Helicobacter pylori infection pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Yamuna Kondapally, M.B.B.S[2]
Overview
Helicobacter pylori (H. pylori) is a bacterium that lives on the lining of the stomach. Although we used to think that spicy food, acid, and stress were the major causes of ulcers, we now know that nine out of ten ulcers are caused by H. pylori. Medicines that reduce stomach acid may make you feel better, but your ulcer may come back. Here's the good news: Since most ulcers are caused by this bacterial infection, they can be cured with the right antibiotics.
Pathophysiology
- The mode of transmission of H.pylori is poorly understood.[1][2][3]
- Person to person transmission is considered to be the most likely route.
- Helicobacter pylori is usually transmitted via the following routes:
- Iatrogenic
- Via tubes and endoscopes that have been in contact with the gastric mucosa of one individual are used for another patient
- Between patient and staff especially among endoscopists and gastroenterologists
- Fecal-oral route
- Fecal contamination of water and food may be the source of infection
- Oral-oral route
- Via saliva
Pathogenesis
Bacterial factors
- Bacterial Virulence factors
- The cytotoxin-associated gene (cag) pathogenecity island (PAI) and cytotoxin-associated gene A (cagA)
- Vacuolating cytotoxins
- Blood group antigen-binding adhesin A (BabA) and H.pylori adhesion
- Bacterial enzymes[5]
- Lipase and protease
- Lipase and protease leads to degradation of protective mucous layer of the stomach
- Protease leads to disintegration of the polymeric structure of mucin
- Phospholipase A2 and lipase leads to loss of mucosal surface hydrophobicity, mucus lipid degradation and lysoophospholipid generation[6][7]
- Lysophospholipids disrupts the phospholipid rich layer at the apical surface of mucous cells
- Urease
- The urease of H.pylori has two sub units, UreA and UreB[8]
- This enzyme produces ammonia, which increases the pH in the microenvironment around the organism, hence protects the bacteria from acid
- Bacterial adherence
Host genetic susceptibility
Environmental cofactors
Bacterial Virulence factors
Following transmission, the H.pylori can directly injure gastric epithelial cells by the secretion of enzymes and by the elaboration of toxins.[5][9]
The pathophysiology of helicobacter pylori infection
- Helicobacter pylori (H. pylori) is a spiral-shaped bacterium that is found in the gastric mucous layer or adherent to the epithelial lining of the stomach. H. pylori causes more than 90% of duodenal ulcers and up to 80% of gastric ulcers.
- Before 1982, when this bacterium was discovered, spicy food, acid, stress, and lifestyle were considered the major causes of ulcers.
- The majority of patients were given long-term medications, such as H2 blockers, and more recently, proton pump inhibitors, without a chance for permanent cure. These medications relieve ulcer-related symptoms, heal gastric mucosal inflammation, and may heal the ulcer, but they do not treat the infection.
- When acid suppression is removed, the majority of ulcers, particularly those caused by H. pylori, recur.
- Since we now know that most ulcers are caused by H. pylori, appropriate antibiotic regimens can successfully eradicate the infection in most patients, with complete resolution of mucosal inflammation and a minimal chance for recurrence of ulcers.
Peptic Ulcer Disease from H. Pylori
A peptic ulcer is a sore or hole in the lining of the stomach or duodenum (the first part of the small intestine). People of any age can get an ulcer and women are affected just as often as men. Over 25 million Americans will suffer from an ulcer at some point during their lifetime. The good news is that most ulcers are caused by an infection with the bacterium, Helicobacter pylori , and can be cured in about two weeks with antibiotics.
- Most ulcers are caused by an infection, not spicy food, acid or stress.
- The most common ulcer symptom is burning pain in the stomach.
- Your doctor can test you for H. pylori infection.
- Antibiotics are the new cure for ulcers.
- Eliminating H. pylori infections with antibiotics means that your ulcer can be cured for good.
References
- ↑ Brown LM (2000). "Helicobacter pylori: epidemiology and routes of transmission". Epidemiol Rev. 22 (2): 283–97. PMID 11218379.
- ↑ Cave DR (1997). "How is Helicobacter pylori transmitted?". Gastroenterology. 113 (6 Suppl): S9–14. PMID 9394753.
- ↑ Transmission http://www.who.int/bulletin/archives/79(5)455.pdf (2001) Accessed on December 27, 2016
- ↑ Atherton JC (2006). "The pathogenesis of Helicobacter pylori-induced gastro-duodenal diseases". Annu Rev Pathol. 1: 63–96. doi:10.1146/annurev.pathol.1.110304.100125. PMID 18039108.
- ↑ 5.0 5.1 Smoot DT (1997). "How does Helicobacter pylori cause mucosal damage? Direct mechanisms". Gastroenterology. 113 (6 Suppl): S31–4, discussion S50. PMID 9394757.
- ↑ Berstad K, Sjödahl R, Berstad A (1994). "Phospholipase A2 activity in gastric juice from patients with active and H. pylori-eradicated healed duodenal ulcer". Aliment Pharmacol Ther. 8 (2): 175–80. PMID 8038348.
- ↑ Mauch F, Bode G, Ditschuneit H, Malfertheiner P (1993). "Demonstration of a phospholipid-rich zone in the human gastric epithelium damaged by Helicobacter pylori". Gastroenterology. 105 (6): 1698–704. PMID 8253346.
- ↑ Smoot DT, Mobley HL, Chippendale GR, Lewison JF, Resau JH (1990). "Helicobacter pylori urease activity is toxic to human gastric epithelial cells". Infect Immun. 58 (6): 1992–4. PMC 258755. PMID 2341188.
- ↑ Jhala NC, Siegal GP, Klemm K, Atkinson BF, Jhala DN (2003). "Infiltration of Helicobacter pylori in the gastric mucosa". Am J Clin Pathol. 119 (1): 101–7. doi:10.1309/YDTX-KE06-XHTH-FNP2. PMID 12520704.