Abstract
Virulence profiles and innate immune responses were studied in Acinetobacter baumannii from nosocomial infections collected over one year in a tertiary care hospital in Mexico. A. baumannii were identified by VITEK 2 System followed by susceptibility tests. Carbapenemase genes, active efflux mechanism to imipenem and meropenem and outer membrane proteins profile were analyzed to evaluate their role on the activity of carbapenem resistance. All isolates were genotyped by pulsed field gel electrophoresis. The ability to form biofilm was determined on a polystyrene surface. The resistance to complement was determined with a pooled human normal serum and TNFα release by infected macrophages was determined by ELISA. The 112 isolates from this study were associated with a 52% of mortality. All were resistance to β-lactams, fluoroquinolones, and trimethroprim-sulfamethoxal, 96 and 90% were resistant to meropenem and imipenem, respectively, but with high susceptibility to polymyxin B, colistin and tigecyclin. Isolates were classified in 11 different clones. Most isolates, 88% (99/112), were metallo-β-lactamases and carbapenemases producers, associated in 95% with the presence of blaOXA-72 gene. Only 4/99 and 1/99 of the carbapenem-resistant isolates were related to efflux mechanism to meropenem or imipenem resistance, respectively. The loss of expression of 22, 29, and/or 33-36-kDa proteins was detected in 8/11 of the clinical isolates with resistance to carbapenem. More than 96% (108/112) of the isolates were high producers of biofilms on biotic surfaces. Finally, all isolates showed variable resistance to normal human serum activity and were high inductors of TNFα release by macrophages. In summary, these results suggest that multidrug-resistant A. baumannii can persist in the hospital environment through its ability to form biofilms. The high mortality observed was due to their ability to survive normal human serum activity and capability to induce potent inflammatory immune response making this nosocomial pathogen a serious threat to hospitalized patients.
Highlights
Over the last few years, infections involving species of Gram-negative non-enteric and multidrug-resistant bacteria have been increasing worldwide [1]
The carbapenem resistance by A. baumannii is due to: a) the production of class B carbapenemases known as metallo-β-lactamases (MBLs) and class D enzymes, b) genetic alterations of penicillin binding proteins, c) overexpression of efflux pumps belonging to the resistance-nodulation-cell division (RND) family and d) the loss of outer membrane proteins associated with the formation of pores [15]
The A. baumannii clinical isolates were obtained from different sources: 50% (56/112) of them were from respiratory sources, 23.2% (26/112) from wound secretions, 14.2% (16/112) from blood culture, 7.1% (8/112) from urine, 3.6% (4/112) from cerebral spinal fluid, 0.9% (1/112) from vascular catheter and 0.9% (1/112) from eye drainage
Summary
Over the last few years, infections involving species of Gram-negative non-enteric and multidrug-resistant bacteria have been increasing worldwide [1]. Among these bacteria, Acinetobacter baumannii has emerged as the most important opportunistic pathogen involved in serious hospital infection outbreaks [2, 3]. Acinetobacter baumannii has emerged as the most important opportunistic pathogen involved in serious hospital infection outbreaks [2, 3] These bacteria have been isolated from different environmental sources, including soil, water, food products, and medical devices as well from the skin of hospital staff. The capability of A. baumannii to form biofilm on biotic or abiotic surfaces partially explains the persistence of these bacteria in the hospital environment [16, 17]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
