A Comprehensive Study of the Relationship between the Production of β-Lactamase Enzymes and Iron/Siderophore Uptake Regulatory Genes in Clinical Isolates of Acinetobacter baumannii

Abstract

Background.The iron/siderophore uptake system (IUS) involved in the Acinetobacter baumannii pathogenicity. However, IUS’s role in antibiotic resistance and the production of β-lactamase enzymes of A. baumannii are unclear. This study aimed to investigate the relationship between the production of β-lactamase enzymes and IUS regulatory genes in clinical isolates of A. baumannii. Methods. A. baumannii isolates were collected from clinical isolates using biochemical tests. The antibiotic resistance patterns and β-lactamase-producing strains were identified using the disk diffusion method (DDM). Also, IUS genes were detected by the polymerase chain reaction (PCR) method. Results. Seventy-two (72) A. baumannii isolates were collected from a different clinical specimen. Gentamicin-resistant strains (43%) had the highest frequency, and aztreonam-resistant strains (12.5%) had the lowest frequency. Also, the distribution of AmpC and MBL producing isolates were 27.7% and 35%, respectively. Moreover, the frequencies of basD, bauA, pld, paaE, entA, feoB, hemO, and tonB genes were as follows: 12.5%, 15.2%, 11.1%, 15.2%, 19.4%, 16.6%, 23.6%, and 6.9%. Further, a strong correlation was observed between the abundance of β-lactamase-producing strains and IUS genes. Conclusions. Based on our knowledge from this study, the association between β-lactamase production and IUS genes in A. baumannii plays an essential role in the emergence of drug-resistant strains.

Detection of blaOXA-145, blaOXA-224, blaOXA-539, and blaOXA-675 Genes and Carbapenem-Hydrolyzing Class D β-Lactamases (CHDLs) in Clinical Isolates of Pseudomonas aeruginosa Collected from West of Iran, Hamadan

“…The zone of inhibition was compared with each other. P. aeruginosa ATCC 15442 was used as a positive control, and P. aeruginosa PAO-1 was used as a negative control [ 1 , 4 ].…”

“…Hydrophobic drugs enter bacterial cells through the phospholipid layer, while hydrophilic drugs enter through porins in Gram-negative bacteria (GNB) [ 1 , 2 ]. Some bacterial species, such as Pseudomonas aeruginosa , have an outer membrane that is less porous than other species, causing the bacteria to be less susceptible to antimicrobial agents [ 3 , 4 ].…”

Antibacterial activity of curcumin and its essential nanoformulations against some clinically important bacterial pathogens: A comprehensive review

“…baumannii is a Gram-negative bacterium with nonfermentative capability, an opportunistic pathogen, and can cause fatal contaminations in the immunodeficient and the severely ill. A. baumannii exhibits resistance to numerous antimicrobial compounds and has the potential to escape the effects of most antibiotics through a union of enzymatic inactivation (β-lactamases, aminoglycoside modifying enzymes), impermeability (porin loss), chromosomal mutations, and active efflux of drugs. 21,124,125 As a result of the absence of new synthetic antimicrobials, much importance is given on natural compounds like curcumin with potential and broad-spectrum antibacterial activity. In connection to this, Betts and Wareham 126 reported that curcumin (256 μg/ml) along with epigallocatechin-3-gallate could effectively kill A. baumannii due to synergistic mechanism and disordering of the Gram-negative outer membrane combined with inhibition of important proteins.…”

“…[110][111][112][113][114][115][116][117][118][119][120] Antibacterial activity of curcumin and its nanoconjugates against A. baumannii is mediated by ROS building, disruption of outer membrane, inhibition of drug efflux pumps, and biofilm response regulator. [122][123][124][125][126][127][128] Curcumin and its various nanoformulations exhibit efficient antibacterial activity against S. mutans in the presence of blue light PDT by ROS generation and bacterial membrane impairment. [131][132][133][134][135][136][137][138][139][140][141][142][143] H. pylori infection and associated gastroduodenal inflammation can be inhibited by curcumin and its essential nanoformulations through inhibition of both NF-ƙB activation, motogenic response, inhibition of inhibitors of NF-κB degradation, and IκB kinase activation, and downregulation of the expression of inflammatory chemokines, inflammatory cytokines, and Toll-like receptors.…”

“…In case of MTB infection, curcumin and its important nanoformulations can cure tuberculosis by directly inhibiting MTB growth as well as modulating the host immune response for immune‐mediated MTB clearance 110–120 . Antibacterial activity of curcumin and its nanoconjugates against A. baumannii is mediated by ROS building, disruption of outer membrane, inhibition of drug efflux pumps, and biofilm response regulator 122–128 . Curcumin and its various nanoformulations exhibit efficient antibacterial activity against S. mutans in the presence of blue light PDT by ROS generation and bacterial membrane impairment 131–143 .…”