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PubMed2003

Infections due to Acinetobacter baumannii in the ICU.

Acinetobacter species are widespread environmental, nonfermentative, aerobic, gram-negative coccobacilli. Most infections due to this organism are opportunistic in nature and occur in patients who spend extended time in the intensive care unit (ICU) due to severe underlying disease, and who need prolonged therapy with mechanical ventilation and antimicrobial agents. Because the only factor amenable to prevention in this setting is antimicrobial therapy, avoidance of unnecessary antibiotics should be a high priority in management of such patients. Nosocomial spread of A. baumannii in the ICU setting has often been attributed to ventilatory equipment and to colonized nursing and respiratory personnel via hand transmission. In fact, the epidemiology of nosocomial respiratory colonization and/or infection with A. baumannii is now commonly much more complex due to the coexistence of epidemic cases with unrelated sporadic cases caused by different strains. This underscores the necessity to use molecular typing to improve the detection of microepidemics amenable to early control. Crude mortality rates of 30 to 75% have been reported for nosocomial infection due to Acinetobacter species, with the highest rates reported in ventilator-dependent patients. As with many other opportunistic gram-negative bacilli, increasing antibiotic resistance has hindered the therapeutic management of nosocomial infection due to Acinetobacter species. A. baumannii are now frequently resistant to most available antibacterial drugs, with some centers reporting up to 80% of strains resistant to all aminoglycosides. Even resistance to imipenem, which was for several years the most effective drug in treating Acinetobacter nosocomial infections, has now been described in several reports. Unfortunately, the unique propensity of Acinetobacter species to develop resistance to multiple antimicrobial agents reinforces concerns about the imminence of a post-antimicrobial era where no effective antibiotics will be available to treat this type of infection.

Journal Article↗
PubMed2002

[Acinetobacter, a nosocomial pathogen. Contribution of experimental models].

EPIDEMIOLOGY: The increasing importance of Acinetobacter as a nosocomial pathogen responsible for outbreaks in intensive care units has been pointed out for twenty years. Today Acinetobacter infections are essentially pneumonia in patients under mechanical ventilation. EXPERIMENTAL MODELS: Most clinical isolates are resistant to b-lactam antibiotics as well as to other drugs. Animal models represent an essential step between in vivo testing an<d clinical studies, necessary to understand physiopathology, pharmacology and efficacy of therapy. The virulence of clinical isolates of Acinetobacter spp has been studied in a mouse model of systemic infection. Pharmacological studies and efficacy of antibiotics have been studied in a mouse model of Acinetobacter pneumonia. HUMAN THERAPEUTICS: The majority of strains are multi-resistant to antibiotics and the infections they cause are difficult to treat. Isolated or combined Sulbactam has often been used with success.

Acinetobacter↗
PubMed1993

Vascular catheter-related bloodstream infection due to Acinetobacter johnsonii (formerly Acinetobacter calcoaceticus var. lwoffi): report of 13 cases.

Although Acinetobacter baumannii (formerly Acinetobacter calcoaceticus var. anitratus) is known to be an important nosocomial pathogen, the clinical impact of other Acinetobacter species is not fully understood. Acinetobacter johnsonii (formerly a subset of A. calcoaceticus var. lwoffii) is considered a commensal on human skin, and infections due to this organism have not been reported previously. During a study period of 18 months, however, 13 patients at 6 hospitals developed catheter-related bloodstream infections caused by A. johnsonii. All patients had an indwelling peripheral or central venous catheter, and 11 patients were receiving a continuous intravenous infusion of heparin via the offending catheter. The clinical course of A. johnsonii bacteremia was usually benign. Infections responded readily to removal of the catheter, with or without administration of appropriate antibiotics. No insertion-site infections were documented. Thus A. johnsonii must be regarded as an organism that can cause rare cases of bloodstream infection in immunocompetent patients.

Acinetobacter Infections↗
PubMed1993

Nosocomial outbreak of Klebsiella infection resistant to late-generation cephalosporins.

OBJECTIVE: To describe the epidemiology, antimicrobial susceptibility, and control of widespread ceftazidime-resistant Klebsiella pneumoniae infections in a North American hospital and circumstances that led to delayed detection. DESIGN: A 2-year epidemiologic, microbiologic, and clinical cohort study. SETTING: A 487-bed general hospital in New York City. PATIENTS AND CLINICAL ISOLATES: Patient records were reviewed retrospectively and prospectively. Isolates were obtained from the Clinical Microbiology Laboratory. RESULTS: Four hundred thirty-two isolates of ceftazidime-resistant Klebsiella pneumoniae were recovered during a 19-month study period. The peak incidence reached 17.3% of all Klebsiella isolates. One hundred fifty-five patients were colonized or infected, representing more than 70 per 1000 average daily census. Infections occurred in 39% of patients from whom ceftazidime-resistant Klebsiella was isolated. These included 14 bacteremias and 17 pulmonary infections among 52 infected patients. The outbreak coincided with increasing use of ceftazidime therapy for multiresistant Acinetobacter infections. Reduction in ceftazidime use and barrier precautions markedly reduced the incidence of colonization and infection. Ceftriaxone, ceftizoxime, cefotaxime, and cephamycins were inhibitory, but not bactericidal, against ceftazidime-resistant Klebsiella and appeared effective by routine disc diffusion tests. In contrast, imipenem provided consistent bactericidal activity. Preliminary studies indicated that the outbreak was caused by one or more plasmid-mediated beta lactamases. CONCLUSIONS: Nosocomial ceftazidime-resistant Klebsiella pneumoniae may be resistant to the bactericidal activity of all cephalosporins and cephamycins. Such isolates appear susceptible to cephalosporins other than ceftazidime by routine disc diffusion testing. Ineffective therapy, delayed detection of resistance, and epidemic spread are potential consequences. Imipenem provides consistent bactericidal activity. Ceftazidime restriction and barrier precautions for colonized and infected patients are effective control measures.

Aged↗
PubMed1998

Outbreak of Acinetobacter spp. bloodstream infections in a nursery associated with contaminated aerosols and air conditioners.

BACKGROUND: Acinetobacter spp. are multidrug-resistant bacteria that grow well in water and cause infections with unexplained, increased summer prevalence. In August, 1996, eight infants acquired Acinetobacter spp. bloodstream infection (A-BSI) while in a nursery in the Bahamas; three infants died and an investigation was initiated. METHODS: A case patient was defined as any newborn in the nursery during August 6 to 13, 1996, with A-BSI. To identify risk factors for A-BSI we conducted a retrospective cohort study and performed environmental cultures and air sampling using settle plates. The genetic relatedness of environmental isolates was assessed by pulsed field gel electrophoresis. RESULTS: Of 33 patients in the nursery 8 (24%) met the case definition. Patients with peripheral iv catheters were more likely to develop A-BSI (8 of 21 vs. O of 10, P < 0.05). Multivariate analysis among patients with iv catheters indicated that only exposure to one nurse was an independent risk factor for developing A-BSI (P < 0.005). Nursery settle plates were more likely to grow Acinetobacter spp. than were settle plates from other hospital areas (8 of 9 vs. 0 of 5, P < 0.005); cultures from nursery air conditioners also grew Acinetobacter spp. Environmental isolates were genetically diverse. After installation of a new air conditioner in May, 1995, A-BSIs occurred more frequently during months of increased absolute humidity or environmental dew point. CONCLUSIONS: Acinetobacter spp. may cause nosocomial BSI and death among infants during periods of polyclonal airborne dissemination; breaks in aseptic technique during i.v. medication administration may facilitate transmission from the environment to the patient. Environmental conditions that increase air conditioner condensate may predispose to airborne dissemination via contaminated aerosols and increase the risk of nosocomial A-BSI.

Acinetobacter↗
PubMed1976

Bacteremic Acinetobacter Herellea pneumonia with survival: case report.

A case of community-acquired pneumonia with Acinetobacter calcoacetium var. anitratus (Herellea vaginicola) is presented. Initial leukopenia and spare leukocytes in the sputum, followed by prolonged leukocytosis and fever, were unusual features of this case. The clinical significance and current antimicrobial drug therapy of acinetobacter infections are discussed.

Acinetobacter↗
PubMed1991

Uropathogens of various childhood populations and their antibiotic susceptibility.

To define the uropathogens of various childhood populations and their antibiotic susceptibility, 646 episodes of urinary tract infections (UTI) were studied. Of the community-acquired UTI 78% were caused by Escherichia coli and 12% by Klebsiella whereas only 65% of hospital-acquired UTI were caused by E. coli (P less than 0.01), and other pathogens, including Pseudomonas, were more common. In children with UTI who did not have an underlying disorder, most infections were caused by E. coli and Klebsiella species. Children with urinary malformations or urinary catheters or those who developed UTI while receiving antibiotic prophylaxis had fewer E. coli infections and more infections caused by other pathogens, including Pseudomonas (P less than 0.01). Children receiving antibiotic prophylaxis had also significantly more Enterococcus and Acinetobacter infections (P less than 0.001), and children with urinary catheters had more Enterobacter infections (P less than 0.05). Isolates of these risk groups showed increased resistance to antibiotics. Only 30-53% were susceptible to trimethoprim-sulfamethoxazole, which is usually recommended for UTI; 19 to 25% and 27 to 66% were susceptible to ampicillin and cephalothin, respectively. In contrast uropathogens of immunocompromised children did not differ significantly from those of children with no underlying disturbances, nor did they show distinct antibiotic susceptibility patterns.

Adolescent↗
PubMed1999

Surveillance of antibiotic resistance in Taiwan, 1998.

For the first national surveillance of antibiotic resistance in Taiwan, we collected in 1998 from 22 hospitals (6 medical centers, 15 regional hospitals, and 1 local hospital) 3,211 isolates in all parts of the country. Besides 50 random successive isolates from inpatients, each hospital was requested to collect 25 isolates each from positive blood cultures, hospital-acquired infections, outpatients and the pediatric department. We re-speciated all the submitted specimens and determined their antibiotic susceptibility patterns. The most common isolates were Enterobacteriaceae (Escherichia coli, Klebsiella pneumoniae), Staphylococcus aureus, and Pseudomonas aeruginosa. Among hospital-acquired infections, Acinetobacter spp. were among those which accounted for over 10% of the isolates. The oxacillin resistance of S. aureus was 82% in isolates from hospital-acquired infections, and 40% from outpatients. Among Enterococcus spp., 85% were either E. faecalis or E. faecium. They were 14% resistant to vancomycin. Among gram-negative bacteria, K. pneumoniae and Acinetobacter baumanii were hospital-acquired isolates that were most clearly more resistant than community acquired isolates. This difference was less apparent in the case of Enterobacter cloacae, Serratia marcescens, and P. aeruginosa. These bacteria were generally more resistant from all sources. Fifty-one percent of Salmonella were resistant to ampicillin; however, these were all sensitive to ciprofloxacin. Isolates from the East were least resistant. Plotting the disc zone diameters of antibiotics within the susceptible range, we identified subpopulations with smaller diameters in the case of vancomycin against S. aureus, ciprofloxacin against E. coli, and ciprofloxacin against Salmonella spp. These findings represent one of the purposes of this surveillance as they may portend developing resistances which bear careful watching in the future.

Ciprofloxacin↗
PubMed2003

Nosocomial multi-drug resistant Acinetobacter baumannii bloodstream infection: risk factors and outcome with ampicillin-sulbactam treatment.

The emergence of multidrug-resistant (MDR) Acinetobacter baumannii poses a therapeutic problem. The aim of this study was to assess the risk factors for nosocomial MDR-A. baumannii bloodstream infection (BSI) and the efficacy of ampicillin-sulbactam (A/S) in its treatment. Of 94 nosocomial A. baumannii BSI during the year 2000, 54% involved MDR strains, 81% of which were genetically related. Various risk factors for MDR-A. baumannii were found, of which intensive-care unit admission and prior aminoglycoside therapy were independently associated with MDR-A. baumannii acquisition on multivariate analysis. Of MDR-A. baumannii BSI cases, 65% received A/S and 35% inadequate antibiotic therapy, whereas of 43 non-MDR cases, 86% were treated according to susceptibility and 14% inappropriately with antibiotics to which these organisms were resistant. Crude mortality was comparable in the adequately treated groups. Respective mortalities among patients treated adequately and inadequately were 41.4 and 91.7% (p<0.001). Among severely ill patients, A/S therapy significantly decreased the risk of death (P=0.02 OR=7.64). MDR-A. baumannii has become highly endemic in our institution. A/S appears to be one of the last effective and safe empirical resorts for treatment of MDR A. baumannii BSI.

Acinetobacter Infections↗
PubMed2006

Molecular investigation of an outbreak of multidrug-resistant Acinetobacter baumannii, with characterisation of class 1 integrons.

We investigated a multidrug-resistant Acinetobacter baumannii outbreak in the Intensive Care Unit (ICU) of a tertiary care hospital in Greece over a 3-month period. Molecular typing of the outbreak isolates from 31 patients revealed that two distinct genotypes were involved. Nine isolates, belonging to both genotypes, were resistant to carbapenems. Samples from the ICU environment and from the hands of personnel were collected to identify possible contamination. Class 1 integrons of 3.1, 2.5 and 2.2 kb were amplified from the clinical and environmental isolates. The 3.1 kb integron carrying five gene cassettes was found for the first time in A. baumannii. The outbreak ceased after implementation of hygienic measures in the ICU, including complete cleaning and disinfection.

Acinetobacter Infections↗
PubMed2004

Acinetobacter skin abscess in a neonate.

Although Acinetobacter is usually a species of low virulence, it is becoming increasingly more important as a cause of hospital outbreaks, particularly on intensive care units. Antibiotic resistance can develop rapidly. This organism has not been reported to cause skin abscesses previously. We describe a case of a neonate who developed an Acinetobacter abscess on our neonatal intensive care unit.

Abscess↗