Acinetobacter baumannii (A. baumannii) is an important Gram-negative pathogenic bacterium, widely distributed in nature[1]. A. baumannii can cause infections of the skin and soft tissue, urinary tract infections, meningitis, bacteremia, and pneumonia, and is less frequently involved in community-acquired infections among predisposed patients[2]. Currently, clinical A. baumannii isolates usually display resistance to all first-line antibiotics, and in many cases, polymyxins, tigecycline, and ampicillin/sulbactam have become the last resort of treatment for extensively drug-resistant isolates[3]. This has led the World Health Organization to classify carbapenem-resistant A. baumannii as a “critical” pathogen among the antibiotic-resistant bacteria of global priority[4].
The global dissemination of A. baumannii is driven by three major international clonal (ICs) lineages, and six additional epidemic clonal lineages. The epidemic A. baumannii lineages are frequently resistant to a broad range of antimicrobials[5]. Moreover, they possess virulence traits which stimulate biofilm growth on abiotic surfaces, tolerance to desiccation, and adherence to human epithelial cells, and contribute to their persistence in the hospital environment and spread among infected patients. ICs 1 and 2 show extensive global dissemination in more than 30 countries, supplemented by a significant repertoire of antimicrobial resistance determinants[6]. IC2 isolates frequently showed higher resistance rates to all antimicrobial agents than the other genotypes, and IC2 is characterized by the acquisition of carbapenem resistance. IC3 in the last decade seems to be less prevalent, with a rather low number of reports worldwide, which were associated with non-human origin[7]. IC5 is the prevalent clonal lineage found in Latin America. Isolates belonging to IC5 presented a broader spectrum of acquired antimicrobial resistance determinants compared to IC4. IC6 was mostly reported in Russia, Belarus, Italy, and South American countries. IC7 was reported in different regions of the world, including Europe, Asia, and North and South America. IC8 A. baumannii clones were documented as single (sporadic) isolates in India, Afghanistan, Germany, Bangladesh, China, and the Philippines[8]. IC9 is currently more specific to the Middle East and North Africa.
A. baumannii has strong invasive virulence factors, such as outer membrane proteins, lipopolysaccharides, and phospholipases. The outer membrane protein A (OmpA) has been demonstrated to bind host epithelial cells and primary monocyte-derived macrophages, translocate into the nucleus by a novel monopartite nuclear localization signal, and induce cell death of host cells in vitro. OmpA has also been shown to stimulate ROS production originating from mitochondria and induces early-onset apoptosis and delayed-onset necrosis in dendritic cells. Phospholipase C (PLC), a key enzyme produced by nosocomial pathogens, catalyzes the breakdown of phospholipids[9], primarily degrading the host cell membrane or mucosal barrier phospholipids, thus causing diseases[10]. Phospholipase D (PLD), a secretory protein, contains two active sites and catalyzes the conversion of phosphatidylcholine to phospholipids acid and choline, thereby enabling bacteria to penetrate deep into the host tissue to evade host attacks[11].
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