1. gastrointestinal block
Role of H pylori in peptic ulcer and drugs used in treatment
By Abdallah Mohamed
Microbiology department

2. Objective
To define peptic ulcer disease and assess its distribution among patients.
To briefly indicate the signs and symptoms.
To know impact of the discovery of H.pylori on the change of diagnosis and management of peptic ulcer.
To understand the various gastric and duodenal diseases caused by H.pylori.
To learn laboratory characteristics of H. pylori and its identification and diagnosis.
To know the pathophysiology of H.pylori inside the stomach and duodenum.
To learn the prevention methods used for H.pylori infection.
To explore and learn the epidemiology and transmission ways of the disease.
Finally, to know the management and treatment regiments used for eradication of H.pylori. .

3. 1983-discovered by Warren and Marshall in Australia
introduction
1983-discovered by Warren and Marshall in Australia
Discovery revolutionised the treatment of duodenal and gastric ulcers
Gram-negative spiral bacillus
Fastidious in terms of growth requirements
strictly micro-aerophilic
require C02 for growth
on charcoal medium
Has a tuft of sheathed unipolar flagella; specially adapted to colonies on mucous membranes

4. Epidemiology Around 50% of world’s population harbor H pylori.
Third world has more rate of infection.
Infections are usually acquired at childhood.
Poor sanitary conditions contribute to high rates.
In USA high prevalence among African-American and Hispanic population-Due to socioeconomic status.
Higher hygiene standards and widespread use of antibiotics behind lower rate of infection in the west.
Overall frequency of H pylori infection is declining.
Prevalence varies greatly among countries and population groups.
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4/21/2019

5. Transmission Contagious with an unknown route of transmission .
Person to person (oral to oral or fecal-oral) route.
Transmission occur mainly within families or community.
Fecal-oral route of infection occur by ingestion contaminated food or water due poor hygiene.
Using same spoons, forks and tooth brushes and kissing children mouth to mouth increases oral-oral route of infection.
Gastric antrum is the most favoured site.
Present in the mucus that overlies the mucosa.
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4/21/2019

6. Peptic ulcer disease (PUD):
H. pylori causes an inflammatory response with neutrophils, lymphocytes, plasma cells, and macrophages within the mucosal layer and causes epithelial cell degeneration and injury
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7. اسم ورقم المقرر – Course Name and No.
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8. Helicobacter pylori is found closely associated with gastric mucosa and causes chronic active gastritis, gastric and duodenal ulcer (Peptic ulcer) and could develop adenocarcinoma and gastric mucosa-associated lymphoid tissue (MALT) lymphoma.
اسم ورقم المقرر – Course Name and No.
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9. Signs and symptoms of a peptic ulcer can include one or more of the following:
abdominal pain, classically epigastric strongly correlated to mealtimes. In case of duodenal ulcers the pain appears aboutthree hours after taking a meal; waterbrash (rush of saliva after an episode of regurgitation to dilute the acid in esophagus - although this is more associated with gastroesophageal reflux disease); nausea and copious vomiting; bloating and abdominal fullness

10. loss of appetite and weight loss;
cont
loss of appetite and weight loss;
hematemesis (vomiting of blood); this can occur due to bleeding directly from a gastric ulcer, or from damage to the esophagus from severe/continuing vomiting.
melena (tarry, foul-smelling feces due to presence of oxidized iron from hemoglobin);
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11. Pathophysiology
To colonize the stomach, H pylori must survive acidity.
Using flagella, H pylori moves through stomach lumen and drill into the mucoid lining of stomach.
Produces adhesions that binds to the epithelial cells.
Produces large amounts of urease enzyme that break down urea into co2 +ammonia.
This in-turn neutalizes gastric acid.
Ammonia is toxic to epithelial cells along with proteases, vacA protein and phospholipases produced by H pylori and could damage epithelial cells.

12. Pathophysiology- cont
Colonization of stomach or duodenum results in chronic gastritis (inflammation of stomach lining).
Inflammation stimulate more production of gastric acid.
This leads to gastric and duodenal ulcers, atrophy and later cancer.
CagA protein was found to contribute to peptic ulcer.
Neutrophil-Activating Protein (NAP) recruits neutrophils to gastric mucosa causing inflammation.
Free radical production in the gastric lining due to H pylori , increases host cell mutation.
H pylori induces the production of TNF-α(tumor necrosis factor alpha) and Interleukin 8 that leads to host cells mutation.
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14. Laboratory characteristics non invasive testing
Culture: on blood or chocolate agar in a moist microaerophilic atmosphere. For isolation from clinical specimens, use campylobacter selective medium. Small colonies grow after 5-7 days at 37˚C.

15. Antigen Detection Test in Stool
Detection of H.pylori antigen in stool appropriate test in patients with H.pylori patients Absence of antigen indicates cure of Infection after Chemotherapy

16. Urea Breath Test
In this test test 13C or 14C C labelled urea is ingested labelled urea is ingested by patients If H.pylori is present the urease activity generates labelled Co that can be detected in the patients exhaled breath
اسم ورقم المقرر – Course Name and No.
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17. Invasive testing
Histological examination of biopsy specimens of gastric/duodenal mucosa take at endoscopy

18. Prevention
Eradication of infection will improve symptoms:
Such as (dyspepsia, gastritis, peptic ulcer and cancer).
Vaccination:
Promising results with studying adjuvant, antigens.
Determining route of immunization (oral or intramuscular).
Dietary methods: (eating broccoli, cabbage, honey, and drinking green tea).
Proper sanitation and clean sources of drinking water).

19. Antibiotic sensitivity
In vitro H.pylori is sensitive to amoxycillin, tetracycline, metronidazole, macrolides (clarithromycin).
However, in vivo their efficacy is often poor due to the low pH of the stomach, their failure to penetrate the gastric mucus and the low concentration of antibiotic obtained in the mucosa of the stomach.
Recently , Metronidazole in developing countries is becoming resistance (80-90%).

20. First line therapy
clarithromycin 500mg b.d. +
amoxicillin 1000mg or metrodiazole 500mg minimum of 7 days
In case of failure
Second line therapy
bismuth subsalicylate/subcitrate 120mg QDS (once a day) + metronidazole 500mg t.d.s. (3 times a day)+ tetracycline 500mg
for a minimum of 7 days
If bismuth is not available, PPI based triple therapies should be used
Subsequent failures should be handled on a case-case basis. Patients failing second-line therapy in primary care should be referred

21. Quadruple Therapies
7days regimen of combination of Amoxycillin , metronidazole, Ranitidine Bismuth Citrate and proton pump inhibitor (Omeprazole) have shown to increase the eradication rate up to 98%. Unfortunately it was followed by side effects such as vaginal candidiasis in 10% of women and Pseudomembranous colitis in 11% of patients.

22. Prevention Eradication of infection will improve symptoms:
Such as (dyspepsia, gastritis, peptic ulcer and cancer).
Vaccination:
Promising results with studying adjuvant, antigens.
Determining route of immunization (oral or intramuscular).
Dietary methods: (eating broccoli, cabbage, honey, and drinking green tea).
Proper sanitation and clean sources of drinking water).
اسم ورقم المقرر – Course Name and No.
4/21/2019

23. End
Thank you four your attention
Any question