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European status of resistance in nosocomial infections.

BACKGROUND: Surveillance studies are mandatory to carefully monitor changing trends in Europe. METHODS: Surveys on antibiotic resistance conducted in European hospitals were reviewed. Data were obtained from own studies, through searches of Medlines, Pubmed, abstracts and posters presented at meetings, from the World Wide Web and from surveillance studies conducted by the pharmaceutical industry. RESULTS: A high prevalence of MRSA was found in most European hospitals, except in northern Europe, and an increasing trend in non-intensive care unit patients was observed. In most European hospitals, the prevalence of infections caused by vancomycin-resistant enterococci remains very low and most outbreaks have occurred in at-risk wards. No major changes of resistance among Enterobacteriaceae were observed. Very few of the major antibiotics are now reliably effective for the treatment of severe nosocomial carbapenem-resistant Acinetobacter infections. CONCLUSIONS: Although antimicrobial resistance appears to be increasing all over Europe, it is difficult to accurately estimate the extent of this emerging problem. One of the main reasons for this can be attributed to the fact that the published susceptibility data are difficult to compare due to the different methods used, population bias, and clonal variation. Increasing antimicrobial resistance necessitates a critical appraisal of the remaining antibiotic treatment options.

Cross Infection↗

[Comparative activity of imipenem, ceftazidime and cefotaxime against Acinetobacter calcoaceticus].

The authors compared the in vitro activity of imipenem, ceftazidime and cefotaxime against 100 strains of Acinetobacter calcoaceticus isolated in 1986 and 1987. The minimal inhibitory and bactericidal concentrations (MICs and MBCs) were determined by the agar dilution and broth microdilution methods respectively, with and without 50 per cent of human serum in the medium to evaluate the possible influence of protein binding. Imipenem was the most active of the three drugs against Acinetobacter, including beta-lactamase producing strains. The MICs 50 and 90 of imipenem were 0.18 micrograms/ml and 0.48 micrograms/ml respectively, as opposed to 5.16 and 14.61 micrograms/ml for ceftazidime, 16 and 75.6 micrograms/ml for cefotaxime. No change was noted in the susceptibility of Acinetobacter to imipenem from 1981 to 1987. The geometric mean MIC of imipenem was 0.25 micrograms/ml. Susceptibility remained unchanged for ceftazidime and cefotaxime but the geometric mean MICs were higher, being 7.29 and 22.8 micrograms/ml respectively. Imipenem had the highest bactericidal activity, with a mean MBC/MIC ratio of 1.16. The presence of human serum did not influence the results, due to the low protein binding of all three antibiotics. It is concluded that imipenem is one of the major antibiotics available for the treatment of nosocomial Acinetobacter infections. However, a few resistant strains have recently been isolated, confirming the need for epidemiological surveillance of bacterial resistance to this antibiotic.

Acinetobacter↗

Prevalence of metallo-beta-lactamase among Pseudomonas aeruginosa and Acinetobacter baumannii isolated from burn wounds and in vitro activities of antibiotic combinations against these isolates.

The prevalence of metallo-beta-lactamases (MBLs) produced by isolates of Pseudomonas aeruginosa and Acinetobacter baumannii and the activities of various antmicrobial combinations against MBL producer strains were investigated. During the period from June 2003 till July 2004, 120 P. aeruginosa and 9 A. baumannii nonduplicate isolates were obtained from burn wounds. Forty strains (37 P. aeruginosa, 3 A. baumannii) were selected because of resistance to carbapenems. Screening for MBL production was performed in the latter isolates by the combined disk method which depends on comparing the zones given by disks containing imipenem with and without ethylenediaminetetraacetic acid (EDTA). Of imipenem resistant P. aeruginosa strains, 21 and 1 of A. baumannii were found metallo-beta-lactamase producers. Disk approximation studies were then performed to test for in vitro activities of various antimicrobial combinations. For a total of 21 P. aeruginosa strains, synergy was demonstrated predominantly by ciprofloxacin in combination with ceftazidime and imipenem, by ofloxacin in combination with astreonam. Against MBL producer A. baumannii strain, synergy was detected only with imipenem-ofloxacin combination. None of the combinations were antagonistic. These results suggest that MBL producing P. aeruginosa and A. baumanni strains have been introduced into burn centers, and to prevent the further spread of MBL producers, it is essential for carbapenem resistant isolates to be screened for MBLs.

Acinetobacter Infections↗

Long-term dissemination of an OXA-40 carbapenemase-producing Acinetobacter baumannii clone in the Iberian Peninsula.

OBJECTIVE: The main objectives of this study were to assess the clonal relatedness of Acinetobacter baumannii carbapenem-resistant isolates recovered from the Iberian Peninsula and to investigate the production of carbapenemases. METHODS: One hundred and sixty-two imipenem-resistant A. baumannii isolates were collected from 1998 to 2003 in three Portuguese university hospitals. An imipenem-resistant isolate (988FFP strain) recovered in 1995 from a smaller hospital unit, was also included, as well as an OXA-40-producing A. baumannii Spanish strain (SM28). Susceptibility tests were carried out by disc diffusion and Etest methods. DNA fingerprints were obtained by PFGE of ApaI-digested chromosomal DNA. Carbapenemase activity was determined by a bioassay and spectrophotometry. The detection of the blaOXA-40 gene was conducted through PCR analysis, cloning and nucleotide sequencing. RESULTS: All the isolates presented a similar multi-resistance pattern, including imipenem (MIC >32 mg/L). The Iberian isolates showed an identical PFGE pattern with minor band variations, including isolate 988FFP collected in 1995. PCR results revealed a blaOXA-type gene in 65 isolates and nucleotide sequence analysis revealed the presence of the blaOXA-40 gene in seven representative Portuguese isolates from the various geographically dispersed hospitals. CONCLUSIONS: Our results indicate that a multi-resistant epidemic clone of A. baumannii, carrying blaOXA-40, is disseminated in the Iberian Peninsula, persisting in Portugal since 1995.

Acinetobacter Infections↗

A case of Acinetobacter calcoaceticus pneumonia.

A case of community acquired pneumonia with Acinetobacter calcoaceticus is presented. Acinetobacter must be considered in the differential diagnosis of Gram negative coccobacillary pneumonia.

Acinetobacter Infections↗

Predictive biomarkers for drug-resistant Acinetobacter baumannii isolates with bla(TEM-1), AmpC-type bla and integrase 1 genotypes.

BACKGROUND AND PURPOSE: We tested whether antibiotic susceptibilities of drug-resistant Acinetobacter baumannii isolates could be used to predict the clinically important genotypes bla(TEM-1), AmpC-type bla, and integrase 1 gene (IntI1). METHODS: We analyzed 401 A. baumannii isolates obtained at Changhua Christian Hospital between April 2001 and March 2002. The isolates were all from blood cultures, and identification of A. baumannii was confirmed by API-20NE. Antibiotic susceptibility testing (phenotype) was performed by disk diffusion method. Polymerase chain reaction was used to detect the genes bla(TEM-1), AmpC-type bla and IntI1. RESULTS: Of 32 A. baumannii isolates, 10 possessed bla(TEM-1), 21 AmpC-type bla, and 26 IntI1. Resistance to ceftazidime (CAZ) predicted bla(TEM-1) genotype with 63.6% sensitivity, 100% specificity, 55.6% positive predictive value (PPV) and 0% negative predictive value (NPV). Trimethoprim-sulfamethoxazole (SXT) and gentamicin (GM) resistance predicted IntI1 genotype with 83.3% sensitivity, 71.4% specificity, 95.2% PPV and 45.4% NPV. No resistance phenotype could predict the AmpC-type bla genotype. CONCLUSIONS: CAZ resistance predicted the bla(TEM-1) genotype with 100% specificity, and SXT and GM resistance predicted the IntI1 genotype with 92.5% PPV. Therefore, antibiotic susceptibilities to CAZ, SXT, and GM can be utilized clinically to detect critical genotypes in A. baumannii.

Acinetobacter Infections↗

Chronic community-acquired Acinetobacter pneumonia that responded slowly to rifampicin in the anti-tuberculous regime.

Acinetobacter baumannii is a well-known cause of hospital-acquired pneumonia. Occasionally, it can present as an acute community-acquired pneumonia with a fulminant course. However, the occurrence of the chronic form of community-acquired Acinetobacter pneumonia is yet to be highlighted. We describe a 62-year-old, HIV negative, non-diabetic male, who was referred for evaluation of consolidation and cavitation in the apicoposterior segment of the left upper lobe for 4 months. For this, he had received anti-tuberculous therapy, which included rifampicin. On investigation, a diagnosis of chronic community-acquired pneumonia due to Acinetobacter baumannii was made. The steady clinico-radiologic improvement observed was attributed to rifampicin in the anti-tuberculous regime. Subsequently, an aspergilloma formed in the cavity.

Acinetobacter Infections↗

Selection of topoisomerase mutations and overexpression of adeB mRNA transcripts during an outbreak of Acinetobacter baumannii.

OBJECTIVES: To investigate the mechanism of ciprofloxacin resistance in isolates of Acinetobacter baumannii during two hospital outbreaks and to determine the expression level of the gene encoding the AdeB efflux pump. METHODS: Isolates were previously typed by PFGE and their MICs determined by broth microdilution. The gyrA and parC genes were sequenced and the adeB gene examined by real-time reverse transcription PCR (RT-PCR). RESULTS: Two clonal lineages were responsible for the two hospital outbreaks. In both outbreaks, ciprofloxacin susceptibility was reduced during the course of the outbreak when compared with the index isolates. Mutations in gyrA and parC were found to have occurred during the outbreak. The MICs of non-fluoroquinolone antibiotics were raised in one clonal lineage and this was associated with a >10-fold increase in mRNA transcripts for adeB. CONCLUSIONS: We have witnessed the appearance of gyrA and parC mutations during outbreaks of A. baumannii. In parallel with these mutations, we observed up-regulation of the adeB gene associated with a decrease in susceptibility to non-fluoroquinolone antibiotics. These data illustrate the propensity for A. baumannii to develop multi-drug resistance rapidly.

Acinetobacter Infections↗

Advances in the management of pneumonia in the intensive care unit: review of current thinking.

Interventions to prevent pneumonia in the intensive care unit should combine multiple measures targeting the invasive devices, microorganisms and protection of the patient. Microbiological investigation is useful for evaluating the quality of the respiratory sample, and permits early modification of the regimen in light of the microbiological findings. Once pneumonia develops, the appropriateness of the initial antibiotic regimen is a vital determinant of outcome. Three questions should be formulated: (1) is the patient at risk of acquiring methicillin-resistant Staphylococcus aureus, (2) is Acinetobacter baumannii a problem in the institution, and (3) is the patient at risk of acquiring Pseudomonas aeruginosa? Antibiotic therapy should be started immediately and must circumvent any pathogen resistance mechanisms developed after previous antibiotic exposure. Therefore, antibiotic choice should be institution-specific and patient-oriented.

Acinetobacter Infections↗