings yielded between 2.6 x 10(1) (for a sporadic strain of var. lwoffii) and 7.2 x 10(2) cfu/finger (for an epidemic strain of var. anitratus). All five test strains survived better on formica than on skin, and from an inoculum of 10(4) cfu, between 6.4 x 10(2) and 2.2 x 10(3) cfu/finger were recoverable 60 min later. After inoculation of formica sheets, both strains of var. lwoffii could still be recovered in low numbers 24 h later, and two of the three strains of var. anitratus 60 h later. These findings suggest the presence of hitherto unrecognized antibacterial activity of skin against Acinetobacter calcoaceticus and suggest that outbreaks may be sustained by hand transmission. The ability of these organisms to survive desiccation on formica supports the proposal that transmission by air, dust or fomites may hitherto have been underestimated for this species.

Acinetobacter↗
PubMed1993

Comparison of three typing methods in hospital outbreaks of Acinetobacter calcoaceticus infection.

During a period of 11 months Acinetobacter baumanii was isolated from 27 patients and 21 environmental samples in the Intensive Care Unit (ICU) and in one surgical unit of a University Hospital. The isolates were characterized by biotyping, antibiograms and plasmid profiles and compared with co-isolates. Plasmid fingerprinting distinguished three outbreaks, whereas other typing methods were less sensitive and discriminatory. Although plasmid profiles seem to be a simple and reproducible marker for epidemiological studies with acinetobacter strains, it might be useful to combine at least two typing methods since plasmids are unstable genetic structures, and not all strains possess plasmids.

Acinetobacter Infections↗
PubMed1995

Genomic fingerprinting Acinetobacter baumannii: amplification of multiple inter-repetitive extragenic palindromic sequences.

Acinetobacter species are important nosocomial pathogens. A rapid and sensitive identification system, capable of providing strain identity at the genetic level, is required to identify outbreak strains and facilitate the early implementation of infection control procedures. Repetitive extragenic palindromic (REP) elements, have been identified in numerous bacteria and these genomic sequences provide useful targets for DNA amplification. A method for amplifying inter-REP DNA sequences, REP-multiple arbitrary amplicon profiling (REP-MAAP), is described and applied to 29 Acinetobacter baumannii from clinical samples. Amplified polymorphic DNA patterns were demonstrated for all isolates and those displaying identical REP-MAAP patterns were considered identical at the genetic level. In the spring of 1993, 10 intensive care unit patients had endotracheal colonization with A. baumannii (five with REP-MAAP I and five with REP-MAAP II patterns). These findings suggested nosocomial transmission of organisms which was terminated by standard infection control measures. No further A. baumannii were detected until the winter of 1993 when isolates of different REP-MAAP groups emerged, suggesting that factors other than nosocomial transmission were implicated.

Acinetobacter↗
PubMed1993

Acinetobacter, an infrequent cause of community acquired bacterial meningitis.

A 19-year-old previously healthy woman developed meningitis due to Acinetobacter calcoaceticus. This is a Gram-negative coccobacillus belonging to the family Neisseriaceae. Most reported cases of Acinetobacter meningitis were hospital-acquired and due to strains highly resistant to amoxycillin. Our patient was treated with amoxycillin and recovered without sequelae.

Acinetobacter Infections↗
PubMed2004

Interhospital transfer of pan-resistant Acinetobacter strains in Johannesburg, South Africa.

BACKGROUND: Acinetobacter species infections are increasingly found to cause nosocomial infections, particularly in intensive care units. These pathogens are difficult to eliminate from the hospital environment, and the emergence of multiple-drug-resistant strains complicates patient treatment. In this retrospective study, several strains were analyzed to study the possible spread of pan-resistant strains. METHODS: Macrorestriction analysis was performed on isolates collected in July 2001 from Johannesburg Hospital and strains collected from a number of hospitals in Johannesburg a year later. RESULTS: A strain endemic to Johannesburg Hospital that was cefepime and ceftazidime sensitive in 2001 developed resistance to these antibiotics within 1 year. This and other resistant strains were found to have spread among academic and private hospitals in the area by July 2002. CONCLUSIONS: The development of resistance is believed to be a response to antibiotic pressure and the spread of resistant strains a result of health care worker and/or patient transfer among hospitals. This snapshot epidemiologic study highlights the need to institute stricter infection control measures to limit the spread of organisms such as Acinetobacter among hospitals.

Acinetobacter↗
PubMed2005

Multi-resistant gram-negative organisms in Maryland: a statewide survey of resistant Acinetobacter baumannii.

Following the development of multi-resistant Acinetobacter baumannii at several area hospitals, a volunteer task force from the Greater Baltimore Chapter of the Association of Professionals in Infection Control and Epidemiology, Inc (APIC) set out to assess the situation throughout the state. A survey was disseminated to all 70 acute, general, and specialty hospitals in Maryland. The response rate was 57%, and multi-resistant Acinetobacter was the most prevalent resistant gram-negative organism reported.

Acinetobacter Infections↗
PubMed2005

Rapid epidemiological analysis of Acinetobacter strains by Raman spectroscopy.

From earlier publications, we noticed that Raman spectra could potentially be used for subspecies identification of microorganisms. Here we evaluated the technique for its use as a typing tool of Acinetobacter species, using a collection of well-characterised strains from five hospital outbreaks. The strains were previously analysed using molecular techniques as cell envelope protein profiling and ribotyping. In this study, we have typed the strains by AFLP analysis and Raman spectroscopy. We compared the results using hierarchical cluster analysis, which showed highly similar groupings by both techniques. There seemed to be some misclassification between two sets of outbreak strains in the Raman analysis. We ascribe this to the clonal relationship between the strains of both outbreaks, described earlier. This results from a highly similar biochemical composition of the strains involved, and hence a highly similar Raman spectrum. We conclude that Raman spectroscopy could be an easy-to-use alternative in epidemiological studies of Acinetobacter strains and a promising starting point for the development of epidemiological studies in general.

Acinetobacter↗
PubMed1994

Clinical and molecular epidemiology of acinetobacter infections sensitive only to polymyxin B and sulbactam.

A nosocomial outbreak of infections due to imipenem-resistant Acinetobacter baumannii occurred in a New York hospital after increased use of imipenem for cephalosporin-resistant klebsiella infections. We identified all A baumannii isolates over 12 months, reviewed corresponding patient records, and compared strains with different antibiotic susceptibility patterns by restriction endonuclease analysis. Environmental surveillance cultures were done before and after institution of control measures. 59 patients harboured imipenem-resistant A baumannii, and 18 were infected. Isolates from patients were resistant to all routinely tested antibiotics, including imipenem. Further studies showed susceptibility to polymyxin B and sulbactam. These isolates were identical by restriction endonuclease analysis to A baumannii isolates susceptible to imipenem alone, or to imipenem and amikacin, but differed from broadly susceptible isolates. Surveillance cultures showed hand and environmental colonisation by imipenem-resistant strains. Infection and colonisation were eliminated by intensive infection control measures, and irrigation of wounds with polymyxin B. Increased use of imipenem against cephalosporin-resistant klebsiella may lead to imipenem resistance among other species, particularly acinetobacter. Such resistance appears to derive from a prior multi-resistant clone, in contrast to one which retains susceptibility to several antibiotics.

Acinetobacter↗
PubMed1997

Community-acquired Acinetobacter pneumonia: a case report.

A 35-year-old male with glucose-6-phosphate dehydrogenase (G6PD) deficiency was admitted because of right chest (pleuritic) pain, fever, cough with scarce production of blood-tinged sputum, and generalized yellowish discolouration of skin for 2 days. Radiographic examination revealed right lower lobe necrotizing pneumonia. Hypotension, dyspnoea and severe haemolysis was noted the next day. Echo-guided lung aspiration and sputum cultures both grew Acinetobacter baumannii. Antibiotic therapy was started immediately, but fever persisted and abscess formation was noted 1 week later. After aggressive supportive and antibiotic therapy, he made a slow but complete recovery from the pneumonia, and was then discharged in a stable condition. Acinetobacter baumannii is a well-known causative agent of nosocomial infections, particularly in intensive units. Community-acquired pneumonia, however, is quite rare, and usually has a fulminant course and high case fatality rate.

Acinetobacter↗