Acinetobacter bacteremia in Hong Kong: prospective study and review.
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The epidemiological characteristics of 18 patients with acinetobacter bacteremia were analyzed. Patients (mean age, 55.5 years) developed bacteremia after an average of 14.1 days of hospitalization. Fifteen of 16 patients survived bacteremia caused by Acinetobacter baumannii. Cultures of blood from the remaining two patients yielded Acinetobacter lwoffii. Most patients (78%) resided in the general ward, while four patients (22%) were under intensive care. Genotyping by arbitrarily primed polymerase chain reaction analysis and the temporal sequence of isolation were more useful than phenotyping by antimicrobial susceptibility in the determination of the source of bacteremia, and the intravascular catheter was the leading infection source (39% of cases). The possibility of an association of glucose with the pathogenesis of acinetobacter infection was raised. (+info)
Risk factors for nosocomial bloodstream infections due to Acinetobacter baumannii: a case-control study of adult burn patients.
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Risk factors for Acinetobacter baumannii bloodstream infection (BSI) were studied in patients with severe thermal injury in a burn intensive care unit where A. baumannii was endemic. Of 367 patients hospitalized for severe thermal injury during the study period, 29 patients with nosocomial A. baumannii BSI were identified (attack rate, 7.9%). Cases were compared with 58 matched controls without A. baumannii BSI. The overall mortality rate was 31% among cases and 14% among controls; only two deaths (7%) were considered directly related to A. baumannii BSI. Molecular typing of A. baumannii blood isolates by means of randomly amplified polymorphic DNA analysis and pulsed-field gel electrophoresis revealed the presence of three different strain types. Multivariate analysis showed that female gender (P = .027), total body surface area burn of > 50% (P = .016), prior nosocomial colonization with A. baumannii at a distant site (P = .0002), and use of hydrotherapy (P = .037) were independently associated with the acquisition of A. baumannii BSI in burn patients. These data underscore the need for effective infection control measures for this emerging nosocomial problem. (+info)
Efficacy of sulbactam alone and in combination with ampicillin in nosocomial infections caused by multiresistant Acinetobacter baumannii.
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From March 1995 to March 1997, sulbactam was prospectively evaluated in patients with non-life-threatening multiresistant Acinetobacter baumannii infections. During this period, 47 patients were treated with sulbactam; of them, five were excluded because they had received < or =48 h of sulbactam therapy. A total of 42 patients, 27 males and 15 females with a mean age of 60+/-15 years, were finally evaluated. Infections were as follows: surgical wound, 19; tracheobronchitis, 12; urinary tract, 7; catheter-related bacteraemia, 2; and pneumonia, 2. Eighteen patients received intravenous sulbactam alone (1 g every 8 h) and 24 patients received intravenous sulbactam/ampicillin (1 g:2 g every 8 h) with no major adverse effects. Of the 42 patients, 39 improved or were cured and showed A. baumannii eradication and one patient had persistence of wound infection after 8 days of sulbactam/ampicillin requiring surgical debridement. Two patients died after 3 days of therapy (one of the deaths was attributable to A. baumannii infection). The in-vitro activity of the sulbactam/ampicillin combination was by virtue of the antimicrobial activity exhibited by sulbactam. Killing curves showed that sulbactam was bacteriostatic; no synergy was observed between ampicillin and sulbactam. Our results indicate that sulbactam may prove effective for non-life-threatening A. baumannii infections. Its role in the treatment of severe infections is unknown. However, the current formulation of sulbactam alone may allow its use at higher doses and provide new potential synergic combinations, particularly for those infections by A. baumannii resistant to imipenem. (+info)
Identification of Acinetobacter baumannii strains with monoclonal antibodies against the O antigens of their lipopolysaccharides.
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Despite the emergence of Acinetobacter baumannii strains as nosocomial pathogens, simple methods for their phenotypic identification are still unavailable. Murine monoclonal antibodies specific for the O-polysaccharide moiety of the lipopolysaccharide (LPS) of two A. baumannii strains were obtained after immunization with heat-killed bacteria. The monoclonal antibodies were characterized by enzyme immunoassay and by Western and dot blot analyses and were investigated for their potential use for the identification of A. baumannii strains. The antibodies reacted with 46 of the 80 A. baumannii clinical isolates that were investigated, and reactivity was observed with 11 of 14 strains which were isolated during outbreaks in different northwestern European cities; no reactivity was observed with Acinetobacter strains of other genomic species, including the closely related genomic species 1 (Acinetobacter calcoaceticus), 3, and 13 sensu Tjernberg and Ursing, or with other gram-negative bacterial strains. The results show that O-antigen-specific monoclonal antibodies such as the ones described are convenient reagents which can be used to identify Acinetobacter strains in clinical and research laboratories. (+info)
Some immunological properties of lipopolysaccharide from Acinetobacter baumannii.
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Acinetobacter baumannii, mainly biotype 9, is an important nosocomial opportunist pathogen in Chile and other countries. The biological basis of its virulence and prevalence is still unknown. As lipopolysaccharide (LPS) is often associated with virulence, some biological properties of purified LPS from seven nosocomial isolates, comprising four isolates of A. baumannii biotype 9, two isolates of biotype 8 and one isolate of biotype 1, were investigated. LPS was extracted and purified from each isolate by the hot phenol-water method, and its ability to elicit a mitogenic response and to induce the synthesis of a tumour necrosis factor (TNF-alpha) in mouse spleen cells was determined. Activity was evaluated in vivo by determining the splenic index in comparison with LPS from Salmonella Typhimurium. All seven LPS samples were mitogenic on the basis of cellular proliferation experiments and six induced synthesis of TNF-alpha. Similar results were obtained in in-vivo experiments in which LPS induced spleen cell growth, as shown by determination of the splenic index. These results suggest that the LPS of A. baumannii might contribute to the pathogenic properties of this species. (+info)
Use of a murine O-antigen-specific monoclonal antibody to identify Acinetobacter strains of unnamed genomic species 13 Sensu Tjernberg and Ursing.
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A monoclonal antibody against the O-antigenic polysaccharide chain of the lipopolysaccharide (LPS) of Acinetobacter strains belonging to the unnamed genomic species 13 Sensu Tjernberg and Ursing (13TU) was obtained after immunization of BALB/c mice with heat-killed bacteria and was characterized by enzyme immunoassay and Western blot analysis, by use of LPS and proteinase K-treated bacterial lysates, analyses in which the antibody was shown to be highly specific for the homologous antigen. In addition, when tested in dot and Western blots, reactivity was observed with 9 of 18 Acinetobacter strains of genomic species 13TU which had been isolated in Germany and Denmark; no reactivity was observed with strains of other genomic species, including the closely related genomic groups 1 (A. calcoaceticus), 2 (A. baumannii), and 3 (unnamed), or with other gram-negative bacteria. The antibody described here represents a convenient reagent for the simple, economical, and accurate differentiation of clinical isolates of genomic species 13TU from other Acinetobacter strains. Although the antibody does not identify all isolates of this genomic group, it is evident that it will be a useful reagent in the development of a serotyping scheme for clinical laboratories. (+info)
Genotypic and phenotypic similarity of multiresistant Acinetobacter baumannii isolates in the Czech Republic.
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The diversity of 103 clinical isolates of the Acinetobacter calcoaceticus-Acinetobacter baumannii complex obtained between 1991 and 1997 from 17 Czech hospitals was studied by ribotyping, biotyping, plasmid profiling and antibiotic susceptibility testing. According to the EcoRI ribotypes, all but one of these isolates were identified to the DNA group level: 77 isolates were allocated to DNA group 2 (A. baumannii), 14 to DNA group 3, 10 to DNA group 13 sensu Tjernberg and Ursing and one to DNA group 1 (A. calcoaceticus). In total, 50 different EcoRI ribotypes and 10 biotypes were observed. Plasmids were found in 92% of the isolates and a high variability in plasmid profiles was found in isolates of the same DNA group. The combination of typing profiles allowed two predominant groups (termed A and B) to be distinguished among the A. baumannii isolates (37 and eight isolates, respectively) that shared a specific ribotype and were highly similar in other properties. These two groups comprised both sporadic and outbreak isolates and were found in most localities. Group A and B isolates were markedly more resistant to antibiotics than most of the remaining isolates, thus representing 85% of all multiresistant isolates. The features of groups A and B corresponded to those of two epidemic clones identified recently among hospital strains in north-western Europe. (+info)
In vivo efficacies of combinations of beta-lactams, beta-lactamase inhibitors, and rifampin against Acinetobacter baumannii in a mouse pneumonia model.
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The effects of various regimens containing combinations of beta-lactams, beta-lactam inhibitor(s), and rifampin were assessed in a recently described mouse model of Acinetobacter baumannii pneumonia (M. L. Joly-Guillou, M. Wolff, J. J. Pocidalo, F. Walker, and C. Carbon, Antimicrob. Agents Chemother. 41:345-351, 1997). Two aspects of the therapeutic response were studied: the kinetics of the bactericidal effect (treatment was initiated 3 h after intratracheal inoculation, and bacterial counts were determined over a 24-h period) and survival (treatment was initiated 8 h after inoculation, and the cumulative mortality rate was assessed on day 5). Two clinical strains were used: a cephalosporinase-producing strain (SAN-94040) and a multiresistant strain (RCH-69). For SAN-94040 and RCH-69, MICs and MBCs (milligrams per liter) were as follows: ticarcillin, 32, 64, 256, and >256, respectively; ticarcillin-clavulanate, 32, 64, and 512, and >512, respectively; imipenem, 0.5, 0.5, 8, and 32, respectively; sulbactam, 0.5, 0.5, 8, and 8, respectively; and rifampin, 8, 8, 4, and 4, respectively. Against SAN-94040, four regimens, i.e., imipenem, sulbactam, imipenem-rifampin, and ticarcillin-clavulanate (at a 25/1 ratio)-sulbactam produced a true bactericidal effect (>/=3-log10 reduction of CFU/g of lung). The best survival rate (i.e., 93%) was obtained with the combination of ticarcillin-clavulanate-sulbactam, and regimens containing rifampin provided a survival rate of >/=65%. Against RCH-69, only regimens containing rifampin and the combination of imipenem-sulbactam had a true bactericidal effect. The best survival rates (>/=80%) were obtained with regimens containing rifampin and sulbactam. These results suggest that nonclassical combinations of beta-lactams, beta-lactamase inhibitors, and rifampin should be considered for the treatment of nosocomial pneumonia due to A. baumannii. (+info)