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Helicobacter pylori ( H. pylori ) is a type of bacteria. Researchers believe that H. pylori is responsible for the majority of peptic ulcers.
H. pylori infection is common in the United States. About 20 percent of people under 40 years old and half of those over 60 years have it. Most infected people, however, do not develop ulcers. Why H. pylori does not cause ulcers in every infected person is not known. Most likely, infection depends on characteristics of the infected person, the type of H. pylori , and other factors yet to be discovered
Peptic ulcers have plagued men throughout the centuries, but the exact cause of the condition was uncertain. In 1940, Dr. A. Stone Freedberg of Harvard Medical School identified unusual curved bacteria in the stomachs of ulcer victims; he suspected that they might be responsible for ulcers but abandoned the research when his team was unable to grow the bacteria in the lab
History of H.pylori
Helicobacter pylori (H.pylori for short) was first discovered in the stomachs of patients with gastritis & stomach ulcers nearly 25 years ago by Dr Barry J. Marshall and Dr J. Robin Warren of Perth, Western Australia. At the time (1982/83) the conventional thinking was that no bacterium can live in the human stomach as the stomach produced extensive amounts of acid which was similar in strength to the acid found in a car-battery. Marshall & Warren literally “re-wrote” the text-books with reference to what causes gastritis & gastric ulcers.
Land Mark Changes in H.pylori
The name of the bacterium was grammatically corrected in 1987 to Campylobacter pylori and, in 1989 the bacterium was renamed Helicobacter pylori and assigned as the type species of a novel genus due to its 16s rRNA sequence. Interest in this bacterium is reflected in the increase in the number of papers on the subject from 20 in 1984 to over 300 in 1990 and over 1000 in 1999 making it one of the most active areas of research in the medical field
Helicobacter pylori is a spiral gram negative bacteria.
It has a multiple polar flagella above the pole and motile
H.pylori grows on
Skirrow”s medium with 1Vancomycin,
Grows in 3 -6 days at 37 0 c
Translucent 1-2 mm in diameter
Optimal growth occurs in Microaerophic environment
Strong producer of
Pathology and Pathogenesis
H.pylori is found in the deep mucus layer
Grows optimally at pH 6.0 to 7.0
But gastric mucosa has a strong buffering in spite of lower pH on the lumen side of stomach
H.pylori also produces a protease that modifies the gastric mucus and further reduces the ability of acid through the mucus
Mechanisms in Pathogenicty
The potential character of H.pylori lie with production of potent Urease activity which yields production of Ammonia and further buffering acid.
H.pylori is quite motile even in mucus finds its way to epithelial surface
H.pylori overlies the gastric type but not intestinal epithelial cells.
Factors contributing to Peptic ulceration
There is a strong association between presence of H.pylori infection and peptic ulceration
Mucosal inflammation and damage involves both bacterial and host factors
H.Pylori causes Peptic ulcer in the Stomach
Factors influencing Pathogenicty
Lipopolysaccharides - damage mucosal cells and Ammonia produced by Urease acitivity may directly damage cells.
Gastritis – Chronic and active inflammation establishes Polymorphonuclear and Mononuclear cell infiltration within the Epithelial and Lamina propria
Events lead to Destruction of epithelium is common.
Glandular atrophy is common.
Upper Gastrointestinal illness
Fever – very occasionally
Acute symptoms lasts for < 1 week,
May extend upto 2 weeks
Infection last for years, decades or even lifetime
Consequences of H.pylori Infection
Association of Duodenal and Gastric ulcers in H.pylori
About 90 % of patients with Duodenal ulcer, and 50- 80 % of gastric ulcers are associated with H.pylori infection.
H.pylori may have greater role in Gastric carcinoma and Lymphomas
Mechanism of Cancer in H.pylori
Specimens for histopathology – Gastric biopsy specimens can be used for Histological examination
Specimens obtained after Gastroscopy, Biopsy, routine stains will demonstrate Gastritis and special stains show curved spiral organisms
Specimens collected in sterile saline mixed are used for culturing
Endoscopy – Gastric Biopsy
Culturing for H.pylori
Culturing of H.pylori needs specific conditions
Chocolate Medium with
Vancomycin, Nalidixic acid
The detection of Antibodies in active infection is useful
But the tests are limited utility as antibodies persist even after H.pylori infection is eradicated.
Several commercial kits are available, but lacks the role in identifying acute infections.
Special Tests for H.pylori
Rapid tests for detection of Urease activity are widely used in presumptive identification of Gastric Biopsy specimens.
Gastric Biopsy can be placed into urea containing medium with color indicator .
If H.pylori is present the Urease rapidly splits urea and resulting shift in pH yields a color change in the medium
Urea Breath Test
H. pylori infection can be detected in the exhaled breath using this special test. This test is positive only if the person has a current infection. Sensitivity and specificity of this test ranges from 94-98 %.
Urea Breath Test
In this test 13 C or 14 C labelled urea is ingested by patients
If H.pylori is present the urease activity generates labelled Co 2 that can be detected in the patients exhaled breath
Antigen Detection Test in Stool
Detection of H.pylori antigen in stool is appropriate test in patients with H.pylori infection
Absence of antigen indicates cure of Infection after Chemotherapy.
Triple therapy has prompt response, contain a combination of following drugs
2 Bismuth subsalicylate or Bismuth sub citrate
3 Amoxicillin or Tetracycles
administered upto 14 days
In 70 – 95 % of patients
Acid suppressing agent is supporting
Other Drug Combination
Proton pump inhibitor directly inhibit
Clarithromycin or Amoxicillin
In Developed countries H.pylori are present in <20 % of the persons below 30 years.
By 60 years prevalence increases to 40 – 60 %
In Developing countries prevalence of infection is higher to 80 % even in younger individuals
Person to person transmission of H.pylori is likely because of interfamilial clustering of infection
Acute epidemics of Gastritis suggest a common source of H.pylori.
Discovery of H.pylori changes the Peptic Ulcer Disease
Barry J. Marshall and J. Robin Warren have been awarded the 2005 Nobel Prize in medicine
Created for Graduate Medical Students in Devloping World Dr.T.V.Rao MD Email [email_address]