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Two outbreaks of multidrug-resistant Acinetobacter baumannii occurred in our hospital. The outbreak strains were eventually isolated from respiratory ventilators, an apparatus used to cool or warm patients, and four continuous veno-venous hemofiltration machines. Removing dust from the machines and replacing all dust filters brought the outbreaks to an end.
A cluster of 4 cases of meningitis due to Acinetobacter calcoaceticus var anitratus occurred during a 5-day period in a neonatal intensive care unit. Three of the infants were preterm and all had a history of other medical problems. Initiation of intravenous therapy with carbenicillin was accompanied by clinical recovery and a bacteriological cure. Intensive bacteriological investigation failed to show a common source for the infections.
Class I integrons were detected in 40.8% (40/98) of Pseudomonas aeruginosa strains and 52.8% (56/106) of Acinetobacter baumannii strains in the Nanjing area of China, including several cassette arrays not previously reported.
Twenty-one patients with multidrug-resistant (MDR) Acinetobacter baumannii and Pseudomonas aeruginosa pneumonia were treated with nebulized polymyxin E (colistin). Overall clinical and microbiological response rates were 57.1% and 85.7%, respectively. Nebulized colistin may be reasonably efficacious and safe for treatment of MDR pneumonia. Its role in therapy warrants further investigation in comparative studies.
OBJECTIVES: To investigate the resistance mechanisms and the genetic relationship of imipenem-resistant Acinetobacter baumannii isolates recovered in the intensive care unit (ICU) of a tertiary care hospital. METHODS: Imipenem-resistant A. baumannii clinical and environmental isolates were collected in the ICU of the Red Cross General Hospital, Athens, Greece between March and October 2002. The isolates were tested by Etest MBL, PCR, RT-PCR and sequencing for carbapenemase-encoding genes, PFGE and synergy experiments using meropenem and the efflux pump inhibitor carbonyl cyanide chlorophenylhydrazone. RESULTS: During the study period, 15 clinical and two environmental imipenem-resistant (MIC 8 to >128 mg/L) A. baumannii isolates were recovered. PFGE showed six different clones that included both clinical and environmental isolates. All 17 isolates were negative by Etest MBL and PCR for genes bla(IMP), bla(VIM), bla(SPM), bla(OXA-23-like) and bla(OXA-24-like). Genes bla(OXA-51-like) and bla(OXA-58-like) were amplified from 15 and 14 isolates, respectively. Sequencing of bla(OXA-51-like) amplicons identified bla(OXA-66) (nine cases) and bla(OXA-69) (six cases), whereas bla(OXA-58-like) sequences were classical bla(OXA-58). Reverse transcriptase-PCR showed that bla(OXA-51-like) genes were expressed in 12 and bla(OXA-58) in 10 isolates; in these isolates, inhibition of OXA enzymes by 200 mM of NaCl reduced carbapenem MICs by up to 4-fold. Overexpression of proton-gradient dependent efflux pumps did not contribute to carbapenem resistance in any isolate. Similarly, although AmpC expression was demonstrated in eight isolates, inhibition of AmpC with cloxacillin did not reduce the MICs of carbapenems significantly. CONCLUSIONS: These findings indicate wide dissemination of OXA-58 carbapenemase, which contributes, at least partially, to the imipenem resistance of unrelated A. baumannii isolates in our ICU.
Colonization of the digestive tract has been supposed to be the source of many hospital-acquired infections, especially nosocomial pneumonia. To assess the relationship between oropharyngeal and gastric colonization and subsequent occurrence of nosocomial pneumonia, we prospectively studied 86 ventilated, intensive care unit (ICU) patients. Oropharyngeal or gastric colonizations were detected and quantified on admission and twice weekly during ICU stay. When nosocomial pneumonia was suspected on clinical grounds (new chest X-ray infiltrate and purulent tracheal secretions), diagnosis was assessed on fiberoptic bronchoscopy with quantitative cultures of a protected specimen brush sampling and/or a plugged telescoping catheter sampling yielding > or = 10(3) cfu/ml of at least one microorganism. Bacterial strains responsible for colonization and infection (Acinetobacter baumannii, Pseudomonas aeruginosa, Enterobacteriaceae, and Staphylococcus aureus) were compared using pulsed-field electrophoresis. A total of 31 cases (36%) of pneumonia were diagnosed. Oropharyngeal colonization, detected either on admission or from subsequent samples, was a predominant factor of nosocomial pneumonia as compared with gastric colonization. For instance, oropharyngeal colonization with A. baumannii yielded a 7.45-fold estimated increased risk of pneumonia as compared with patients not yet or not identically colonized (p = 0.0004). DNA genomic analysis demonstrated that an identical strain was isolated from oropharyngeal or gastric samples and bronchial samples in all but three cases of pneumonia, due to S. aureus. These findings provide better knowledge of the pathophysiology of nosocomial pneumonia in mechanically ventilated patients.
OBJECTIVE: To study the risk factors of Acinetobacter baummanii in nosocomial infections, and to verify the nature of Acinetobacter baumannii strains isolated from intensive care unit (ICU). METHODS: A hundred and fourty patients associated with nosocomial infection of Acinetobacter baummanii from four teaching hospitals were selected and compared with controls through a case control study to identify risk factors. The strains isolated from the ICU were typed by polymerase chain reaction (PCR) with the primer M(13) following electrophoresis in agarose gel. RESULTS: The odds ratios (ORs) were: state of the illness (OR = 8.69), using immunosuppressant (OR = 4.85), mechanical ventilation (OR = 3.68) and treatment with 3 kinds of antibiotics (OR = 3.014). Data from PCR studies indicated that these strains were sharing identical band pattern from the five strains. CONCLUSION: Risk factors for nosocomial infection with Acinetobacter baummanii included state of an illness, immunosuppressant, mechanical ventilation, and treatment with antibiotics. A multidrug-resistant strains of Acinetobacter baumannii was identified in ICU.
The outer membrane protein (OMP) profiles of 23 blood isolates of Acinetobacter baumannii representing all the different antimicrobial susceptibility patterns observed during a 3-year period in a Spanish hospital were studied. OMPs extracted from envelopes of sonicated cells after solubilisation with 2% of N-lauryl-sarcosinate were analysed by sodium dodecyl sulphate-polyacrylamide gel electrophoresis (SDS-PAGE) using the Laemmli's buffers. Eight running gel systems differing in the concentration of polyacrylamide (8%, 10% and 12%) and in the absence or presence of urea (4 M and 6 M) were used in a preliminary study analysing the OMP profiles of four clonally unrelated strains of A. baumannii. When this study was completed, the OMPs of the 23 A. baumannii were analysed in 10% SDS-polyacrylamide gels with 6 M urea and in 12% SDS-polyacrylamide gels. Ten OMP profiles were observed in 10% SDS-polyacrylamide gels with 6 M urea, whereas only 5 OMP profiles were visualised using 12% SDS-polyacrylamide gels. The OMP profiles obtained in 10% SDS-polyacrylamide gels with 6 M urea only partially correlated with those observed in 12% SDS-polyacrylamide gels. In conclusion, the use of 10% SDS-polyacrylamide gels with 6 M urea is recommended for the study of OMP profiles of A. baumannii.
Acinetobacter calcoaceticus, a gram-negative bacterium ubiquitous in soil, water and sewage, is a rare cause of endocarditis in children. The first case of Acinetobacter endocarditis in an infant is described. This patient had underlying tetralogy of Fallot with absent pulmonary valve. A review of the literature in English revealed only four other cases of Acinetobacter endocarditis in children; three of whom had underlying congenital heart disease. Like the other reported cases, this patient responded well to antibiotic treatment. Subsequently this patient underwent corrective cardiac surgery but died of post-operative complications.
Described here is the case of a 23-year-old male with Acinetobacter baumannii sepsis and acute renal failure requiring continuous venovenous hemodialysis treated successfully with intravenous polymyxin B. The drug was administered as a loading dose of 2.5 mg/kg, followed by 2 doses of 1 mg/kg on days 4 and 8, then 0.8 mg/kg daily to complete a 24-day course. A discussion of dosing recommendations for polymyxins in dialysis is presented.
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A 19-year-old previously healthy woman developed meningitis due to Acinetobacter calcoaceticus. This is a Gram-negative coccobacillus belonging to the family Neisseriaceae. Most reported cases of Acinetobacter meningitis were hospital-acquired and due to strains highly resistant to amoxycillin. Our patient was treated with amoxycillin and recovered without sequelae.
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The Acinetobacter calcoaceticus-Acinetobacter baumannii complex includes some of the most clinically relevant species of the genus Acinetobacter due to their capacity to cause epidemic nosocomial outbreaks as well as their increasing resistance to antibiotics. Susceptibility of Acinetobacter strains varies greatly depending on origin, thus highlighting the importance of local analyses of susceptibility profiles. Two hundred twenty-one strains of the A. calcoaceticus-A. baumannii complex were identified using biochemical tests and were biotyped. Strain susceptibility to imipenem, meropenem, colistin and sulbactam was studied using agar dilution. Eight different biotypes were found, type 1 accounting for 69.2% of the strains. MIC(50) and MIC(90) to imipenem, meropenem, colistin and sulbactam were 4 and 8 mg/l, 16 and 32 mg/l, 0.5 and 1mg/l, and 8 and 16 mg/l, with susceptibility rates of 64.3, 22.6, 98.2 and 73.8%, respectively. Biotype 1 was the most resistant. A statistically significant difference was observed for the mean MIC of the four predominant biotypes to imipenem, meropenem and sulbactam but not to colistin.
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We report a case of a 52-year-old man with post-surgical meningitis due to a multi-drug resistant Acinetobacter baumannii. Despite therapy with intravenous amikacin and imipenem the meningitis progressed. Upon institution of combination therapy with amikacin by the intravenous and intrathecal (IT) routes, and intravenous colistin the patient experienced successful clinical and microbiological outcomes.