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Treatment of Acinetobacter spp infections.

Acinetobacter spp. are predominantly nosocomial pathogens of growing importance. One of their important features is antimicrobial resistance that includes beta-lactams, aminoglycosides and quinolones. Imipenem, considered the most effective drug against Acinetobacter spp., is not universally active against clinical isolates and therapeutic options are necessary. In vitro studies demonstrate the activity of beta-lactamase inhibitors with direct antimicrobial activity, polymyxins, doxycycline and rifampin. Synergy of various combinations has been demonstrated in vitro. Experimental models of infection in mice and rabbits show the efficacy of rifampin and doxycycline. Colistin did not lead to good results in a mouse pneumonia model. There are no randomised, controlled studies on the treatment of Acinetobacter spp. infections. Retrospective comparative studies suggest that ampicillin-sulbactam may be comparable to imipenem in the treatment of pneumonia and bacteraemia. There are a few uncontrolled studies using ampicillin-sulbactam and one study with colistin with results that suggest that they may be acceptable options to treat multi-resistant infections.

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An outbreak of acinetobacter infection associated with the use of a ventilator spirometer.

Although respiratory therapy equipment is a well-known source of nosocomial infection, ventilator spirometers have not been previously implicated. We report 17 Acinetobacter calcoaceticus variety anitratus infections traced to contaminated spirometers. Isolates from infected patients were recovered from urine, sputum, wounds, and blood. A review of attack rates for Acinetobacter was prompted by a dramatic increase in blood culture isolates. Prospective surveillance of intensive care environment, personnel, and patients established that Bennett MA-1 spirometers constituted the major reservoir of infecting organisms. Despite daily sterilization, 30% of spirometers in use were found to be contaminated. The hands of 12% of intensive care nurses and 10% of respiratory therapists cultured were found to be colonized. In addition to the infected patients, 28 other patients on spirometer-equipped ventilators were judged to be colonized by Acinetobacter following examination of sputa and/or mouthwashings. Following discontinuation of spirometer use and following increased emphasis on proper handwashing, the incidence of Acinetobacter infections dropped dramatically. Antibiosis in the intensive care environment and a deterioration in aseptic awareness serve to make Acinetobacter an environmental opportunist of increasing importance.

Acinetobacter Infections↗

Impact of Acinetobacter infection on the mortality of burn patients.

BACKGROUND: Acinetobacter calcoaceticus-baumannii complex (Acb) is recognized as an important cause of nosocomial infections. Although Acb can be associated with multidrug resistance, its impact on mortality in burn patients has not been fully elucidated. STUDY DESIGN: In a retrospective cohort study assessing medical records and microbiology laboratory data at a US military tertiary care burn center, we evaluated all patients admitted to the burn center between January 2003 and November 2005. Data collected included age, severity of burn, comorbidities, length of stay, and survival to hospital discharge. In addition, microbiology data were reviewed to determine which patients were infected with Acb during this time frame. These data were then used to compare patients infected with Acb to patients not infected. Multivariate analysis using logistic regression was performed to determine which patient characteristics were associated with increased mortality. RESULTS: There were 802 patients included in the study. Fifty-nine patients met the case definition for infection. An additional 52 patients were found to be colonized with Acb. Patients with Acb infection had more severe burns and comorbidities, and had longer lengths of stay compared with patients without Acb or those with Acb colonization. Mortality in infected patients was higher compared with those without infection (relative risk = 2.86, p = 0.001). On multivariate analysis, infection with Acb was not statistically associated with mortality. CONCLUSIONS: Multidrug-resistant Acb is a common cause of nosocomial infection in the burn patient population. Despite this, it does not independently affect mortality.

Acinetobacter Infections↗

Clinical and molecular epidemiology of acinetobacter infections sensitive only to polymyxin B and sulbactam.

A nosocomial outbreak of infections due to imipenem-resistant Acinetobacter baumannii occurred in a New York hospital after increased use of imipenem for cephalosporin-resistant klebsiella infections. We identified all A baumannii isolates over 12 months, reviewed corresponding patient records, and compared strains with different antibiotic susceptibility patterns by restriction endonuclease analysis. Environmental surveillance cultures were done before and after institution of control measures. 59 patients harboured imipenem-resistant A baumannii, and 18 were infected. Isolates from patients were resistant to all routinely tested antibiotics, including imipenem. Further studies showed susceptibility to polymyxin B and sulbactam. These isolates were identical by restriction endonuclease analysis to A baumannii isolates susceptible to imipenem alone, or to imipenem and amikacin, but differed from broadly susceptible isolates. Surveillance cultures showed hand and environmental colonisation by imipenem-resistant strains. Infection and colonisation were eliminated by intensive infection control measures, and irrigation of wounds with polymyxin B. Increased use of imipenem against cephalosporin-resistant klebsiella may lead to imipenem resistance among other species, particularly acinetobacter. Such resistance appears to derive from a prior multi-resistant clone, in contrast to one which retains susceptibility to several antibiotics.

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[Ecological aspects and prophylaxis of Acinetobacter baumannii nosocomial infection].

Acinetobacter Baumannii is an aerobic strit gram negative bacteria cause of epidemic infection in intensive care units this bacteria is isolated from the patient and its environment. The detection of AB infection require the isolation of patients and decontamination of the material despite the virulence of the germ, these measures are necessary due to the rapid extension of epidemic in the absence of adequate means.

Acinetobacter Infections↗

Evaluation of adherence, hemagglutination, and presence of genes codifying for virulence factors of Acinetobacter baumannii causing urinary tract infection.

Acinetobacter baumannii is a strictly aerobic bacterium which causes severe infections, however its pathogenic characteristics are not well defined. Thirteen A. baumannii strains isolated from urine of hospitalized and nonhospitalized patients with different ages were investigated for the presence of virulence factors. The isolates belonged to biotypes 2, 6, and 9 and were sensitive to imipenem. The majority of them showed resistance to amikacin, ceftazidime, ceftriaxone, ciprofloxacin, gentamicin, norfloxacin, and trimethoprim-sulfamethoxazole. None of A. baumannii strains presented genes codifying for 17 different virulence factors previously described in uropathogenic Escherichia coli, when tested by polymerase chain reaction (PCR). Nine isolates agglutinated human group AB erythrocytes, in presence of mannose, but none of them agglutinated group O erythrocytes. Adherence to polystyrene was observed in 7 isolates, and this result did not correlate with that obtained in hemagglutination assay. All the isolates were able to grow in iron-limiting conditions, showing that A. baumannii produces some type of siderophore. However, the genes iutA and fyuA, from iron uptake system of E. coli and Yersinia sp., respectively, were not present in the isolates, suggesting the presence of a different type of siderophore. The fimbriae of A. baumannii strains that mediates the adherence are possibly mannose-resistant, even though the mechanism of adherence to human epithelial cells still remains to be elucidated.

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