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PubMed1996

Outbreak of gentamicin-resistant Acinetobacter baumanii in an intensive care unit: clinical, epidemiological and microbiological features.

The clinical, epidemiological and microbiological features of an outbreak of infection and colonisation caused by gentamicin-resistant Acinetobacter baumanii (GRAB) in an 18-bed intensive care unit (ICU) of a 680-bed adult teaching hospital are described. A retrospective review of medical, laboratory and infection control records was followed by prospective surveillance. Typing of isolates was performed by restriction enzyme analysis (REA) of chromosomal DNA. The incidence of GRAB in the ICU increased from 1.26 cases per 1000 occupied bed days (OBDs) for January to June 1993, to 6.62 per 1000 OBDs for July to December 1993 (Chi square = 4.8, P < 0.05), confirming the existence of an outbreak. For the two year period, 1993 and 1994, a total of 45 cases of GRAB infection or colonisation was identified. Males and females were equally represented, with an age range of 16-79 years and a mean age of 51 years. Admitting diagnoses varied, with multiple trauma and head injury predominating (ten cases). For 35 of the 45 cases the initial site of GRAB isolation was sputum or other respiratory tract specimen. Specific treatment for GRAB was initiated in 23 patients, however no deaths were directly attributable to GRAB infection. The period of time between admission to the ICU and first isolation of GRAB ranged from three to 70 days with a median of nine days. Overall, ten (11%) of 91 staff hand samples and one of 37 (3%) environmental samples yielded GRAB. All GRAB isolates produced similar biochemical profiles and antibiotic resistance patterns, except for a group of five which were ciprofloxacin resistant. Thirty patient isolates, all ten staff hand isolates and the environmental isolate produced identical REA patterns. The remaining five patient isolates (all ciprofloxacin resistant) which were available for typing produced a different REA pattern. Our study has documented a moderate-sized outbreak of GRAB in an ICU setting. Typing of isolates using REA was useful in delineating outbreak strains. Carriage of GRAB on staff hands was demonstrated as the most likely source of infection. Despite institution of infection control measures GRAB now appears endemic in the ICU.

Acinetobacter↗
PubMed2001

Prospective study of antibacterial susceptibility, risk factors and outcome of 157 episodes of Acinetobacter baumannii bacteremia in 1999 in Slovakia.

This study prospectively investigated all 157 cases of Acinetobacter baumannii bacteremia occurring in major university hospitals or tertiary care institutions in Slovakia during 1999 in order to determine the antimicrobial susceptibility, risk factors and outcome. Resistance to meropenem was 7.4, gentamicin 35.6, amikacin 26.5, cefepime 20.4 and ciprofloxacin 32.7%, but was only 17.3% to cefoperazone/sulbactam or ampicillin/sulbactam. Antimicrobial susceptibility of A. baumanii was lowest among isolates from cancer patients (ceftazidime 58%, piperacillin/tazobactam 52% and azthreonam 48%; p < or = 0.01-0.001). In univariate analysis, several risk factors, such as wound infection (p < or = 0.01) and ventilatory support (p < or = 0.0001), were significantly related to A. baumannii bacteremia in surgical patients. Neutropenia (p < or = 0.0001), antineoplastic chemotherapy (p < or = 0.0001) and prior antibiotic therapy (p < or = 0.0006) were significant risk factors for A. baumannii bacteremia in cancer patients. In addition, ventilatory support and surgery (p < or = 0.0001) and prior antibiotic therapy (p < or = 0.01) were significantly related to A. baumannii bacteremia in children. Colonization at other body sites (p < or = 0.05), diabetes mellitus (p < or = 0.04) and decubital ulcers/burns (p < or = 0.002) as underlying disease were significantly related to death due to A. baumannii bacteremia. In a multiple logistic regression model, decubital ulcers/burns as underlying disease (p < or = 0.0006; relative risk 5.08) and nosocomial pneumonia (p < or = 0.045; relative risk 5.08) were independent predictors of mortality. Mortality was similar between cancer and surgical patients but significantly lower in children vs. adults (p < or = 0.009).

Acinetobacter↗
PubMed2004

Serological and molecular evidence of Rickettsia helvetica in Denmark.

Recent seroepidemiological studies and examinations of Ixodes ricinus ticks in Europe have demonstrated the presence of an emerging tick-borne infection with Rickettsia helvetica. We conducted a serosurvey in 168 Danish patients seropositive for borreliosis reflecting their exposure to I. ricinus ticks. A total of 21 patients (12.5%) had positive antibody titres to R. helvetica including 4 cases of seroconversion. None of the samples were positive for antibodies to Ehrlichia. We conclude that in humans exposed to I. ricinus ticks in Denmark the risk of acquiring rickettsial infection is for the first time demonstrated. In the same region of Denmark we collected 570 I. ricinus ticks from various sources, and examinations by PCR for Rickettsia were performed. Positive reactions were obtained in 23 ticks (4%), and R. helvetica was identified in all 13 of those for which sequencing was performed.

Animals↗
PubMed2005

Treatment of pan-drug resistant Acinetobacter baumannii.

The objective of this study was to investigate the role of sulbactam in the treatment of pan-drug resistant Acinetobacter baumannii (PDRAB). We studied 89 patients with PDRAB infection treated with different antibiotic regimens. Group A (n = 39) were treated with carbapenem with sulbactam and group B (n = 30) with second and third generation cephalosporins, antipseudomonas penicillins, or fluoroquinolones with aminoglycosides. We also studied the MICs for 48 PDRAB strains by using antimicrobial agents with and without sulbactam. The clinical outcomes of the 2 groups did not differ significantly, either in terms of resolution of infection (25/59, 42% in group A vs 12/30, 40% in group B) or survival (35/59, 59% vs 17/30, 57%). However, the MICs indicated that 16 of the 48 strains were sensitive to imipenem/sulbactam, compared with only 2 of the 48 to imipenem alone. The addition of sulbactam thus reversed the response in 30% (14/46) of strains initially resistant or only intermediate sensitive to imipenem. The MICs for meropenem/sulbactam were in the sensitive range for 8 of 48 strains compared to only 3 of the meropenem alone, indicating an 11% (5/45) reversal rate when sulbactam was added to meropenem. For the 38 isolates initially resistant to both carbapenems alone, imipenem/sulbactam reversed the resistance in 16% (6/38), while meropenem/sulbactam did so in only 3% (1/38). Thus, the carbapenem-sulbactam combinations did not clearly improve clinical outcome, but they did demonstrate lower MICs for the PDRAB strains tested. It may be that aggressive, early treatment of A. baumannii infections with these agents might prevent the emergence of PDRAB strains.

Acinetobacter Infections↗
PubMed2006

Prevalence and antibiotic susceptibility of Acinetobacter baumannii, Pseudomonas aeruginosa and Klebsiella pneumoniae in Estonian intensive care units in comparison with European data.

This prospective cohort study was performed from April to December 2003 for the purpose of collecting a maximum of 50 non-duplicate isolates of Acinetobacter baumannii, Pseudomonas aeruginosa, and Klebsiella pneumoniae from each of 4 ICUs to determine minimum inhibitory concentrations. The most prevalent species were Enterobacteriaceae (13%), K. pneumoniae and A. baumannii (both 12%). 60% of A. baumannii strains were susceptible to ampicillin/sulbactam and cefepime, 95% to meropenem and imipenem, and 75% to amikacin. 79% of P. aeruginosa strains were piperacillin/tazobactam, 58% ceftazidime, 81% meropenem, 72% imipenem, 69% ciprofloxacin and 97% amikacin susceptible. The susceptibility of K. pneumoniae to meropenem and imipenem was 99%, to ciprofloxacin was 91% and to amikacin was 98%. Gram-negative bacteria (especially K. pneumoniae and A. baumannii) were prevalent in our ICUs compared to other European studies. Carbapenem susceptibility of Estonian strains was higher, but P. aeruginosa sensitivity to ceftazidime was lower, compared to other EU countries.

Acinetobacter Infections↗
PubMed2001

Risk factors for Acinetobacter baumannii nosocomial bacteremia in critically ill patients: a cohort study.

Nosocomial bacteremia caused by Acinetobacter baumannii (AB) is of increasing concern in critically ill patients, and the risk factors for this infection are not well established. An inception cohort study in a 40-bed medical and surgical intensive care unit (ICU) at a single institution was conducted during a 2-year period to determine the risk factors for AB nosocomial bacteremia. Risk factors related to the underlying diseases, the clinical picture at admission, and those acquired during the stay in the ICU were recorded upon admission and daily throughout the ICU stay. We defined an "invasive procedures index" as the number of invasive procedures performed every day during the ICU stay before the onset of AB bacteremia divided by the number of days in the ICU before the onset of AB bacteremia. Risk factors that were independently associated with AB bacteremia were immunosuppression, unscheduled admission to the hospital, respiratory failure at ICU admission, previous antimicrobial therapy, previous sepsis in the ICU, and the invasive procedures index.

Acinetobacter↗
PubMed2003

Treatment of multidrug-resistant Acinetobacter baumannii ventilator-associated pneumonia (VAP) with intravenous colistin: a comparison with imipenem-susceptible VAP.

We prospectively evaluated the efficacy and toxicity of intravenously administered colistin in 35 episodes of ventilator-associated pneumonia (VAP) due to multidrug-resistant Acinetobacter baumannii. Microbiological diagnosis was performed with use of quantitative culture. In 21 patients, the episodes were caused by a strain susceptible exclusively to colistin (the CO group) and were all treated with this antimicrobial intravenously. In 14 patients, the episodes were caused by strains that remained susceptible to imipenem and were treated with imipenem-cilastatin (the IM group). Acute Physiology and Chronic Health Evaluation II scores at the time of admission and Sequential Organ Failure Assessment scores at time of diagnosis were similar in both groups. VAP was considered clinically cured in 57% of cases in both groups. In-hospital mortality rates were 61.9% in the CO group and 64.2% in the IM group, and the VAP-related mortality rates were 38% and 35.7%, respectively. Four patients in the CO group and 6 in the IM group developed renal failure. Neurophysiological evaluation was performed during 12 episodes in the CO group, but it revealed no signs of neuromuscular blockade. Intravenous colistin appears to be a safe and effective alternative to imipenem for the management of VAP due to carbapenem-resistant strains of A. baumannii.

Acinetobacter Infections↗
PubMed2003

Considerations in control and treatment of nosocomial infections due to multidrug-resistant Acinetobacter baumannii.

We sought to control infection due to multidrug-resistant Acinetobacter baumannii (MDR-Ab) by identifying isolates as clonally related, leading to enhanced infection-control measures, including cohorting, surveillance, contact precaution, initial therapy with ampicillin/sulbactam and local polymyxin B, and, more recently, therapy with synergistic antibiotic combinations. Class restriction of cephalosporins has been associated with a reduction in cephalosporins-cephamycin-carbapenem resistance among nosocomial Klebsiella isolates. This has been supplemented by restriction of carbapenem use after an initial 24-h period in an effort to reduce the selection of porin-deficient, carbapenem-resistant A. baumannii and Pseudomonas aeruginosa. Evidence is reviewed suggesting that eradication of MDR-Ab nosocomial colonization may prevent subsequent infection. Relatively few standard antibacterial drugs remain active against MDR-Ab. Published clinical results of therapy with these agents are reviewed, and in vitro evidence of synergy between them is presented that suggests that combination therapy should be studied for enhanced clinical activity.

Acinetobacter Infections↗
PubMed2003

Molecular epidemiology and mechanisms of carbapenem resistance in Acinetobacter baumannii endemic in New York City.

Multidrug-resistant Acinetobacter baumannii has emerged as a serious nosocomial pathogen in certain areas. In Brooklyn, New York, citywide surveillance revealed that approximately 2 of every 3 isolates were resistant to carbapenem antibiotics. Genetic fingerprinting revealed that 2 strains accounted for 82% of these resistant isolates. Compared with carbapenem-susceptible isolates, carbapenem-resistant isolates had reduced expression of 47-, 44-, and 37-kDa outer-membrane proteins. No specific carbapenemase was found; however, carbapenem-resistant isolates expressed greater levels of a class C cephalosporinase. Although expression of penicillin-binding proteins varied among strains, no consistent pattern appeared to account for carbapenem resistance. An efflux pump, present in several strains, did not appear to contribute to carbapenem resistance. Clonal spread of carbapenem-resistant A. baumannii has occurred in hospitals in Brooklyn. The preliminary findings for a small number of strains suggest that diminished production of outer-membrane porins, together with increased expression of a class C cephalosporinase, appear to be important factors leading to carbapenem resistance in this region.

Acinetobacter Infections↗
PubMed2005

Nebulized colistin in the treatment of pneumonia due to multidrug-resistant Acinetobacter baumannii and Pseudomonas aeruginosa.

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.

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↗
PubMed2006

The epidemiology and control of Acinetobacter baumannii in health care facilities.

Acinetobacter baumannii is a ubiquitous pathogen capable of causing both community and health care-associated infections (HAIs), although HAIs are the most common form. This organism has emerged recently as a major cause of HAI because of the extent of its antimicrobial resistance and its propensity to cause large, often multifacility, nosocomial outbreaks. The occurrence of outbreak is facilitated by both tolerance to desiccation and multidrug resistance, contributing to the maintenance of these organisms in the hospital environment. In addition, the epidemiology of A. baumannii infection is often complex, with the coexistence of epidemic and endemic infections, the latter of which often is favored by the selection pressure of antimicrobials. The only good news is that potentially severe A. baumannii infection, such as bacteremia or pneumonia in patients in the intensive care unit who are undergoing intubation, do not seem to be associated with a higher attributable mortality rate or an increased length of hospital stay.

Acinetobacter Infections↗
PubMed1999

The emergence of resistant strains of Acinetobacter baumannii: clinical and infection control implications.

A prospective study was undertaken to determine colonization rates, susceptibility profiles, and outcomes in patients with clinical isolates of Acinetobacter baumannii. Fifty percent of patients became colonized with A. baumannii, and 29% of these patients had clinical and colonizing isolates with discordant susceptibility profiles, without apparent relation to antibiotic use. Barrier infection control measures are necessary to prevent nosocomial transmission.

Acinetobacter↗
PubMed2000

An outbreak of Acinetobacter baumannii: the importance of cross-transmission.

OBJECTIVE: To investigate an outbreak of nosocomial infections due to multidrug-resistant (MDR) Acinetobacter baumannii and to analyze the contribution of cross-transmission in the rise in infection rates. DESIGN: Epidemiological investigation; molecular typing using pulsed-field gel electrophoresis (PFGE); matched case-control study to identify risk factors for infection. SETTING: A 34-bed surgical intensive care unit at a tertiary-care hospital. PATIENTS: Eighteen patients who developed MDRA baumannii nosocomial infection were matched to 36 patients who were admitted to the same surgical intensive care unit (SICU) room and did not develop an infection during the outbreak period. RESULTS: Prior to the outbreak, the baseline attack rate of MDR A baumannii nosocomial infections was 3 per 100 patients per month. From February 1 through March 22, 1998, the attack rate rose to 16 per 100 patients per month, with a total of 18 infections. All isolates had indistinguishable PFGE patterns. Seventy environmental cultures were negative for MDR A baumannii. Following intense infection control education, the attack rate decreased to 4 per 100 patients per month. By conditional logistic regression, cases were exposed to a significantly higher number of patients with MDR A baumannii infections compared to controls (odds ratio, 1.1; 95% confidence interval, 1.01-1.2; P=.02), even after adjusting for length of SICU admission and exposure to antibiotics and invasive devices. CONCLUSION: Cross-transmission between patients contributed to the rise in rates of MDRA baumannii infections. A common environmental source was not detected.

Acinetobacter↗
PubMed2001

An outbreak of imipenem-resistant Acinetobacter baumannii in critically ill surgical patients.

OBJECTIVE: To describe an outbreak of imipenem-resistant Acinetobacter baumannii (IR-Ab) and the measures for its control, and to investigate risk factors for IR-Ab acquisition. DESIGN: An observational and a case-control study. SETTING: A surgical intensive care unit (ICU) in a university tertiary care hospital. METHODS: After admission to the ICU of an IR-Ab-positive patient, patients were prospectively screened for IR-Ab carriage upon admission and then once a week. Environmental cleaning and barrier safety measures were used for IR-Ab carriers. A case-control study was performed to identify factors associated with IR-Ab acquisition. Cases were patients who acquired IR-Ab. Controls were patients who were hospitalized in the ICU at the same time as cases and were exposed to IR-Ab for a similar duration as cases. The following variables were investigated as potential risk factors: baseline characteristics, scores for severity of illness and therapeutic intervention, presence and duration of invasive procedures, and antimicrobial administration. RESULTS: Beginning in May 1996, the outbreak involved 17 patients over 9 months, of whom 12 acquired IR-Ab (cases), 4 had IR-Ab isolates on admission to the ICU, and 1 could not be classified. Genotypic analysis identified two different IR-Ab isolates, responsible for three clusters. Ten of the 12 nosocomial cases developed infection. Control measures included reinforcement of barrier safety measures, limitation of the number of admissions, and thorough environmental cleaning. No new case was identified after January 1997. Eleven of the 12 cases could be compared to 19 controls. After adjustment for severity of illness, a high individual therapeutic intervention score appeared to be a risk factor for IR-Ab acquisition. CONCLUSION: The outbreak ended after strict application of control measures. Our results suggest that high work load contributes to IR-Ab acquisition.

Acinetobacter↗
PubMed2001

Environmental contamination by multidrug-resistant Acinetobacter baumannii in an intensive care unit.

Contamination in an intensive care unit caused by multidrug-resistant Acinetobacter baumannii complex (MRAB)-colonized patients was evaluated using environmental and patient cultures. MRAB occurred in 21% of patients' cultures, 2.1% of 513 areas surrounding MRAB-patients, and one of 372 common areas. No transmission to other patients occurred. Barrier precautions and ethanol disinfection may prevent dissemination.

Acinetobacter Infections↗
PubMed2001

Infrequent isolation of multiresistant Acinetobacter baumannii from the staff tending a colonized patient with severe burns.

A patient with severe burns who was colonized by multiresistant Acinetobacter baumannii was cared for in contact isolation by staff intensively trained on hospital hygiene. Of the 1,907 postexposure cultures from the staff and 425 environmental samples, only 0.7% and 4%, respectively, yielded this microorganism. These data show that strict hygienic measures may limit staff colonization and contamination of the environment byA baumannii.

Acinetobacter↗