Helicobacter pylori detection and susceptibility profile using feces could optimize guided therapy, when endoscopy is not necessary. This study evaluated the performances of three tests: AllPlexH.pylori&ClariR, RIDAGENEHelicobacterpylori and AmplidiagH.pylori+ClariR assays on stool samples. Stool samples from a documented cohort (50 positive and 25 negative) were analyzed. The gold standard was a composite based on PCR targeting H. pylori and 23S rDNA mutations (A2142C, A2142G, A2143G) on gastric biopsies; and biopsy culture for H.pylori and susceptibility testing. For AllPlex, RidaGene and Amplidiag assays respectively: 55 (73.3%), 75 (100%), 54 (72%) samples could be analyzed; (for detection of H. pylori), sensitivity was 36% (95%CI]28;52%[); 32% (95%CI]21;46%[) and 93% (95%CI]87;100%[); specificity was 100% (95%CI]81;100%[), 83% (95%CI]68;91%[) and 57% (95%CI]33;79%[). (for the Clarithromycin resistance), sensitivity was 18% (95%CI]5;48%[), 25% (95%CI]9;53%[) and 67% (95%CI]39;86%[); specificity was 100% (95%CI]92;100%[). 92% (95%CI]83;97%[) and 97% (95%CI]89;99%[). Innovative technologies could become invaluable tools for mass testing after improvement.

Helicobacter pylori strains containing the cag pathogenicity island (PAI) deliver an effector protein (CagA) and non-protein substrates into gastric cells through a process that requires the Cag type IV secretion system (T4SS). The Cag T4SS outer membrane core complex (OMCC) contains multiple copies of five proteins, two of which are species-specific proteins. By using modifications of a previously described OMCC immunopurification method and optimized mass spectrometric methods, we have now isolated additional cag PAI-encoded proteins that are present in lower relative abundance. Four of these proteins (CagW, CagL, CagI, and CagH) do not exhibit sequence relatedness to T4SS components in other bacterial species. Size exclusion chromatography analysis of immunopurified samples revealed that CagW, CagL, CagI, and CagH co-elute with OMCC components. These four Cag proteins are copurified with the OMCC in immunopurifications from a Δcag3 mutant strain (lacking peripheral OMCC components), but not from a ΔcagX mutant strain (defective in OMCC assembly). Negative stain electron microscopy analysis indicated that OMCC preparations isolated from ΔcagW, cagL::kan, ΔcagI, and ΔcagH mutant strains are indistinguishable from wild-type OMCCs. In summary, by using several complementary methods, we have identified multiple species-specific Cag proteins that are associated with the Cag T4SS OMCC and are required for T4SS activity.

Helicobacter pylori (H. pylori) infection remains a significant public health concern in developing countries, especially among pediatric populations where data are limited. In war-torn regions like the Eastern Democratic Republic of Congo, the impact of H. pylori infection on children's health may be exacerbated due to disrupted healthcare systems and limited resources.

This mixed-methods study, incorporating both cross-sectional and prospective cohort designs, was conducted at Samaritan Doctor's Pediatric Centre between January 2020 and December 2022. The study enrolled 323 children aged 0 to 15 years presenting with gastrointestinal symptoms. Sociodemographic and clinical characteristics were assessed via questionnaire, and H. pylori stool antigen rapid tests were performed. Multivariate regression analyses were conducted. Participants were followed up and outcomes recorded after 30 days.

Of the 323 participants, 119 (36.80%) tested positive for H. pylori infection. Independent factors associated with H. pylori infection included age between 37 and 59 months (aOR: 9.76, 95% CI: 2.62-36.40, p = 0.001), caretaker's occupation (aOR: 2.58, 95% CI: 1.19-5.54, p = 0.016), presence of pets at home (aOR: 0.371, 95% CI: 0.18-0.74, p = 0.005), drinking unsafe water (aOR: 0.13, 95% CI: 0.04-0.42, p = 0.001), anemia (aOR: 4.80, 95% CI: 1.12-20.53, p = 0.034), and presence of red blood cells in stool (aOR: 30.84, 95% CI: 13.97-68.10, p < 0.0001). Thirty days post-initial treatment with first-line medications (omeprazole, clarithromycin, and amoxicillin), 19.30% of patients remained positive for H. pylori.

Children with occult blood in stool and microcytic anemia should be tested for H. pylori using stool antigen tests. Treatment with clarithromycin should be guided by local antibiotic resistance data. Hygiene education, including safe water practices and managing pet contact, is crucial due to their association with H. pylori infection.

Helicobacter pylori (H. pylori) infection affects around half of the global population and is a globally highly prevalent pathogen that is closely linked not only to gastrointestinal diseases such as chronic atrophic gastritis, functional dyspepsia and peptic ulcer but also to the development and progression of a variety of extra-gastrointestinal diseases. Numerous studies have shown the correlation between H. pylori infection and iron-deficiency anemia (IDA). The prevalence of H. pylori infection is higher in individuals with IDA, and the hemoglobin level of patients with IDA can be increased to different degrees or even returned to normal following active H. pylori eradication. However, this conclusion is still controversial. In this paper, a comprehensive literature search was conducted using the PubMed/MEDLINE/Web of Science database, combining the following terms: "Helicobacter pylori," "Helicobacter pylori infection," "iron deficiency anemia," "iron deficiency," "iron absorption," "iron malabsorption," "serum iron," "hemoglobin," "pathogenesis," "mechanism," and "eradication therapy." Through extensive literature searches, the correlation between H. pylori infection and IDA, its potential mechanism, and the efficacy of H. pylori eradication therapy in IDA patients have been comprehensively discussed. We conclude that the majority of existing studies have confirmed the correlation between H. pylori infection and IDA, indicating that patients with H. pylori infection are more likely to develop IDA and that the prevalence of H. pylori infection is higher in individuals with IDA. Compared with iron supplementation alone, combining H. pylori eradication with iron supplementation is more effective in treating IDA, particularly in unexplained or refractory IDA cases. These findings provide valuable insights for clinicians managing patients with unexplained or refractory IDA.

Gastric cancer and ulcers are responsible for almost 1 million deaths globally each year, disproportionately affecting low- and middle-income populations. Helicobacter pylori (H. pylori) infection is a major risk factor for both gastric cancer and peptic ulcers, with infection rates surpassing 70% in developing countries and reaching 88% in Jordan. Despite strong evidence linking H. pylori infection to gastric cancer, particularly with CagA-positive strains, public awareness of H. pylori infection, its transmission routes, and associated health risks remains insufficient.

This study aimed to assess the knowledge, attitudes, and practices (KAP) related to H. pylori-induced stomach ulcers and cancer in a Jordanian population, focusing on early detection and eradication efforts. A survey was administered to 398 participants to evaluate their understanding of H. pylori and its role in gastric disease.

The findings revealed that 64.3% of respondents were aware of H. pylori, with 75.9% recognizing its association with gastric ulcers. However, awareness of the transmission routes and potential complications is limited. The frequent use of antacids for symptom relief also highlights the need for better awareness of appropriate treatments.

Public health education targeting these knowledge gaps could help reduce the incidence of H. pylori-related complications, including gastric cancer, especially in high-prevalence areas such as Jordan. Addressing these deficits and promoting preventive strategies, such as improved hygiene and regular medical check-ups, could facilitate early detection and improve health outcomes for individuals at risk of H. pylori-induced infection.

Recent studies have shown a noticeable increase in global Helicobacter pylori (H. pylori) resistance, with clarithromycin resistance surpassing 15% in various areas. However, inadequate epidemiological monitoring, especially in developing countries, and the absence of uniform testing methods lead to discrepancies between regions and a possible underestimation of resistance levels. The complexity of treating H. pylori is driven by its highly dynamic genome, which is prone to frequent mutations contributing to phenotypical resistance. The usual course of action in empirical treatment involves using a combination of various drugs simultaneously, leading to significant resistance selection pressure and potential side effects. The emergence of H. pylori strains resistant to multiple drugs is closely tied to failures in first-line treatment, highlighting the need to prevent further resistance by using optimal initial empirical therapy or regimens guided by antibiotic susceptibility testing, requiring a collection of mixed samples and multiple isolates for accurate assessment. The emergence of new treatments like potassium-competitive acid blockers offers a hopeful approach to decrease antimicrobial usage while still ensuring effectiveness in comparison to traditional therapies with proton pump inhibitors. Additionally, the use of probiotics is under investigation to identify specific strains and formulations that may mitigate therapy-associated adverse effects.

Helicobacter pylori, causing chronic systemic infection, may colonize in middle ear milieu and conduce to effusion collection. Many investigations on relationship between pathogenesis of otitis media with effusion (OME) and Helicobacter pylori yielded conflicting results. We investigated Helicobacter pylori presence in effusion and adenoid samples of children having OME and in middle ear and adenoid samples of children with healthy middle ears to elucidate its role on OME pathogenesis.

This prospective case-control study included 300 patients aged 1-12 years. One-hundred effusion samples collected from 100 children undergoing ventilation tube insertion and adenoidectomy due to chronic OME and adenoid hypertrophy formed study group, and 100 adenoid samples collected from adenoids of these children formed Group-1. One-hundred healthy-looking middle ear irrigation solutions collected from 100 children undergoing cochlear implantation formed Group-2. One-hundred adenoid samples collected from 100 children having no effusion and only undergoing adenoidectomy formed Group-3. After DNA isolation of samples, Helicobacter pylori 16 S rRNA and 23 S rRNA gene for clarithromycin-resistance were investigated by real time-polymerase chain reaction (Rt-PCR).

The median age of 300 children was 5, and 179 were boys and 121 were girls. Helicobacter pylori was detected by Rt-PCR in none (%0) of the 400 samples (200 middle ear, 200 adenoid).

In this largest sample-size study utilizing updated molecular methods to date, negative results indicate that Helicobacter pylori does not play role as an active pathogen in polymicrobiality of OME, and adenoids do not serve as a reservoir for Helicobacter pylori in this process.

Gastric cancer is highly correlated with Helicobacter pylori (H. pylori) infection. Approximately 50 % of the population worldwide is infected with H. pylori. However, current treatment regimens face severe challenges including drug resistance and gut microbiota disruption. An integrative treatment with slight negative influences on intestinal flora, conforming with concepts of integrative prevention of gastric cancer, is urgently needed. Non-antibiotic responsive biomaterials can respond to different stimuli, including pH, enzymes, light, ultrasound and magnetism, under which biomaterials are specifically activated to perform antibacterial capabilities, while neutral intestinal microenvironments differ from gastric microenvironments or inflammatory sites and have no or minimal irradiation via precisely controlled exogenous stimuli, which may not only overcome antibiotic resistance but also avoid gut microbiota disorders. First, the latest progress in responsive biomaterials against H. pylori without gut microbiome disturbance and their anti-H. pylori performances are profoundly summarized. Second, the mechanisms against planktonic bacteria, biofilms and intracellular bacteria are discussed respectively. Finally, the strategies of specific and targeted H. pylori elimination by responsive biomaterials are introduced. Additionally, the challenges and the focus of future research on translation into clinical application are fully proposed. Antibiotic-free responsive biomaterials for specific and targeted H. pylori eradication represent an innovative approach.

Germ-free mice experiments indicate that human gut microbiota influence blood pressure (BP), but no studies have prospectively examined if infant gut microbiota affects their future childhood BP. We aim to investigate prospective associations of infant gut microbiota diversity and composition with childhood BP, examining effect measure modification by breastfeeding and mediation by a child's body mass index.

In the Copenhagen Prospective Studies on Asthma in Childhood 2010 cohort, we measured infant gut microbiota (16S rRNA V4) at 1 week, 1 month, and 1 year and child BP at 3 and 6 years. We assessed α diversity-BP, β diversity-BP, and microbe abundances-BP associations using linear regression, permutational multivariate analysis of variance, and beta-binomial count regression, respectively. Data from 526 children showed that α diversity and several Bifidobacterium spp. had protective associations with BP but only in children breastfed for ≥6 months. For instance, a 1-unit increment in 1 month Shannon index was associated with 1.86 mm Hg (95% CI, 0.66-3.05) lower 6-year systolic BP in children breastfed ≥6 months but a 0.73 (95% CI, -1.00 to 2.45) higher 6-year systolic BP in those breastfed <6 months (P-interaction=0.02). Greater abundance of 2 Bifidobacterium microbes at 1 week was negatively associated with 6-year systolic BP when breastfeeding ≥6 months (P-interaction<0.1). Further, abundance of 8 microbes at 1week or 1 month was linked to 3-year or 6-year BP (false discovery rate P<0.05), with 5 of them independent of a child's body mass index. Lastly, 1-week unweighted UniFrac distance and 1-year weighted UniFrac distance were associated with BP after adjustment (P<0.05).

Gut microbiota features at 1 week and 1 month of life were associated with BP at 6 years. Breastfeeding duration modified key associations including those for α diversity and Bifidobacteria.

Helicobacter pylori is the primary causative agent of peptic ulcer disease, among other gastrointestinal ailments, and currently affects over half of the global population. Although some treatments exist, growing resistance to these drugs has prompted efforts to develop novel approaches to fighting this pathogen. To generate many of the nucleotides essential to biochemical processes, H. pylori relies exclusively on the de novo biosynthesis of these molecules. Recent drug-discovery efforts have targeted the first committed step of this pathway, catalysed by a class 2 dihydroorotate dehydrogenase (DHODH). However, these initiatives have been limited by the lack of a crystal structure. Here, we detail the crystal structure of H. pylori DHODH (HpDHODH) at 2.25 Å resolution (PDB entry 6b8s). We performed a large-scale bioinformatics search to find evolutionary homologs. Our results indicate that HpDHODH shows high conservation of both sequence and structure in its active site. We identified key polar interactions between the HpDHODH protein and its requisite flavin mononucleotide (FMN) cofactor, identifying amino-acid residues that are critical to its function. Most notably, we found that HpDHODH maintains several structural features that allow it to associate with the inner membrane and utilize ubiquinone to achieve catalytic turnover. We discovered a hydrophobic channel that runs from the putative membrane interface on the N-terminal microdomain to the core of the protein. We predict that this channel establishes a connection between the ubiquinone pool in the membrane and the FMN in the active site. These findings provide a structural explanation for the competitive inhibition of ubiquinone by pyrazole-based compounds that was determined biochemically in other studies. Understanding this mechanism may facilitate the development of new drugs targeting this enzyme and push the effort to find a resistance-free treatment for H. pylori.

Nearly half of the world population is infected by Helicobacter pylori (H. pylori). Bismuth-containing quadruple therapy (BQT) has shown favorable outcomes. This study compares 10-day and 14-day BQT regimens to evaluate their efficacy, safety, and compliance rates.

We searched electronic databases from their inception until May 2024 to retrieve all randomized controlled trials (RCTs) that compared 10-day and 14-day BQT regimens for H. pylori eradication. Meta-analysis was performed using Review Manager 5.4. Dichotomous outcomes were compared using the risk ratio (RR).

Seven RCTs and a total of 2424 patients were included in the meta-analysis. There was no significant difference in the intention-to-treat eradication rate (RR 0.97; 95% CI 0.94, 1.01) and the per-protocol eradication rate (RR 0.96; 95% CI 0.93, 1.00) between the 10-day BQT and 14-day BQT groups. Commonly reported adverse events in both groups were epigastric pain and discomfort, nausea, and vomiting. There was no significant difference in the risk of adverse events between the two groups (RR 0.85; 95% CI 0.70, 1.03). There was no significant difference in the compliance rate between the two groups (RR 1.02; 95% CI 1.00, 1.04).

The eradication rates, risk of adverse events, and compliance rates were comparable between the two groups. Future research comparing similar drug doses with larger sample sizes and longer patient follow-ups can improve the quality of results.

Helicobacter pylori (H. pylori) infection have been closely associated with several extra-gastrointestinal disorders. Outer membrane vesicles (OMVs), as lipid-membrane-bounded nanoparticles, are usually shed from Gram-negative both in vitro and in vivo. H. pylori is also capable of producing OMVs, which can enter the systemic circulation and be delivered to various cells, tissues or organs, eliciting a range of inflammatory and immune modulation responses. In this current review, we summarize the biogenesis and functions of H. pylori OMVs, describe the contribution of H. pylori OMVs to the generation and progression of extra-gastrointestinal diseases, such as neuronal damage, Alzheimer disease, hepatic fibrosis and atherosclerosis. We also explored the effect of H. pylori OMVs in inflammatory and immune modulation of diverse immune cells, including macrophages, mononuclear cells and dendritic cells. By elucidating the molecular mechanism of H. pylori OMVs-mediated extra-gastrointestinal diseases and immunomodulatory effect, it may promote the development of efficient treatments and vaccinations against H. pylori.

Helicobacter pylori (H. pylori) infection is one of the major risk factors of stomach cancer. Strains carrying the oncogenic cytotoxin CagA (cytotoxin-associated gene A) induce epithelial-mesenchymal transition (EMT) and contribute to tumor progression and metastasis. However, the mechanism in which CagA induces EMT has not been defined. In this study, using genetic methods in Drosophila, we identified Semaphorin 5A (SEMA5A) as a new target for CagA. We showed that infection with CagA-positive H. pylori downregulated the expression level of SEMA5A to induce expression of EMT-driving transcription factor Snail and mesenchymal marker N-cadherin, and promote invasive behavior in gastric epithelial cells. Furthermore, we demonstrated that transient over-expression of SEMA5A in H. pylori-infected cells inhibited CagA-mediated gain of mesenchymal phenotype. These results suggest that SEMA5A could be a key mediator of EMT and gastric carcinogenesis caused by CagA-positive H. pylori infection.

Despite a decline in global incidence, gastric cancer (GC) remains a major health concern. The development of GC is a sequential, multistage maladaptive process involving numerous different factors. Understanding the complexity of GC development is crucial for early detection, effective treatment, and, ultimately, prevention. In this respect, identifying the impact of risk factors contributing to the emergence or progression of GC, such as Helicobacter pylori infection, host and bacterial genetics, alcohol consumption, smoking, and preserved foods, will aid in combatting this disease. In this review, we focus on recent developments in understanding the role of the microbiome, dysfunctional molecular pathways, and immune evasion in gastric pathophysiology. We also highlight challenges and advances in treatment of GC.

Sarcina ventriculi (SV) is a Gram-positive cocci that thrives in the acidic stomach environment and may cause gastrointestinal symptoms. A 65-year-old woman with a history of Helicobacter pylori gastritis and diabetes presented with abdominal pain, vomiting, diarrhea, and weight loss. Initial esophagogastroduodenoscopy revealed pyloric stenosis with thickened prepyloric gastric folds, and endoscopic biopsy revealed SV without malignancy. Owing to persistent symptoms, endoscopic ultrasound was done with repeat biopsies and was nondiagnostic. Subsequently, a robotic gastrojejunostomy was done due to persistent gastric outlet obstruction symptoms. Surgical specimens revealed signet ring cell carcinoma. This case highlights the importance of suspecting underlying malignancy in patients with SV and the necessity of comprehensive diagnostic evaluation when endoscopic findings are inconclusive.

Helicobacter infection is a key cause of gastric B cell mucosa-associated lymphoid tissue (MALT) lymphoma. This study examined the role of B cell-activating factor (BAFF), a major driver of B cell proliferation and many B cell disorders, in this malignancy using a model in which conditional knockout mice for NOD-like receptor family CARD domain-containing 5 (Nlrc5) are infected with Helicobacter felis. Gastric BAFF production was significantly increased in H. felis-infected Nlrc5mø-KO mice compared to wild-type. Blocking BAFF signalling, before or after the onset of Helicobacter-induced gastritis, significantly reduced MALT development, with fewer gastric B cell follicles and reduced gland hyperplasia. BAFF blockade also reshaped the immune cell landscape in the stomach, resulting in fewer CD4+ T cells, Tregs, macrophages and dendritic cells. Using a cell culture model, we identified the protein-coding BAFF transcripts that are upregulated in NLRC5-deficient macrophages stimulated with either H. felis or the NLRC5 agonist, lipopolysaccharide. Among the upregulated variants, TNFSF13B (BAFF)-206 acts as a transcription factor and is reported to enhance BAFF production in autoimmune diseases and cancer. Altogether, these findings implicate the NLRC5-BAFF signalling axis in Helicobacter-induced B cell MALT lymphoma, highlighting BAFF inhibition as a potential therapeutic approach.

Helicobacter pylori (H. pylori) infection increases the risks of chronic gastritis, peptic ulcer diseases, and the incidence of gastric cancer. However, antibiotic resistance and adverse effects led to the emergence of alternative treatments such as probiotics supplementation. This systematic review and network meta-analysis aims to assess the efficacy and safety of incorporating probiotics into the various eradication regimens for H. pylori.

We searched PubMed, Embase, Scopus, Cochrane, and Web of Science from inception to May 2023, for randomized controlled trials (RCTs) comparing standard therapy (triple or quadrable therapy). for H. pylori with or without probiotic supplementation. Dichotomous data was reported using an odds ratio (OR) for intention-to-treat (ITT) and risk ratios (RR) for side effects with a 95 % confidence interval (CI).

We included 91 RCTs involving 13,680 patients. Adding probiotics to standard treatment was associated with a higher H. pylori eradication rate in the ITT analysis (78.75 % vs 62.43 %, OR = 1.62, 95 % CI: 1.41 to 1.87, P < 0.0001), and per-protocol (PP) analysis (80.33 % vs 72.63 %, OR = 1.60, 95 % CI: 1.34 to 1.91, P < 0.0001). Meanwhile, dyspepsia, gastric ulcer, and peptic ulcer were comparable in both groups. The probiotics group was associated with significantly fewer side effects including, abdominal pain (RR = 0.68, 95 % CI: 0.54 to 0.86), bad taste (RR = 0.64, 95 % CI: 0.53 to 0.78), diarrhea (RR = 0.49, 95 % CI: 0.40 to 0.61), epigastric pain/bloating (RR = 0.76, 95 % CI: 0.65 to 0.88), headache/dizziness (RR = 0.46, 95 % CI: 0.29 to 0.74), (RR = 0.65, 95 % CI: 0.55 to 0.77), or nausea/vomiting (RR = 0.69, 95 % CI: 0.56 to 0.83). The network meta-analysis showed that, compared to the placebo, Bifidobacterium longum had the highest efficacy in eradicating H. pylori (ITT: 81.06 % vs 64.88 %, PP: 88 % vs 75.71 %) (OR = 2.52, 95 % CI: 1.18 to 5.49).

Adding probiotics to standard H. pylori therapy not only increased the rate of eradication but also reduced some of the adverse reactions throughout therapy, particularly nausea, vomiting, diarrhea, abdominal pain, epigastric pain/bloating, and taste issues.

Helicobacter pylori (HP) is a Gram-negative bacterium that infects approximately fifty percent (50%) of individuals worldwide. The coccoid form of HP, a dormant state with altered morphology, has been associated with persistent infections and antibiotic resistance. This study aimed to investigate the prevalence of the coccoid form of HP in patients living with obesity. Sleeve gastrectomy specimens from obese patients and gastric biopsies from non-obese individuals were analyzed. Immunohistochemistry (IHC) staining and histopathological examination were performed to identify and quantify the coccoid forms of HP. Statistical analysis was conducted to compare the results between the two groups. The study included 53 obese patients and 62 non-obese individuals. The percentage of coccoid forms of HP was significantly higher in obese patients compared to non-obese individuals (median 50% vs. 10%, p < 0.001). Type of gastritis was also significantly different between the groups. Obese patients exhibited a higher prevalence of the coccoid form of HP in their gastric mucosa. This finding suggests that the gastric microenvironment in obesity may favor the formation of the coccoid form, potentially impacting the colonization and pathogenicity of HP. The higher prevalence of the coccoid form in obese patients has important clinical implications, as it is more resistant to antibiotics and difficult to eradicate. Alternative treatment strategies may be necessary to effectively manage HP infections in this population. Furthermore, the presence of the coccoid form may increase the risk of HP-associated diseases in obese individuals. Further research is needed to elucidate the underlying mechanisms and explore novel treatment approaches for HP infection in the context of obesity.

Gastric cancer remains a significant global health challenge, with Helicobacter pylori (H. pylori) recognized as a major etiological agent, affecting an estimated 50% of the world's population. There has been a rapidly expanding knowledge of the molecular and pathogenetic mechanisms of H. pylori over the decades. This review summarizes the latest research advances to elucidate the molecular mechanisms underlying the H. pylori infection in gastric carcinogenesis. Our investigation of the molecular mechanisms reveals a complex network involving STAT3, NF-κB, Hippo, and Wnt/β-catenin pathways, which are dysregulated in gastric cancer caused by H. pylori. Furthermore, we highlight the role of H. pylori in inducing oxidative stress, DNA damage, chronic inflammation, and cell apoptosis-key cellular events that pave the way for carcinogenesis. Emerging evidence also suggests the effect of H. pylori on the tumor microenvironment and its possible implications for cancer immunotherapy. This review synthesizes the current knowledge and identifies gaps that warrant further investigation. Despite the progress in our previous knowledge of the development in H. pylori-induced gastric cancer, a comprehensive investigation of H. pylori's role in gastric cancer is crucial for the advancement of prevention and treatment strategies. By elucidating these mechanisms, we aim to provide a more in-depth insights for the study and prevention of H. pylori-related gastric cancer.

Current evidence on the associations between insulin resistance (IR) and Helicobacter pylori (H. pylori) infection remains limited. This study aimed to investigate the association between non-insulin-based surrogate markers of IR, including the triglyceride glucose (TyG) index, triglyceride to high-density lipoprotein cholesterol (TG/HDL-C) ratio, and the metabolic score for IR (METS-IR), and H. pylori infection in U.S.

This cross-sectional study involving 939 U.S. participants from the National Health and Nutrition Examination Survey (NHANES) 1999-2000. The associations between three IR surrogate markers and H. pylori infection were respectively investigated using logistic regression model, restricted cubic spline (RCS) curve and subgroup analysis.

Three IR surrogate markers levels were significantly elevated in H. pylori infection participants. There was a positive association between three IR surrogate markers and H. pylori infection, even after adjusting for potential confounding variables by three different models. In subgroup analysis, the adjusted association between three IR surrogate markers and H. pylori infection were more likely to be observed in female and Non-Hispanic White. Additionally, the RCS curve revealed a positive linear correlation between TyG index and H. pylori infection across all three models, and between METS-IR and H. pylori infection in Model 3. However, a positive nonlinear correlation was observed between TG/HDL-C ratio and H. pylori infection in all three models.

These findings suggest that non-insulin-based IR surrogate markers including TyG index, TG/HDL-C ratio, and METS-IR were all positively associated with H. pylori infection. These markers may serve as the potential indicators for identifying the risk of H. pylori infection in U.S.

Not applicable.

Gastric cancer (GC) is one of the most common cancers in the world. It is a multi-factorial disease influenced by both genetic and environmental factors such as diet, obesity, radiation exposure, and infectious agents. Viral infections usually lead to chronic inflammation, which can initiate the development of cancers. To date, only a few studies have been published about Epstein-Barr virus (EBV) and human papillomavirus (HPV) infections in the context of the development of GC. In particular, research on the development of cancer among people under 45 years of age, including the impacts of EBV and HPV, is rare, and clear results have not been obtained. The aim of this study was to analyze the frequency of occurrence of EBV and HPV in GC, particularly in early-onset gastric cancer (EOGC). Tissue material from 135 patients with GC, including 84 men and 51 women, was examined. RT-PCR was performed to detect EBV, and PCR was performed to detect HPV. There were no significant impacts of EBV and HPV infections on any subtype of GC. There was also no statistically significant dependence of gender and location of the tumor on any subtype of GC. Further research on the impacts of infectious agents such as EBV and HPV on GC should be conducted using larger populations.

In this study, we analyzed bioaerosol emission characteristics and potential risks of antimicrobial resistance (AMR) during composting using the impaction culture method and metagenomic sequencing. The results showed that the highly saturated water vapor in the emission gas mitigated particulate matter emission during the thermophilic period. About the bioaerosols, the airborne aerobic bacterial emissions were suppressed as composting enters the mature period, and the airborne fungi are usually present as single-cell or small-cell aggregates (< 3.3 µm). In addition, the microbial community structure in bioaerosols was stable and independent of composting time. Most importantly, the PM2.5 in bioaerosols contained large amounts of antibiotic resistance genes (ARGs), potential pathogens, and multidrug resistant pathogens, which were diverse and present in high concentrations. Among them, ARGs concentrations encoding 21 antibiotics ranged from - 4.50 to 0.70 ppm/m3 (Log10 ARGs). Among the 89 potential human pathogens detected, Escherichia coli, Salmonella enterica, Klebsiella pneumoniae, and Staphylococcus aureus were the only culturable potentially multidrug resistant pathogens carrying multiple ARGs encoding resistance at high concentrations (- 0.57 to 1.15 ppm/m3 (Log10 ARGs)), and were more likely to persist and multiply in oligotrophic environments. Our findings indicate that composting technology can transfer AMR from solid compost to gas phase and increase the risk of AMR transmission.

Accurate detection of Helicobacter pylori and its antimicrobial resistance is essential for eradication of the infections. The aim of this study was to compare five different CE-IVD marked assays in detection of H. pylori from 268 clinical stool samples. Samples were considered positive for H. pylori when at least three of the five tests were positive. Amplified IDEIA Hp StAR (Oxoid) and Premier Platinum HpSA PLUS (Meridian Bioscience Inc.) assays showed sensitivity of 100% [95% CI (confidence interval): 87-100] and LIAISON® Meridian H. pylori SA (DiaSorin) of 83.3% (95% CI: 66-93). Specificities of the assays were 94.5% (95% CI: 91-97), 95.4%; (95% CI: 92-97), and 97.1% (95% CI: 94-99) respectively. Amplidiag® H. pylori + ClariR (Mobidiag) assay showed 93.3% (95% CI: 78-99) and Allplex™ H. pylori & ClariR Assay (Seegene Inc.) 36.7% (95% CI: 22-55) sensitivity, while specificity of both was 97.9% (95% CI: 95-99). The Amplidiag® and Allplex™ assays concordantly detected clarithromycin resistance in positive for H. pylori samples. The Amplidiag® assay showed the highest accuracy, namely 97.4% (95% CI: 95-99). These data provide helpful information for planning laboratory diagnostics of H. pylori and detection of clarithromycin resistance from stool samples.

Helicobacter pylori (H. pylori) infection can cause a wide range of gastrointestinal disorders, including chronic nonatrophic gastritis, multifocal atrophic gastritis, peptic ulcer disease, gastric adenocarcinoma, and extra-nodal B-cell lymphoma. Although the prevalence of H. pylori infection has decreased among adults, it is still very common. Approximately 90% of gastric adenocarcinomas are associated with H. pylori infection. Despite the established link between H. pylori infection and noncardiac gastric cancer, and the increasing incidence of gastric cancer in Kazakhstan, there are limited data on the prevalence of H. pylori in the country. This may be due to the difficulty of detecting H. pylori and the unavailability of diagnostic methods. This review presents the current data of diagnostic tests for the detection of H. pylori in Kazakhstan with a focus on limitations and practical significance.

Helicobacter pylori ( H. Pylori ) is considered a main causative organism of gastric ulcers, gastric cancer and duodenal ulcers. The current treatment relies on a combination of antimicrobial agents and acid suppressant agents, but the eradication effect is not satisfactory. To clarify the concentration of antibiotics at the lesion site, we investigate the clinical efficacy and drug tissue distribution of the combination therapy of furazolidone and tetracycline in eradicating H. Pylori.

Patients with H. pylori infection (n = 60) were randomized to either group A or B. Bismuth potassium citrate capsules 220 mg, omeprazole enteric-coated capsules 20 mg, amoxicillin capsules 1000 mg, each twice per day, and furazolidone tablets 500 mg were administered to group A. Group B was treated with bismuth potassium citrate capsules 220 mg, omeprazole enteric-coated capsules 20 mg, amoxicillin capsules 1000 mg, and tetracycline tablets 500 mg each twice per day for 2 weeks. The serum and gastric juice, gastric antrum, gastric horn, and gastric body samples were taken under a gastroscope on the 14th day. The antimicrobial concentrations in serum and tissue samples were determined by high-performance liquid chromatography.

In the negative group of furazolidone, the concentrations of gastric antrum, gastric body, and gastric angle were significantly higher than those in the positive group ( P = 0.017, 0.015, and 0.028). The concentrations of furazolidone in gastric fluid, gastric antrum, gastric angle, and gastric body were ∼421 times, 82 times, 17 times, and 51 times higher than those in serum, respectively. The concentrations of tetracycline in the serum and gastric angle of the tetracycline negative group were significantly higher than those in the positive group ( P = 0.036 and 0.042), and the tetracycline concentrations in the gastric horn and gastric body were about 4 and 6 times higher than those in the serum, respectively. The concentration of amoxicillin in group B was higher than that in group A, especially in serum, gastric juice, gastric angle, and gastric body ( P < 0.05).

Furazolidone is mainly concentrated and sequentially distributed in gastric juice, gastric antrum, and gastric body tissue, and tetracycline is mainly distributed in serum, gastric angle, and gastric body, whereas amoxicillin is mainly distributed in serum, gastric juice, gastric angle, and gastric body. Improving the concentration and tissue distribution of antibacterial drugs in the human gastric mucosa is the key to ensuring the ideal eradication rate of quadruple therapy.

There are many well-established relationships between pathogens and human disease, but far fewer when focusing on non-communicable diseases (NCDs). We leverage data from The UK Biobank and TriNetX to perform a systematic survey across 20 pathogens and 426 diseases, primarily NCDs. To this end, we assess the association between disease status and infection history proxies. We identify 206 pathogen-disease pairs that replicate in both cohorts. We replicate many established relationships, including Helicobacter pylori with several gastroenterological diseases and connections between Epstein-Barr virus with multiple sclerosis and lupus. Overall, our approach identified evidence of association for 15 pathogens and 96 distinct diseases, including a currently controversial link between human cytomegalovirus (CMV) and ulcerative colitis (UC). We validate this connection through two orthogonal analyses, revealing increased CMV gene expression in UC patients and enrichment for UC genetic risk signal near human genes that have altered expression upon CMV infection. Collectively, these results form a foundation for future investigations into mechanistic roles played by pathogens in NCDs. All results are easily accessible on our website, https://tf.cchmc.org/pathogen-disease.

Lipoproteins are crucial for maintaining the structural integrity of bacterial membranes. In Gram-negative bacteria, the localization of lipoprotein (Lol) system facilitates the transport of these proteins from the inner membrane to the outer membrane. In Helicobacter pylori, an ε-proteobacterium, lipoprotein transport differs significantly from the canonical and well-studied system in Escherichia coli, particularly due to the absence of LolB and the use of a LolF homodimer instead of the LolCE heterodimer. This study presents the crystal structure of the H. pylori lipoprotein chaperone LolA (LolA-HP) and its interaction with lipopeptide antibiotics such as polymyxin B and colistin. Isothermal titration calorimetry revealed that, unlike LolA from Vibrio cholerae and Porphyromonas gingivalis, LolA-HP does not bind to these antibiotics. Structural comparisons showed that LolA-HP has a deeper hydrophobic cleft but lacks the negative electrostatic potential critical for binding polymyxins. These findings offer insights into the structural diversity of LolA across bacterial species and its potential as a target for antibacterial agents.

Helicobacter pylori (H. pylori) is a major cause of peptic ulcer disease (PUD) and upper gastrointestinal bleeding. Testing for and eradication of H. pylori reduces the risk of future PUD-related complications including readmission for gastrointestinal bleeding. Our aim was to determine the most cost-effective testing strategy for H. pylori in patients hospitalized with bleeding peptic ulcers.

We developed a Markov cohort model to compare the following 6 H. pylori testing strategies: no testing, histology, rapid urease test, stool antigen test, urea breath test (UBT), and serology. Histology and rapid urease test require biopsies, while stool antigen test, UBT, and serology do not. We assumed a 17% H. pylori prevalence in patients admitted with bleeding ulcers. Model outcomes included hospitalizations for rebleeds, number needed to treat to avoid another hospitalization, life expectancy, total cost, quality-adjusted life years, and incremental cost-effectiveness ratios.

Compared to no testing, UBT resulted in a gain of 0.02 quality-adjusted life years, total cost savings of $2140 per patient, and 1675 hospitalizations avoided per 10,000 patients per year. Additionally, the number needed to treat to avoid an additional hospitalization over 35 years was 167. UBT was the preferred strategy as it was both less costly and more effective than no testing.

Our findings suggest that UBT is the cost-effective strategy to identify H. pylori in patients admitted with PUD. Noninvasive H. pylori testing at the point of care or during inpatient admission should be considered, as it presents limited risk to patients and offers potential clinical benefits.

Helicobacter pylori disturbs the stomach lining during long-term colonization of its human host, with sequelae including ulcers and gastric cancer1,2. Numerous H. pylori virulence factors have been identified, showing extensive geographic variation1. Here we identify a 'Hardy' ecospecies of H. pylori that shares the ancestry of 'Ubiquitous' H. pylori from the same region in most of the genome but has nearly fixed single-nucleotide polymorphism differences in 100 genes, many of which encode outer membrane proteins and host interaction factors. Most Hardy strains have a second urease, which uses iron as a cofactor rather than nickel3, and two additional copies of the vacuolating cytotoxin VacA. Hardy strains currently have a limited distribution, including in Indigenous populations in Siberia and the Americas and in lineages that have jumped from humans to other mammals. Analysis of polymorphism data implies that Hardy and Ubiquitous coexisted in the stomachs of modern humans since before we left Africa and that both were dispersed around the world by our migrations. Our results also show that highly distinct adaptive strategies can arise and be maintained stably within bacterial populations, even in the presence of continuous genetic exchange between strains.

Background/objectives: Bismuth is commonly used in Helicobacter pylori (H. pylori) eradication therapy. However, few studies have examined the in vitro susceptibility of H. pylori to bismuth. Moreover, the exact mechanism of action of bismuth on H. pylori remains unclear. The aim of this study was to identify the anti-bacterial effect of bismuth as well as to evaluate potential synergistic effects between bismuth and various antibiotics. Methods: The minimum inhibitory concentrations (MICs) of three bismuth preparations, bismuth subsalicylate, bismuth potassium citrate, and colloidal bismuth subcitrate (CBS, De-Nol) were determined for H. pylori strains using the agar dilution technique. Agar plates of varying pH values from 5.0 to 8.0 were used to investigate whether acidity influences the anti-bacterial effect of bismuth. A checkerboard assay was performed to assess the synergism between CBS and antibiotics (amoxicillin, clarithromycin, and metronidazole). Results: Twelve H. pylori strains, including three reference strains (H. pylori 26695, J99, and ATCC 43504), and nine clinically isolated strains were tested. The MICs for bismuth subsalicylate, bismuth potassium citrate, and CBS ranged from 4 to 32 μg/mL, 2 to 16 μg/mL, and 1 to 8 μg/mL, respectively. The bismuth MICs for the reference strains were similar at pH 5-8. In the checkerboard assay, no interactions between CBS and any of the antibiotics were observed in the reference H. pylori strains. Conclusions: Bismuth showed in vitro susceptibility against H. pylori. The enhanced eradication efficacy of bismuth-containing regimens appears to be due to mechanisms other than direct synergy with antibiotics.

Cadmium (Cd) and lead (Pb) exposure have been identified as risk factors for Helicobacter pylori seropositivity, possibly due to the immune suppression by Cd and Pb. Physical activity (PA) can induce an immune response. However, whether PA can reduce the effect of Cd and Pb on H pylori infection remains elusive. This study aims to investigate the association of blood Cd and Pb levels with H pylori infection and explore the intermediary effects of PA. This cross-sectional survey was conducted using the National Health and Nutrition Examination Survey (NHANES) of the 1999 to 2000 cycle (n = 9965). Participants without clear serological testing data, or absent in PA, blood Cd, and Pb information were excluded. Collinearity analysis was performed to remove the variables with high collinearity. Restricted cubic spline curve analysis was adopted to assess the nonlinear association of Cd and Pb with H pylori infection. The logistic regression analysis, generalized linear models, sensitivity analysis, and P for trend test were used to further analyze their relationship. Then, we analyzed the association of Cd and Pb with H pylori infection in 2 PA groups. Totally 3638 participants were divided into H pylori-negative (n = 2545) and H pylori-positive group (n = 1093). Pb exhibited a linear relationship but Cd had a nonlinear relationship with H pylori infection. Besides, the elevation of Cd and Pb both independently predicted H pylori infection after adjusting various variables (P < .05). The robust relationship was confirmed by the P for trend test (P for trend < .05). Under Cd exposure, the risk of H pylori infection was lower in the active PA group than in the inactive group (P < .05). A reverse result was found under the Pb exposure (P < .05). Exposure to Cd and Pb are positively linked to H pylori infection. PA may alleviate the effect of Cd on H pylori infection but may enhance H pylori infection under Pb exposure. Therefore, PA should be recommended in the appropriate season or region.

The rapid urease test (RUT) is widely used to detect Helicobacter pylori infection; however, it is not preferred as a monitoring strategy after eradication owing to its low sensitivity. In this study, we evaluated the diagnostic performance of RUT using the sweeping method, which overcomes the limitations of conventional tissue sampling methods after eradication.

Patients who received H pylori eradication treatment were enrolled. Each of the sweeping and conventional methods was performed on the same patients to compare diagnostic performance. Urea breath test (UBT), histology, and polymerase chain reaction were performed to determine true infection. Logistic regression analysis was conducted to investigate reasons for discrepancies between the results of the 2 methods.

In 216 patients, the eradication success rate was 68.1%, and the sensitivity and specificity of the sweeping method were 0.812 and 0.912, respectively, whereas those of the conventional method were 0.391 and 0.993, respectively (P < .05 for all). The area under the receiver operating characteristic curve for the sweeping method was higher than that for the conventional method (0.862 vs 0.692, P < .001). The mean time to H pylori detection for the sweeping method was 4.7 ± 4.4 minutes and 12.3 ± 16.1 minutes for the conventional method (P < .001). The risk for inconsistent results between the 2 methods was the highest for UBT values of 1.4‰ to 2.4‰ (odds ratio, 3.8; P = .016).

The RUT with the sweeping method could potentially replace the tissue sampling method as a test to confirm H pylori eradication and be an alternative option to UBT for patients requiring endoscopy.

Helicobacter pylori infection has been thought to be associated with liver diseases, although the exact mechanisms remain elusive. This study identified H. pylori-induced liver inflammation and tissue damage in infected mice and examined the exosome-mediated mechanism underlying H. pylori infection's impact on liver injury. Exosomes were isolated from H. pylori-infected gastric epithelial GES-1 cells (Hp-GES-EVs), and the crucial virulence factor CagA was identified within these exosomes. Fluorescent labeling demonstrated that Hp-GES-EVs can be absorbed by liver cells. Treatment with Hp-GES-EVs enhanced the proliferation, migration, and invasion of Hep G2 and Hep 3B cells. Additionally, exposure to Hp-GES-EVs activated NF-κB and PI3K/AKT signaling pathways, which provides a reasonable explanation for the liver inflammation and neoplastic traits. Using a mouse model established via tail vein injection of Hp-GES-EVs, exosome-driven liver injury was evidenced by slight hepatocellular erosion around the central hepatic vein and elevated serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and IL-6. Administering the exosome inhibitor GW4869 via intraperitoneal injection in mice resulted in a reduction of liver damage caused by H. pylori infection. These findings illuminate the exosome-mediated pathogenesis of H. pylori-induced liver injury and offer valuable insights into the extra-gastrointestinal manifestations of H. pylori infection.

Infection by pathogenic microbes is widely hypothesized to be a risk factor for the development of neurocognitive disorders and dementia, but evidence remains limited. We analyzed the association of seropositivity to 11 common pathogens and cumulative infection burden with neurocognitive disorder (mild cognitive impairment and dementia) in a population-based cohort of 475 older individuals (mean age = 67.6 y) followed up over 3-5 years for the risk of MCI-dementia. Specific seropositivities showed a preponderance of positive trends of association with MCI-dementia, including for Plasmodium, H. pylori, and RSV (p < 0.05), as well as Chickungunya, HSV-2, CMV and EBV (p > 0.05), while HSV-1 and HHV-6 showed equivocal or no associations, and Dengue and VZV showed negative associations (p < 0.05) with MCI-dementia. High infection burden (5 + cumulated infections) was significantly associated with an increased MCI-dementia risk in comparison with low infection burden (1-3 cumulative infections), adjusted for age, sex, and education. Intriguingly, for a majority (8 of 11) of pathogens, levels of antibody titers were significantly lower in those with MCI-dementia compared to cognitive normal individuals. Based on our observations, we postulate that individuals who are unable to mount strong immunological responses to infection by diverse microorganisms, and therefore more vulnerable to infection by greater numbers of different microbial pathogens or repeated infections to the same pathogen in the course of their lifetime are more likely to develop MCI or dementia. This hypothesis should be tested in more studies.

Antibiotics are currently used for the treatment of Helicobacter pylori (H. pylori), which is confirmed to be the major cause of gastric disorders. However, the long-term consumption of antibiotics has already caused antibiotic resistance and side effects in vivo. Therefore, there is an emerging need for searching for safe and effective anti-H. pylori agents. Inspired by the excellent bioactivities of cinnamic acid, a series of cinnamic acid derivatives (compounds 1-30) were synthesized and determined for H. pylori inhibition. The initial screening revealed that compound 23, a 2,4-dinitro cinnamic acid derivative containing 4-methoxyphenol, showed excellent H. pylori inhibition with an MIC value of 4 μM. Further studies indicated that compound 23 showed anti-bacterial activity and had a bactericidal effect on H. pylori due to the destruction of the bacterial structure. Molecular docking analysis revealed that the 2,4-dinitro groups in cinnamic acid moiety formed hydrogen bonding with amino acid residues in an active pocket of H. pylori protein. Interestingly, the ester moiety fitted into the hydrophobic pocket, attaining additional stability to compound 23. Above all, the present study reveals that compound 23 could be considered a promising anti-H. pylori agent to treat H. pylori causing gastritis.

This study aimed to investigate the risk factors associated with central serous chorioretinopathy (CSC) and analyze the relationship between vascular endothelial growth factor (VEGF), high-sensitivity C-reactive protein (hs-CRP), erythrocyte sedimentation rate (ESR), and CSC.

A total of 109 patients diagnosed with CSC (CSC group) at our ophthalmology clinic from February 2017 to February 2021 were included, with 103 volunteers from our hospital's health examination center serving as the control group. Additionally, the new multimodal imaging classification of 109 CSC patients was further divided into simple CSC (57 cases) and complex CSC (52 cases). Demographic data, underlying diseases, medical history, and medication history were collected. Levels of VEGF, hs-CRP, and ESR were measured, and multifactorial logistic regression analysis was performed to identify factors influencing CSC. Receiver operating characteristic (ROC) curve analysis was conducted to assess the diagnostic value of VEGF, hs-CRP, and ESR in CSC.

The CSC group showed a higher proportion of males, smoking history, alcohol consumption, comorbid obstructive sleep apnea, hypothyroidism, renal disease, Helicobacter pylori infection, steroid use, and shift work compared to the control group (P < 0.05). VEGF, hs-CRP, and ESR levels were significantly higher in the CSC group than in the control group (P < 0.05). The levels of VEGF, hs-CRP, and ESR in the complex CSC group were higher than those in the simple CSC group (P < 0.05). Male gender, shift work, Helicobacter pylori infection, hypothyroidism, elevated VEGF, hs-CRP, and ESR were identified as risk factors for CSC (P < 0.05). The combined diagnostic value of VEGF, hs-CRP, and ESR (area under the ROC curve: 0.886) was higher than that of individual markers (0.722, 0.728, and 0.703, respectively) (P < 0.05).

Male gender, shift work, Helicobacter pylori infection, hypothyroidism, and elevated levels of VEGF, hs-CRP, and ESR are risk factors for CSC. The combined use of VEGF, hs-CRP, and ESR demonstrates higher diagnostic efficiency in identifying CSC.

The metabolic state of bacteria significantly contributes to their resistance to antibiotics; however, the specific metabolic mechanisms conferring antimicrobial resistance in Helicobacter pylori remain largely understudied. Employing transcriptomic and non-targeted metabolomics, we characterized the metabolic reprogramming of H. pylori when challenged with antibiotic agents. We observed a notable increase in both genetic and key proteomic components involved in fatty acid biosynthesis. Inhibition of this pathway significantly enhanced the antibiotic susceptibility of the sensitive and multidrug-resistant H. pylori strains while also disrupting their biofilm-forming capacities. Further analysis revealed that antibiotic treatment induced a stringent response, triggering the expression of the hp0560-hp0557 operon regulated by Sigma28 (σ28). This activation in turn stimulated the fatty acid biosynthetic pathway, thereby enhancing the antibiotic tolerance of H. pylori. Our findings reveal a novel adaptive strategy employed by H. pylori to withstand antibiotic stress.

Rates of antimicrobial-resistant Helicobacter pylori infection are rising globally, but little is known about contemporary resistance patterns, virulence factors, and phylogenetic patterns of isolates within Australia. We aimed to characterize antimicrobial resistance and genetic mutations associated with adverse clinical outcomes.

Whole genome sequencing, culturing, and antibiotic sensitivity data for refractory H. pylori isolates at Australian centers were collected between 2013 and 2022. Phylogenetic origins, antibiotic resistance mutations, and virulence factors were examined with phenotypic resistance profiles.

One hundred thirty-five isolates underwent culture, with 109 of these undergoing whole genome sequencing. Forty-three isolates were isolated from patients in South Australia and 66 from Western Australia. Isolates originated primarily from hpEurope (59.6%), hpEastAsia (25.7%), and hpNEAfrica (6.4%). Antimicrobial resistance to clarithromycin was seen in 85% of isolates, metronidazole in 52%, levofloxacin in 18%, rifampicin in 14%, and amoxicillin in 9%. Most isolates (59%) were multi-drug resistant. Resistance concordance between genetically determined resistance and phenotypic resistance was 92% for clarithromycin and 94% for levofloxacin. Analysis of virulence factors demonstrated cag pathogenicity island (cagPAI) in 67% of isolates and cagA in 61%, correlating with isolate genetic origin. The most virulent s1m1 vacuolating cytotoxin A genotype was present in 26% of isolates.

Refractory H. pylori isolates in Australia emanate from multiple global origins. Strong concordance between genetic and phenotypic antibiotic resistance profiles raises the possibility of utilizing genetic profiling in clinical practice. The dynamic landscape of H. pylori in Australia warrants the establishment of a national database to monitor H. pylori resistance and evolving virulence.