Acinetobacter baumannii: an evolving and cunning opponent

Abstract

Acinetobacter baumannii is one of the most common multidrug-resistant pathogens causing nosocomial infections. The prevalence of multidrug-resistant A. baumannii infections is increasing because of several factors, including unregulated antibiotic use. A. baumannii drug resistance rate is high; in particular, its resistance rates for tigecycline and polymyxin—the drugs of last resort for extensively drug-resistant A. baumannii—has been increasing annually. Patients with a severe infection of extensively antibiotic-resistant A. baumannii demonstrate a high mortality rate along with a poor prognosis, which makes treating them challenging. Through carbapenem enzyme production and other relevant mechanisms, A. baumannii has rapidly acquired a strong resistance to carbapenem antibiotics—once considered a class of strong antibacterials for A. baumannii infection treatment. Therefore, understanding the resistance mechanism of A. baumannii is particularly crucial. This review summarizes mechanisms underlying common antimicrobial resistance in A. baumannii, particularly those underlying tigecycline and polymyxin resistance. This review will serve as a reference for reasonable antibiotic use at clinics, as well as new antibiotic development.

First Report of Ocellatin-VT from the Skin Secretion of Leptodactylus vastus Lutz (Amphibia: Leptodactylidae)

“…A. baumannii is responsible for several cases of nosocomial infections and has become one of the most common MDR pathogens, also causing great concern because of its resistance to the last resort drugs tigecycline and polymyxin [31]. Finding new potential antibiotics against this bacterium is a priority in biomedicine and biotechnology [32].…”

Pan-Genome Plasticity and Virulence Factors: A Natural Treasure Trove for Acinetobacter baumannii

“…In this regard, LPS modification or mutation in LPS bisynthesis genes, efflux pumps (promoted efflux), outer membrane proteins (OMPs/porins) (decrease in OMPs’ permeability) and secretion systems (T2SS, T4SS and T6SS) contribute to antibiotic resistance through transportation via bacterial cell membranes; antibiotic inactivation via enzymes (e.g., monooxygenase and β-lactamase enzymes); alterations and modifications in antibiotic target sites, such as mutations in antibiotic target enzymes (including DNA gyrase (single mutations in parC (topoisomerase IV encoding gene)) and/or in gyrA (DNA topoisomerase IV encoding gene) against fluoroquinolones), mutations in Penicillin-binding proteins (PBPs)), ribosomal protection proteins (RPPs) in the occurrence of non-covalent modifications of bacterial ribosomes against antibiotics (e.g., tetracycline), production of ribosome methylase enzymes (via plasmid-transposon-borne genes) against lincosamides, and 16S rRNA methylase enzymes against aminoglycosides. Plasmids are important MGEs directly participating in antibiotic-resistant genes via HGTs [ 3 , 62 , 63 , 64 , 65 ].…”

A review on drug resistance patho-mechanisms in ESKAPE bacterial pathogens

“…This species exhibits a high propensity for incorporating foreign DNA through a horizontal gene transfer. Consequently, Acinetobacter baumannii often possesses a substantial number of β-lactamases due to its ability to integrate exogenous genetic materials (Shi et al, 2024). β-lactamases of class A are inhibited by clavulanate, penicillins, and cephalosporins, and they cause β-lactam resistance.…”