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Anton Y Peleg - One of the best experts on this subject based on the ideXlab platform.
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acinetobacter Baumannii evolution of antimicrobial resistance treatment options
Seminars in Respiratory and Critical Care Medicine, 2015Co-Authors: Yohei Doi, Anton Y Peleg, Gerald L MurrayAbstract:The first decade of the 20th century witnessed a surge in the incidence of infections due to several highly antimicrobial-resistant bacteria in hospitals worldwide. Acinetobacter Baumannii is one such organism that turned from an occasional respiratory pathogen into a major nosocomial pathogen. An increasing number of A. Baumannii genome sequences have broadened our understanding of the genetic makeup of these bacteria and highlighted the extent of horizontal transfer of DNA. Animal models of disease combined with bacterial mutagenesis have provided some valuable insights into mechanisms of A. Baumannii pathogenesis. Bacterial factors known to be important for disease include outer membrane porins, surface structures including capsule and lipopolysaccharide, enzymes such as phospholipase D, iron acquisition systems, and regulatory proteins. A. Baumannii has a propensity to accumulate resistance to various groups of antimicrobial agents. In particular, carbapenem resistance has become commonplace, accounting for the majority of A. Baumannii strains in many hospitals today. Carbapenem-resistant strains are often resistant to all other routinely tested agents. Treatment of carbapenem-resistant A. Baumannii infection therefore involves the use of combinations of last resort agents such as colistin and tigecycline, but the efficacy and safety of these approaches are yet to be defined. Antimicrobial-resistant A. Baumannii has high potential to spread among ill patients in intensive care units. Early recognition and timely implementation of appropriate infection control measures is crucial in preventing outbreaks.
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galleria mellonella as a model system to study acinetobacter Baumannii pathogenesis and therapeutics
Antimicrobial Agents and Chemotherapy, 2009Co-Authors: Anton Y Peleg, Sebastian Jara, Divya Monga, George M Eliopoulos, Robert C Moellering, Eleftherios MylonakisAbstract:Nonmammalian model systems of infection such as Galleria mellonella (caterpillars of the greater wax moth) have significant logistical and ethical advantages over mammalian models. In this study, we utilize G. mellonella caterpillars to study host-pathogen interactions with the gram-negative organism Acinetobacter Baumannii and determine the utility of this infection model to study antibacterial efficacy. After infecting G. mellonella caterpillars with a reference A. Baumannii strain, we observed that the rate of G. mellonella killing was dependent on the infection inoculum and the incubation temperature postinfection, with greater killing at 37 degrees C than at 30 degrees C (P = 0.01). A. Baumannii strains caused greater killing than the less-pathogenic species Acinetobacter baylyi and Acinetobacter lwoffii (P < 0.001). Community-acquired A. Baumannii caused greater killing than a reference hospital-acquired strain (P < 0.01). Reduced levels of production of the quorum-sensing molecule 3-hydroxy-C(12)-homoserine lactone caused no change in A. Baumannii virulence against G. mellonella. Treatment of a lethal A. Baumannii infection with antibiotics that had in vitro activity against the infecting A. Baumannii strain significantly prolonged the survival of G. mellonella caterpillars compared with treatment with antibiotics to which the bacteria were resistant. G. mellonella is a relatively simple, nonmammalian model system that can be used to facilitate the in vivo study of host-pathogen interactions in A. Baumannii and the efficacy of antibacterial agents.
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prokaryote eukaryote interactions identified by using caenorhabditis elegans
Proceedings of the National Academy of Sciences of the United States of America, 2008Co-Authors: Anton Y Peleg, George M Eliopoulos, Robert C Moellering, Emmanouil Tampakakis, Beth Burgwyn Fuchs, Eleftherios MylonakisAbstract:Prokaryote–eukaryote interactions are ubiquitous and have important medical and environmental significance. Despite this, a paucity of data exists on the mechanisms and pathogenic consequences of bacterial–fungal encounters within a living host. We used the nematode Caenorhabditis elegans as a substitute host to study the interactions between two ecologically related and clinically troublesome pathogens, the prokaryote, Acinetobacter Baumannii, and the eukaryote, Candida albicans. After co-infecting C. elegans with these organisms, we observed that A. Baumannii inhibits filamentation, a key virulence determinant of C. albicans. This antagonistic, cross-kingdom interaction led to attenuated virulence of C. albicans, as determined by improved nematode survival when infected with both pathogens. In vitro coinfection assays in planktonic and biofilm environments supported the inhibitory effects of A. Baumannii toward C. albicans, further showing a predilection of A. Baumannii for C. albicans filaments. Interestingly, we demonstrate a likely evolutionary defense by C. albicans against A. Baumannii, whereby C. albicans inhibits A. Baumannii growth once a quorum develops. This counteroffensive is at least partly mediated by the C. albicans quorum-sensing molecule farnesol. We used the C. elegans–A. Baumannii–C. albicans coinfection model to screen an A. Baumannii mutant library, leading to the identification of several mutants attenuated in their inhibitory activity toward C. albicans. These findings present an extension to the current paradigm of studying monomicrobial pathogenesis in C. elegans and by use of genetic manipulation, provides a whole-animal model system to investigate the complex dynamics of a polymicrobial infection.
Yohei Doi - One of the best experts on this subject based on the ideXlab platform.
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colistin resistant acinetobacter Baumannii beyond carbapenem resistance
Clinical Infectious Diseases, 2015Co-Authors: Zubair A Qureshi, Robert K Ernst, Lauren E Hittle, Jessica A Ohara, Jesabel I Rivera, Alveena Syed, Ryan K Shields, Anthony W Pasculle, Yohei DoiAbstract:Background. With an increase in the use of colistin methansulfonate (CMS) to treat carbapenem-resistant Acinetobacter Baumannii infections, colistin resistance is emerging. Methods. Patientswithinfection orcolonizationdue tocolistin-resistantA.Baumanniiwere identifiedat ahospital system in Pennsylvania. Clinical data were collected from electronic medical records. Susceptibility testing, pulsed-field gel electrophoresis (PFGE), and multilocus sequence typing (MLST) were performed. To investigate the mechanism of colistin resistance, lipid A was subjected to matrix-assisted laser desorption/ionization mass spectrometry. Results. Twenty patients with colistin-resistant A. Baumannii were identified. Ventilator-associated pneumonia was the most common type of infection. Nineteen patients had received intravenous and/or inhaled CMS for treatment of carbapenem-resistant, colistin-susceptible A. Baumannii infection prior to identification of colistin-resistant isolates. The 30-day all-cause mortality rate was 30%. The treatment regimen for colistin-resistant A. Baumannii infection associated with the lowest mortality rate was a combination of CMS, a carbapenem, and ampicillin-sulbactam. The colistin-susceptible and -resistant isolates from the same patients were highly related by PFGE, but isolates from different patients were not, suggesting evolution of resistance during CMS therapy. By MLST, all isolates belonged to the international clone II, the lineage that is epidemic worldwide. Phosphoethanolamine modification of lipid Awas present in all colistin-resistant A. Baumannii isolates. Conclusions. Colistin-resistant A. Baumannii occurred almost exclusively among patients who had received CMS for treatment of carbapenem-resistant, colistin-susceptible A. Baumannii infection. Lipid A modification by the addition of phosphoethanolamine accounted for colistin resistance. Susceptibility testing for colistin should be considered for A. Baumannii identified from CMS-experienced patients.
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acinetobacter Baumannii evolution of antimicrobial resistance treatment options
Seminars in Respiratory and Critical Care Medicine, 2015Co-Authors: Yohei Doi, Anton Y Peleg, Gerald L MurrayAbstract:The first decade of the 20th century witnessed a surge in the incidence of infections due to several highly antimicrobial-resistant bacteria in hospitals worldwide. Acinetobacter Baumannii is one such organism that turned from an occasional respiratory pathogen into a major nosocomial pathogen. An increasing number of A. Baumannii genome sequences have broadened our understanding of the genetic makeup of these bacteria and highlighted the extent of horizontal transfer of DNA. Animal models of disease combined with bacterial mutagenesis have provided some valuable insights into mechanisms of A. Baumannii pathogenesis. Bacterial factors known to be important for disease include outer membrane porins, surface structures including capsule and lipopolysaccharide, enzymes such as phospholipase D, iron acquisition systems, and regulatory proteins. A. Baumannii has a propensity to accumulate resistance to various groups of antimicrobial agents. In particular, carbapenem resistance has become commonplace, accounting for the majority of A. Baumannii strains in many hospitals today. Carbapenem-resistant strains are often resistant to all other routinely tested agents. Treatment of carbapenem-resistant A. Baumannii infection therefore involves the use of combinations of last resort agents such as colistin and tigecycline, but the efficacy and safety of these approaches are yet to be defined. Antimicrobial-resistant A. Baumannii has high potential to spread among ill patients in intensive care units. Early recognition and timely implementation of appropriate infection control measures is crucial in preventing outbreaks.
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clinical outcomes of hospital acquired infection with acinetobacter nosocomialis and acinetobacter pittii
Antimicrobial Agents and Chemotherapy, 2014Co-Authors: Jesabel I Rivera, Sarunyou Chusri, Virasakdi Chongsuvivatwong, Kachornsakdi Silpapojakul, Kamonnut Singkhamanan, Edward Mcneil, Yohei DoiAbstract:The role of Acinetobacter nosocomialis and Acinetobacter pittii, which belong to the A. calcoaceticus-A. Baumannii complex, in hospital-acquired infections is increasingly recognized. Here we describe a retrospective cohort study of hospital-acquired A. calcoaceticus-A. Baumannii complex infections at a university hospital in Thailand. A total of 222 unique cases were identified between January 2010 and December 2011. The genomospecies of the A. calcoaceticus-A. Baumannii complex isolates were classified as follows: A. Baumannii, 197 (89%); A. nosocomialis, 18 (8%); and A. pittii, 7 (3%). All A. nosocomialis and A. pittii isolates were susceptible to imipenem and meropenem. The patients infected with A. nosocomialis and A. pittii had lower 30-day mortality than those infected with carbapenem-susceptible A. Baumannii (P = 0.025) and carbapenem-resistant A. Baumannii (P = 0.013). The factors influencing 30-day mortality were infection with non-Baumannii A. calcoaceticus-A. Baumannii complex (hazard ratio [HR], 0.12; 95% confidence interval [CI], 0.03 to 0.51; P = 0.004), infection with carbapenem-resistant A. Baumannii (HR, 1.57; 95% CI, 0.89 to 2.79; P = 0.105), appropriate empirical antimicrobial therapy (HR, 0.38; 95% CI, 0.23 to 0.61; P < 0.001), and higher acute physiology and chronic health evaluation II (APACHE II) score (HR, 1.15; 95% CI, 1.10 to 1.19; P < 0.001). In Galleria mellonella assays, the survival rates were significantly higher for the larvae infected with A. nosocomialis or A. pittii than for those infected with either carbapenem-susceptible A. Baumannii or carbapenem-resistant A. Baumannii, but no differences in survival rates were observed between carbapenem-susceptible A. Baumannii and carbapenem-resistant A. Baumannii. These findings suggest intrinsic differences in virulence between non-Baumannii A. calcoaceticus-A. Baumannii complex species and A. Baumannii but not between carbapenem-susceptible and resistant A. Baumannii.
Luther E Lindler - One of the best experts on this subject based on the ideXlab platform.
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an outbreak of multidrug resistant acinetobacter Baumannii calcoaceticus complex infection in the us military health care system associated with military operations in iraq
Clinical Infectious Diseases, 2007Co-Authors: Paul T Scott, Kimberly A Moran, Ed Hulten, Joel Fishbain, Scott Riddell, Clinton K Murray, Gregory Deye, David Craft, Arjun Srinivasan, Luther E LindlerAbstract:Background. We investigated an outbreak of multidrug-resistant Acinetobacter Baumannii-calcoaceticus complex infection among US service members injured in Iraq. Methods. The investigation was conducted in Iraq and Kuwait, in the 2 military hospitals where the majority of injured service members were initially treated. After initially characterizing the outbreak, we evaluated 3 potential sources of infection for the period March 2003 to December 2004. The evaluation included screening samples that were obtained from the skin of patients for the presence of colonization and assessing the soil and health care environments for the presence of A. baumanii-calcoaceticus complex organisms. Isolates obtained from samples from patients in US Military treatment facilities, as well as environmental isolates, were genotypically characterized and compared using pulsed-field gel electrophoresis. Results. A. baumanii-calcoaceticus complex organisms were present on the skin in only 1 (0.6%) of 160 patients who were screened and in 1 (2%) of 49 soil samples. A. baumanii-calcoaceticus complex isolates were recovered from treatment areas in 7 of the 7 field hospitals sampled. Using pulsed-field gel electrophoresis, we identified 5 cluster groups in which isolates from patients were related to environmental isolates. One cluster included hospitalized patients who had not been deployed to Iraq. Among the clinical isolates, only imipenem, polymyxin B, and colistin demonstrated reliable in vitro antimicrobial activity. Generally, the environmental isolates were more drug susceptible than were the clinical isolates. Conclusions. Our findings suggest that environmental contamination of field hospitals and infection transmission within health care facilities played a major role in this outbreak. On the basis of these findings, maintaining infection control throughout the military health care system is essential. Novel strategies may be required to prevent the transmission of pathogens in combat field hospitals. Acinetobacter Baumannii-calcoaceticus complex (ABC)
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an outbreak of multidrug resistant acinetobacter Baumannii calcoaceticus complex infection in the us military health care system associated with military operations in iraq
Clinical Infectious Diseases, 2007Co-Authors: Paul T Scott, Kimberly A Moran, Ed Hulten, Joel Fishbain, Scott Riddell, Clinton K Murray, Gregory Deye, David Craft, Arjun Srinivasan, Luther E LindlerAbstract:BACKGROUND: We investigated an outbreak of multidrug-resistant Acinetobacter Baumannii-calcoaceticus complex infection among US service members injured in Iraq. METHODS: The investigation was conducted in Iraq and Kuwait, in the 2 military hospitals where the majority of injured service members were initially treated. After initially characterizing the outbreak, we evaluated 3 potential sources of infection for the period March 2003 to December 2004. The evaluation included screening samples that were obtained from the skin of patients for the presence of colonization and assessing the soil and health care environments for the presence of A. baumanii-calcoaceticus complex organisms. Isolates obtained from samples from patients in US Military treatment facilities, as well as environmental isolates, were genotypically characterized and compared using pulsed-field gel electrophoresis. RESULTS: A. baumanii-calcoaceticus complex organisms were present on the skin in only 1 (0.6%) of 160 patients who were screened and in 1 (2%) of 49 soil samples. A. baumanii-calcoaceticus complex isolates were recovered from treatment areas in 7 of the 7 field hospitals sampled. Using pulsed-field gel electrophoresis, we identified 5 cluster groups in which isolates from patients were related to environmental isolates. One cluster included hospitalized patients who had not been deployed to Iraq. Among the clinical isolates, only imipenem, polymyxin B, and colistin demonstrated reliable in vitro antimicrobial activity. Generally, the environmental isolates were more drug susceptible than were the clinical isolates. CONCLUSIONS: Our findings suggest that environmental contamination of field hospitals and infection transmission within health care facilities played a major role in this outbreak. On the basis of these findings, maintaining infection control throughout the military health care system is essential. Novel strategies may be required to prevent the transmission of pathogens in combat field hospitals.
Eric P Skaar - One of the best experts on this subject based on the ideXlab platform.
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acinetobacter Baumannii coordinates urea metabolism with metal import to resist host mediated metal limitation
Mbio, 2016Co-Authors: Lillian J Juttukonda, Walter J Chazin, Eric P SkaarAbstract:ABSTRACT During infection, bacterial pathogens must adapt to a nutrient metal-limited environment that is imposed by the host. The innate immune protein calprotectin inhibits bacterial growth in vitro by chelating the divalent metal ions zinc (Zn 2+ , Zn) and manganese (Mn 2+ , Mn), but pathogenic bacteria are able to cause disease in the presence of this antimicrobial protein in vivo. One such pathogen is Acinetobacter Baumannii, a Gram-negative bacterium that causes pneumonia and bloodstream infections that can be complicated by resistance to multiple antibiotics. A. Baumannii inhibition by calprotectin is dependent on calprotectin Mn binding, but the mechanisms employed by A. Baumannii to overcome Mn limitation have not been identified. This work demonstrates that A. Baumannii coordinates transcription of an NRAMP family Mn transporter and a urea carboxylase to resist the antimicrobial activities of calprotectin. This NRAMP family transporter facilitates Mn accumulation and growth of A. Baumannii in the presence of calprotectin. A. Baumannii is found to utilize urea as a sole nitrogen source, and urea utilization requires the urea carboxylase encoded in an operon with the NRAMP family transporter. Moreover, urea carboxylase activity is essential for calprotectin resistance in A. Baumannii. Finally, evidence is provided that this system combats calprotectin in vivo , as deletion of the transporter impairs A. Baumannii fitness in a mouse model of pneumonia, and this fitness defect is modulated by the presence of calprotectin. These findings reveal that A. Baumannii has evolved mechanisms to subvert host-mediated metal sequestration and they uncover a connection between metal starvation and metabolic stress. IMPORTANCE Acinetobacter Baumannii is a bacterium that causes bloodstream, wound, urinary tract, and pneumonia infections, with a high disease burden in intensive care units. Treatment of A. Baumannii infection is complicated by resistance to most antibiotics in use today, and resistance to last-resort therapies has become commonplace. New treatments for A. Baumannii infection are desperately needed, but our current understanding of the bacterial factors required to cause infection is limited. We previously found that the abundant innate immune protein calprotectin inhibits the growth of A. Baumannii by withholding essential metals . Despite this, A. Baumannii is still able to infect wild-type mice, which produce calprotectin during infection. Here, we identify factors employed by A. Baumannii during infection to overcome calprotectin-mediated metal sequestration. Moreover, we expose a connection between metal starvation and metabolism that may be a “chink in the armor” of A. Baumannii and lead to new treatment options.
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toll like receptor 9 contributes to defense against acinetobacter Baumannii infection
Infection and Immunity, 2015Co-Authors: Michael J Noto, Kelli L Boyd, William J Burns, Matthew G Varga, Richard M Peek, Eric P SkaarAbstract:Acinetobacter Baumannii is a common nosocomial pathogen capable of causing severe diseases associated with significant morbidity and mortality in impaired hosts. Pattern recognition receptors, such as the Toll-like receptors (TLRs), play a key role in pathogen detection and function to alert the immune system to infection. Here, we examine the role for TLR9 signaling in response to A. Baumannii infection. In a murine model of A. Baumannii pneumonia, TLR9(-/-) mice exhibit significantly increased bacterial burdens in the lungs, increased extrapulmonary bacterial dissemination, and more severe lung pathology compared with those in wild-type mice. Following systemic A. Baumannii infection, TLR9(-/-) mice have significantly increased bacterial burdens in the lungs, as well as decreased proinflammatory cytokine and chemokine production. These results demonstrate that TLR9-mediated pathogen detection is important for host defense against the opportunistic pathogen Acinetobacter Baumannii.
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inactivation of phospholipase d diminishes acinetobacter Baumannii pathogenesis
Infection and Immunity, 2010Co-Authors: Anna C Jacobs, Eric P Skaar, Indriati Hood, Kelli L Boyd, Patrick D Olson, John M Morrison, Steven D Carson, Khalid Sayood, Peter C Iwen, Paul M DunmanAbstract:Acinetobacter Baumannii is an emerging bacterial pathogen of considerable health care concern. Nonetheless, relatively little is known about the organism's virulence factors or their regulatory networks. Septicemia and ventilator-associated pneumonia are two of the more severe forms of A. Baumannii disease. To identify virulence factors that may contribute to these disease processes, genetically diverse A. Baumannii clinical isolates were evaluated for the ability to proliferate in human serum. A transposon mutant library was created in a strain background that propagated well in serum and screened for members with decreased serum growth. The results revealed that disruption of A. Baumannii phospholipase D (PLD) caused a reduction in the organism's ability to thrive in serum, a deficiency in epithelial cell invasion, and diminished pathogenesis in a murine model of pneumonia. Collectively, these results suggest that PLD is an A. Baumannii virulence factor.
Jeronimo Pachon - One of the best experts on this subject based on the ideXlab platform.
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platelet activating factor receptor initiates contact of acinetobacter Baumannii expressing phosphorylcholine with host cells
Journal of Biological Chemistry, 2012Co-Authors: Younes Smani, Jose Ibanezmartinez, Fernando Docoboperez, Rafael Lopezrojas, Juan Dominguezherrera, Jeronimo PachonAbstract:Abstract Adhesion is an initial and important step in Acinetobacter Baumannii causing infections. However, the exact molecular mechanism of such a step between A. Baumannii and the host cells remains unclear. Here, we demonstrated that the phosphorylcholine (ChoP)-containing outer membrane protein of A. Baumannii binds to A549 cells through platelet-activating factor receptor (PAFR), resulting in activation of G protein and intracellular calcium. Upon A. Baumannii expressing ChoP binding to PAFR, clathrin and β-arrestins, proteins involved in the direction of the vacuolar movement, are activated during invasion of A. Baumannii. PAFR antagonism restricts the dissemination of A. Baumannii in the pneumonia model. These results define a role for PAFR in A. Baumannii interaction with host cells and suggest a mechanism for the entry of A. Baumannii into the cytoplasm of host cells.
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efficacy of rifampin and its combinations with imipenem sulbactam and colistin in experimental models of infection caused by imipenem resistant acinetobacter Baumannii
Antimicrobial Agents and Chemotherapy, 2010Co-Authors: Maria Eugenia Pachonibanez, C Pichardo, A Garciacuriel, Fernando Docoboperez, Rafael Lopezrojas, Juan Dominguezherrera, M E Jimenezmejias, Luis Jimenez, Jeronimo PachonAbstract:There are currently no defined optimal therapies available for multidrug-resistant (MDR) Acinetobacter Baumannii infections. We evaluated the efficacy of rifampin, imipenem, sulbactam, colistin, and their combinations against MDR A. Baumannii in experimental pneumonia and meningitis models. The bactericidal in vitro activities of rifampin, imipenem, sulbactam, colistin, and their combinations were tested using time-kill curves. Murine pneumonia and rabbit meningitis models were evaluated using the A. baummnnii strain Ab1327 (with MICs for rifampin, imipenem, sulbactam, and colistin of 4, 32, 32, and 0.5 mg/liter, respectively). Mice were treated with the four antimicrobials and their combinations. For the meningitis model, the efficacies of colistin, rifampin and its combinations with imipenem, sulbactam, or colistin, and of imipenem plus sulbactam were assayed. In the pneumonia model, compared to the control group, (i) rifampin alone, (ii) rifampin along with imipenem, sulbactam, or colistin, (iii) colistin, or (iv) imipenem plus sulbactam significantly reduced lung bacterial concentrations (10.6 ± 0.27 [controls] versus 3.05 ± 1.91, 2.07 ± 1.82, 2.41 ± 1.37, 3.4 ± 3.07, 6.82 ± 3.4, and 4.22 ± 2.72 log 10 CFU/g, respectively [means ± standard deviations]), increased sterile blood cultures (0% versus 78.6%, 100%, 93.3%, 93.8%, 73.3%, and 50%), and improved survival (0% versus 71.4%, 60%, 46.7%, 43.8%, 40%, and 85.7%). In the meningitis model rifampin alone or rifampin plus colistin reduced cerebrospinal fluid bacterial counts (−2.6 and −4.4 log 10 CFU/ml). Rifampin in monotherapy or with imipenem, sulbactam, or colistin showed efficacy against MDR A. Baumannii in experimental models of pneumonia and meningitis. Imipenem or sulbactam may be appropriate for combined treatment when using rifampin.
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treatment of multidrug resistant acinetobacter Baumannii meningitis with ampicillin sulbactam
Clinical Infectious Diseases, 1997Co-Authors: M E Jimenezmejias, Jeronimo Pachon, Baltazar Becerril, J Palominonicas, A Rodriguezcobacho, M P RevueltaAbstract:: The clinical features and the outcomes of eight cases of nosocomial Acinetobacter Baumannii meningitis treated with ampicillin/sulbactam are reported. All the patients had fever, neck stiffness or meningeal signs, and a low consciousness level, and in their cerebrospinal fluid (CSF), pleocytosis, a low glucose level, and an elevated protein level were noted. For all CSF isolates of A. Baumannii, the MIC of ampicillin/sulbactam was < or = 8/4 microg/mL. The MICs of sulbactam by microdilution in two cases were 4 microg/mL. All isolates were resistant to cefotaxime, ceftriaxone, ceftazidime, ureidopenicillins, ciprofloxacin, and gentamicin. Seven isolates were resistant to imipenem. A. Baumannii was isolated from other samples in seven episodes. All patients were treated with ampicillin/sulbactam (seven with 2 g/l g every 6 hours and one with 2 g/l g every 8 hours). Six patients were cured and two patients died of meningitis. There were no side effects with the ampicillin/sulbactam treatment. In conclusion, ampicillin/sulbactam may be effective as therapy for meningitis caused by A. baumanii resistant to imipenem and other beta-lactam drugs.
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bacteremia due to acinetobacter Baumannii epidemiology clinical findings and prognostic features
Clinical Infectious Diseases, 1996Co-Authors: Jose Miguel Cisneros, Jeronimo Pachon, Maria J Reyes, B Becerril, F J Caballero, Jose Garcia L Garmendia, Carlos Ortiz, Adelaido R CobachoAbstract:The number of nosocomial infections caused by Acinetobacter Baumannii has increased in recent years. During a 12-month study, there were 1.8 episodes of A. Baumannii bacteremia per 1,000 adults admitted to a hospital in Seville, Spain. Seventy-nine patients were included in the study. A. Baumannii bacteremia occurred after a mean (± SD) hospitalization of 18 ± 20 days. In all cases the infections were acquired nosocomially ; 71% were acquired in intensive care units. Ampicillin/sulbactam was found to be the most active agent against A. Baumannii. The most common source of the bacteremia was the respiratory tract (32 cases [71%]). Twenty patients (25%) had septic shock, and 24 (30%) had disseminated intravascular coagulation (DIC). Treatment with imipenem or ampicillin/sulbactam was most effective (cure rates, 87.5% and 83%, respectively). The deaths of 27 patients (34%) were related to A. Baumannii bacteremia. The presence of DIC (odds ratio [OR] = 116.4 ; P <.0001) and inappropriate antimicrobial treatment (OR = 15.2 ; P <.01) were independently associated with mortality. We conclude that most A. Baumannii isolates are multiresistant and that nosocomial A. Baumannii bacteremia may cause severe clinical disease that is associated with a high mortality.
