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PubMed1990

[Comparative activity of imipenem, ceftazidime and cefotaxime against Acinetobacter calcoaceticus].

The authors compared the in vitro activity of imipenem, ceftazidime and cefotaxime against 100 strains of Acinetobacter calcoaceticus isolated in 1986 and 1987. The minimal inhibitory and bactericidal concentrations (MICs and MBCs) were determined by the agar dilution and broth microdilution methods respectively, with and without 50 per cent of human serum in the medium to evaluate the possible influence of protein binding. Imipenem was the most active of the three drugs against Acinetobacter, including beta-lactamase producing strains. The MICs 50 and 90 of imipenem were 0.18 micrograms/ml and 0.48 micrograms/ml respectively, as opposed to 5.16 and 14.61 micrograms/ml for ceftazidime, 16 and 75.6 micrograms/ml for cefotaxime. No change was noted in the susceptibility of Acinetobacter to imipenem from 1981 to 1987. The geometric mean MIC of imipenem was 0.25 micrograms/ml. Susceptibility remained unchanged for ceftazidime and cefotaxime but the geometric mean MICs were higher, being 7.29 and 22.8 micrograms/ml respectively. Imipenem had the highest bactericidal activity, with a mean MBC/MIC ratio of 1.16. The presence of human serum did not influence the results, due to the low protein binding of all three antibiotics. It is concluded that imipenem is one of the major antibiotics available for the treatment of nosocomial Acinetobacter infections. However, a few resistant strains have recently been isolated, confirming the need for epidemiological surveillance of bacterial resistance to this antibiotic.

Acinetobacter↗

PubMed1985

[Comparative in vitro study of the activity of 5 quinolones against Acinetobacter calcoaceticus].

The authors compared the in vitro activity of ofloxacin, pefloxacin, ciprofloxacin, norfloxacin and nalidixic acid against 143 clinical isolates of Acinetobacter calcoaceticus. Minimal inhibitory concentrations (MICs) were determined by the agar dilution method. Minimal bactericidal concentrations (MBCs) were measured using microplates. Ciprofloxacin, ofloxacin and pefloxacin were substantially active in vitro. MICs 50 were respectively 0.72, 0.69 and 1.05 micrograms/ml. Geometric means were 0.98, 1.03 and 1.64 micrograms/ml. Norfloxacin and nalidixic acid were slightly less active, with MICs 50 of 7.85 and 17.87 micrograms/ml and geometric means of 10.72 and 28.3 micrograms/ml respectively. Fifty percent of strains were killed by 1.5 micrograms/ml of pefloxacin; the greatest bactericidal in vitro activity was exhibited by ciprofloxacin whose MBC 50 was 0.60 micrograms/ml. Bactericidal activity of ofloxacin was comparable with a MBC 50 of 0.68 micrograms/ml. A significant difference was observed between the two varieties of Acinetobacter: Acinetobacter calcoaceticus var. Iwoffi was more susceptible to tested drugs than the anitratum variety. In short, new quinolone antimicrobial agents may be active in the treatment of nosocomial hospital infections due to Acinetobacter calcoaceticus which is one of the most resistant pathogens to currently available beta-lactams and aminoglycosides.

Acinetobacter↗

PubMed1997

[E-test to study small inhibitor concentrations, bacterial diversity and to identify presumptively beta-lactamases in strains of Pseudomonas aeruginosa and Acinetobacter baumannii associated with +nosocomial infections].

BACKGROUND: Pseudomonas aeruginosa and Acinetobacter baumanii are two important nosocomial agents that require permanent testing of their antimicrobial susceptibility. AIM: To use E-test to determine minimal inhibitory concentrations, estimate bacterial diversity and presumably identify B-lactamases of strains of Pseudomonas aeruginosa and Acinetobacter baumanii isolated from nosocomial infections. MATERIALS AND METHODS: Sixty eight strains of Pseudomonas aeruginosa and Acinetobacter baumanii isolated in a teaching hospital were analyzed with E-test strips to determine their minimal inhibitory concentrations for different antimicrobials. RESULTS: More than 75% of Acinetobacter baumanii were resistant to Piperacillin, Cefpirome, Cefepime, Gentamicin or Amikacin, 40% of strains were resistant to Ceftazidime, 27 and 53% of isolates had a decreased susceptibility to Meropenem and Piperacillin-tazobactam respectively. Twenty eight to 54% of Pseudomonas aeruginosa strains were resistant to Cefepime, Cefpirome, Ciprofloxacin and Gentamicin. Eighteen and 10% of strains were resistant to Meropenem and Imipenem respectively. Less than 10% of strains were resistant to Amikacin, Azireonam, Piperacillin-tazobactam or Ceftazidime. Most of beta-lactam resistance of Pseudomonas aeruginosa was associated to decreased susceptibility or resistance to Cefpirome, Cefepime or to Meropenem-Imipenem and did not match clearly with known beta-lactamase profiles. CONCLUSIONS: The knowledge of susceptibility of these bacteria responsible for nosocomial infections, will help to plan the appropriate use of antimicrobials.

Acinetobacter↗

PubMed1998

Acinetobacter sepsis in newborns.

OBJECTIVE: To evaluate the clinico-epidemiological profile of Acinetobacter sepsis in neonates. DESIGN: Retrospective study. SETTING: Level II Neonatal Care Unit. SUBJECTS: 79 neonates with blood culture positive for Acinetobacter. METHODS: Relevant information was collected on a predesigned proforma from the case records and analyzed for clinical and epidemiological characteristics. RESULTS: The incidence of Acinetobacter septicemia was 11.1/1000 live births. Fifty-five babies were hospital born, 24 were outborn. Out of these, 64.6% babies were born at term and 40.5% had a birth weight of 2500 g or more. A cluster of 53 cases was seen between May and September 1995. In cases with early onset sepsis (onset < 7 days of postnatal age), difficulty in breathing (n = 54), chest retraction (n = 35) and refusal to feed (n = 46) were seen more commonly as compared to late onset sepsis (p < 0.05). Complications observed included meningitis, bleeding manifestations and necrotising enterocolitis in three, six and five babies, respectively. The organism was sensitive to ciprofloxacin (96.2%), amikacin (92.4%) and gentamicin (87.3%). A response rate of 52.4% was observed with Ciprofloxacin in babies not responding to cefotaxime and amikacin combination. The overall mortality was 13.9%. CONCLUSION: Nosocomial Acinetobacter sepsis may affect fullterm, appropriate for gestational age babies. Clinical presentation is indistinguishable from Gram negative septicemia. Life threatening complications can also occur. Ciprofloxacin may prove to be useful drug in resistant cases.

Acinetobacter Infections↗

PubMed1998

[Bacteria of the Acinetobacter genus].

Bacteria of the Acinetobacter genus received little attention for many years because of their weak pathogenic potential and changing taxonomy. Since the introduction starting in the 1980s of an ever increasing number of antimicrobials, these organisms have demonstrated their ability to adapt. They are causing an increasing number of nosocomial infections, most notably in intensive care units. The selection pressure exerted by antimicrobials and the use of increasingly invasive diagnostic and therapeutic procedures are the main factors that promote emergence of Acinetobacter in high-risk patients. Acinetobacter exhibit a high level of resistance to antimicrobials and are capable of persisting in hostile environments (humidity or dryness, presence of some antiseptics). As a result, they can cause nosocomial outbreaks. Identification of carriers and colonized patients, rigorous isolation, and scrupulous cleaning procedures are effective control measures. Despite these efforts, however, Acinetobacter baumannii now contributes a significant proportion of nosocomial infections.

Acinetobacter↗

PubMed2026

Occurrence of blaOXA-72 in a clinical isolate of carbapenem-resistant Acinetobacter pittii ST206 in Japan.

The development of carbapenem resistance in Acinetobacter spp., which are recognized as significant opportunistic pathogens, is of critical importance as it poses challenges to therapy and the control of healthcare-associated infections in clinical settings. This study investigated the genetic characteristics of a carbapenem-resistant A. pittii clinical isolate from a university hospital using whole-genome sequencing. The A. pittii strain SU8507, which was detected in the abdominal drainage fluid of a patient, exhibited resistance to imipenem (MIC: 128 μg/mL) and meropenem (MIC: 64 μg/mL) and produced positive results by the CIMTris method. A. pittii SU8507, belonging to ST206, harbored the blaOXA-72 and new variants of intrinsic blaOXA-213-like gene blaOXA-1222, which lacks an upstream insertion sequence element, and blaADC-1-like gene blaADC-343. The blaOXA-72 gene, flanked by XerC/XerD-like recombination sites, was located on a plasmid pSU8507, sized at 10,913 bp, carrying 13 predicted protein-coding genes. Complete pSU8507 containing mobA, repB, and the yoeB-yefM toxin-antitoxin genes, showed 98.9% nucleotide sequence identity and 75% coverage with plasmid pA2702 of the A. baylyi strain A2702, but a low BLAST MAX score. SU8507 harbored virulence genes involved in biofilm formation, types II and VI secretion systems, type IV pilus system, and serum resistance. This study describes the first isolation of an OXA-72-producing, carbapenem-resistant A. pittii clinical isolate in Japan. Given that the isolation rate of carbapenem-resistant Acinetobacter spp. Remains low in Japan, it is crucial to expand the scope of rapid, accurate carbapenemase detection to include not only A. baumannii, but also non-baumannii Acinetobacter spp.

Humans↗

PubMed2006

Analysis of antibiotic resistance genes in multidrug-resistant Acinetobacter sp. isolates from military and civilian patients treated at the Walter Reed Army Medical Center.

Military medical facilities treating patients injured in Iraq and Afghanistan have identified a large number of multidrug-resistant (MDR) Acinetobacter baumannii isolates. In order to anticipate the impact of these pathogens on patient care, we analyzed the antibiotic resistance genes responsible for the MDR phenotype in Acinetobacter sp. isolates collected from patients at the Walter Reed Army Medical Center (WRAMC). Susceptibility testing, PCR amplification of the genetic determinants of resistance, and clonality were determined. Seventy-five unique patient isolates were included in this study: 53% were from bloodstream infections, 89% were resistant to at least three classes of antibiotics, and 15% were resistant to all nine antibiotics tested. Thirty-seven percent of the isolates were recovered from patients nosocomially infected or colonized at the WRAMC. Sixteen unique resistance genes or gene families and four mobile genetic elements were detected. In addition, this is the first report of bla(OXA-58)-like and bla(PER)-like genes in the U.S. MDR A. baumannii isolates with at least eight identified resistance determinants were recovered from 49 of the 75 patients. Molecular typing revealed multiple clones, with eight major clonal types being nosocomially acquired and with more than 60% of the isolates being related to three pan-European types. This report gives a "snapshot" of the complex genetic background responsible for antimicrobial resistance in Acinetobacter spp. from the WRAMC. Identifying genes associated with the MDR phenotype and defining patterns of transmission serve as a starting point for devising strategies to limit the clinical impact of these serious infections.

Acinetobacter↗

PubMed2001

Acinetobacter bacteraemia in a teaching hospital, 1989-1998.

Background: The mortality rate from bacteraemia is one of the highest among infections in hospitals, especially in the intensive care unit (ICU). Recently, an increase in nosocomial bacteraemia caused by gram-negative resistant pathogens has been observed. In this work we review the clinical and laboratory findings of adult patients with Acinetobacter bacteraemia in order to identify risk factors associated with mortality. Methods: A retrospective review of the medical records of patients with Acinetobacter bacteraemia identified by blood cultures from the Diagnostic Microbiology Laboratory was conducted between January 1989 and March 1998. Results: We identified 59 cases of Acinetobacter bacteraemia. Most of the infections (71%) were nosocomial; the majority occurred in the Department of Internal Medicine (28.8%), followed by Haematology (27%) and the ICU (23%). A. lwoffii was isolated in 52.5% of cases and A. baumannii in 47.5%. The related mortality was 17%. Staying in the ICU was associated with A. baumannii bacteraemia (P<0.004). An intravascular catheter was the leading source of infection (37%). Main risk factors were mechanical ventilation (28%), parenteral nutrition (23%) and the presence of a urinary catheter (22%). In the multivariate analysis the independent prognostic factors for mortality were the presence of shock (P<0.05) and the severity of the underlying disease, according to the classification of McCabe (P<0.05). Conclusions: The incidence of Acinetobacter bacteraemia has increased in the last decade, mainly since 1995. The development of septic shock and the severity of the underlying disease appear to be associated with an increase in mortality.

Journal Article↗

PubMed1998

Molecular epidemiology of quinolone resistance in Acinetobacter spp.

OBJECTIVE: To determine whether similar mutations to quinolone resistance in the gyrA subunit of DNA gyrase and the parC subunit of topoisomerase IV are occurring independently in genotypically unrelated clinical isolates of Acinetobacter spp., or whether worldwide clonal spread of particular resistant strains is occurring. METHODS: The genotypic relationships of 25 nosocomial isolates of Acinetobacter spp. from 15 locations in 11 different countries worldwide were examined by randomly amplified polymorphic DNA analysis. Quinolone resistance-determining regions of gyrA and parC were amplified by PCR and mutations were analyzed by restriction digestion with Hinfl and DNA sequencing. RESULTS: Twenty-four of the 25 Acinetobacter isolates were genotypically heterogeneous and 12 were resistant to both nalidixic acid and ciprofloxacin. Analysis of conserved gyrA and parC regions showed that all isolates with a ciprofloxacin MIC of 4 mg/L had a substitution of Ser83 with either Leu or Phe in the GyrA protein. Five of six isolates with ciprofloxacin MICs of 64 mg/L had additional substitutions of Ser80 with Leu in the ParC protein. CONCLUSIONS: Similar mutations to quinolone resistance, predominantly at codons 82--83 of gyrA, are occurring independently in genotypically distinct isolates of Acinetobacter spp. from different worldwide locations. Most isolates with high ciprofloxacin MICs also exhibited secondary mutations in parC at codons 79--80.

Journal Article↗

PubMed1986

Enrichment for Hydrogen-Oxidizing Acinetobacter spp. in the Rhizosphere of Hydrogen-Evolving Soybean Root Nodules.

Field soybean plants were inoculated with Hup wild-type or H(2) uptake-negative (Hup) mutants of Bradyrhizobium japonicum. For two consecutive summers we found an enrichment for acinetobacters associated with the surfaces of the H(2)-evolving nodules. Soybean root nodules that evolved H(2) had up to 12 times more Acinetobacter spp. bacteria associated with their surfaces than did nodules incapable of evolving H(2). All of the newly isolated strains identified as Acinetobacter obtained from the surfaces of root nodules, as well as known established Acinetobacter strains, were capable of oxidizing H(2), a property not previously described for this alkane-degrading soil bacterium.

Journal Article↗

PubMed1988

Role of Cations in Accumulation and Release of Phosphate by Acinetobacter Strain 210A.

Cells of the strictly aerobic Acinetobacter strain 210A, containing aerobically large amounts of polyphosphate (100 mg of phosphorus per g [dry weight] of biomass), released in the absence of oxygen 1.49 mmol of P(i), 0.77 meq of Mg, 0.48 meq of K, 0.02 meq of Ca, and 0.14 meq of NH(4) per g (dry weight) of biomass. The drop in pH during this anaerobic phase was caused by the release of 1.8 protons per PO(4) molecule. Cells of Acinetobacter strain 132, which do not accumulate polyphosphate aerobically, released only 0.33 mmol of P(i) and 0.13 meq of Mg per g (dry weight) of biomass but released K in amounts comparable to those released by strain 210A. Stationary-phase cultures of Acinetobacter strain 210A, in which polyphosphate could not be detected by Neisser staining, aerobically took up phosphate simultaneously with Mg, the most important counterion in polyphosphate. In the absence of dissolved phosphate in the medium, no Mg was taken up. Cells containing polyphosphate granules were able to grow in a Mg-free medium, whereas cells without these granules were not. Mg was not essential as a counterion because it could be replaced by Ca. The presence of small amounts of K was essential for polyphosphate formation in cells of strain 210A. During continuous cultivation under K limitation, cells of Acinetobacter strain 210A contained only 14 mg of phosphorus per g (dry weight) of biomass, whereas this element was accumulated in amounts of 59 mg/g under substrate limitation and 41 mg/g under Mg limitation. For phosphate uptake in activated sludge, the presence of K seemed to be crucial.

Journal Article↗

PubMedDate not supplied

Acinetobacter endocarditis in children: a case report and review of the literature.

Acinetobacter calcoaceticus, a gram-negative bacterium ubiquitous in soil, water and sewage, is a rare cause of endocarditis in children. The first case of Acinetobacter endocarditis in an infant is described. This patient had underlying tetralogy of Fallot with absent pulmonary valve. A review of the literature in English revealed only four other cases of Acinetobacter endocarditis in children; three of whom had underlying congenital heart disease. Like the other reported cases, this patient responded well to antibiotic treatment. Subsequently this patient underwent corrective cardiac surgery but died of post-operative complications.

Acinetobacter Infections↗

PubMedDate not supplied

Infective endocarditis of an interventricular patch caused by Acinetobacter haemolyticus.

A case of infective endocarditis caused by Acinetobacter haemolyticus affecting and interventricular patch is reported. The patient, a 21-year-old man with a Fallot's tetralogy who had undergone cardiovascular surgery several years before, received imipenem and gentamicin for 6 and 4 weeks respectively and showed a good response without needing surgical treatment. Endocarditis by Acinetobacter species is very unusual and, to our knowledge, this is the first reported case of infective endocarditis caused by A. haemolyticus. As the clinical characteristics and the response to antibiotics appear to be similar to those reported for infective endocarditis by Acinetobacter lwoffi, prosthetic infective endocarditis by A. haemolyticus is apparently not always an indication for surgical treatment.

Acinetobacter↗

PubMed1999

Six-year prospective study of risk and prognostic factors in patients with nosocomial sepsis caused by Acinetobacter baumannii.

In this prospective study, the risk factors associated with nosocomial sepsis Caused by Acinetobacter baumannii or Pseudomonas aeruginosa were compared. Prior use of broad-spectrum antibiotics, urinary tract catheter, prior surgery, and mechanical ventilation were significantly associated with nosocomial sepsis caused by Acinetobacter baumannii. The mean prognostic factors significantly associated with mortality were known focus of infection, multiresistant Acinetobacter baumannii, and inappropriate antibiotic treatment. Adequate knowledge of these findings is important to ensure appropriate management of patients and rational use of antibiotics.

Acinetobacter↗

PubMed2005

Safety and efficacy of colistin in Acinetobacter and Pseudomonas infections: a prospective cohort study.

OBJECTIVE: To assess renal dysfunction and outcome in patients treated exclusively with colistin vs. other antibiotics. DESIGN AND SETTING: Prospective cohort study in a mixed ICU in a university-affiliated hospital. PATIENTS: 185 patients infected with Acinetobacter baumannii and Pseudomonas aeruginosa after an ICU stay longer than 48 h: 55 in the colistin group and 130 in the noncolistin group, similar in age, APACHE II, medical status, and SOFA score. MEASUREMENTS AND RESULTS: We recorded data on epidemiology and severity of illness, site of infection, renal function before and after treatment, clinical cure, and mortality. Clinical cure was defined as simultaneous normalization of central temperature (< or = 38 degrees), leukocyte count (< or = 10,000/mm3), and PaO2/FIO2 ratio (>187). Before treatment creatinine was 0.9+/-0.2 in the colistin group and 0.9+/-0.1 in the noncolistin group; after treatment the value was 1.0+/-0.3 in both groups. The most frequent infection was ventilator-associated pneumonia: 53% vs. 66% in colistin and noncolistin groups, respectively, Acinetobacter was the cause in 65% and 60% and Pseudomonas in 35% and 53%. In the noncolistin group 81% of patients were treated with carbapenems. Inadequate empirical antimicrobial treatment was more frequent in the colistin group (100% vs. 8%), but there were no differences in the frequency of clinical cure on day 6 of treatment (15% and 17%) or in mortality (29% and 24%). CONCLUSIONS: Colistin appears to be as safe and as effective as other antimicrobials for treatment of sepsis caused by Acinetobacter and Pseudomonas in critically ill patients.

APACHE↗

PubMed1990

A study of the relationships between antibiotic resistance phenotypes, phage-typing and biotyping of 117 clinical isolates of Acinetobacter spp.

Two typing systems were used to conduct an epidemiological study of Acinetobacter and to establish their relationship to antibiotic resistance phenotypes. Biotyping was performed with biochemical tests according to the new definition of Acinetobacter baumannii (18 biotypes). Phage typing included two complementary systems: 125 phage-types and 25 subtypes. Resistance phenotype analysis included 11 antibiotics. The results of the study showed that: (1) nine phage-types or subtypes (67%) and two groups of atypical phage-types (5%) or of untypable strains (28%), could be defined; (2) all strains that were resistant to carboxy/ureido-penicillins and cephalosporins (62%) belonged to biotypes 6 or 9; among them 70% belonged to phage-types 17 or 124; (3) imipenem resistance was observed in five isolates of biotype 9 and one of biotype 6; (4) a phenotype including resistance to third generation cephalosporins (but not carboxypenicillins) and to amikacin (but not tobramycin) represented 8.5% of the isolates; 90% of them belonged to biotype 1 and were not phage-typable; (5) 15% of the isolates were not identified as A. baumannii; among them five Acinetobacter haemolyticus strains all had the same resistance phenotype: amikacin-tobramycin-kanamycin-netilmicin resistant; they were however, susceptible to beta-lactams and to gentamicin. There was a clear relationship between biotypes 6 and 9 and phage-types 17 and 124 which were the strains most resistant to beta-lactams and aminoglycosides and were predominant in the survey. The three typing systems were complementary but it seems that antibiotic resistance phenotypes and one of the two other typing systems would be required in parallel to provide suitable information for epidemiological purposes.

Acinetobacter↗

PubMed1995

Outbreak caused by two multi-resistant Acinetobacter baumannii clones in a burns unit: emergence of resistance to imipenem.

Since early 1992 an increased number of tobramycin- and imipenem-resistant Acinetobacter spp. were observed causing colonization, wound infections, and bacteraemias in a burns and plastic surgery unit. This raised the question of whether this outbreak was caused by a single or by multiple Acinetobacter spp. clones. To study this, 97 Acinetobacter spp. isolates from clinical samples from different hospital units as well as isolates from the environment and the hands of the staff were characterized by antibiogram, plasmid profile and ribotyping. Two dominant multi-resistant A. baumannii clones were identified; one of them was sensitive to polymyxin B only. There was a close correlation between the results obtained by plasmid profiling and ribotyping. No common environmental source or significant hand carriage, or spread of these strains outside the unit were detected. The burns patients were the most likely reservoir, and strain transmission occurred in spite of strict control measures.

Acinetobacter↗

PubMed1995

Identification and biotyping of Acinetobacter spp. isolated in Chilean hospitals.

Two hundred and eighty-one isolates of Acinetobacter spp. obtained from clinical specimens in hospitals from five Chilean cities were identified to species level and biotyped. Respiratory tract and wound secretions were the main sources of the isolates. Acinetobacter baumannii was the most frequent species (96.8%), followed by Acinetobacter genospecies 3 (2.8%). Twelve different biotypes of A. baumannii strains were found of which biotypes 9, 8 and 6 were the most frequent. Isolates of other biotypes were rare. These results differ from most other Latin American and European countries.

Acinetobacter↗