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HELICOBACTER PYLORI
INFECTIONS
Dr Raman Ghimire
OUTLINES
• Introduction
• Microbiology
• Pathogenesis
• Indications for tests
• Investigations
• Treatment guidelines
• MCQs
INTRODUCTION
• Helicobacter pylori infection is the most common bacterial infection
worldwide
• In developing countries, 70 to 90% of the population carries H. pylori
• H pylori may be detected in 90% of individuals with PUD
• No specific clinical signs and symptoms have been described
• 85% -asymptomatic
10% -peptic ulcer
1% - gastric cancer
• H. pylori infection is associated with Idiopathic Thrombocytopenic Purpura
( anti-CagA antibodies that cross-react with platelet antigens)
• H. pylori infection is protective against GERD ,Oesophageal CA, Asthma
• EXTRA-GASTRIC DISEASES:
Parkinsonism, MS, GBS,alzheimer’s
Rosacea, Psoriasis ,chronic utricaria
IDA, ITP ,B12 def
open-angle glaucoma , central serous chorioretinitis , blepharitis
CAD, stroke
DM, metabolic syndrome
NAFLD
Mode of transmission:
 feco-oral
 oral-oral routes
 iatrogenic (unsterilized endoscopy equipment)
• No substantial reservoir of H. pylori aside from the human
stomach
• Gastric infection and H. pylori in the mouth (Periodontal disease )
• Dental plaque has been reported to be a reservoir for H. pylori.
MICROBIOLOGY
• Gram-negative ,microaerophilic,
spiral shaped bacilli
• Motile: 4-6 lophotrichous flagella
• Demonstrated by Gram stain,
Giemsa stain, H&E stain, Warthin–
Starry silver stain
• Culture: Columbia blood agar,
Brucella broth
• Produces oxidase, catalase
and urease
• UREA urease CO2 + AMMONIA
Virulence factors:
 cytotoxin-associated gene A antigen (CagA)
cag pathogenicity island (cagPAI): cag A gene + T4SS
absent in 40% of strains
risk of gastric CA
enters the cell: interferes with transduction pathway, antiapoptotic
 vacuolating cytotoxin (VacA)
coded by Vac A gene
absent in 60% of strains
induces inflammation $ injury to gastric mucosa
 Lipopolysaccharides
 Adhesins : Ice A , Bab A, Sap A ,Dup A ,Oip A
 Enzymes: Urease, proteinase, mucinase ,lipase
PATHOGENESIS
INDICATION FOR TESTING H. PYLORI
• All patients; with active or past history of PUD
(unless previous cure of HPI has been documented),
low-grade gastric mucosa-associated lymphoid tissue (MALToma )
history of endoscopic resection of early gastric cancer
• Patients with dyspepsia who are undergoing upper endoscopy
(gastric biopsy specimens)
• Patients on long-term, low-dose aspirin
• Patients initiating long-term therapy with NSAIDs
• Patients with unexplained iron deficiency anemia following standard workup
• Adults with idiopathic thrombocytopenic purpura
• Post-treatment testing to prove eradication of HPI
 urea breath test,
 fecal antigen test
 biopsy-based testing
at least 4 weeks following completion of antimicrobial therapy
and after proton pump inhibitors have been withheld for 1-2
weeks.
American College of Gastroenterology (ACG),2017 guidelines for the treatment
of H pylori infection (HPI) include the following recommendations for testing
for H pylori [26] :
TESTS FOR H. PYLORI
95-98
1.INVASIVE:
 Endoscopy + biopsy sample required
 Expensive
 Drug sensitivity can be done in Culture
 Histology provides additional information about gastric mucosa
 Can be used to start antimicrobial therapy and confirm eradication
2.NON-INVASIVE:
Easy & cheaper
Sample : blood, stool , breath
 Can be used to start antimicrobial therapy and confirm eradication
except serology test
serology test cannot differentiate new or old infection
TREATMENT
MCQs
1. All of the following can be used as confirmation for
eradication of H. pylori EXCEPT:
A. urea breath test
B. fecal antigen test
C. biopsy-based testing
D. serology
Ans: D
2. Which of the following is true regarding H. pylori
A. Gram positive
B. Non –motile
C. carcinogenic effect via the CagA protein
D. Levofloxacin based therapy are not used for treament
Ans : C
Gram negative ,motile
Levofloxacin based therapy is used
REFERENCES
• The 2017 American College of Gastroenterology (ACG) guidelines
for the treatment of H pylori infection (HPI)
• Pathogenesis of Helicobacter pylori Infection
Johannes G. Kusters,* Arnoud H. M. van Vliet, and Ernst J. Kuipers
• Helicobacter pylori: Toward effective eradication
Susan Collazo, RN, MSN, ACNP
• Diagnosis of Helicobacter pylori by invasive test: histology
Ju Yup Lee and Nayoung Kim
• Helicobacter pylori infection: Host immune response, implications
on gene expression and microRNAs
Aline Cristina Targa Cadamuro, Ana Flávia Teixeira Rossi, Nathália Maciel Maniezzo,
Ana Elizabete Silva
THANK YOU

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Helicobacter pylori infections

  • 2. OUTLINES • Introduction • Microbiology • Pathogenesis • Indications for tests • Investigations • Treatment guidelines • MCQs
  • 3. INTRODUCTION • Helicobacter pylori infection is the most common bacterial infection worldwide • In developing countries, 70 to 90% of the population carries H. pylori • H pylori may be detected in 90% of individuals with PUD • No specific clinical signs and symptoms have been described • 85% -asymptomatic 10% -peptic ulcer 1% - gastric cancer
  • 4. • H. pylori infection is associated with Idiopathic Thrombocytopenic Purpura ( anti-CagA antibodies that cross-react with platelet antigens) • H. pylori infection is protective against GERD ,Oesophageal CA, Asthma • EXTRA-GASTRIC DISEASES: Parkinsonism, MS, GBS,alzheimer’s Rosacea, Psoriasis ,chronic utricaria IDA, ITP ,B12 def open-angle glaucoma , central serous chorioretinitis , blepharitis CAD, stroke DM, metabolic syndrome NAFLD
  • 5. Mode of transmission:  feco-oral  oral-oral routes  iatrogenic (unsterilized endoscopy equipment) • No substantial reservoir of H. pylori aside from the human stomach • Gastric infection and H. pylori in the mouth (Periodontal disease ) • Dental plaque has been reported to be a reservoir for H. pylori.
  • 6. MICROBIOLOGY • Gram-negative ,microaerophilic, spiral shaped bacilli • Motile: 4-6 lophotrichous flagella • Demonstrated by Gram stain, Giemsa stain, H&E stain, Warthin– Starry silver stain • Culture: Columbia blood agar, Brucella broth • Produces oxidase, catalase and urease • UREA urease CO2 + AMMONIA
  • 7. Virulence factors:  cytotoxin-associated gene A antigen (CagA) cag pathogenicity island (cagPAI): cag A gene + T4SS absent in 40% of strains risk of gastric CA enters the cell: interferes with transduction pathway, antiapoptotic  vacuolating cytotoxin (VacA) coded by Vac A gene absent in 60% of strains induces inflammation $ injury to gastric mucosa  Lipopolysaccharides  Adhesins : Ice A , Bab A, Sap A ,Dup A ,Oip A  Enzymes: Urease, proteinase, mucinase ,lipase
  • 9.
  • 10. INDICATION FOR TESTING H. PYLORI • All patients; with active or past history of PUD (unless previous cure of HPI has been documented), low-grade gastric mucosa-associated lymphoid tissue (MALToma ) history of endoscopic resection of early gastric cancer • Patients with dyspepsia who are undergoing upper endoscopy (gastric biopsy specimens) • Patients on long-term, low-dose aspirin • Patients initiating long-term therapy with NSAIDs • Patients with unexplained iron deficiency anemia following standard workup • Adults with idiopathic thrombocytopenic purpura
  • 11. • Post-treatment testing to prove eradication of HPI  urea breath test,  fecal antigen test  biopsy-based testing at least 4 weeks following completion of antimicrobial therapy and after proton pump inhibitors have been withheld for 1-2 weeks. American College of Gastroenterology (ACG),2017 guidelines for the treatment of H pylori infection (HPI) include the following recommendations for testing for H pylori [26] :
  • 12. TESTS FOR H. PYLORI 95-98
  • 13. 1.INVASIVE:  Endoscopy + biopsy sample required  Expensive  Drug sensitivity can be done in Culture  Histology provides additional information about gastric mucosa  Can be used to start antimicrobial therapy and confirm eradication 2.NON-INVASIVE: Easy & cheaper Sample : blood, stool , breath  Can be used to start antimicrobial therapy and confirm eradication except serology test serology test cannot differentiate new or old infection
  • 15.
  • 16. MCQs 1. All of the following can be used as confirmation for eradication of H. pylori EXCEPT: A. urea breath test B. fecal antigen test C. biopsy-based testing D. serology Ans: D
  • 17. 2. Which of the following is true regarding H. pylori A. Gram positive B. Non –motile C. carcinogenic effect via the CagA protein D. Levofloxacin based therapy are not used for treament Ans : C Gram negative ,motile Levofloxacin based therapy is used
  • 18. REFERENCES • The 2017 American College of Gastroenterology (ACG) guidelines for the treatment of H pylori infection (HPI) • Pathogenesis of Helicobacter pylori Infection Johannes G. Kusters,* Arnoud H. M. van Vliet, and Ernst J. Kuipers • Helicobacter pylori: Toward effective eradication Susan Collazo, RN, MSN, ACNP • Diagnosis of Helicobacter pylori by invasive test: histology Ju Yup Lee and Nayoung Kim • Helicobacter pylori infection: Host immune response, implications on gene expression and microRNAs Aline Cristina Targa Cadamuro, Ana Flávia Teixeira Rossi, Nathália Maciel Maniezzo, Ana Elizabete Silva

Editor's Notes

  1. Basis for pathogenesis , diagnostic tests
  2. functions like a molecular syringe, injecting CagA, peptidoglycans and other factors into host epithelial cells
  3. CORPUS – BODY
  4. PPI decreases PH $ so urease activity is decreased
  5.  antimicrobial effect of PPIs on H pylori or pH-dependent suppression of H pylori urease activity Bacterial culture is very difficult. It is not used for diagnosis; it is used in patients with resistant infection and for experimental purposes.
  6. Concomitant –non bismuth quadruple ANILIA –NITROZOXANIDE – PRAZIQUANTEL GROUP