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Peptic Ulcer and Helicobacter pylori infection:

Peptic Ulcer and Helicobacter pylori infection:. In 1982, Barry Marshall and Robin Warren , reported that H.pylori is associated with chronic gastritis and gastric ulcers , conditions that were not previously believed to have a microbial cause.

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Peptic Ulcer and Helicobacter pylori infection:

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  1. Peptic Ulcer and Helicobacterpylori infection: In 1982,Barry Marshall and Robin Warren, reported that H.pyloriis associated with chronicgastritis and gastriculcers, conditions that were not previously believed to have a microbial cause. However, over 80 percent of individuals infected with the bacterium are asymptomatic patients. More than 50% of the world's population harbor H. pylori in their upper gastrointestinal tract.

  2. Microscopy: H. pylori is a curved rod,helix-shaped, Gram-negativebacterium measuring about (3 L*0.5 D ) micrometers . All Species are Pleomorphic; Bacillary, spiral, and Coccoidal shape. All are motile by four to six lophotrichous flagella. Helicobacterpylori species arenon-Spore formers, and most strains have a glycocalyx.

  3. Cultural characteristics: All Helicobacterpylorispecies are FastidiousMicroaerophilic in nature. The cultivation Enrichment -media: - Brain heart infusion broth supplemented by fetal calf serum (10%) or/and Bovine serum albumin. - Brucella broth supplemented by fetal calf serum (10%). The selective Enriched media: - Columbia chocolate agar supplemented by 5-10% hemolyzed sheep blood, and specific antibiotics combination ( 5mg/L trimethoprim, 6mg/L vancomycin, and 6mg/L amphotericin B).

  4. N Both Enrichment and Enriched media should be inoculated by the clinical specimens and incubated at 37ᵒC with a microaerophilic atmosphere ( 10% CO2, 5% O2, and 85% N2) for up to 8days( humidity should be > 95%). Colony morphology: -H. pylori species produce a specific colonies with the following characteristics : small(0.5-2mm), round, convex, translucent, with entericmargin and non-hemolytic activity.

  5. Biochemical identification: All Helicobacterpylori species show immediate positive oxidase , catalase, and urease (++++) reactions. All species are also demonstrating alkaline phosphatase, gamma – glutamylaminopeptidase , and ornithine decarboxylase activities.

  6. Biotyping of Helicobacterpylori: Almost all strains of Helicobacterpylori are sensitive to Cephalothin and resistant to Nalidixic acid.

  7. Helicobacter pylori Virulence factors: Outer membrane proteins: 1-The adhesinsprotein : adhesion to host cell. 2- Porins proteins, iron transporters, and Flagella proteins. The Lipopolysaccharide(LPS)- O antigen: mimic Lewis blood group antigen found on the gastric epithelium The Exotoxins: The Vacuolating(Vac A) toxins: : gastric mucosal injury. The Secretory Enzymes: 1- The Urease: Neutralize gastric acid, and mucosal injury. 2- The mucinase, lipase, protease: mucosal injury. The Flagella : motility. The effector cytotoxin : The cytotoxinassociatedgeneA (Cag A): cause uncontrolled host cell growth and apoptosis inhibition.

  8. Helicobacter pylori Virulence factors: N

  9. Pathogenesis and clinical picture: Transmission :1- Person to Person (Oral-Oral or Fecal-Oral). 2- Waterborne mainly within People living in crowded condition, inadequate sanitation practices, and poor hygiene. 3-Iatrogenic transmission: mediated by contaminated Endoscopy. 1-Primary infection: -H. pylori enters the stomach. - To avoid being carried into the lumen, H. pylori senses the pH- gradient and swims away from the acidic microenvironment. - The microbe invades the mucus layer .

  10. N - Ammonia will neutralize gastric acid and damage the epithelial cells of gastric mucosa. The microbial toxins will also destroy epithelial mucosa. Colonization of gastric mucosa stimulates chemotaxis of phagocytes, lymphocytes and cellular immunity. Antrum Gastritis ( acute infection). Corpus Gastritis ( acute infection). Both types of gastritis could lead to gastric ulceration. (gastric acid concentration reduced) Duodenal ulceration : (mainly chronic infection): (gastric acid concentration increased). Duodenal atrophy: ( chronic infection): (gastric acid concentration decreased). - The risk of stomach cancer increased by chronic infection.

  11. a 2- Secondary infection:Latency.

  12. Pathogenesis and clinical picture: a

  13. N The secondary and chronic infections caused by Toxigenic Helicobacter pylori strains(Cag A +++) could be complicated by: 1- Adenocarcinoma of the stomach. 2- MALToma of the stomach: It is a rare type of Non-Hodgkin’s lymphoma of the stomach (B-cell Lymphoma). Chronic ulceration of stomach and duodenum could be converted into Bleeding ulceration.

  14. Clinical picture of H. pylori: n

  15. n n

  16. Diagnosis: 1- Clinical diagnosis: A- Endoscopy: gastritis, ulcers, bleeding ulcer, atrophy. B- CLO test: Rapid diagnostic test. C- Carbon urea breath test: 13C-UREA swallowed, 13-CO2 exhaled. 2-Laboratory diagnosis: A-Microbiology: tissue biopsy: culture for isolation of H. pylori. : antibiotic sensitivity by Microbroth dilution method. B-Serology: detection of anti-Helicobacter antibodies or Anti-Cag A antibodies in serum. C-Histology: biopsy tissue prepared for Giemsa stain and silver stain for H. pylori. H&E stain.

  17. Laboratory diagnosis: Gastric antrum: H&E Stain Gastric antrum: Giemsa stain.

  18. Clinical and Laboratory diagnosis: Warthin-Starry’s silver stain Immunohistochemistry stain for H.pylori. The CLO test.

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