Helicobacter pylori has been evolving with human beings for well over 50,000 years, since they migrated out of Africa. H. pylori colonization has been implicated in a variety of gastroduodenal diseases including:
- gastritis,
- gastric cancer,
- and duodenal and peptic ulcer.
H. pylori has also been detected by stool PCR in cases of:
- dyspepsia,
- abdominal pain,
- and chronic gastrointestinal symptoms.
It is infamous for its causal link to ulcers and gastric cancer, which resulted in a Nobel prize awarded to Robin Warren and Barry Marshall in 2005. However, some sources are suggesting its role, at least in part, as a commensal organism. H. pylori may protect its host from certain atopic disorders, as well as other diseases such as:
- esophageal cancer reflux,
- and obesity.
Population data shows that H. pylori virulence varies geographically. It is associated with high rates of cancer in certain regions, but not in others. The difference may lie in H. pylori’s genetics. Host immune status and acid secretion seem to be other important factors contributing to H. pylori’s colonization and pathogenesis. The H. pylori virulence factors that are most well recognized are vacA and cagA. The presence of cagA-positive H.pylori strains has been significantly associated with gastric cancer and peptic ulcer. The gene codes for a type IV secretion system which allows the bacterium to inject the cagA protein into the host cell. Once inside the host’s gastric epithelial cells, cagA can disrupt cell signaling, leading to abnormal proliferation, motility, and changes in the cytoskeleton. These changes to normal cell signaling can initiate cancer. The presence of vacA has been associated with gastric cancer, peptic ulcer, and duodenal ulcer. The vacA gene is present in all strains of H.pylori but is polymorphic, which leads to different levels of vacuolating toxin. VacA toxins interact with certain receptors on host cells, setting off a chain of events including mitochondrial damage, inhibition of T-lymphocytes, and interference of antigen presentation.
Numerous papers suggest the clinical utility of PCR testing for H. pylori. Detection of H.pylori in biopsy specimens by PCR has proven superior to other methods. It has shown sensitivity and specificity reaching that of the diagnostic “gold standard,” which is endoscopy with biopsy and urease test. H.pylori genotyping may be useful for resistant H. pylori infections that have failed to respond to triple antibiotic therapy. In one study of RT-PCR, authors stated it was a “highly accurate noninvasive method to detect H. pylori infection in stool and at the same time allows for culture-independent clarithromycin susceptibility testing.”
H. pylori may be asymptomatic and require no treatment or only supportive care to improve the intestinal mucosa and gastrointestinal lining. Information on the cagA and vacA genes may help determine whether treating a positive H. pylori result is necessary.
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H. pylori colonization has been implicated in a variety of gastroduodenal diseases including:
- gastritis,
- gastric cancer,
- and duodenal and peptic ulcer.
H. pylori has also been detected by stool PCR in cases of:
- dyspepsia,
- abdominal pain,
- and chronic gastrointestinal symptoms.
It is infamous for its causal link to ulcers and gastric cancer, which resulted in a Nobel prize awarded to Robin Warren and Barry Marshall in 2005. However, some sources are suggesting its role, at least in part, as a commensal organism. H. pylori may protect its host from certain atopic disorders, as well as other diseases such as:
- esophageal cancer reflux,
- and obesity.
Symptoms:
Most people with H. pylori infection will never have any signs or symptoms. It's not clear why this is, but some people may be born with more resistance to the harmful effects of H. pylori.
When signs or symptoms do occur with H. pylori infection, they may include:
- An ache or burning pain in your abdomen
- Abdominal pain that's worse when your stomach is empty
- Nausea
- Loss of appetite
- Frequent burping
- Bloating
- Unintentional weight loss
Potential treatment:
H. pylori infections are usually treated with at least two different antibiotics at once, to help prevent the bacteria from developing a resistance to one particular antibiotic. Your doctor also will prescribe or recommend an acid-suppressing drug, to help your stomach lining heal. Your doctor may recommend that you undergo testing for H. pylori at least four weeks after your treatment. If the tests show the treatment was unsuccessful, you may undergo another round of treatment with a different combination of antibiotic medications.
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Adenovirus 40/41, Akkermansia muciniphila, Ancylostoma duodenale, Anti-gliadin IgA, Ascaris lumbricoides, b-Glucuronidase, Bacillus spp., Bacteroides fragilis, Bacteroidetes, Bifidobacterium spp., Blastocystis hominis, C. difficile, Toxin A, C. difficile, Toxin B, Calprotectin, Campylobacter, Candida albicans, Candida spp., Chilomastix mesnili, Citrobacter freundii, Citrobacter spp., Clostridia (class), Cryptosporidium, Cyclospora spp., Cytomegalovirus, Desulfovibrio spp., Dientamoeba fragilis, E. coli O157, Elastase-1, Endolimax nana, Entamoeba coli, Entamoeba histolytica, Enterobacter spp., Enterococcus faecalis, Enterococcus faecium, Enterococcus spp., Enterohemorrhagic E. coli (EHEC), Enteroinvasive E. coli/Shigella, Enterotoxigenic E. coli LT/ST, Eosinophil Activation Protein (EDN/EPX), Epstein-Barr Virus, Escherichia spp., Faecalibacterium prausnitzii, Firmicutes, Firmicutes:Bacteroidetes Ratio, Fusobacterium spp., Geotrichum spp., Giardia, Helicobacter pylori, Klebsiella pneumoniae, Klebsiella spp., Lactobacillus spp., M. avium subsp. paratuberculosis, Methanobacteriaceae (family), Microsporidium spp., Morganella spp., Necator americanus, Norovirus GI/II, Occult Blood - FIT, Pentatrichomonas hominis, Prevotella spp., Proteus mirabilis, Proteus spp., Pseudomonas aeruginosa, Pseudomonas spp., Rhodotorula spp., Rodotorula spp., Roseburia spp., Salmonella, Secretory IgA, Shiga-like Toxin E. coli stx1, Shiga-like Toxin E. coli stx2, Staphylococcus aureus, Staphylococcus spp., Steatocrit, Streptococcus spp., Taenia spp., Trichuris trichiura, Vibrio cholerae, Virulence Factor, babA, Virulence Factor, cagA, Virulence Factor, dupA, Virulence Factor, iceA, Virulence Factor, oipA, Virulence Factor, vacA, Virulence Factor, virB, Virulence Factor, virD, Yersinia enterocolitica, Zonulin