Abstract
Acinetobacter baumannii is a Gram-negative ESKAPE microorganism that poses a threat to public health by causing severe and invasive (mostly nosocomial) infections linked with high mortality rates. During the last years, this pathogen displayed multidrug resistance (MDR), mainly due to extensive antibiotic abuse and poor stewardship. MDR isolates are associated with medical history of long hospitalization stays, presence of catheters, and mechanical ventilation, while immunocompromised and severely ill hosts predispose to invasive infections. Next-generation sequencing techniques have revolutionized diagnosis of severe A. baumannii infections, contributing to timely diagnosis and personalized therapeutic regimens according to the identification of the respective resistance genes. The aim of this review is to describe in detail all current knowledge on the genetic background of A. baumannii resistance mechanisms in humans as regards beta-lactams (penicillins, cephalosporins, carbapenems, monobactams, and beta-lactamase inhibitors), aminoglycosides, tetracyclines, fluoroquinolones, macrolides, lincosamides, streptogramin antibiotics, polymyxins, and others (amphenicols, oxazolidinones, rifamycins, fosfomycin, diaminopyrimidines, sulfonamides, glycopeptide, and lipopeptide antibiotics). Mechanisms of antimicrobial resistance refer mainly to regulation of antibiotic transportation through bacterial membranes, alteration of the antibiotic target site, and enzymatic modifications resulting in antibiotic neutralization. Virulence factors that may affect antibiotic susceptibility profiles and confer drug resistance are also being discussed. Reports from cases of A. baumannii coinfection with SARS-CoV-2 during the COVID-19 pandemic in terms of resistance profiles and MDR genes have been investigated.
Highlights
Antimicrobial or antibiotic resistance (AMR) has emerged as a substantial and triggering phenomenon with increasing costs for healthcare systems worldwide
Carbapenems were the preferred treatment of multidrug resistant (MDR) A. baumannii infections, but their prior use has led to increased incidence of carbapenem resistance during the last years [12]
According to MicroBIGG-E, resistance to aminoglycosides (AG) in A. baumannii can result through three distinct mechanisms (Table 2) [97]: aminoglycoside-modifying enzymes (AMEs) that weaken AG binding capacity, target site alteration by 16S rRNA methyltransferases, and limited AG uptake subsequent to loss of permeability or overactivity of efflux pumps
Summary
Antimicrobial or antibiotic resistance (AMR) has emerged as a substantial and triggering phenomenon with increasing costs for healthcare systems worldwide. Acinetobacter baumannii belongs to the Moraxellaceae family and is a Gram-negative bacterium that predominantly causes nosocomial infections. These infections are diverse and may include hospital-acquired and ventilator-associated pneumonia (HAP, VAP), urinary tract infections, meningitis, bacteremia, and gastrointestinal and skin/wound infections [3,4,5,6,7]. Increased incidence of carbapenem resistant A. baumannii isolates has been observed in Northern and Eastern. Carbapenems were the preferred treatment of multidrug resistant (MDR) A. baumannii infections, but their prior use has led to increased incidence of carbapenem resistance during the last years [12].
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