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PubMed1998

Specificity of rabbit antisera against lipopolysaccharide of Acinetobacter.

Acinetobacter has been reported to be involved in hospital-acquired infections with increasing frequency. However, clinical laboratories still lack simple methods that allow the accurate identification of Acinetobacter strains at the species level. For this study, proteinase K-digested whole-cell lysates from 44 clinical and environmental isolates were investigated by sodium dodecyl sulfate-polyacrylamide gel electrophoresis and immunoblotting with hyperimmune rabbit sera to examine the possibility of developing a serotyping scheme based on the O antigen of Acinetobacter lipopolysaccharide (LPS). The antisera, obtained by immunization of rabbits with 13 of the heat-killed isolates investigated, were characterized by Western blotting and enzyme immunoassay by using proteinase K-digested whole-cell lysates and phenol-water-extracted LPS as antigens. In both assays, the antisera were shown to be highly specific for the homologous antigen. In addition, assignment of Acinetobacter LPS to the smooth or the rough phenotype was shown not to be reliable when it was based only on the results obtained with silver-stained gels. O-antigen reactivity, determined by Western blot analysis, was observed with 11 of the 31 isolates, most of which belonged to the species Acinetobacter baumannii (DNA group 2) and the unnamed DNA group 3. Interestingly, some O antigens were found in a DNA group different from that of the strain used for immunization. The results indicate that O serotyping of Acinetobacter strains is feasible and thus may provide a simple method for the routine identification of these opportunistic pathogens.

Acinetobacter↗
PubMedDate not supplied

Isolation, characterization, and plasmid pUPI126-mediated indole-3-acetic acid production in acinetobacter strains from rhizosphere of wheat.

Thirty-seven strains of Acinetobacter isolated and characterized from rhizosphere of wheat were screened for indole-3-acetic acid (IAA) production. Only eight Acinetobacter strains showed IAA production. The genus Acinetobacter was confirmed by chromosomal DNA transformation assay. Biotyping of eight strains was carried out and they were found to be genospecies of A. junii, A. baumannii, A. genospecies 3, and A. haemolyticus. Five of eight strains produced IAA at the early stationary phase: A. haemolyticus (A19), A. baumannii (A18, A16, A13), and Acinetobactergenospecies 3 (A15). A. junii A6 showed maximum IAA production at log phase and A. genospecies 3 and A. baumannii (A28, A30) at late stationary phase. IAA was extracted by ethyl acetate and purified by preparative thin-layer chromatography. Purified IAA was confirmed by 1H-nuclear magnetic resonance and infrared spectrum analysis. Pot experiments showed a significant increase in plant growth inoculated with eight Acinetobacter genospecies as compared to control plants. IAA production was found to be encoded by plasmid pUPI126. All eight strains of Acinetobacter contain a plasmid pUPI126 with a molecular weight of 40 kb. Plasmid pUPI126 was transformed into Escherichia coli HB101 at a frequency of 5 x 10(-5), and E. coli HB101 (pUPI126) transformants also showed IAA activity. PUPI126 also encoded resistance to selenium, tellurium, and lead. This is the first report of plasmid-encoded IAA production in the genus Acinetobacter.

Acinetobacter↗
PubMedDate not supplied

Infections caused by Acinetobacter species and their susceptibility to 14 antibiotics in Lagos University Teaching Hospital, Lagos.

Acinetobacter spp are well recognised as causes of nosocomial infections particularly in patients with immature or defective body defence system. Information concerning these organisms are lacking in this environment. For this reason the pattern of infection and the antimicrobial susceptibility profiles of these organisms isolated over a one-year period were studied. A total of 58 (3%) of the 2001 isolates from all clinical specimens received in the laboratory during the year were Acinetobacter spp. The 58 Acinetobacter spp constituted 5.5% of all the 1051 NLF-GNB isolated, and caused 4.6% of all the 1261 nosocomial infections. Thirty-seven (63%) and 17 (30%) of the Acinetobacter isolates were from wound infections and UTI respectively. All the infections were nosocomially acquired and were associated with compromised host immunity, defective body defence, surgery or urinary catheterization; with Acinetobacter baumannii being the predominant species. There was an apparent male predominance over females by a ratio of 1. 9:1 in the infections, particularly from 45 years and above. One hundred percent and 96.6% of the isolates were susceptible to cefoperazone-sulbactam and travofloxacin respectively. Forty-five (77.6%) were susceptible to cefotaxime, 49 (84.5%) to ampicillin-sulbactam, 34 (58.6%) to ceftazidime, 38 (65.6%) to ticarcillin-clavulanic acid and 41 (70.7%) to ciprofloxacin. Generally the Acinetobacter spp showed multiple resistance to the range of antibiotics tested. All the isolates produced beta-lactamase.

Acinetobacter Infections↗
PubMed2004

[The isolation of acinetobacter strain from burn wound and the analysis of its antibiotic resistance].

OBJECTIVE: To investigate the distribution and drug resistance of acinetobacter isolated from burn wounds. METHODS: The acinetobacter strains were isolated and identified by routine methods. Based on the recommendation of NCCLS, AmpC enzyme was determined by cefoxiti three-dimensional test, ESBLs by disk diffusion method and bacterial susceptibility by Kirby-Bauer agar diffusion method. RESULTS: Among the 69 strains of acinetobacter clinically isolated from burn wounds, 52 were baumannii (75.6%). The acinetobacter strains were identified to be highly resistant to 17 kinds of antibiotics. The drug resistance rate of beta-lactamase-producing strains (68.25%) was higher than that of non-beta-lactamase-producing strains (20.33%). The strains isolated in our burn ward exhibited multiple drug resistance which was mainly due to the production of many kinds of beta-lactamases. Among the 38 strains of beta-lactamase-producing acinetobacter, those producing AmpC beta-lactamase (AmpC BLA) accounted for 42.1%. CONCLUSION: Acinetobacter strain was one of the pathogens in burn wound infection, and its isolation and identification of its drug resistance could be beneficial to the doctors to make right choice of antibiotics.

Acinetobacter↗
PubMed1975

Gas chromatography of bacterial whole cell methanolysates. VII. Fatty acid composition of Acinetobacter in relation to the taxonomy of Neisseriaceae.

The cellular fatty acids of seventeen Acinetobacter strains were determined. Most acids identified were previously found in neisseriae and moraxellae. Specific for Acinetobacter was 2-hydroxydodecanoid acid and a few minor unidentified components. The fatty acid data were analysed by numerical methods and compared with previous results obtained for neisseriae and moraxellae. The findings were consistent with genetic evidence for some affinities of genus Acinetobacter to genus Moraxella and "false neisseriae". Occasionally, a high resemblance in fatty acid pattern was demonstrated between a Moraxella strain and certain strains of Acinetobacter, and also between an Acinetobacter strain and certain "true neisseriae". Still, the acinetobacters constituted one single cluster separated from the other genera of Neisseriaceae.

Acinetobacter↗
PubMed1998

[Surface characteristics and antimicrobial sensitivity of clinical strains of Acinetobacter spp].

BACKGROUND: The treatment of nosocomial infections caused by Acinetobacter baumannii has been hindered by the easiness of this species to acquire antimicrobial resistance. AIM: To study surface hydrophobicity, the presence of capsule and antimicrobial susceptibility of nosocomial Acinetobacter spp strains. MATERIAL AND METHODS: Ninety four Acinetobacter spp strains isolated from a public hospital of Santiago, between July 1995 and April 1996, were studied. RESULTS: Compared to Acinetobacter genospecies 3 isolates, A baumannii isolates exhibited greater antimicrobial resistance, was uniformly susceptible to imipenem and highly resistant to other antimicrobials of clinical use. Most strains of biotypes 8 and 9 were hydrophilic and encapsulated, whereas those of infrequent biotypes and of Acinetobacter genospecies 3 were, with few exceptions, hydrophobic and not encapsulated. CONCLUSIONS: Capsule production might confer a greater virulence to Acinetobacter baumannii biotypes 8 and 9, and explain their higher prevalence in the studied hospital.

Acinetobacter↗
PubMedDate not supplied

DNA amplification fingerprinting (DAF) applied to the investigation of Acinetobacter baumanii isolated from intensive care unit patients.

Acinetobacter are important emerging nosocomial pathogens. In this paper thirteen Acinetobacter baumanii from intensive care patients were isolated. These were initially typed using the API-20 NE biotyping system and antibiogram analysis. Results obtained using these methods failed to convincingly characterise the organisms. In this report a method to characterise these Acinetobacter baumanii isolates is described, which utilises a modified polymerase chain reaction (PCR), capable of generating genomic fingerprints, known as DNA amplification fingerprinting (DAF). Purified chromosomal DNA of cultured clinical isolates of Acinetobacter baumanii were subjected to DAF using the M13 universal sequencing primer. Polymorphic DNA bands produced, were visualised after agarose gel electrophoresis and ethidium bromide staining. Results demonstrated that six of the thirteen clinical isolates represented one group and a second group of two isolates displayed identical fingerprint patterns. The remaining four organisms were all unique. This genotype based method is rapid, simple, reproducible and may have potential as a means of specifically typing Acinetobacter spp. allowing the route(s) of nosocomial transmission to be identified and to assess the efficiency of instituted infection control measures.

Acinetobacter↗
PubMed1999

Molecular and antibiogram relationships of Acinetobacter isolates from two contrasting hospitals in the United Kingdom and South Africa.

The aim of this study was to compare the molecular relationships and antibiograms of nosocomial isolates of Acinetobacter spp. from two acute-care hospitals in Nottingham, UK, and Soweto, South Africa, with different hospital infection control problems and procedures. In contrast to Nottingham, where randomly amplified polymorphic DNA fingerprinting demonstrated that a single multiresistant strain of Acinetobacter baumannii has predominated in the hospital intensive care unit over an 11-year period, the Soweto isolates formed a heterogeneous group of unrelated molecular clusters of different antibiograms, with numerous different strains of Acinetobacter baumannii, Acinetobacter sp. 3 and Acinetobacter sp. 13TU apparently being endemic throughout the Soweto hospital. The contrasting results illustrate the need to maintain exemplary infection control procedures in hospitals where high standards have been achieved and warn of what might result if such measures are diminished.

Acinetobacter↗
PubMed1984

A decade of nosocomial Acinetobacter.

A review of nosocomial infections (NI) from January 1971 to April 1981 was conducted in a university-affiliated hospital to examine NI caused by Acinetobacter and to determine whether a rising trend in rates could be detected. Acinetobacter accounted for 85 of 6115 (1.4%) NI. Sites of infection were respiratory tract (42.2%), blood (17.8%), peritoneum (16.7%), urinary tract (10%), surgical wounds (7.8%), central nervous system (3.3%), and skin or eye (2.2%). All patients who developed NI from Acinetobacter were receiving systemic antimicrobial therapy; 58.8% were in the intensive care unit (ICU). The highest rates of Acinetobacter infection occurred in the early 1970s (2.3%); the lowest occurred from 1978 to 1981 (0.94%), p approximately 0.06. This decrease primarily resulted from two factors: a reduction in cross-infections, probably related to a structural change in the ICU from open-bed ward to single rooms, and the elimination of peritoneal infections traced to contamination of dialysate solution. We conclude that in this institution no rise in the proportion of NI caused by Acinetobacter has occurred over the past decade; if anything, there is a downward trend.

Acinetobacter↗
PubMed2006

In vitro activity of cefepime combined with sulbactam against clinical isolates of carbapenem-resistant Acinetobacter spp.

The aim of this study was to assess the in vitro activity of cefepime combined with sulbactam against carbapenem-resistant clinical isolates of Acinetobacter spp. The checkerboard method was used to determine whether combinations act synergistically against these strains. Twenty-three Acinetobacter baumannii and one Acinetobacter junii found to be carbapenem resistant were included in the study. The susceptibility results for cefepime and sulbactam were interpreted according to the guidelines of the Clinical and Laboratory Standards Institute. Pseudomonas aeruginosa ATCC 27853 and Escherichia coli ATCC 25922 were used as quality control strains. The combination of cefepime and sulbactam demonstrated the following interactions: 33.3% (8/24) synergism; 58.3% (14/24) partial synergism; 4.2% (1/24) additive; 4.2% (1/24) indifference; and no antagonism (minimum and maximum fractional inhibitory concentration index 0.25 and 1.5, respectively). According to our in vitro study results, combinations of cefepime with sulbactam have moderate synergistic activity against some carbapenem-resistant strains of Acinetobacter spp., which could be beneficial for the treatment of infections due to multidrug-resistant strains of Acinetobacter spp.

Acinetobacter↗
PubMed2004

Antibiotic susceptibility and REP-PCR fingerprints of Acinetobacter spp. isolated from a hospital ten years apart.

The antibiotic susceptibility profiles and the repetitive extragenic palindromic sequence-based polymerase chain reaction (REP-PCR)-determined genotypes of 109 Acinetobacter strains collected from the University Malaya Medical Center (UMMC), Kuala Lumpur, Malaysia, in 1987 (N=21) and 1996-1998 (N=88) were established. Twelve antibiotic susceptibility profiles of antibiotics used at the UMMC were obtained. In descending order of effectiveness, imipenem, amikacin and ciprofloxacin were the most effective against the Acinetobacter strains. Compared with 1987 isolates, the isolates obtained in 1996-1998 had decreased susceptibility to these antibiotics and were tolerant to the antibiotics up to an MIC90 of > or =256 mg/L. REP-PCR DNA fingerprints of all the isolates revealed the presence of four Acinetobacter spp. lineages; 92% of all the isolates belonged to two dominant lineages (genotypes 1 and 4). Genotype 4 isolates predominant in 1987 showed increased resistance and antibiotic tolerance to imipenem, amikacin and ciprofloxacin compared with the 1996-1998 isolates. In contrast, genotype 1 isolates from 1996-1998 were mainly sensitive to these antibiotics. These findings demonstrate the presence of at least two independent Acinetobacter spp. lineages in the same hospital, and suggest the possibility that genotype 4 Acinetobacter spp. acquired the resistance phenotype in situ, whereas most of the genotype 1 isolates were probably introduced to the hospital in recent years.

Acinetobacter↗
PubMed1997

Outbreak of septicaemia in neonates caused by Acinetobacter junii investigated by amplified ribosomal DNA restriction analysis (ARDRA) and four typing methods.

Septicaemia caused by Acinetobacter occurred in six infants in the neonatal unit. A total of 18 acinetobacters were isolated from blood cultures, cultures of intravascular catheters, and surveillance cultures. Twelve isolates from the six affected infants were identified as Acinetobacter junii by the use of a novel method, amplified ribosomal DNA restriction analysis (ARDRA). Typing of the organisms using the biochemical profiles of the API 20NE system, antibiogram typing, cell envelope protein electrophoresis, and PCR fingerprinting with two primer sets, ERIC1/ERIC2 and ERIC2/ 1026, showed that these 12 isolates were indistinguishable, whereas the remaining six isolates were different. The six infants recovered after therapy with ciprofloxacin alone in five cases and with a combination of ciprofloxacin and gentamicin in one case. This study showed that A. junii is capable of causing a serious, though non-fatal infection in neonates. The combined use of genotypic and phenotypic methods allowed the rapid separation of epidemic from non-epidemic isolates. It is concluded that for a better understanding of the role of the various Acinetobacter genomic species in human pathology, identification of acinetobacters according to the recent taxonomy is imperative.

Acinetobacter↗
PubMed2003

Phenotypic antimicrobial resistance patterns in Pseudomonas aeruginosa and Acinetobacter: results of a Multicenter Intensive Care Unit Surveillance Study, 1995-2000.

Susceptibility data from the Intensive Care Unit (ICU) Surveillance Study for 10,361 isolates of Pseudomonas aeruginosa and 2,573 isolates of Acinetobacter tested at centers in the United States during 1995 to 2000 were analyzed. In all years, amikacin was the most active antimicrobial agent against P. aeruginosa, and imipenem was the most active agent against Acinetobacter. Resistance of both organisms to common therapeutic agents tested throughout the analysis period increased from 1995 to 2000, although the increase was not consistent for all drugs from year to year. The increases were higher among Acinetobacter, and for both organisms, the increase in resistance was greatest for ciprofloxacin. Among all P. aeruginosa tested in 1999 and 2000, resistance to ciprofloxacin was 9-11% higher for isolates from patients on general hospital wards than those from ICUs. Of the 3424 ICU isolates of P. aeruginosa tested in 1999 and 2000, 77 (2.2%) were multidrug-resistant (i.e., resistant to piperacillin, ceftazidime, imipenem, and gentamicin). Twenty (3.9%) isolates of Acinetobacter in 1999 and seven (1.9%) in 2000 were resistant to imipenem, ceftazidime, piperacillin-tazobactam, ciprofloxacin, and amikacin. Although resistance in both P. aeruginosa and Acinetobacter increased, multidrug-resistant (to > or =4 agents) strains were uncommon.

Acinetobacter↗
PubMed2005

Acinetobacter as a causative agent in preseptal cellulitis.

BACKGROUND: The bacterial genus Acinetobacter, once viewed as inconsequential, has been increasingly implicated as a significant pathogen. Acinetobacter is becoming progressively more resistant to older and newer-generation antibiotics. The primary species encountered in infections is Acinetobacter baumannii. CASE REPORT: A 39-year-old woman came in for treatment of a preseptal cellulitis and conjunctivitis. She was referred to W.W. Hastings Optometry Clinic eleven days after first being diagnosed with a hordeolum that developed into a preseptal cellulitis, despite the use of oral cephalexin anazithromycin. After being referred, the patient was placed on oral regimen of gatifloxacin and topical ciprofloxacin. The patient gradually improved over the next 10 days, with full resolution occurring 21 days after the first presentation. Culturing revealed the offending organism to be Acinetobacter. DISCUSSION: Most ocular infections are still caused by common organisms such as Staphylococcus. However, atypical bacteria such as Acinetobacter are responsible for a minority of infections. Careful consideration of patient history and clinical signs must be made to differentiate preseptal cellulitis and orbital cellulitis. CONCLUSION: This case emphasizes that clinicians need to be aware of emerging and resistant bacteria in ocular infections. Infections that do not respond to traditional therapy should be treated aggressively with the latest-generation antibiotics. Ocular infections that do not resolve in a timely manner should be cultured for the offending organism and these organisms should be tested for susceptibility to anti-microbial drugs.

Acinetobacter↗
PubMed2002

Carbapenem-resistant Acinetobacter and role of curtains in an outbreak in intensive care units.

Multiple-antibiotic-resistant Acinetobacter baumanii, including meropenem resistance, was first isolated from a patient in the general intensive care unit of a tertiary-referral university teaching hospital in Birmingham in December 1998. Similar strains were subsequently isolated from 12 other patients, including those on another intensive care unit within the hospital. The outbreak followed an increase in the use of meropenem in both the units. Environmental screening revealed the presence of the multiple-resistant Acinetobacter species on fomite surfaces in the intensive care unit and bed linen. The major source appeared to be the curtains surrounding patients' beds. Typing by pulsed field gel electrophoresis demonstrated that the patients' isolates and those from the environment were indistinguishable. Rigorous infection control measures including increased frequency of cleaning of the environment with hypochlorite (1000 ppm) and twice-weekly changing of curtains were implemented, along with restriction of meropenem use in the units. Isolation of the multiple-resistant Acinetobacter spp. subsequently diminished and it was not detected over a follow-up period of 18 months. To our knowledge, this is the first reported outbreak of carbapenem-resistant Acinetobacter spp. from the UK. This outbreak also highlights environmental sources, particularly dry fabrics such as curtains, as an important reservoir for dissemination of acinetobacters.

Acinetobacter↗
PubMed2000

Endemic carbapenem-resistant Acinetobacter species in Brooklyn, New York: citywide prevalence, interinstitutional spread, and relation to antibiotic usage.

Acinetobacter species are problematic nosocomial pathogens. In November 1997, pathogens isolated by microbiology laboratories were collected from 15 hospitals in Brooklyn, New York. Acinetobacter species accounted for 10% of gram-negative isolates. Only half of Acinetobacter species were susceptible to carbapenems; 11 hospitals had at least 1 isolate resistant to carbapenems. Other Acinetobacter susceptibility rates were as follows: polymyxin, 99%; amikacin, 87%; ampicillin/sulbactam, 47%; ceftazidime, 25%; and ciprofloxacin 23%. Overall, 10% were resistant to all commonly used antibiotics. Genetic analysis by use of pulsed-field gel electrophoresis of 12 carbapenem-resistant isolates revealed 4 strains that were recovered from >1 hospital, which suggests interinstitutional spread. Antibiotic usage data from 11 hospitals revealed that the use of third-generation cephalosporins was associated significantly with the percentage of carbapenem-resistant strains (P=.03). Resistant Acinetobacter species have become endemic in Brooklyn, New York. Citywide strategies that involve surveillance, infection-control practices, and the reduction of antibiotic usage may be necessary to control the spread of these pathogens.

Acinetobacter↗
PubMed2001

Antibiotic resistance is a major risk factor for epidemic behavior of Acinetobacter baumannii.

OBJECTIVE: To study the presence of bacterial factors in clinical isolates of Acinetobacter species in order to identify markers of epidemic potential. DESIGN: Case-control study. METHODS: Forty-six isolates of Acinetobacter species, including 23 epidemic and 23 sporadic strains from different outbreaks in nine European countries, were compared for the presence of the following factors: hemagglutination, presence of capsules and fimbriae, binding to salivary mucins, resistance to drying, and antibiogram typing. Genotyping of all strains was performed by amplified fragment-length polymorphism (AFLP). RESULTS: All outbreak strains except two (91%) were identified as Acinetobacter baumannii. Binding to salivary mucins and resistance to antibiotics were significantly associated with epidemic behavior. Antibiogram typing showed clustering of predominantly A baumannii strains within one group, and these strains were significantly more resistant to antibiotics than sporadic strains. AFLP genotyping revealed a great heterogeneity among the different European Acinetobacter strains. Cluster analysis of AFLP fingerprints showed several small clusters of different A baumannii outbreak strains. AFLP genotyping could not identify a common epidemic marker within the strains studied. CONCLUSIONS: Antibiogram typing can be used in routine clinical laboratories as a screening method to recognize potentially epidemic A baumannii strains. Several other factors were found, both in different outbreaks as well as in sporadic Acinetobacter isolates. These characteristics were unable to predict epidemic behavior and therefore cannot be used as discriminative epidemic markers. AFLP genotyping demonstrated no common clonal origin of European epidemic A baumannii strains. This indicates that any clinical A baumannii isolate with resistance to multiple antibiotics can be a potential nosocomial outbreak strain.

Acinetobacter↗
PubMed2006

Outbreak of infection with Acinetobacter strain RUH 1139 in an intensive care unit.

OBJECTIVE: To investigate a nosocomial outbreak of infection with Acinetobacter strain RUH 1139, in the unit of high neonatal risk at University Hospital of The Andes (Merida, Venezuela). METHODS: Twenty-eight Acinetobacter strains were detected by biochemical testing and further identified to the species level by examination of the gene encoding 16S ribosomal DNA, using restriction analysis and gene sequencing. The epidemiological relationship between the strains was established by means of repetitive extragenic palindromic polymerase chain reaction (REP-PCR) and pulsed-field gel electrophoresis (PFGE), and antimicrobial susceptibilities were determined by disk diffusion. RESULTS: The spread of an epidemic strain of Acinetobacter RUH 1139 among 16 patients over a period of 3 months was demonstrated using antimicrobial susceptibility testing, PFGE, and REP-PCR. The epidemic strain was also isolated in 2 of the sampled parenteral nutrition solutions. All the patients involved in the infection outbreak had received parenteral solution. Moreover, strains of Acinetobacter RUH 1139 with another PFGE pattern and of A. baumannii were sporadically isolated before and during the outbreak. CONCLUSION: This is the first description of an outbreak of infection with this genospecies of Acinetobacter in which parenteral nutrition solution was potentially the infection source.

Acinetobacter↗