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Patients with polymicrobial infections were also allowed in some studies . However, it is the extreme diversity in controls that really distinguishes one study from another, as controls included patients with no A. Baumannii infection or colonization but infection with other organisms allowed , no A. Baumannii infection only but colonization allowed , no infection with drug-resistant A.

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Baumannii bacteremia has been analyzed. Several studies report that receipt of inactive empirical therapy is an independent predictor of increased mortality , whereas others have not been able to confirm these findings . Such differences may relate to the small patient numbers included in these studies and the resulting lack of statistical power.

Baumannii complex cannot be separated by currently available commercial identification systems; in fact, A. Baumannii, Acinetobacter genomic species 3, and Acinetobacter genomic species 13TU are uniformly identified as A. Baumannii by the most widely used identification systems. In referring to these species, it therefore seems appropriate to use the term A.

Some authors have suggested that eradication of colonization be performed by techniques such as selective digestive tract decolonization or use of topical or aerosolized polymyxins . However, we are hesitant to recommend these interventions due to the possible risks of polymyxin-resistant organisms. Rather, we would prefer greater assessment for colonized patients, greater attention to environmental decontamination, and improved hand hygiene as a means for prevention of patient-to-patient transfer. Further studies are still required to define the efficacy of these infection control interventions in the prevention of A. Even in the face of sequence-based methods that are now available and are challenging PFGE as the gold standard for typing of many bacterial species, for Acinetobacter PFGE still remains the reference method of choice. It is a rather laborious method that requires several days before generating a typing result, but the necessary equipment is now standard not only in most reference laboratories but also in hospital-based laboratories.

This method—using EcoRI, ClaI, and SalI for restriction of purified chromosomal DNA, followed by electrophoresis, blotting, and hybridization with a digoxigenin-11-UTP-labeled cDNA probe derived from E. Coli rRNA—has also been used to type strains in several studies investigating the epidemiology of acinetobacters . However, the discriminatory power of ribotyping is limited, and PFGE and other methods are less labor-intensive and more discriminatory . More accurate typing results with a discriminatory power comparable to that of PFGE have been obtained using an automated ribotyping system (RiboPrinter; DuPont Qualicon, Wilmington, DE) . Automated ribotyping generates typing results more rapidly than PFGE does, but it is expensive and requires specialized equipment that is available in only a few laboratories that perform high-throughput molecular epidemiology investigations.

These data suggest that caution should be used in considering tigecycline treatment for A. Baumannii infection in sites where drug levels may be suboptimal, such as the bloodstream . Despite MBLs being less commonly identified in A. Baumannii than the OXA-type carbapenemases, their hydrolytic activities toward carbapenems are significantly more potent (100- to 1,000-fold) .

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The cerebrospinal fluid penetration of sulbactam in patients with inflamed meninges is reported to be 2 to 32% of serum levels , with peak serum levels reaching approximately 42 to 60 mg/liter after an intravenous (i.v.) dose of 1 g . Thus, assuming that the susceptibility breakpoint for sulbactam is ≤4 μg/ml, inadequate dosing may explain the variable clinical response. Baumannii infections, we recommend dosing of at least 6 g/day of sulbactam in divided doses, assuming normal renal function. Recently, dosing of up to 12 g/day was reported for the treatment of hospital-acquired pneumonia caused by sulbactam-resistant A.

Baumannii, with OXA-23 contributing to this phenotype . As seen in other countries, strains within institutions are often clonally related . Also, interhospital spread of multidrug-resistant A.