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Nontraditional dosing of ampicillin-sulbactam for multidrug-resistant Acinetobacter baumannii meningitis.

A 52-year-old man was admitted to a local hospital with headache, nausea, vomiting, dizziness, photophobia, and confusion after a sudden fall. Progressive changes in neurologic function were noted despite neurosurgical intervention and broad-spectrum antimicrobial coverage. Cerebral spinal fluid (CSF) culture identified Acinetobacter baumannii that was resistant to traditionally recommended therapies of amikacin and imipenem-cilastatin. The organism demonstrated minimum inhibitory concentrations of greater than 32 microg/ml and 8 microg/ml, respectively, for these two agents. Ampicillin 2 g-sulbactam 1 g every 3 hours was administered based on history of therapeutic failure of traditional dosing in our thermal injury population. Repeat CSF cultures after 12 days of ampicillin-sulbactam therapy were negative. After 35 days, the patient's A. baumannii infection was completely resolved. The patient experienced no adverse drug events or toxicity with this high-dosage regimen.

Acinetobacter↗

Use of interrepeat PCR fingerprinting to investigate an Acinetobacter baumannii outbreak in an intensive care unit.

An epidemiological investigation of an outbreak of Acinetobacter baumannii among patients on 2 closely related intensive care units (ICU) was performed by molecular typing with interrepeat polymerase chain reaction (interrepeat PCR). 31 A. baumannii isolates obtained from 15 ICU patients were characterized. All patients were infected or colonized with A. baumannii. After identification of the outbreak, 6 environmental isolates were collected from tap-water, sinks and cleaning detergents. PCR fingerprinting identified 3 genotypes among the outbreak-related strains. One predominant genotype was demonstrated in 14/15 patients and this genotype was also found among all environmental isolates. The cluster of A. baumannii represented an outbreak of 1 genotype, suggesting cross-contamination. The finding of the identical genotype among all environmental strains indicated a common environmental source causing the outbreak. The outbreak was controlled after reimplementation of an effective disinfection of workplace surfaces. This survey proved interrepeat PCR to be a rapid and reliable method to differentiate A. baumannii strains, thereby allowing epidemiological surveillance of large amounts of strains and early interventions to control outbreaks.

Acinetobacter↗

Community-acquired Acinetobacter radioresistens bacteremia in an HIV-positive patient.

We describe the first case of community-acquired bacteremia caused by Acinetobacter radioresistens; the patient was a 32-year-old HIV-positive neutropenic woman. Ambiguous Gram staining and poor biochemical reactivity of blood culture isolates misguided early diagnosis and therapy. Bacterial identification was based on 16S rDNA sequence analysis. A. radioresistens can be considered as a cause of opportunistic infection in immunodeficient patients.

AIDS-Related Opportunistic Infections↗

Pandrug-resistant Acinetobacter baumannii causing nosocomial infections in a university hospital, Taiwan.

The rapid emergence (from 0% before 1998 to 6.5% in 2000) of pandrug-resistant Acinetobacter baumannii (PDRAB) was noted in a university hospital in Taiwan. To understand the epidemiology of these isolates, we studied 203 PDRAB isolates, taken from January 1999 to April 2000: 199 from 73 hospitalized patients treated at different clinical settings in the hospital and 4 from environmental sites in an intensive-care unit. Pulsed-field gel electrophoresis analysis and random amplified polymorphic DNA (RAPD) generated by arbitrarily primed polymerase chain reaction of these 203 isolates showed 10 closely related genotypes (10 clones). One (clone 5), belonging to pulsotype E and RAPD pattern 5, predominated (64 isolates, mostly from patients in intensive care). Increasing use of carbapenems and ciprofloxacin (selective pressure) as well as clonal dissemination might have contributed to the wide spread of PDRAB in this hospital.

Acinetobacter↗

VIM- and IMP-type metallo-beta-lactamase-producing Pseudomonas spp. and Acinetobacter spp. in Korean hospitals.

We determined the occurrence of acquired metallo-b-lactamase (MBL)-producing bacteria in Korean hospitals. Among the isolates nonsusceptible to imipenem that were collected from 28 hospitals from 2000 to 2001, 44 (11.4%) of 387 Pseudomonas spp. and 38 (14.2%) of 267 Acinetobacter spp. produced MBL and had alleles of blaVIM-2 or blaIMP-1. MBL-producing isolates were detected in 60.7% of the hospitals.

Acinetobacter↗

Multidrug-resistant Acinetobacter baumannii.

To understand the epidemiology of multidrug-resistant (MDR) Acinetobacter baumannii and define individual risk factors for multidrug resistance, we used epidemiologic methods, performed organism typing by pulsed-field gel electrophoresis (PFGE), and conducted a matched case-control retrospective study. We investigated 118 patients, on 27 wards in Israel, in whom MDR A. baumannii was isolated from clinical cultures. Each case-patient had a control without MDR A. baumannii and was matched for hospital length of stay, ward, and calendar time. The epidemiologic investigation found small clusters of up to 6 patients each with no common identified source. Ten different PFGE clones were found, of which 2 dominated. The PFGE pattern differed within temporospatial clusters, and antimicrobial drug susceptibility patterns varied within and between clones. Multivariate analysis identified the following significant risk factors: male sex, cardiovascular disease, having undergone mechanical ventilation, and having been treated with antimicrobial drugs (particularly metronidazole). Penicillins were protective. The complex epidemiology may explain why the emergence of MDR A. baumannii is difficult to control.

Acinetobacter Infections↗

VEB-1 Extended-spectrum beta-lactamase-producing Acinetobacter baumannii, France.

VEB-1 extended-spectrum beta-lactamase-producing Acinetobacter baumannii was responsible for an outbreak in hospitals in France. A national alert was triggered in September 2003 when 4 hospitals reported clusters of A. baumannii infection with similar susceptibility profiles. Case definitions and laboratory guidelines were disseminated, and prospective surveillance was implemented; strains were sent to a single laboratory for characterization and typing. From April 2003 through June 2004, 53 hospitals reported 290 cases of A. baumannii infection or colonization; 275 isolates were bla(VEB-1)-positive and clonally related. Cases were first reported in 5 districts of northern France, then in 10 other districts in 4 regions. Within a region, interhospital spread was associated with patient transfer. In northern France, investigation and control measures led to a reduction of reported cases after January 2004. The national alert enabled early control of new clusters, demonstrating the usefulness of early warning about antimicrobial drug resist.

Acinetobacter Infections↗

Whole-Genome Analysis Reveals Antimicrobial Resistance and Population Structure of Environmental and Veterinary Acinetobacter baumannii.

Acinetobacter (A.) baumannii is an important multidrug-resistant pathogen increasingly recognized across animal and environmental settings, and carbapenem-resistant A. baumannii (CRAB) is classified as a critical-priority pathogen by the World Health Organization. This study investigated the antimicrobial resistance (AMR) and genomic characteristics of 122 A. baumannii isolates comprising 72 veterinary and 50 environmental isolates collected in Andhra Pradesh, India. Antimicrobial susceptibility testing, whole-genome sequencing (WGS), resistance and virulence gene profiling, multilocus sequence typing (MLST), core-genome analysis, single nucleotide polymorphism (SNP) phylogeny, and pan-genome analysis were performed. Overall, 58.2% of isolates were multidrug-resistant (MDR), and 41.8% were extensively drug-resistant (XDR). Sequence type (ST) 52 predominated among veterinary isolates, whereas ST2 was more frequent among environmental isolates. The presence of carbapenem-resistant isolates along with the ST2 lineage enhances the similarity to clinical A. baumannii. Several intrinsic resistance genes, including blaOXA-23, armA, aph(3″)-Ib, aph(6)-Id, tet(B), mph(E), and msr(E), were more prevalent in the ST2-associated population. Virulence-associated determinants were widely conserved. Core-genome MLST (cgMLST) and core-genome SNP (cgSNP) analyses identified highly related isolates within both lineages, while pairwise SNP differences were 0-7. Pan-genome analysis identified 4204 gene clusters and distinct accessory gene patterns between ST2 and ST52. These findings indicate that resistance gene distribution was closely associated with lineage structure and support integrated genomic surveillance of A. baumannii across animal and environmental reservoirs.

Acinetobacter baumannii↗

The resistance mechanisms of b-lactam antimicrobials in clinical isolates of Acinetobacter baumannii.

BACKGROUND: Despite increasing importance of Acinetobacter baumannii in nosocomial infections and rapid development of multi-antimicrobial resistance in this strain, the resistance mechanisms of beta-lactam antimicrobials in A. baumannii were not clearly defined. In order to observe the resistance mechanisms against beta-lactams and carbapenem, we characterized the production of beta-lactamases and outermembrane protein (OMP) profiles for the 44 clinical isolates of A. baumannii. METHODS: The MICs of antimicrobials were determined by agar dilution test. The secondary beta-lactamases were characterized by isoelectric focusing, polymerase chain reactions and nucleotide sequencing, and the production of chromosomal beta-lactamases was quantitated by spectrophotometric method. For two strains with an elevated MIC of carbapenem, outermembrane protein (OMP) profile was analyzed by ultracentrifugation of the sonicated bacteral cells and SDS-PAGE. RESULTS AND CONCLUSION: Twenty two or 4 of 44 strains produced TEM-1-like beta-lactamase or PER-1 extended-spectrum beta-lactamase, respectively. However, when we analyzed the MICs of several beta-lactams with the beta-lactamase production, the resistance level of beta-lactam was mainly determined by the production of chromosomal beta-lactamase, not by the secondary beta-lactamases in the clinical isolates of A. baumannii. In two strains with an elevated MIC of imipenem, a decrease or loss of about 35 kDa and 22 kDa proteins in OMP was observed, which suggested that the change of OMP played a role in carbapenem resistance.

Acinetobacter↗

[Acinetobacter baumannii pandrug-resistant: update in epidemiological and antimicrobial managing issues].

In the last two decades Acinetobacter baumannii has emerged as a major relevant world nosocomial pathogen. A. baumannii can be a causal agent of diseases like pneumonia, bacteremia, meningitis, soft tissue and urinary tract infections, associating to high mortality. Several national and foreign communications reveal the isolation of A. baumannii resistant to almost all commercially available antimicrobial agents, drastically limiting the therapeutic options. To optimize the therapy of these infections, the need of development of new antibacterial agents is raised as is the revival of certain forgotten compounds, as the polymyxins. In order to check and evaluate the information on the management of multi-resistant A. baumannii infections, we performed a systematical review of the medical scientific literature, that included Medline and LILACS, identifying and categorizing the clinical relevancy of the sources gathered to the date of this investigation. Clinically relevant epidemiological aspects, microbiological information and clinical studies in patients with pandrug (AB-PDR) or multidrug resistant (AB-MDR) A. baumannii infections were reviewed. The response adapted to the management of AB-PDR infection is complex, its eradication needs adherence to suitable practices of infection control and the prudent and effective use of antimicrobial therapy. Potential options of therapy could be colistin, betalactam associations with sulbactam and tetracyclines, but there are no random and controlled studies in the matter.

Acinetobacter Infections↗

Influence of iron on growth and extracellular products of Acinetobacter baumannii.

Iron is an important nutrient required by bacteria for optimal growth. Acquisition of iron from the host where iron is restricted is an important mediator of bacterial pathogenesis. In iron deplete chemically defined medium (CDM-Fe) growth of Acinetobacter baumannii was restricted as compared to iron replete medium (CDM + Fe). Bacteria developed four high molecular weight outer membrane proteins (OMPs) of 88, 84, 80 and 77 kDa in CDM-Fe medium which were absent in CDM + Fe medium, and are known iron regulated outer membrane proteins (IROMPs). A. baumannii secreted siderophores extracellularly into the medium which act as iron chelators which had been demonstrated in the supernatants of CDM-Fe media. The siderophore was of catechol type. This shows that A. baumannii under iron restricted conditions express IROMPs along with production of catechol type siderophore in order to acquire iron from the external milieu.

Acinetobacter↗

Acinetobacter calcoaceticus-baumannii complex bacteremia: analysis of 82 cases.

Eighty-two cases of Acinetobacter calcoaceticus-baumannii complex bacteremia were identified during a 33-month period, from November 1993 to July 1996, at the Veterans General Hospital, Taipei. All cases were due to hospital-acquired infections, with 28 cases of polymicrobial bacteremia. Most patients had severe debilitating conditions: 26 had malignancies, 40 required stay in Intensive Care Unit and 17 had undergone major operations. The main predisposing factors included central venous catheterization, endotracheal intubation or tracheostomy, prior antibiotic therapy and prolonged hospitalization. Amikacin, tobramycin, and ceftazidime were the most effective agents in vitro against A. calcoaceticus-baumannii complex. 32 patients (39 %) died during hospitalization, 19 of the cases (23 %) directly attributed to septicemia. Factors that adversely influenced mortality included polymicrobial bacteremia, inappropriate antimicrobial therapy and prior antibiotic treatment. Of particular interest is the fact that none of the patients who did not receive appropriate antimicrobial therapy survived. Early diagnosis and appropriate antibiotic therapy are critical for improving the prognosis of A. calcoaceticus-baumannii complex bacteremia.

Acinetobacter Infections↗

Acinetobacter meningitis following head trauma.

A case of acinetobacter meningitis following head injury in a patient who developed cerebrospinal fluid otorrhea, and did not have any neurosurgical procedure, is presented. Previously reported cases are cited, with a review of the literature. Pefloxacin monotherapy is associated with a poor clinical response.

Acinetobacter Infections↗

[New findings on the genus Acinetobacter].

The author reviewed recent data on the genus Acinetobacter. It is an evaluation of their participation in nosocomial infections, antibiotic resistance, virulence factors as well as the possibilities of modifications of their virulence after treatment with antibiotics.

Acinetobacter↗

[Evolution of antimicrobial susceptibility of Acinetobacter baumannii clinical isolates].

Acinetobacter baumannii is a microorganism frequently implicated in colonization and infection in hospitalized patients. An increase of resistance has been observed in recent years making these infections difficult to treat. The in vitro activity of 24 antibiotics, 15 betalactam agents and nine nonbetalactams, was studied in 156 A. baumannii clinical isolates. The strains were collected from different clinical samples obtained from inpatients (92%) and 8% were from outpatients. Evolution of susceptibility from January 1995 to December 1997 was studied. MIC of the following antibiotics was determined by the agar dilution method: ampicillin, ticarcillin, piperacillin, ampicillin-sulbactam, amoxicillin- clavulanic acid, ticarcillin-clavulanic acid, piperacillin-tazobactam, cefotaxime, ceftazidime, cefepime, imipenem, meropenem, clavulanic acid, sulbactam, tazobactam, amikacin, gentamicin, tobramycin, ofloxacin, doxycycline, fosfomycin, rifampin, azithromycin and colistin. Low antimicrobial susceptibility was observed in most A. baumannii strains. Colistin, imipenem, meropenem and ampicillin-sulbactam showed the greatest susceptibility (100, 88.4, 88.4 and 84.6%, respectively). A. baumannii strains from inpatients showed a lower antimicrobial susceptibility than strains from outpatients, who showed a high percentage of susceptibility to most antibiotics. Rifampin and azithromycin showed certain in vitro activity against the most susceptible A. baumannii strains. A progressive decrease in susceptibility to most antibiotics was observed during the period studied. Carbapenem-resistant A. baumannii emerged in 1996 and increased in 1997.

Acinetobacter↗

[Antibacterial activity of aminoglycosides against nosocomial strains of Acinetobacter baumannii isolated between 1990 and 1999].

The antibacterial activity of selected aminoglycosides against 487 nosocomial strains of Acinetobacter baumannii isolated from Chilean hospitals between 1990 and 1998 was investigated. Plasmid profiles were determined for some resistant isolates. A high frequency of resistant strains was found for all aminoglycosides assayed, with values ranging from 47% for amikacin (1990-1992) to 88% for gentamicin (1993-1994). The cure of a plasmid greater than 30 kb was associated with the loss of amikacin, kanamycin and neomycin resistance in some isolates. This result suggests that plasmid may harbor the genes encoding for the combination of aminoglycoside-modifying enzymes AAC(6')I+APH(3'). Gentamicin resistance was not lost among cured strains, suggesting it may be encoded by genes located on the bacterial chromosome or transposons inserted on the chromosome.

Acinetobacter↗

[Activity of imipenem and meropenem against strains of Acinetobacter baumannii isolated from various Chilean hospitals].

The activity of two carbapenem compounds, imipenem and meropenem, against 447 strains of Acinetobacter baumannii isolated between 1990 and 1998 in different Chilean hospitals was determined. MIC ranges, MIC(50) and MIC(90), were determined by an agar dilution method. Similar antibacterial activities were observed for both antibacterials; however, a slight increase in the MIC(50) of imipenem and meropenem, and in the MIC(90) of meropenem was found among strains isolated from 1997-1998. Although A. baumannii remains susceptible to these antibiotics, the MIC(50) and MIC(90) have increased in recent years.

Acinetobacter↗