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PubMed2000

Monitoring precursor 16S rRNAs of Acinetobacter spp. in activated sludge wastewater treatment systems.

Recently, Cangelosi and Brabant used oligonucleotide probes targeting the precursor 16S rRNA of Escherichia coli to demonstrate that the levels of precursor rRNA were more sensitive to changes in growth phase than the levels of total rRNA (G. A. Cangelosi and W. H. Brabant, J. Bacteriol. 179:4457-4463, 1997). In order to measure changes in the levels of precursor rRNA in activated sludge systems, we designed oligonucleotide probes targeting the 3' region of the precursor 16S rRNA of Acinetobacter spp. We used these probes to monitor changes in the level of precursor 16S rRNA during batch growth of Acinetobacter spp. in Luria-Bertani (LB) medium, filtered wastewater, and in lab- and full-scale wastewater treatment systems. Consistent with the previous reports for E. coli, results obtained with membrane hybridizations and fluorescence in situ hybridizations with Acinetobacter calcoaceticus grown in LB medium showed a more substantial and faster increase in precursor 16S rRNA levels compared to the increase in total 16S rRNA levels during exponential growth. Diluting an overnight culture of A. calcoaceticus grown in LB medium with filtered wastewater resulted in a pattern of precursor 16S rRNA levels that appeared to follow diauxic growth. In addition, fluorescence in situ hybridizations with oligonucleotide probes targeting total 16S rRNA and precursor 16S rRNA showed that individual cells of A. calcoaceticus expressed highly variable levels of precursor 16S rRNA when adapting from LB medium to filtered sewage. Precursor 16S rRNA levels of Acinetobacter spp. transiently increased when activated sludge was mixed with influent wastewater in lab- and full-scale wastewater treatment systems. These results suggest that Acinetobacter spp. experience a change in growth activity within wastewater treatment systems.

Acinetobacter↗
PubMed1999

Genetic analysis of a chromosomal region containing vanA and vanB, genes required for conversion of either ferulate or vanillate to protocatechuate in Acinetobacter.

VanA and VanB form an oxygenative demethylase that converts vanillate to protocatechuate in microorganisms. Ferulate, an abundant phytochemical, had been shown to be metabolized through a vanillate intermediate in several Pseudomonas isolates, and biochemical evidence had indicated that vanillate also is an intermediate in ferulate catabolism by Acinetobacter. Genetic evidence supporting this conclusion was obtained by characterization of mutant Acinetobacter strains blocked in catabolism of both ferulate and vanillate. Cloned Acinetobacter vanA and vanB were shown to be members of a chromosomal segment remote from a supraoperonic cluster containing other genes required for completion of the catabolism of ferulate and its structural analogs, caffeate and coumarate, through protocatechuate. The nucleotide sequence of DNA containing vanA and vanB demonstrated the presence of genes that, on the basis of nucleotide sequence similarity, appeared to be associated with transport of aromatic compounds, metabolism of such compounds, or iron scavenging. Spontaneous deletion of 100 kb of DNA containing this segment does not impede the growth of cells with simple carbon sources other than vanillate or ferulate. Additional spontaneous mutations blocking vanA and vanB expression were shown to be mediated by IS1236, including insertion of the newly discovered composite transposon Tn5613. On the whole, vanA and vanB appear to be located within a nonessential genetic region that exhibits considerable genetic malleability in Acinetobacter. The overall organization of genes neighboring Acinetobacter vanA and vanB, including a putative transcriptional regulatory gene that is convergently transcribed and overlaps vanB, is conserved in Pseudomonas aeruginosa but has undergone radical rearrangement in other Pseudomonas species.

Acinetobacter↗
PubMed1995

Occurrence and antigenic heterogeneity of L-2,4-diaminobutyrate decarboxylase in Acinetobacter species.

We have previously reported that a novel enzyme, L-2,4-diaminobutyrate decarboxylase (DABA DC), which is responsible for the formation of 1,3-diaminopropane, occurs in two Acinetobacter species. The present study extends this observation to additional Acinetobacter species and strains (6 reference strains and 30 clinical isolates). Furthermore, the DABA DC protein was detected in every strain by Western blot analysis with the antiserum against the enzyme purified from A. baumannii ATCC 19606. However, only the DABA DCs in the A. calcoaceticus and Acinetobacter genospecies 3 in addition to A. baumannii strains strongly cross-reacted with the antiserum, suggesting antigenic heterogeneity among the DABA DC proteins in Acinetobacter species. Therefore, immunological testing of the DABA DC protein may provide an additional method for differentiating and identifying Acinetobacter strains.

Acinetobacter↗
PubMed1999

Risk factors for an outbreak of multi-drug-resistant Acinetobacter nosocomial pneumonia among intubated patients.

INTRODUCTION: Acinetobacter baumanii is a Gram-negative coccobacillus that is normally a commensal pathogen but can be a nosocomial pathogen. An epidemiologic study was performed to investigate an outbreak of A baumanii that occurred in our medical intensive care unit (MICU) from March to September 1995. METHODS: A case-control study was performed by retrospective chart review, comparing case patients to randomly selected patients who were mechanically ventilated in the MICU for at least 1 week during the outbreak. A case patient was defined as any patient with an Acinetobacter infection in which the epidemic strain was considered to be a pathogen. The epidemic strain was defined by its antibiogram. Case patients and control patients were compared for age, gender, underlying disease, acute physiology and chronic health evaluation III score, length of MICU stay, prior antibiotic use, presence of fever, sepsis, type of pulmonary infiltrate, and outcome. Environmental and hand-washing studies also were performed during the period of the outbreak. Molecular typing was performed on available bloodstream isolates. RESULTS: There were 15 cases of A baumanii nosocomial pneumonia. Fifty percent were bacteremic; one chart was unavailable for review. Twenty-nine patients were identified as control patients. The mean age for case patients was 50 (range, 21 to 84). The mean duration of time from admission to the ICU to infection was 12.8 days (range, 4 to 40). Sepsis developed in 35% of the case patients. Forty-three percent of the case patients died during their hospitalization, with two of those deaths attributed to Acinetobacter infection. Univariate analysis showed that prior use of ceftazidime was associated with infection with Acinetobacter (11/14 case patients compared to 11/29 control patients; p < 0.01). Pulsed-field gel electrophoresis revealed two strains to be responsible for the outbreak. Hand washing was performed before patient contact by only 10% of health-care workers, and only 32% washed their hands after patient contact. CONCLUSION: The use of ceftazidime was associated with an increased risk of nosocomial pneumonia with resistant strains of Acinetobacter. Health-care workers need to improve compliance with hand-washing recommendations.

Acinetobacter Infections↗
PubMed1980

An outbreak of acinetobacter infection associated with the use of a ventilator spirometer.

Although respiratory therapy equipment is a well-known source of nosocomial infection, ventilator spirometers have not been previously implicated. We report 17 Acinetobacter calcoaceticus variety anitratus infections traced to contaminated spirometers. Isolates from infected patients were recovered from urine, sputum, wounds, and blood. A review of attack rates for Acinetobacter was prompted by a dramatic increase in blood culture isolates. Prospective surveillance of intensive care environment, personnel, and patients established that Bennett MA-1 spirometers constituted the major reservoir of infecting organisms. Despite daily sterilization, 30% of spirometers in use were found to be contaminated. The hands of 12% of intensive care nurses and 10% of respiratory therapists cultured were found to be colonized. In addition to the infected patients, 28 other patients on spirometer-equipped ventilators were judged to be colonized by Acinetobacter following examination of sputa and/or mouthwashings. Following discontinuation of spirometer use and following increased emphasis on proper handwashing, the incidence of Acinetobacter infections dropped dramatically. Antibiosis in the intensive care environment and a deterioration in aseptic awareness serve to make Acinetobacter an environmental opportunist of increasing importance.

Acinetobacter Infections↗
PubMedDate not supplied

[Peculiarities of ethanol metabolism in an Acinetobacter sp. mutant strain defective in exopolysaccharide synthesis].

Activities of the key enzymes of ethanol metabolism were assayed in ethanol-grown cells of an Acinetobacter sp. mutant strain unable to synthesize exopolysaccharides (EPS). The original EPS-producing strain could not be used for enzyme analysis because its cells could not to be separated from the extremely viscous EPS with a high molecular weight. In Acinetobacter sp., ethanol oxidation to acetaldehyde proved to be catalyzed by the NAD(+)-dependent alcohol dehydrogenase (EC 1.1.1.1.). Both NAD+ and NADP+ could be electron accepters in the acetaldehyde dehydrogenase reaction. Acetate is implicated in the Acinetobacter sp. metabolism via the reaction catalyzed by acetyl-CoA-synthetase (EC 6.2.1.1.). Isocitrate lyase (EC 4.1.3.1.) activity was also detected, indicating that the glyoxylate cycle is the anaplerotic mechanism that replenishes the pool of C4-dicarboxylic acids in Acinetobacter sp. cells. In ethanol metabolism by Acinetobacter sp., the reactions involving acetate are the bottleneck, as evidenced by the inhibitory effect of sodium ions on both acetate oxidation in the intact cells and on acetyl-CoA-synthetase activity in the cell-free extracts, as well as by the limitation of the C2-metabolism by coenzyme A. The results obtained may be helpful in developing a new biotechnological procedure for obtaining ethanol-derived exopolysaccharide ethapolan.

Acetaldehyde↗
PubMed2003

[Study on risk factors and molecular typing of Acinetobacter baummanii in nosocomial infections].

OBJECTIVE: To study the risk factors of Acinetobacter baummanii in nosocomial infections, and to verify the nature of Acinetobacter baumannii strains isolated from intensive care unit (ICU). METHODS: A hundred and fourty patients associated with nosocomial infection of Acinetobacter baummanii from four teaching hospitals were selected and compared with controls through a case control study to identify risk factors. The strains isolated from the ICU were typed by polymerase chain reaction (PCR) with the primer M(13) following electrophoresis in agarose gel. RESULTS: The odds ratios (ORs) were: state of the illness (OR = 8.69), using immunosuppressant (OR = 4.85), mechanical ventilation (OR = 3.68) and treatment with 3 kinds of antibiotics (OR = 3.014). Data from PCR studies indicated that these strains were sharing identical band pattern from the five strains. CONCLUSION: Risk factors for nosocomial infection with Acinetobacter baummanii included state of an illness, immunosuppressant, mechanical ventilation, and treatment with antibiotics. A multidrug-resistant strains of Acinetobacter baumannii was identified in ICU.

Acinetobacter baumannii↗
PubMed1991

[Quantitation of Acinetobacter calcoaceticus in mixed bacterial cultures by an enzyme immunoassay].

An enzyme-linked immunosorbent assay using polyclonal antibodies from rabbits has been developed for quantification of Acinetobacter calcoaceticus. Bacteria were added to the wells of a microtiter plate coated with anti-Acinetobacter immunoglobulin. For detecting bound cells the peroxidase-labelled immunoglobulin fraction was used. Over a distinct range there is a linear correlation between bound bacteria and measured absorbance allowing a quantification of bacteria in an order from 10(7) to 10(8) per milliliter. The specificity of the assay was evaluated by the heterologous bacteria Pseudomonas putida, Pseudomonas aeruginosa, Proteus vulgaris, Escherichia coli and Citrobacter freundii. Only a minimal cross-reactivity was observed. Within a certain range of error it is possible to quantitate Acinetobacter calcoaceticus in mixtures with one or several other bacterial species. Mixed with bacteria of one other species the differences to the value for Acinetobacter calcoaceticus alone do not exceed +/- 10% with a tendency to lower values. Mixed with several other species only negative differences up to -15% were obtained. Treatment of Acinetobacter calcoaceticus with 0.5% formaldehyde results in a loss of reactivity up to 15%. In conclusion, the enzyme-linked immunosorbent assay is a useful method for quantitating bacteria not only with respect to the high sensitivity, specificity and good reproducibility but also for the minimal technical equipment and the short assay time.

Acinetobacter calcoaceticus↗
PubMed1990

[Nosocomial bacteremia caused by Acinetobacter].

Forty episodes of nosocomial Acinetobacter calcoaceticus bacteremia produced by the Anitratus type over a period of 4 years were analyzed and compared with a control group of 28 patients with bacteremia produced by gram negative bacilli. Although most of acinetobacter bacteremia were endemic an outbreak involving 12 cases were observed in an intensive care unit during the study period. Thirteen patients presented a transient bacteremia. When the site of origin of the infection could be established the respiratory system was the most commonly involved (5 cases). Polymicrobial bacteremia was present in 11 patients (27.5%). Gram-positive cocci were the most commonly associated microorganisms. Most of isolated Acinetobacter strains were resistant to cotrimoxazole, beta-lactams, and aminoglycosides but were uniformly sensitive to ciprofloxacin and imipenem. The overall mortality was 22.5%. As compared with the control group, Acinetobacter bacteremia occurred more frequently during the first week of hospitalization and involved patients with less severe underlying diseases in whom three or more potential risk factors were detected. The entering site of infection was commonly unknown and the antibiotic treatment was inappropriate in most of the cases of Acinetobacter bacteremia.

Acinetobacter Infections↗
PubMed1989

[Nosocomial infections caused by Acinetobacter. Epidemiology and therapeutic difficulties].

Nosocomial infections due to Acinetobacter calcoaceticus are not easy to treat particularly in intensive-care and surgical units. Our study included 33 cases of nosocomial infections which developed during 1987 in the surgical intensive care unit and in the urology department. Acinetobacter was isolated from various types of nosocomial infections: urinary tract infections (43 per cent); septicaemia (15 per cent); surgical infections (27 per cent) and respiratory tract infections (15 per cent). Forty eight per cent of the patients received an antibiotic therapy and 52 per cent had no specific treatment. The following beta-lactam antibiotics were studied: ticarcilline, mezlocilline, cefotaxime and ceftazidime, and 83 per cent of the strains were TICRMEZRCTXR (phenotype IV). All the strains except one were imipenem susceptible. The study of aminoglycoside resistance in Acinetobacter showed that 91 per cent of the strains were gentamicin resistant (GENR); 25.5 per cent were gentamicin, and amikacin resistant and tobramycin susceptible (GENR AMKR TOBS, phenotype IV), and 45 per cent were GENR TOBR AMKR (phenotype V). Acinetobacter strains were resistant and 63 per cent pefloxacin resistant. Co-trimoxazole resistant strains represented 65 per cent of the strains. Should major antibiotics be used to treat nosocomial infections due to multiresistant Acinetobacter strains? Are prophylaxis, aseptic and surgical procedures sufficient to control these infections?

Acinetobacter Infections↗
PubMed1982

[In vitro activity of ceftazidime compared with five beta-lactamase stable compounds against clinical strains of Acinetobacter calcoaceticus ].

Acinetobacter calcoaceticus is recognized as one of the most resistant nosocomial pathogens. Clinical isolates of Acinetobacter are usually resistant to most beta-lactam antibiotics. The objective of this study was to evaluate the in vitro activity of ceftazidime, a new broad spectrum highly potent beta-lactam antibiotic, able to inhibit especially Pseudomonas and Providencia. Its activity against 96 clinical strains of Acinetobacter was compared with the activity of 5 recent beta-lactam antibiotics which are resistant to beta-lactamase degradation (cefoxitine, Cefotaxime, moxalactam, cefotiam, cefamandole). The results of this comparative study of the in vitro activity of the 6 beta-lactam antibiotics exhibit a higher activity of ceftazidime: 50 p. cent of the strains were inhibited at a concentration of 4 micrograms/ml while the other drugs inhibited 50 p. cent of the strains at concentrations superior to 10 micrograms/ml; the geometric mean was 7 micrograms/ml for ceftazidime while for the other drugs it was more than 10 micrograms/ml and for 3 of them, the geometric mean was more than 40 micrograms/ml. Otherwise one could notice a bimodal distribution of the strains which suggests the presence of 2 populations of Acinetobacter, respectively inhibited with 4 micrograms/ml (susceptible) and 64 or 128 micrograms/ml (resistant). Finally this study shows that ceftazidime is one of the most active compounds against clinical isolates of Acinetobacter calcoaceticus among the 3rd generation of cephalosporins.

Acinetobacter↗
PubMed1980

Evolutionary divergence of co-selected beta-ketoadipate enol-lactone hydrolases in Acinetobacter calcoaceticus.

Muconolactone isomerase (EC 5.3.3.4) and beta-ketoadipate enol-lactone hydrolase (EC 3.1.1.24) mediate consecutive catabolic steps in bacteria. Separately inducible beta-ketoadipate enol-lactone hydrolases I and II are formed in representatives of Acinetobacter calcoaceticus. When subjected to DEAE-cellulose chromatography, Acinetobacter enol-lactone hydrolase I displays heterogeneous behavior which, in whole or in part, appears to be due to modifications of sulfhydryl groups in the protein; the enzyme is unusual in that its NH2-terminal amino acid is cysteine. Comparison of the NH2-terminal amino acid sequence of Acinetobacter enollactone hydrolase I, reported here, with the corresponding amino acid sequences of Acinetobacter enollactone hydrolase II and Pseudomonas enol-lactone hydrolase indicates that all three proteins have diverged widely from a common evolutionary origin. Sequence comparisons suggest that divergence of the Acinetobacter enol-lactone hydrolase structural genes was achieved by substitution with DNA derived from an ancestral muconolactone isomerase structural gene.

Acinetobacter↗
PubMed1993

[Test of using plasmid DNA profile analysis for identification of Acinetobacter species].

The analysis regarded 32 strains of Acinetobacter genus isolated from a variety of samples from human and animal sources (hospital environment, nonhospital source, water, burns). The genus Acinetobacter is heterogeneous and has a complex taxonomy. For this reason, plasmid profile analysis has been used as a method of identification to study the genetic diversity of natural populations. Strains having an identical plasmid profile were pooled in the same plasmid group. According to these criteria, 32 isolates were grouped in 11 classes. Within the 11 plasmid groups, 2 were found in A. baumannii, 3 in A. lwoffii, 2 in A. johnsonii, 3 in A. haemolyticus and 1 in A. junii. Most frequently isolated species of Acinetobacter from burns was A. baumannii (11 out of the 13 isolates). Plasmid profile analysis of those strains revealed a presence of only one plasmid group. Plasmid profile analysis of Acinetobacter strains can be an useful technique for characterizing isolates in epidemiologic studies as a complementary method. It can be used directly as a very rapid and convenient technique to type Acinetobacter strains.

Acinetobacter↗
PubMed1997

Purification and some properties of ribulose 1,5-bisphosphate carboxylases/oxygenases from Acinetobacter sp. strain JC1 and Hydrogenophaga pseudoflava.

Ribulose 1,5-bisphosphate carboxylases/oxygenases (RuBisCOs) of two carboxydobacteria, Acinetobacter sp. strain JC1 and Hydrogenophaga pseudoflava, grown on carbon monoxide were purified and partially characterized. RuBisCO of Acinetobacter sp. JC1 was purified 5-fold in eight steps to homogeneity, with a yield of 1.6%. The final specific activity of the purified enzyme was 39.5 nmol CO2 incorporated per min per mg protein. The molecular weight of the native enzyme was determined to be 520,000. Sodium dodecyl sulfate-gel electrophoresis revealed two nonidentical subunits of molecular weights 53,500 and 15,000. The Km and Vmax for CO2 were 36.7 microM and 296.1 nmol per min per mg protein, respectively, and those for ribulose 1,5-bisphosphate were 3.7 microM and 770 nmol per min per mg protein, respectively. The enzyme of H. pseudoflava was purified 55-fold in eight steps to homogeneity, with a yield of 3.6%. The final specific activity was 304.3 nmol CO2 incorporated per min per mg protein. The molecular weight of the enzyme was estimated to be 505,000. The enzyme was found to have two kinds of nonidentical subunits of molecular weights 51,500 and 14,000. The Km and Vmax for CO2 were found to be 16.4 microM and 777.8 nmol per min per mg protein, respectively, and those for ribulose 1,5-bisphosphate were 0.1 microM and 436.2 nmol per min per mg protein, respectively. The N-terminal amino acid sequences of the large and small subunits of Acinetobacter sp. JC1 enzyme were Ala-Asp-Arg-Trp-Asn-Ala-Gly-Val-IIe-Pro-Tyr-Ala-Glu-Met-Gly and Met-Arg-Ile-Thr-Glu-Gly-Thr-Phe-Ser-Tyr-Leu-Pro-Asp-Phe-Thr, respectively. The sequences of the H. pseudoflava enzyme were Ala-Thr-Lys-Thr-Tyr-Asu-Ala-Gly-Val-Lys-Glu-Tyr-Trp-Ser-Thr and Met-Ser-Met-Gln-Asp-Tyr-His-Ser-Arg-Leu-Ser-Asp-Pro-Ala-Ile, respectively. The peptide map of RuBisCO from Acinetobacter sp. JC1 grown on carbon monoxide was different from that of the bacterium grown on methanol. The two RuBisCOs, however, were found to be identical in N-terminal residue and antigenic property. The RuBisCO of Acinetobacter sp. JC1 was found to share no immunological properties with those of H. pseudoflava, Oligotropha carboxidovorans and Pseudomonas carboxydohydrogena.

Acinetobacter↗
PubMed2000

Acinetobacter.

Members of the genus Acinetobacter are oxidase negative, aerobic Gram-negative coccobacilli, which have evolved taxonomically from former strains of the Mima-Herrelia group. Their natural habitat is human skin and mucous membranes, water, soil, vegetation, and sewage. The most common multiresistant nosocomial pathogen among 19 genospecies is the A. calcoaceticus-baumannii complex ( A. baumannii). This species is not a common component of normal human acinetobacter colonization, and its ecological origin remains unknown. Outbreaks of nosocomial acinetobacter infection are due to spread of one or a few clones among patients, personnel, and the inanimate hospital environment. Thus, strict implementation of infection control procedures is the major technique for prevention and suppression of such outbreaks. Surveillance cultures of personnel and the environment; molecular genotyping of isolates; cohorting of colonized or infected patients and staff; and topical application of polymyxin B to colonized wounds have been used to enhance standard infection control procedures. Antimicrobial resistance to beta lactam antibiotics in Acinetobacter is due primarily to a combination of chromosomal beta lactamase production and reduced outer membrane permeability. Carbapenem resistance is an increasing phenomenon and restriction of late-generation cephalosporin and carbapenem utilization should be considered in outbreak control. Effective therapy of multiresistant Acinetobacter infection may require a variety of potentially synergistic antibiotic combinations.

Journal Article↗
PubMed2003

Infections due to Acinetobacter baumannii in the ICU.

Acinetobacter species are widespread environmental, nonfermentative, aerobic, gram-negative coccobacilli. Most infections due to this organism are opportunistic in nature and occur in patients who spend extended time in the intensive care unit (ICU) due to severe underlying disease, and who need prolonged therapy with mechanical ventilation and antimicrobial agents. Because the only factor amenable to prevention in this setting is antimicrobial therapy, avoidance of unnecessary antibiotics should be a high priority in management of such patients. Nosocomial spread of A. baumannii in the ICU setting has often been attributed to ventilatory equipment and to colonized nursing and respiratory personnel via hand transmission. In fact, the epidemiology of nosocomial respiratory colonization and/or infection with A. baumannii is now commonly much more complex due to the coexistence of epidemic cases with unrelated sporadic cases caused by different strains. This underscores the necessity to use molecular typing to improve the detection of microepidemics amenable to early control. Crude mortality rates of 30 to 75% have been reported for nosocomial infection due to Acinetobacter species, with the highest rates reported in ventilator-dependent patients. As with many other opportunistic gram-negative bacilli, increasing antibiotic resistance has hindered the therapeutic management of nosocomial infection due to Acinetobacter species. A. baumannii are now frequently resistant to most available antibacterial drugs, with some centers reporting up to 80% of strains resistant to all aminoglycosides. Even resistance to imipenem, which was for several years the most effective drug in treating Acinetobacter nosocomial infections, has now been described in several reports. Unfortunately, the unique propensity of Acinetobacter species to develop resistance to multiple antimicrobial agents reinforces concerns about the imminence of a post-antimicrobial era where no effective antibiotics will be available to treat this type of infection.

Journal Article↗
PubMed1999

Detection of integrons in worldwide nosocomial isolates of Acinetobacter spp.

OBJECTIVE: To examine the distribution of integrons in genotypically unrelated worldwide multiresistant clinical isolates of Acinetobacter spp. METHODS: The presence and genetic location of class 1, 2 and 3 integrons were examined in a genotypically heterogeneous collection of 25 nosocomial isolates of Acinetobacter spp., from 15 locations in 11 different countries worldwide, by hybridization and PCR-based methods. Class 1 integron structures were characterized genetically by a PCR mapping technique. RESULTS: Class 1 integrons were detected in 17 of the 25 Acinetobacter isolates examined. Only one isolate contained a class 2 integron. No class 3 integrons were detected. The integrons varied in size and in the number of inserted cassettes, but similar integrons were found in genotypically distinct isolates from different locations worldwide. These structures were integrated into the chromosome in all isolates where they were detected, although some integrons were capable of subsequent transfer or mobilization. Genes coding for aminoglycoside-modifying enzymes formed the predominant cassettes identified within the integrons. CONCLUSIONS: Clinical isolates of Acinetobacter spp. from diverse locations seem to share resistance mechanisms acquired from other genera by a variety of mechanisms, including dissemination of integrons. Once integrons are incorporated into the bacterial genome, Acinetobacter spp. are potentially able to act as a reservoir of resistance genes for other species and genera.

Journal Article↗
PubMed2001

The Increasing Role of Acinetobacter Species As Nosocomial Pathogens.

Among gram-negative organisms playing a significant role in nosocomial infections, Acinetobacter species have attracted increasing attention in intensive care units during the past two decades. Acinetobacter species are implicated in a wide spectrum of infections (eg, bacteremia, nosocomial pneumonia, urinary tract infections, secondary meningitis, superinfections in burn patients). One of the most striking features of Acinetobacter species is their extraordinary ability to develop multiple resistance mechanisms against major antibiotic classes. They have become resistant to broad-spectrum beta-lactams (third-generation cephalosporins, carboxypenicillins, and increasingly to carbapenems); they produce a wide range of aminoglycoside-inactivating enzymes; and most strains are resistant to fluoroquinolones. In Acinetobacter nosocomial infections, the major problems confronting clinicians in intensive care units are related to the severity of Acinetobacter nosocomial infections and to resistance to major antibiotic classes of these organisms.

Journal Article↗