MICROBIOLOGY


ammonia to bicarbonate, increasing the local pH.5


Pathogenesis of H. pylori involves a range of virulence factors that enable it to adhere to the gastric epithelium, evade host defences, and cause tissue damage. Key virulence factors include the cytotoxin-associated gene A (cagA) and vacuolating cytotoxin A (vacA), both of which contribute to inflammation and cellular damage. Chronic infection results in persistent inflammation, which can exacerbate tissue damage over time, contributing to gastritis, peptic ulcers, and, in some cases, gastric cancer. In fact, CagA, a protein injected into the host epithelial cells, was the first bacterial protein found to be directly involved in oncogenesis. The bacterium is classified as a Group 1 carcinogen by the World Health Organization due to its strong association with gastric malignancies.6 Current treatment guidelines in the UK, whilst based on local resistance data, generally recommend a first-line triple therapy consisting of a proton pump inhibitor (PPI), clarithromycin, and either amoxicillin or metronidazole for 7–14 days. However, the rising prevalence of clarithromycin resistance is significantly impacting the efficacy of this regimen, with treatment success rates falling below 80% in some cases.7


This has led to the


recommendation of alternative regimens, such as quadruple therapy (adding bismuth or a second antibiotic) in areas with high resistance rates or in cases of treatment failure. The reliance on empiric prescribing for


H. pylori infections presents significant challenges. Empiric treatment generally assumes susceptibility to clarithromycin, which may not reflect the actual resistance profile of the infection. This approach increases the likelihood of treatment failure, necessitating repeat courses of antibiotics and exposing patients to prolonged symptoms and potential complications. Furthermore, ineffective treatments contribute to the broader issue of AMR by promoting the selection of resistant strains. Recent UK studies estimate that clarithromycin resistance in H. pylori exceeds 20%, with some reports indicating rates over 70%.8,9 These findings highlight the urgent need for diagnostics that guide therapy based on resistance profiles rather than assumptions.


Current diagnostic approaches In the UK, the diagnosis of H. pylori and assessment of antibiotic resistance relies on several established methods. These include: n Urea breath test (UBT): a non-invasive test that detects H. pylori infection by measuring labelled carbon dioxide in the patient’s breath after ingestion of a urea solution. While highly sensitive for detecting active infection, it does not provide information about antibiotic resistance.


n Stool antigen test: a cost-effective and non-invasive method that detects H. pylori antigens in stool samples. Like the UBT, it confirms infection but lacks the ability to identify resistance patterns.


n Endoscopy with biopsy: the gold standard for diagnosing H. pylori, involving histopathology, culture, and susceptibility testing. This method allows for direct observation of the gastric mucosa and resistance profiling through culture. However, it is invasive, labour intensive, and has a longer turnaround time.


n Serology: used to detect antibodies against H. pylori. While useful in certain contexts, it cannot distinguish between active and past infections, nor does it provide resistance data.


These current approaches do have a number of limitations and disadvantages which should be taken into account. Most non-invasive methods (UBT, stool antigen) do not offer insights into resistance, making them inadequate for guiding tailored treatments, while culture and susceptibility testing, though comprehensive, are slow and resource intensive. The current reliance on empiric therapy – due to diagnostic limitations – contributes to resistance development, as ineffective antibiotics may be prescribed. These limitations highlight the need for advanced molecular diagnostics that combine infection detection with resistance profiling in a single, streamlined test.


Combating AMR with molecular diagnostics


Molecular diagnostics (MDx) offer a solution to these challenges by providing rapid and accurate detection of active infection and resistance markers. MDx can


Recent UK studies estimate that clarithromycin resistance in H. pylori exceeds 20%, with some reports indicating rates over 70%


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deliver results in hours, enabling timely and informed treatment decisions. Key benefits of MDx include:


n High sensitivity and specificity: molecular tests are more sensitive and specific than classical methods due to their ability to amplify and detect even small amounts of bacterial DNA, ensuring accurate results even in low bacterial load scenarios.


n Comprehensive information: molecular diagnostics provide not only detection of active infection but also resistance profiling in a single, streamlined process, offering clinicians critical data to guide targeted treatments.


n Reduced turnaround times: MDx significantly shortens diagnostic time compared to most classical methods, often providing results within hours instead of days. This allows clinicians to initiate appropriate therapy more quickly, reducing patient wait times and potentially improving clinical outcomes.


n Labour savings: automated platforms streamline testing, minimising manual effort and reducing the risk of errors. This can enhance overall operational efficiency.


n Broader healthcare savings: by reducing the need for repeat visits and failed treatments, molecular diagnostics help free valuable bed space, lower overall healthcare costs, and improve resource allocation within the healthcare system.


By incorporating MDx into routine diagnostics, healthcare providers can not only improve patient outcomes but also transform antimicrobial stewardship by reducing resistance spread and optimising treatment efficiency.10


Introducing Seegene’s H. pylori and ClariR panel Seegene’s H. pylori & ClariR panel represents a significant advancement in the molecular detection of H. pylori and its resistance markers. The panel is designed to simultaneously detect H. pylori infection and mutations in the 23S rRNA gene that confer clarithromycin resistance. Key features include: n Comprehensive targeting: the panel identifies three distinct mutations associated with clarithromycin resistance (A2142G, A2142C, and A2143G), ensuring robust coverage of clinically relevant resistance mechanisms.


n Efficiency and speed: results are available within hours (~4-hour TAT), supporting faster clinical decision- making compared to traditional culture methods, which can take days.


n Broad sample type compatibility: the MAY 2025 WWW.PATHOLOGYINPRACTICE.COM


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