The critical role of the T6SS in the drug resistance and pathogenicity of A. baumannii necessitates strengthened surveillance and the prompt implementation of effective measures.
Abstract
The Type VI secretion system (T6SS) is a multi-component transmembrane apparatus that is crucial for substance acquisition and pathogenicity of bacteria. In this study we investigated Acinetobacter baumannii, a causative agent of bacteremia, to explore the mechanisms of T6SS in drug resistance and pathogenicity by contrasting virulence, drug sensitivity, conjugation, transformation, competition, and cell adhesion capacities. A total of 136 non-repetitive A. baumannii strains were collected, and 80.1% of patients received treatment in intensive care unit. Forty strains (29.4%) were classified as hypervirulent A. baumannii (hvAB), which exhibited a higher prevalence of the virulence gene abaI, a reduced capacity for biofilm formation, and a lower prevalence of the outer membrane protein gene carO. T6SS-positive strains exhibited enhanced antimicrobial resistance, elevated frequencies of resistance genes (blaOXA−23−like, blaTEM, adeB, adeR, adeS) and the virulence gene csuE. Differences were observed between strains with T6SS deletion and those with an intact T6SS concerning the HigAB toxin-antitoxin system and the RSF1010-like IncQ plasmid. T6SS may down-regulate the expression of effector genes due to the insertion sequence ISAba13. The critical role of the T6SS in the drug resistance and pathogenicity of A. baumannii necessitates strengthened surveillance and the prompt implementation of effective measures.
It is suggested that the abaI gene boosts capsule production and pathogenicity of A. baumannii, providing new insights for clinical management of drug-resistant A. baumannii diseases and a foundation for new antimicrobial drugs.
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