To better understand the genetic reasons causing Acinetobacter baumannii's growing resistance to antimicrobial drugs, particularly carbapenems, more research is required. With an emphasis on the genes and mutations that make up this resistance, as well as the function of mobile and proprietary genetic elements in transmitting and sustaining resistance, this study attempts to present a comprehensive review of the scientific literature on the molecular analysis of gene clusters linked to carbapenem resistance in this bacterial family. The study used data from clinical colonies and a thorough review of published literature from around the world. It examined the genetic distribution and variety of resistance gene clusters, found related genetic clusters, and talked about the distinctions between chromosome-based and plasmid-inoculated resistance factors using genetic and genomic analysis methods and techniques. Additionally, the study looked at the combined analysis of factors that enhance susceptibility to infection, such as inflammatory or harmful factors, and resistance factors. According to the findings, the most common beta-lactamase genes are blaOXA-type ones, especially blaOXA-23 and blaOXA-51-like. These genes frequently co-occur with other resistance genes and novel variations, demonstrating the diversity and ongoing development of resistance genes. With the common presence of elements like ISAba1, which increases the expression of carbapenemase genes, mobile genetic elements—such as transposons, mutants, and plasmids—play a crucial role in the transfer and expression of resistance genes. The majority are represented by global genotypes, especially the IC2/ST2 clinical lines, while the appearance of novel variants underscores the shifting epidemiological dynamics. In addition to chromosomal inactivation, horizontal gene dissemination on plasmids is linked to the broader spread of resistance, which is most likely the result of stable gene expression. Research has also shown that resistance genes work in concert with inflammatory and infectious characteristics, like genes that create biofilms and capsules, to increase the pathogenic potential of bacteria. In summary, this review offers a thorough understanding of the genetic composition and mechanisms underlying the bacterium's resistance to carbapenem, highlighting the significance of implementing unified surveillance, genomic, and sequence analysis strategies as crucial instruments for more effective treatment and infection control choices.
Marhoon et al. (Tue,) studied this question.