Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Acinetobacter”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 163 records · Page 9Linked to original sources
PubMed1985

An outbreak of infections with Acinetobacter calcoaceticus in burn patients: contamination of patients' mattresses.

During a 21-month period Acinetobacter calcoaceticus was the most common organism causing infections in a university burn center. Forty-three of 103 patients admitted became infected with this organism. Risk factors associated with burn wound colonization with Acinetobacter included larger burns and Foley catheter use; however, only a longer duration of hospitalization was an independent discriminator of colonization. Infection-control measures, including strict isolation and closure and repainting of the burn unit, did not prevent the transmission of Acinetobacter. An investigation found that wet mattresses served as environmental reservoirs of Acinetobacter. This finding led to a policy of discarding each patient's mattress on the day of the patient's discharge from the burn unit. Life table analysis demonstrated that this intervention led to a reduced risk of burn wound colonization with Acinetobacter (P less than .05) and ultimately resulted in the complete elimination of the organism from the burn unit.

Acinetobacter↗
PubMed1998

Outbreak of Acinetobacter spp. bloodstream infections in a nursery associated with contaminated aerosols and air conditioners.

BACKGROUND: Acinetobacter spp. are multidrug-resistant bacteria that grow well in water and cause infections with unexplained, increased summer prevalence. In August, 1996, eight infants acquired Acinetobacter spp. bloodstream infection (A-BSI) while in a nursery in the Bahamas; three infants died and an investigation was initiated. METHODS: A case patient was defined as any newborn in the nursery during August 6 to 13, 1996, with A-BSI. To identify risk factors for A-BSI we conducted a retrospective cohort study and performed environmental cultures and air sampling using settle plates. The genetic relatedness of environmental isolates was assessed by pulsed field gel electrophoresis. RESULTS: Of 33 patients in the nursery 8 (24%) met the case definition. Patients with peripheral iv catheters were more likely to develop A-BSI (8 of 21 vs. O of 10, P < 0.05). Multivariate analysis among patients with iv catheters indicated that only exposure to one nurse was an independent risk factor for developing A-BSI (P < 0.005). Nursery settle plates were more likely to grow Acinetobacter spp. than were settle plates from other hospital areas (8 of 9 vs. 0 of 5, P < 0.005); cultures from nursery air conditioners also grew Acinetobacter spp. Environmental isolates were genetically diverse. After installation of a new air conditioner in May, 1995, A-BSIs occurred more frequently during months of increased absolute humidity or environmental dew point. CONCLUSIONS: Acinetobacter spp. may cause nosocomial BSI and death among infants during periods of polyclonal airborne dissemination; breaks in aseptic technique during i.v. medication administration may facilitate transmission from the environment to the patient. Environmental conditions that increase air conditioner condensate may predispose to airborne dissemination via contaminated aerosols and increase the risk of nosocomial A-BSI.

Acinetobacter↗
PubMed2000

Distribution and in-vitro transfer of tetracycline resistance determinants in clinical and aquatic Acinetobacter strains.

Following characterisation by phenotypic tests and amplified ribosomal DNA restriction analysis (ARDRA), 50 tetracycline-resistant (MIC > or = 16 mg/L) Acinetobacter strains from clinical (n = 35) and aquatic (n = 15) samples were analysed by PCR for tetracycline resistance (Tet) determinants of classes A-E. All the clinical strains were A. baumannii; most (33 of 35) had Tet A (n = 16) or B (n = 17) determinants, and only two did not yield amplicons with primers for any of the five tetracycline resistance determinants. The aquatic strains belonged to genomic species other than A. baumannii, and most (12 of 15) did not contain determinants Tet A-E. Strains negative for Tet A-E were also negative for Tet G and M; further analysis of two aquatic strains with specific primers for Tet O and Tet Y and degenerate primers for Tet M-S-O-P(B)-Q also showed negative results. Transfer of tetracycline resistance was tested for 20 strains with three aquatic Acinetobacter strains and Escherichia coli K-12 as recipients. Transfer of resistance was demonstrated between aquatic strains from distinct ecological niches, but not from clinical to aquatic strains, nor from any Acinetobacter strain to E. coli K-12. Most transconjugants acquired multiple relatively small plasmids (<36 kb). Transfer did not occur when DNA from the donor strains was added to the recipient cultures and was not affected by deoxyribonuclease I, suggesting a conjugative mechanism. It is concluded that Tet A and B are widespread among tetracycline-resistant A. baumannii strains of clinical origin, but unknown genetic determinants are responsible for most tetracycline resistance among aquatic Acinetobacter spp. These differences, together with the inability of clinical strains to transfer tetracycline resistance in vitro to aquatic strains, contra-indicate any important flow of tetracycline resistance genes between clinical and aquatic acinetobacter populations.

Acinetobacter↗
PubMed2000

Simplified phenotypic tests for identification of Acinetobacter spp. and their antimicrobial susceptibility status.

Acinetobacter spp. have been found to be responsible for an increasing number of nosocomial infections. During a 16-month period, 22 patients hospitalised mainly in the respiratory intensive care unit (RICU), paediatric and other medical wards were investigated either for infection or colonisation by Acinetobacter spp. Of the 45 isolates of Acinetobacter detected among the total of 425 non-fermenters encountered, 24 representative isolates were selected for extended phenotypic identification. Four environmental isolates were also included in the study. These 28 isolates were typed by biotyping and antibiotyping, which helped in delineating the Acinetobacter spp. into 12 phenotypes and two distinct antibiotypes respectively. A sudden increase of cases of acinetobacter infection suggested that three outbreaks during the study period were due to phenotypes 1 and 2 of A. calcoaceticus-A. baumannii complex (Acb). Strains of Acb-complex showed multiple drug resistance and were sensitive only to netilmicin. A comparatively high proportion of resistance to amikacin (48%) was also detected among these strains by the agar dilution method. The RICU environment was recognised as an important reservoir for the resistant outbreak strain (Acb-1) which was probably leading to persistent colonisation and recurrent infections.

Acinetobacter↗
PubMed2001

Clinical importance of extended-spectrum beta-lactamase (PER-1-type)-producing Acinetobacter spp. and Pseudomonas aeruginosa strains.

Recently, an extended-spectrum beta-lactamase (PER-1) was found to be disseminated among Acinetobacter spp. and Pseudomonasaeruginosa isolates in Turkey. A population-based cohort study was conducted to elucidate predictive mortality factors in patients with nosocomial infections caused by Acinetobacter spp. and P. aeruginosa, with particular reference to PER-1-type extended-spectrum beta-lactamase (ESBL) production. The study group comprised 16 and 21 non-survivors and 82 and 126 survivors in cohorts infected with Acinetobacter and P. aeruginosa, respectively. In the Acinetobacter-infected cohort, nosocomial pneumonia, hypotension and infection with a PER-positive isolate were independent predictors of mortality. In the P. aeruginosa-infected cohort, impaired consciousness, a PER-positive isolate, male sex and (with a negative relative risk) urinary tract infection were independent predictors of death. This study demonstrated the relationship of PER-1-type ESBL-producing Acinetobacter spp. and P. aeruginosa with poor clinical outcome.

Acinetobacter↗
PubMed1996

The epidemiology of acinetobacter infections in Hong Kong.

A retrospective survey was conducted of the characteristics of acinetobacter infections in Hong Kong--seasonal and geographic distributions, frequency of isolation from various body sites, antimicrobial susceptibility and molecular epidemiology. Most (80%) isolates of Acinetobacter spp. belonged to DNA groups 2 (A. baumannii) or 13, as defined by growth at 44 degrees C. An increased isolation rate in summer was related to higher ambient temperatures. The notion that acinetobacters are opportunist nosocomial pathogens was supported by the body site- and ward-specific distributions, which were similar to those of Pseudomonas aeruginosa and in marked contrast to those of coagulase-negative staphylococci and Escherichia coli. Typing of Acinetobacter isolates by arbitrary-primed polymerase chain reaction revealed extensive genotypic polymorphism, suggesting that numerous unrelated strains were circulating between patients. In view of the association with a high incidence of polymicrobial bacteraemia and multiresistance to antibiotics, a careful selection of appropriate antibiotics in combination is necessary for empirical therapy of infections caused by Acinetobacter spp.

Acinetobacter↗
PubMed1998

Molecular epidemiology of aminoglycoside resistance in Acinetobacter spp.

Most aminoglycoside resistance in Acinetobacter spp. involves production of aminoglycoside-modifying enzymes. Previous studies have shown that the genes encoding these enzymes can be present on plasmids, transposons or within integron-type structures. To determine whether particular mechanisms of aminoglycoside resistance have developed in strains from specific geographical locations (with subsequent clonal spread), or whether common mechanisms have been acquired by genotypically distinct clinical isolates of Acinetobacter spp. throughout the world, a genotypically heterogeneous collection of 24 multiresistant clinical isolates of Acinetobacter spp. from 15 hospitals in 11 countries worldwide was studied. All were resistant to two or more aminoglycoside antibiotics. The full aminoglycoside resistance profile was determined for each isolate, allowing a putative enzyme content to be inferred, with subsequent confirmation of enzyme content and genetic location by polymerase chain reaction (PCR) and hybridisation techniques. All produced at least one aminoglycoside-modifying enzyme, most commonly AAC(3)-I and ANT(3'')-I in various combinations. Other enzymes found were AAC(3)-II, AAC(6')-I, ANT(2''), APH(3')-I and APH(3')-VI. None was confined to strains from a particular geographical area. Nine isolates transferred resistance mediated by AAC(3)-I, ANT(2'')-I, APH(3')-I or APH(3)'-VI by conjugation to a sensitive strain of A. baumannii, but most resistance was non-transferable. PCR mapping revealed an integron location in six isolates for the aac(3)-Ia gene and in three isolates for the ant(3'')-Ia gene. Overall, the study demonstrated that similar aminoglycoside-modifying enzymes are found in unrelated isolates of Acinetobacter spp., and that particular genes are not restricted to specific areas of the world. The demonstration of certain genes on plasmids and integrons emphasises the probable importance of these structures in the dissemination of certain types of aminoglycoside resistance in Acinetobacter spp.

Acinetobacter↗
PubMed2006

Alert surveillance of intensive care unit-acquired Acinetobacter infections in a Sicilian hospital.

The epidemiological impact of Acinetobacter baumannii nosocomial infections in a Sicilian intensive care unit (ICU) was investigated to determine the Acinetobacter-specific infection rates, to estimate the preventable proportion of Acinetobacter infections, i.e., those resulting from cross-transmission, and to investigate the molecular epidemiology of antimicrobial resistance in Acinetobacter. The impact of Acinetobacter nosocomial infection in the ICU was determined to be 3.0 new cases per 100 admissions. Site-specific rates confirmed that ICU-acquired pneumonia was the most important infection type. The incidence rate, adjusted by the number of patient-days, was 3.3 infections/1000 patient-days. The estimated preventable proportion of A. baumannii nosocomial infections in the ICU was 66.7%. A class 1 integron, characterised by its gene cassette content, was present in all A. baumannii isolates of four different pulsed-field gel electrophoresis types, and was associated significantly with clones implicated in cross-transmission episodes. Furthermore, the same integron was detected in two genetically distinct isolates responsible for recurrent infection in the same patient, suggesting the occurrence of horizontal gene transfer in vivo. Even in an endemic setting with low infection rates, spread of A. baumannii was caused mainly by infection control shortcomings that require appropriate surveillance and control policies.

Acinetobacter Infections↗
PubMed1997

Widespread detection of PER-1-type extended-spectrum beta-lactamases among nosocomial Acinetobacter and Pseudomonas aeruginosa isolates in Turkey: a nationwide multicenter study.

We studied the prevalence and molecular epidemiology of PER-1-type beta-lactamases among Acinetobacter, Klebsiella, and Pseudomonas aeruginosa strains isolated over a 3-month period in eight university hospitals from distinct regions of Turkey. A total of 72, 92, and 367 Acinetobacter, Klebsiella, and P. aeruginosa isolates were studied, respectively. The presence of blaPER was determined by the colony hybridization method and later confirmed by isoelectric focusing. We detected PER-1-type beta-lactamases in 46% (33/72) of Acinetobacter strains and in 11% (40/367) of P. aeruginosa strains but not in Klebsiella strains. PER-1-type enzyme producers were highly resistant to ceftazidime and gentamicin, intermediately resistant to amikacin, and susceptible or moderately susceptible to imipenem and meropenem. Among PER-1-type-beta-lactamase-positive isolates, five Acinetobacter isolates and six P. aeruginosa isolates from different hospitals were selected for ribosomal DNA fingerprinting with EcoRI and SalI. The EcoRI-digested DNAs were later hybridized with a digoxigenin-labelled PER-1 probe. The ribotypes and the lengths of blaPER-carrying fragments were identical in four Acinetobacter strains. A single isolate (Ac3) harbored a PER gene on a different fragment (approximately 4.2 kbp) than the others (approximately 3.4 kbp) and showed a clearly distinguishable ribotype. Ribotypes of P. aeruginosa strains obtained with EcoRI showed three patterns. Similarly, in Pseudomonas strains two different EcoRI fragments harbored blaPER (approximately 4.2 kbp in five isolates and 3.4 kbp in one isolate). PER-1-type beta-lactamases appear to be restricted to Turkey. However, their clonal diversity and high prevalence indicate a high spreading potential.

Acinetobacter↗
PubMed2001

Characterization of OXA-25, OXA-26, and OXA-27, molecular class D beta-lactamases associated with carbapenem resistance in clinical isolates of Acinetobacter baumannii.

Carbapenem resistance in Acinetobacter spp. is increasingly being associated with OXA-type beta-lactamases with weak hydrolytic activity against imipenem and meropenem. Such enzymes were characterized from Acinetobacter isolates collected in Belgium, Kuwait, Singapore, and Spain. The isolates from Spain and Belgium had novel class D beta-lactamases that were active against carbapenems. These were designated OXA-25 and OXA-26, respectively, and had >98% amino acid homology with each other and with the OXA-24 enzyme recently described by others from an Acinetobacter isolate collected elsewhere in Spain. The isolate from Singapore had OXA-27 beta-lactamase, another novel class D type with only 60% homology to OXA-24, -25, and -26, but with 99% homology to OXA-23 (ARI-1), described previously from an Acinetobacter baumannii isolate collected in Scotland. Sequence data were not obtained for the carbapenem-hydrolyzing OXA enzyme from the isolate from Kuwait; nevertheless, the enzyme was phenotypically similar to OXA-25 and -26. The enzymes OXA-23, -24, -25, -26, and -27 retained the STFK and SXV motifs typical of class D beta-lactamases, but the YGN motif was altered to FGN. The KTG motif was retained by OXA-27 and -23 but was replaced by KSG in OXA-24, -25, and -26. OXA-25 and -26 enzymes were strongly active against oxacillin, but unusually for an OXA-type beta-lactamase, OXA-27 had apparently weak activity, although measurement was complicated by biphasic kinetics. None of the new enzymes was transmissible to Escherichia coli recipients. Many Acinetobacter isolates are multiresistant to other antibiotics, and the emergence of class D enzymes with carbapenem-hydrolyzing activity is a disturbing development for antimicrobial chemotherapy.

Acinetobacter↗
PubMed1997

Survival of Acinetobacter baumannii on dry surfaces.

Acinetobacter spp. have frequently been reported to be the causative agents of hospital outbreaks. The circumstances of some outbreaks demonstrated the long survival of Acinetobacter in a dry, inanimate environment. In laboratory experiments, we compared the abilities of five Acinetobacter baumannii strains, three Acinetobacter sp. strains from the American Type Culture Collection (ATCC), one Escherichia coli ATCC strain, and one Enterococcus faecium ATCC strain to survive under dry conditions. Bacterial solutions of the 10 strains were inoculated onto four different material samples (ceramic, polyvinyl chloride, rubber, and stainless steel) and stored under defined conditions. We investigated the bacterial counts of the material samples immediately after inoculation, after drying, and after 4 h, 1 day, and 1, 2, 4, 8, and 16 weeks of storage. A statistical model was used to distribute the 40 resulting curves among four types of survival curves. The type of survival curve was significantly associated with the bacterial strain but not with the material. The ability of the A. baumannii strains to survive under dry conditions varied greatly and correlated well with the source of the strain. Strains isolated from dry sources survived better than those isolated from wet sources. An outbreak strain that had caused hospital-acquired respiratory tract infections survived better than the strains from wet sources, but not as well as strains from dry sources. Resistance to dry conditions may promote the transmissibility of a strain, but it is not sufficient to make a strain an epidemic one. However, in the case of an outbreak, sources of Acinetobacter must be expected in the dry environment.

Acinetobacter↗
PubMed2004

Multidrug-resistant Acinetobacter infections: an emerging challenge to clinicians.

OBJECTIVE: To review and evaluate clinically relevant epidemiology, microbiology, and clinical studies regarding the treatment of multidrug-resistant Acinetobacter infections. DATA SOURCES: Pertinent literature was identified by a MEDLINE search (1966-September 2003) and through secondary bibliographies of pertinent articles. STUDY SELECTION AND DATA EXTRACTION: All English-language articles identified from data sources were evaluated for clinical relevance. DATA SYNTHESIS: Acinetobacter baumannii has emerged as a worldwide problem as a nosocomial pathogen in hospitalized patients. Acinetobacter spp. can cause a multitude of infections including pneumonia, bacteremia, meningitis, urinary tract infections, and skin and soft tissue infections, and the mortality associated with these infections is high. Isolates resistant to almost all commercially available antimicrobials have been identified, thus limiting treatment options. The development of new agents and reappraisal of older compounds (ie, polymyxins, ampicillin/sulbactam) are necessary as we consider the optimal treatment of these multidrug-resistant organisms. CONCLUSIONS: There is no simple answer to the treatment of Acinetobacter infections. Eradication of Acinetobacter spp. requires adherence to good infection control practices and prudent antibiotic use, as well as effective antimicrobial therapy. Alternative therapies such as colistin, ampicillin/sulbactam, and tetracycline are potential options, but prospective, randomized, controlled trials are still lacking.

Acinetobacter Infections↗
PubMed2006

Comparison of efficacy of cefoperazone/sulbactam and imipenem/cilastatin for treatment of Acinetobacter bacteremia.

Multiple antibiotic resistance threatens successful treatment of Acinetobacter baumannii infections worldwide. Increasing interest in the well-known activity of sulbactam against the genus Acinetobacter has been aroused. The purpose of this study was to compare the outcomes for patients with Acinetobacter bacteremia treated with cefoperazone/sulbactam versus imipenem/cilastatin. Forty-seven patients with Acinetobacter baumannii bacteremia were analyzed through a retrospective review of their medical records for antibiotic therapy and clinical outcome. Thirty-five patients were treated with cefoperazone/sulbactam, and twelve patients with imipenem/cilastatin. The percentage of favorable response after 72 hours was not statistically different between cefoperazone/sulbactam group and imipenem/cilastatin group. The mortality rate was not statistically different, too. Cefoperazone/sulbactam was found to be as useful as imipenem/cilastatin for treating patients with Acinetobacter bacteremia.

Acinetobacter↗
PubMed1998

[Adherence of Acinetobacter baumannii to rat tracheal tissue].

BACKGROUND: Acinetobacter baumannii is an important nosocomial pathogen whose virulence factors have not been fully elucidated. AIM: To study the adherence and hemagglutinating capacity of several biotypes of Acinetobacter baumannii. MATERIAL AND METHODS: Thirty nine strains of Acinetobacter baumannii isolated from hospitalized patients were studied. The adherence of these strains to small pieces of rat tracheal tissue was studied. Additionally, their ability to hemagglutinate human erythrocytes and the effect of D-mannose and D-galactose on the adherence and hemagglutinating capacity was assessed. Transmission electron microscopy of strains was performed looking for the presence of fimbriae. RESULTS: All strains exhibited adherence to tissues. All strains had also D-mannose and D-galactose resistant hemagglutinating ability. Fimbriae were found in Acinetobacter baumannii and E coil cells. CONCLUSIONS: Adherence of Acinetobacter baumannii to rat tracheal tissue, apparently not related to the presence of fimbriae, may be a virulence mechanism of this bacterium.

Acinetobacter↗
PubMed2002

[Acinetobacter].

Acinetobacter spp. are increasingly important nosocomial pathogens and are capable of rapid adaptation to the hospital environment. National surveillance of nosocomial infection in Japan from July 2000 to June 2001 showed that 1.5% of blood-stream infections has occurred by Acinetobacter spp. The greatest impact of Acinetobacter has been a causative agent of nosocomial pneumonia, particularly ventilator-associated cases. Recent trends indicate increasing antimicrobial resistance of Acinetobacter isolates, posing a serious threat to hospitalized patients. Especially, carbapenem-resistance including muti-resistant metallo-beta-lactamase producing isolates has been identified in Japan and other countries. Hand-washing policy and practices with daily decontamination of medical-devices or hand-contact environment should control nosocomial infection by Acinetobacter.

Acinetobacter↗
PubMed2004

[Clinical features of ventilator-associated pneumonia caused by acinetobacter].

OBJECTIVE: To investigate the clinical features of ventilator-associated pneumonia (VAP) caused by acinetobacter. METHODS: The clinical manifestations of 45 cases with ventilator-associated pneumonia caused by acinetobacter between 1995 and 2002 were analyzed. Bacterial susceptibility of acinetobacter strains was determined by Kerby-Bauer method. RESULTS: The mean age of the subjects was 58 +/- 13 years with 31 patients older than 60 years. All the patients had underlying diseases, most of which were respiratory diseases (37.8%), nervous system diseases (22.2%), and trauma (22.2%). Thirteen cases (28.9%) were mixed infections with other bacteria. The main manifestations were fever, purulent secretion, and solidification in the lung. X-ray revealed inflammatory infiltration in lower lobes of both sides. The mortality was 37.8%. The in vitro activity tests of 28 antibiotics against the acinetobacter strains showed that they were multiresistant. Polymysin B, imipenem, minocycline, ofloxacin, and amikacin were relatively active. CONCLUSION: The patients with VAP caused by acinetobacter usually had underlying diseases without unique features and high mortality, and the isolated strains were often mutiresistant. It is necessary to make early diagnosis, select the appropriate agents, and improve the disinfection of the breath loop in the ventilator.

Acinetobacter↗
PubMedDate not supplied

[In vitro activity of 9 antibiotics and 3 beta-lactamase inhibitors against 107 clinical isolates of Acinetobacter baumanii].

BACKGROUND: Acinetobacter sp. is an important cause of nosocomial infections and it is often resistant to many antibiotics. In our hospital it often causes infections in patients on the intensive care unit. The aim of this study was to know the susceptibility of Acinetobacter sp. strains isolated in our hospital. METHODS: The in vitro activities of nine antimicrobial agents (ticarcillin, piperacillin, ceftazidime, imipenem, meropenem, gentamicin, tobramycin, amikacin and colistin) and three beta-lactamase inhibitors (sulbactam, clavulanate and tazobactam) against 107 clinical isolates of Acinetobacter baumannii were studied. MICs were determined by a dilution agar method, except for colistin, which we used the disk-diffusion agar method. RESULTS: Of the antimicrobial agents tested imipenem and colistin were highly active against all isolates (100% susceptibility), meropenem presented good activity (96.3% susceptibility), ticarcillin presented moderated activity (84.1% susceptibility). Most of the strains were resistant to ceftazidime (4.7% susceptibility), piperacillin (3.7% susceptibility) and the aminoglycosides (amikacin 21.5% susceptibility, gentamicin 2.8% susceptibility and tobramycin 4.7% susceptibility). Sulbactam was the most active agent among the beta-lactamase inhibitors studied (CMI90 = 4 micrograms/ml). CONCLUSIONS: Recent trends indicate increasing antimicrobial resistance of Acinetobacter baumannii, posing a serious threat to hospitalized patients. An strict attention to maintain a good housekeeping and control of the environment and of the antimicrobial usage, appears the measures most likely to control the spread of Acinetobacter baumannii in hospitals.

Acinetobacter↗
PubMed2004

Susceptibility of the Acinetobacter calcoaceticus-A. baumannii complex to imipenem, meropenem, sulbactam and colistin.

The Acinetobacter calcoaceticus-Acinetobacter baumannii complex includes some of the most clinically relevant species of the genus Acinetobacter due to their capacity to cause epidemic nosocomial outbreaks as well as their increasing resistance to antibiotics. Susceptibility of Acinetobacter strains varies greatly depending on origin, thus highlighting the importance of local analyses of susceptibility profiles. Two hundred twenty-one strains of the A. calcoaceticus-A. baumannii complex were identified using biochemical tests and were biotyped. Strain susceptibility to imipenem, meropenem, colistin and sulbactam was studied using agar dilution. Eight different biotypes were found, type 1 accounting for 69.2% of the strains. MIC(50) and MIC(90) to imipenem, meropenem, colistin and sulbactam were 4 and 8 mg/l, 16 and 32 mg/l, 0.5 and 1mg/l, and 8 and 16 mg/l, with susceptibility rates of 64.3, 22.6, 98.2 and 73.8%, respectively. Biotype 1 was the most resistant. A statistically significant difference was observed for the mean MIC of the four predominant biotypes to imipenem, meropenem and sulbactam but not to colistin.

Acinetobacter↗