Introduction: Acinetobacter baumannii is a major pathogen causing infections in intensive care units (ICUs). In this study, we aimed to evaluate the presence of A. baumannii in an ICU environment and gloves from ICU workers and to characterize the antimicrobial resistance of the isolates in comparison with those isolated from ICU patients at the same hospital. Methods: ICU samples were collected from March to November 2010. Isolates biochemically characterized as Acinetobacter calcoaceticusAcinetobacter baumannii complex were evaluated by PCR targeting the 16S rDNA and bla OXA-51 genes. Antimicrobial susceptibility was determined using the disk diffusion method, and carbapenem-resistant isolates were also evaluated for the minimum inhibitory concentration of imipenem using broth microdilution. The presence of the bla OXA-23 gene was evaluated in isolates with reduced susceptibility to carbapenems. Results: A. baumannii was detected in 9.5% (84) of the 886 samples collected from the ICU environment, including from furniture, medical devices, and gloves, with bed rails being the most contaminated location (23.8%; 20/84). Multidrug-resistant (MDR) A. baumannii was found in 98.8% (83/84) of non-clinical and 97.8% (45/46) of clinical isolates. Reduced susceptibility to carbapenems was detected in 83.3% (70/84) of non-clinical and 80.4% (37/46) of clinical isolates. All isolates resistant to carbapenems harbored bla . Conclusions: We found a strong similarity between the antimicrobial susceptibility profiles of non-clinical and clinical A. baumannii isolates. Such data highlight the ICU environment as a potential origin for the persistence of MDR A. baumannii, and hence the ICU may be a source of hospital-acquired infections caused by this microorganism.

Objectives Carbapenemase-producing Klebsiella pneumoniae (CP-Kp) is a major cause of infections in transplanted patients and has been associated with high mortality rates in this group. There is a lack of information about the Brazilian structure population of CP-Kp isolated from transplanted patients. By whole-genome sequencing (WGS), we analyzed phylogeny, resistome, virulome of CP-Kp isolates, and the structure of plasmids encoding bla KPC– 2 and bla NDM– 1 genes. Methods One K. pneumoniae isolated from each selected transplanted patient colonized or infected by CP-Kp over a 16-month period in a hospital complex in Porto Alegre (Brazil) was submitted for WGS. The total number of strains sequenced was 80. The hospital complex in Porto Alegre comprised seven different hospitals. High-resolution SNP typing, core genome multilocus sequence typing (cgMLST), resistance and virulence genes inference, and plasmid reconstruction were performed in 80 CP-Kp. Results The mortality rate of CP-Kp colonized or infected transplanted inpatients was 21.3% (17/80). Four CP-Kp epidemic clones were described: ST11/KPC-2, ST16/KPC-2, and ST15/NDM-1, all responsible for interhospital outbreaks; and ST437/KPC-2 affecting a single hospital. The average number of acquired resistance and virulence genes was 9 (range = 2–14) and 27 (range = 6–36), respectively. Two plasmids carrying the bla KPC – 2 were constructed and belonged to IncN and IncM types. Additionally, an IncFIB plasmid carrying the bla NDM– 1 was described. Conclusion We detected intrahospital and interhospital spread of mobile structures and international K . pneumoniae clones as ST11, ST16, and ST15 among transplanted patients, which carry a significant range of acquired resistance and virulence genes and keep spreading across the world.

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