The study identifies that metronidazole resistance in Helicobacter pylori NCTC11637 is caused by the inactivation of the rdxA gene through the insertion of mini-IS605 and deletion of adjacent sequences.

The study identifies three enzymes involved in the reductive activation of nitazoxanide, nitrofurans, and metronidazole in Helicobacter pylori: RdxA, FrxA, and Por. These enzymes play a critical role in the antimicrobial activity of these drugs.

The study identified mutations in the rdxA and frxA genes as contributing to metronidazole resistance in Helicobacter pylori, with some cases showing resistance without mutations in these genes.

The paper discusses the molecular mechanisms of antibiotic resistance in Helicobacter pylori, focusing on mutations in the 23S rRNA gene, rdxA, frxA, PBP1, and PBP4 that confer resistance to clarithromycin, metronidazole, and amoxicillin.

The study identified rdxA gene mutations as a key factor in metronidazole resistance among Helicobacter pylori strains in The Gambia.

The study identifies the rdxA gene in Helicobacter bizzozeronii as a contingency gene involved in metronidazole resistance through a frame length extension of the C-terminal cysteine-containing conserved region. Loss of function mutations in rdxA, particularly the disruption of the conserved region IACLXALGK, are sufficient to produce clinically significant resistance to metronidazole.

The study validated a high-throughput multiplex genetic detection system (HMGS) for identifying, quantifying, and analyzing virulence and drug resistance genes in Helicobacter pylori. Four drug resistance genes (23S rRNA, rdxA, gyrA, and pbp1A) were characterized for their roles in resistance to clarithromycin, metronidazole, levofloxacin, and amoxicillin, respectively.

The study identified mutations in gyrA and gyrB associated with levofloxacin resistance and a mutation in frxA associated with metronidazole resistance in Helicobacter pylori.

Mutational inactivation of rdxA and frxA and point mutations in the 23S rRNA are the primary causes of metronidazole and clarithromycin resistance in H. pylori. Overexpression of the efflux pump gene hefA contributes to multidrug resistance.

The study identified genetic determinants of antibiotic resistance in Cambodian Helicobacter pylori clinical isolates, including mutations in 23S rRNA for clarithromycin resistance, gyrA for levofloxacin resistance, pbp1 for amoxicillin resistance, and rdxA for metronidazole resistance.

The study identifies several genes and mutations associated with antimicrobial resistance in H. pylori, including rdxA and frxA for metronidazole resistance, 23S rRNA for clarithromycin resistance, gyrA for levofloxacin resistance, and rpoB for rifampicin resistance.

The study identified various AMR genes and mutations in H. pylori isolates, including 23S rRNA mutations for clarithromycin resistance, gyrA mutations for levofloxacin resistance, pbp1, pbp2, and pbp3 mutations for amoxicillin resistance, rdxA mutations for metronidazole resistance, 16S rRNA mutations for tetracycline resistance, and rpoB mutations for rifampin resistance.

The study identified antibiotic resistance genes rdxA, pbp1A, gyrA, and cla in Helicobacter pylori isolates from raw meat, contributing to resistance against metronidazole, amoxicillin, levofloxacin, and clarithromycin.

The study identified several genes and mutations associated with antimicrobial resistance in Helicobacter pylori clinical isolates from the Democratic Republic of Congo, including pbp1A, 23S_rRNA, gyrA, gyrB, rdxA, and frxA, which are linked to resistance against amoxicillin, clarithromycin, levofloxacin, and metronidazole.

The study identified mutations in 23S rRNA, gyrA, and rdxA genes associated with resistance to clarithromycin, levofloxacin, and metronidazole in Helicobacter pylori strains from Mexico. The prevalence of these mutations varied over time and between different populations.

The study identifies FBPAII and rpoBC as novel secreted proteins in antibiotic-sensitive Helicobacter pylori strains, highlighting their potential roles in antibiotic resistance mechanisms.

The study shows that increasing the temperature to 41°C reduces metronidazole resistance in Helicobacter pylori, with significant downregulation of rdxA and sod genes, and upregulation of fur.

The study compared culture-based and molecular-based susceptibility testing for six antibiotics in H. pylori using clinical isolates and formalin-fixed, paraffin-embedded gastric biopsies. It found that next-generation sequencing accurately predicted resistance to clarithromycin, levofloxacin, rifabutin, and tetracycline, while showing fair agreement for metronidazole and amoxicillin.

The study identified several mutations in genes associated with antibiotic resistance in Helicobacter pylori isolates from Myanmar, including pbp1-A for amoxicillin, 23S rRNA for clarithromycin, gyrA and gyrB for levofloxacin, and rdxA and frxA for metronidazole.

The study identified mutations in 23S rRNA, PBP-1A, gyrA, and rdxA genes in H. pylori strains, which were associated with resistance to clarithromycin, amoxicillin, levofloxacin, and metronidazole, respectively.

The study identified several AMR genes and mutations in H. pylori strains associated with resistance to clarithromycin, levofloxacin, and metronidazole. Key findings include mutations in 23S rRNA, gyrA, gyrB, rdxA, frxA, and fdxB genes that confer resistance to these antibiotics.

The study identified mutations in GyrA, GyrB, Pbp1, rdxA, and 23S rRNA as the genetic determinants of resistance to levofloxacin, amoxicillin, metronidazole, and clarithromycin in Helicobacter pylori clinical isolates.

Jinghua Weikang capsule (JWC) reverses metronidazole (MTZ) resistance in H. pylori 26,695–16R by targeting biofilm formation and efflux pump gene expression. A G210T point mutation in the rdxA gene was identified as the cause of MTZ resistance.

The study identified a high prevalence of metronidazole resistance in H. pylori isolates from Morocco, with 62.7% of isolates showing resistance. Deletions in the rdxA gene were associated with metronidazole resistance.

The paper discusses the mechanisms of antibiotic resistance in Helicobacter pylori, focusing on genes and mutations associated with resistance to amoxicillin, clarithromycin, furazolidone, levofloxacin, and metronidazole. Key findings include the identification of specific mutations in 23S rRNA, gyrA, gyrB, PBP1A, porD, oorD, RdxA, and other genes that contribute to resistance against these antibiotics.

The study identified antibiotic resistance genes such as gyrA, cmeDEF, rdxA, and frxA in Helicobacter pylori strains from Pakistan, highlighting the prevalence of resistance to metronidazole, clarithromycin, and levofloxacin.

The study developed a next-generation sequencing panel (NGS-PHET) to identify antibiotic resistance genes and mutations in Helicobacter pylori, enabling personalized eradication treatment. Key findings include resistance-conferring variants in hprrna23s, hprrna16s, pbp1, rdxa, frxa, frxb, gyra, and gyrb, along with caga positivity.

The study identified a high prevalence of metronidazole resistance in Helicobacter pylori isolates from Moroccan children, primarily due to mutations in the rdxA gene.

The study identified several AMR genes and mutations in H. pylori strains from Hainan Province, China, including 23S rRNA (A2143G) for clarithromycin resistance, gyrA (N87K, D91N) for levofloxacin resistance, rdxA (R16H/C, M21A) for metronidazole resistance, pbp1A (Thr593Ala, Thr556Ser, Asn562Tyr, Phe366Leu, Val374Leu, Ser414Arg) for amoxicillin resistance, 16S rRNA (AGA926_928>GGA, AGA926_928>AGC, AGA926_928>GGC, AGA926_928>TGA) for tetracycline resistance, porD (A356G, C357T, G353A) and oorD (A41G, A122G, A335G, C349A, C349G) for furazolidone resistance.

The study developed a machine learning model to predict antibiotic resistance in Helicobacter pylori using genome-wide genetic variation data, identifying key mutations and genes associated with resistance to metronidazole, clarithromycin, levofloxacin, amoxicillin, and multidrug resistance.

The study identified various mutations in the gyrA and rdxA genes associated with resistance to fluoroquinolones and metronidazole in Helicobacter pylori, respectively. These mutations were analyzed through in silico methods to understand their potential roles in antibiotic resistance.

The study identified several mutations in 23S rRNA, gyrA, pbp1 A, and rdxA genes associated with resistance to clarithromycin, levofloxacin, amoxicillin, and metronidazole in H. pylori isolates from Vietnam.

The study identified several AMR genes and mutations in 141 clinical Helicobacter pylori isolates from Eastern China, including 23S rRNA (A2143G), infB (C110T), gyrA (T261A), gyrB (G1033A), pbp1A (1785_1786insAGC), rdxA (G278A), frxA (T184A), recA (G946A), 16S rRNA (A928C), and oorD (G22A) associated with resistance to clarithromycin, levofloxacin, amoxicillin, metronidazole, tetracycline, and furazolidone.