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PubMed2004

Annual trends in antibiotic resistance of nosocomial Acinetobacter baumannii strains and the effect of synergistic antibiotic combinations.

Acinetobacter baumannii is becoming increasingly resistant to antibiotics often requiring combination therapy. Annual changes of resistance to selected antimicrobials of 150 A. baumannii strains, isolated as nosocomial pathogens between 1994 and 2000 were investigated. The synergistic effects of antimicrobials were studied using a microdilution checkerboard technique in eight selected isolates resistant to third-generation cephalosporins and beta-lactam/beta-lactamase inhibitor combinations and to at least one aminoglycoside. Rates of resistance of cefepime, ceftazidime, ampicillin/sulbactam, amikacin and ciprofloxacin (before 1996 and between 1996-2000) were 29.7% - 72.6, 37.8% - 81.4%, 35.1% - 72.6%, 8.1% - 56.6%, 5.4% - 46.0% respectively (p < 0.001 for each one). Synergy was observed in at least one of the combinations of antibiotics from seven of eight isolates (87%), no antagonism was detected with any combination. Ceftazidime-amikacin (50%) and ampicillin/sulbactam-tobramycin (50%) were the most effective combinations. Due to the effectiveness of sulbactams to Acinetobacter, ampicillin/sulbactam-tobramycin combination is recommended as the first line of choice.

Acinetobacter Infections↗
PubMed2005

Treatment of nosocomial meningitis due to a multidrug resistant Acinetobacter baumannii with intraventricular colistin.

We report a case of serious nosocomial meningitis due to a multidrug-resistant Acinetobacter baumannii in a 23-year-old woman who had a posterior fossa craniotomy with upper cervical laminectomy for excision of a meningioma at the level of foramen magnum. Post-operatively, she had neck pain with continuous fever and deterioration in the level of consciousness and convulsions. The CSF was turbid and had neutrophil pleocytosis. A multidrug-resistant Acinetobacter baumannii was isolated from the blood and CSF. The patient failed high doses of imipenem, ciprofloxacin and systemic colistin but responded well to intraventricular injections of colistin 125,000 units twice daily for 3 weeks. No apparent side effects were noticed. We have reviewed other similar cases reported in the literature.

Acinetobacter Infections↗
PubMed2004

Outbreak of nosocomial meningitis caused by Acinetobacter baumannii in neurosurgical patients.

An outbreak of nosocomial meningitis caused by Acinetobacter baumannii, which developed postoperatively in seven neurosurgical patients is described. The clinical isolates of A. baumannii were typed by biochemical profiles and antibiogram patterns, and by random amplified polymorphic DNA polymerase chain reaction (RAPD-PCR) and amplified fragment length polymorphism (AFLP) fingerprinting. The implicated strain was multi-drug resistant, however, susceptibility to imipenem and netilmicin was detected. An extensive search for the environmental source of the epidemic strain was carried out. Two of several isolates from hospital environment, corresponded to the A. baumannii outbreak strain, one being cultured from the suctioning equipment used in the care of these patients. The introduction of multiresistant epidemic A. baumannii into a neurosurgical unit is a severe risk factor for patients undergoing neurosurgical procedures. Genotypic typing methods are important for definitive identification of these strains in patients and their environment.

Acinetobacter Infections↗
PubMed2004

[Carbapenemase detection in Acinetobacter baumannii clones resistant to imipenem].

INTRODUCTION: The aim of this study was to detect carbapenemases in imipenem-resistant Acinetobacter baumannii isolates obtained in the microbiology department of a Basque Country Public Health Service hospital over a period of 19 months, and to genetically characterize the resistant clones. METHODS: Susceptibility tests to imipenem, meropenem, ticarcillin, ceftazidime, cefotaxime, cefepime and aztreonam were done by determining the minimum inhibitory concentration on agar plates. A tRNA technique was used for species identification and PCR with primers ERIC2, AP3 and M13 for genetic typing of resistant isolates. Carbapenemase production was detected by the Hodge test and metallo-beta-lactamase by the EDTA test and Etest MBL. RESULTS: A total of 76 isolates were resistant to imipenem and 49 of these were resistant to all the betalactam antibiotics tested. Genetic typing showed three predominant clones, denominated I (9 isolates), II (48 isolates) and III (8 isolates). Hodge and EDTA tests were positive in 45 and 8 isolates belonging to clone II, 8 and 4 belonging to clone I and 7 and 3 belonging to clone III, respectively. The Etest confirmed 7 results (45% of the 17 positive EDTA test isolates). CONCLUSION: Our results show that one factor contributing to the high level of imipenem resistance in the isolates analyzed is dissemination of a predominant, multiresistant clone able to produce OXA-type carbapenemases and metallo-beta-lactamases.

Acinetobacter Infections↗
PubMed2004

[Clonal diversity and antimicrobial susceptibility of Acinetobacter baumannii isolated in Spain. A nationwide multicenter study: GEIH-Ab project (2000)].

INTRODUCTION: A nationwide multicenter study was performed in Spain to evaluate the clonal diversity and antimicrobial susceptibility of Acinetobacter baumannii clinical isolates. METHODS: A total of 221 consecutive A. baumannii isolates recovered from clinical samples from 25 Spanish hospitals during November 2000 were studied. Isolate identification was performed by phenotyping methods and by amplified rDNA restriction analysis. Clonal relationships among A. baumannii isolates were determined by pulsed field gel electrophoresis. MICs of amikacin (AK), ampicillin (AP), cephalothin (CF), cefoxitin (FX), ceftazidime (CZ), ciprofloxacin (CP), cotrimoxazole (T/S), doxycycline (DX), gemifloxacin (GX), gentamicin (GN), imipenem (IP), meropenem (MP), minocycline (MI), piperacillin (PP), polymyxin B (PB), rifampicin (RI), tetracycline (TT), sulbactam (SB) and tobramycin (TO) were determined by microdilution (NCCLS guidelines). RESULTS: Seventy-nine A. baumannii clones were differentiated. MIC50/MIC90 (mg/L) values for the 221 A. baumannii isolates were PP: > 512/> 512; AP, CF, FX: > 256/> 256; TT, GN: > 128/> 128; CZ: 128/> 256; CP: > 64/> 64; FP: 64/256; AK: 32/256; DX: 32/64; GX: > 16/> 16; TO: 16/128; SB, T/S: 16/64; MP: 8/> 128; IP: 4/128; RF: 4/8; MI: 2/16 and PB: 1/2. Percentages of susceptible isolates were PB: 100%; MI: 65.8%; IP: 52.5%, RF: 49.3%; SB: 46.7%; MP: 43.1%; AK: 34.7%; DX: 32.0%; TO: 21.3% and CZ, FP, GN, T/S, TT, GX, CP, AP, PP, CF and FX: < 20%. CONCLUSIONS: A. baumannii isolates show high clonal variability in Spain. The most active antimicrobial agents against this organism were polymyxin B, minocycline, rifampicin, imipenem, sulbactam, meropenem, amikacin and doxycycline.

Acinetobacter Infections↗
PubMed2004

Risk factors for acquisition of imipenem-resistant Acinetobacter baumannii: a case-control study.

Risk factors for the nosocomial occurrence of imipenem-resistant Acinetobacter baumannii (IRAB) were determined. A case-control study design was used for a comparison of two groups of A. baumannii-positive patients with control patients. Nosocomial IRAB was isolated from the first group of A. baumannii-positive patients, and imipenem-susceptible A. baumannii (ISAB) was isolated from the second group. The control patients were randomly selected in a 4:1 ratio from the same medical or surgical services from which the A. baumannii-positive patients were receiving care when the isolation of IRAB occurred. Risk factors analyzed included demographic variables, comorbid conditions, variables related to hospitalization, and the antimicrobials used. IRAB was isolated from 104 patients, and ISAB was isolated from 387 patients between January and December 2000. The risk factors for IRAB were a previous intensive care unit (ICU) stay (odds ratio [OR], 21.54; 95% confidence interval [CI], 10.73 to 43.23) and prior exposure to imipenem (OR, 9.18; 95% CI, 3.99 to 21.13) or third-generation cephalosporins (OR, 2.11; 95% CI, 1.13 to 3.95). Risk factors for ISAB were a previous ICU stay (OR, 8.05; 95% CI, 5.67 to 11.44) and exposure to third-generation cephalosporins (OR, 2.07; 95% CI, 1.47 to 2.91). Our results suggest that the nosocomial occurrence of IRAB or ISAB is strongly related to an ICU stay, and IRAB occurrence may be favored by the selection pressure of imipenem.

Acinetobacter Infections↗
PubMed2004

Dissemination of a clone of unusual phenotype of pandrug-resistant Acinetobacter baumannii at a university hospital in Taiwan.

From December 2002 to February 2003, 15 isolates of pandrug-resistant unidentified Acinetobacter species were recovered from seven patients treated on different wards or intensive care units. Both 16S-23S rRNA intergenic spacer PCR-restriction fragment length polymorphism profiles and sequence analysis of these isolates identified them as Acinetobacter baumannii. This pandrug-resistant A. baumannii strain with an unusual phenotype could persist in humans for long periods and was widely disseminated throughout the hospital.

Acinetobacter Infections↗
PubMed2005

Widespread transfer of resistance genes between bacterial species in an intensive care unit: implications for hospital epidemiology.

A transferable plasmid encoding SHV-12 extended-spectrum beta-lactamase, TEM-116, and aminoglycoside resistance was responsible for two sequential clonal outbreaks of Enterobacter cloacae and Acinetobacter baumannii bacteria. A similar plasmid was present among isolates of four different bacterial species. Recognition of plasmid transfer is crucial for control of outbreaks of multidrug-resistant nosocomial pathogens.

Acinetobacter Infections↗
PubMed2003

[Community-acquired Acinetobacter baumannii pneumonia].

OBJECTIVES: Description of two cases of community-acquired Acinetobacter baumannii pneumonia. PATIENTS AND METHODS: Two patients, one with a history of diabetes mellitus type 2 and pulmonary thromboembolism 2 years earlier and the second without known risk factors except for the age, were admitted to hospital because of community-acquired A. baumannii pneumonia with cavitation and with favorable final evolution. CONCLUSION: A. baumannii is an infrequent cause of community-acquired pneumonia, although it should be suspected in patients with debilitating illness and in patients who do not evolve favorably on the first days of the admission with conventional treatment.

Acinetobacter Infections↗
PubMed2005

Spread of a single clone Acinetobacter baumannii strain in an intensive care unit of a teaching hospital in Turkey.

Acinetobacter baumannii is an important nosocomial pathogen, especially in immunocomprimised patients and those hospitalized in intensive care units. After the first isolation of A. baumannii strains from the bronchial aspirates of two patients in the intensive care unit (ICU) of our hospital as a pure culture, screening studies were performed to define possible source(s). A. baumannii strains isolated from bronchial aspirates and blood cultures of the patients in ICU were collected as a possible part of the outbreak. A total of 23 screening samples collected from equipment (7), hands (4) and gloves (2) of the staff, and from ten different body regions of the patients in the ICU were cultured. Antimicrobial susceptibility test of the isolates was performed by the standardized disk-diffusion method. All isolates were subtyped by antibiogram, arbitrarily primed polymerase chain reaction (AP-PCR) and pulsed-field gel electrophoresis (PFGE) typing methods. A total of 26 A. baumannii strains including eight clinical and 18 screening isolates were identified. All isolates were susceptible only to meropenem, tobramycin, and imipenem. There was at least a 96% resistance rate to the other antibiotics tested. Antibiogram typing showed that 24 of the 26 isolates were epidemiologically related, two were unique. AP-PCR yielded two types, one of which had 21 isolates, the other had five. PFGE fingerprinting revealed that all isolates were clonally related, including four closely related and 22 indistinguishable strains. Based on the results of PFGE which has been accepted as a reference method it can be concluded that A. baumannii strains isolated from our intensive care unit originated from a single type of strain.

Acinetobacter Infections↗
PubMedDate not supplied

[Genetic variety of Acinetobacter baumannii in an intensive care unit for burn patients].

The genetic structure of A. baumannii hospital isolates, formed in the course of 2002 - 2004 in an intensive care unit for burn patients (St. Petersburg) was studied. The prolonged circulation of only some clonal strains was shown, 35% of the isolates belonged to dominating strains. Phenotypically, all cultures were characterized by resistance to the preparations of the cephalosporin row and gentamicin. The presence of class 1 integron with variable segment sized 2.5 kbp was found in the genotype of four isolates with the use the polymerase chain reaction. The restriction analysis revealed its similarity with integron, detected earlier (in 1989 - 2001 ) in A. baumannii in European hospitals abroad.

Acinetobacter Infections↗
PubMed2005

The acute-phase response and serum amyloid A inhibit the inflammatory response to Acinetobacter baumannii Pneumonia.

BACKGROUND: Acinetobacter baumannii is an emerging pathogen in nosocomial pneumonia. Trauma and postsurgical patients display a profound acute-phase protein response and are susceptible to pneumonia. METHODS: To study the way in which the acute-phase response induced by sterile tissue injury influences pulmonary host defense, mice were injected subcutaneously with turpentine or saline in both hind limbs either 2 or 5 days before intranasal inoculation with A. baumannii. RESULTS: Turpentine-injected mice demonstrated strong increases in levels of the acute-phase proteins serum amyloid A (SAA) and serum amyloid P. The inflammatory response to A. baumannii was significantly impaired in turpentine-injected mice, as shown by decreased local cytokine and chemokine levels, reduced neutrophil influx and lung myeloperoxidase activity, less pulmonary inflammation on histological examination, and lower total protein levels in their bronchoalveolar lavage fluid, which was associated with reduced bacterial clearance of A. baumannii. The late acute-phase protein response still caused lower pulmonary cytokine levels and neutrophil recruitment. Furthermore, previous injection of SAA, a major acute-phase protein, also reduced inflammatory responses to A. baumannii pneumonia. CONCLUSIONS: These data suggest that the acute-phase response and SAA inhibit the local inflammatory response to A. baumannii pneumonia, which may facilitate bacterial outgrowth.

Acinetobacter Infections↗