Abstract
Acinetobacter baumannii is an opportunistic pathogen which is undoubtedly known for a high rate of morbidity and mortality in hospital-acquired infections. A. baumannii causes life-threatening infections, including; ventilator-associated pneumonia (VAP), meningitis, bacteremia, and wound and urinary tract infections (UTI). In 2017, the World Health Organization listed A. baumannii as a priority-1 pathogen. The prevalence of A. baumannii infections and outbreaks emphasizes the direct need for the use of effective therapeutic agents for treating such infections. Available antimicrobials, such as; carbapenems, tigecycline, and colistins have insufficient effectiveness due to the appearance of multidrug-resistant strains, accentuating the need for alternative and novel therapeutic remedies. To understand and overcome this menace, the knowledge of recent discoveries on the virulence factors of A. baumannii is needed. Herein, we summarized the role of various virulence factors, including; outer membrane proteins, efflux pumps, biofilm, penicillin-binding proteins, and siderophores/iron acquisition systems. We reviewed the recent scientific literature on different A. baumannii virulence factors and the effective antimicrobial agents for the treatment and management of bacterial infections.
Highlights
Acinetobacter baumannii are non-motile, aerobic Gram-negative, glucose non-fermentative, catalase-positive, non-fastidious, oxidative-negative coccobacilli [1].The phylogenetic classification and interpretation of the taxonomy of the genus Acinetobacterhas established over 60 known species within the genus (Figure 1) [2]
A. baumannii is associated with hospital-acquired infections (HAI) world wide [3]
Hospital-acquired pneumonia, meningitis, and skin and soft tissue infections are amongst the diverse infections caused by A. baumannii [4]
Summary
Acinetobacter baumannii are non-motile, aerobic Gram-negative, glucose non-fermentative, catalase-positive, non-fastidious, oxidative-negative coccobacilli [1]. Animal infection models have reported A. baumannii strains with increased pathogenicity [10,11]. This might be due to phenotypic and genetic adaptations that could increase the resistance and virulence potential of A. baumannii [12,13]. K1 surface antigen protein 1, acinetobactin transporters, capsular polysaccharides, outer membrane porins, and iron acquisition systems are some of the factors which, along with acquired antibiotics resistance, have promoted A. baumannii as a significant nosocomial pathogen [17,18]. A. baumannii has been reported to have a range of virulence genes that code for biofilmformation and its adherence on biotic and abiotic surfaces [19]. We review the virulence factors of A. baumannii to assess the relationships between antimicrobial resistance, virulence, and the therapeutic options
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