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Dr.T.V.Rao MD    Dr.T.V.Rao MD   1
Dr.T.V.Rao MD   2
Campylobacters causes Important     Zoonotic Infections                           Dr.T.V.Rao MD        3
History of Campylobacter First isolated as Vibrio fetus in 1909 from  spontaneous abortions in livestock                 ...
General Characteristics      Common to Superfamily Gram-negative Helical (spiral or curved) morphology; Tend to be  pleo...
Campylobacter jejuni                     Bacteria commonly found in animal feces. It is one of the most common causes of...
Morphology & Physiology of Campylobacter  Small, thin (0.2 - 0.5 um X 0.5 - 5.0 um),   helical (spiral or curved) cells w...
Motility – A Darting type                     Distinctive rapid  darting motility  • Long sheathed    polar flagellum   ...
Growth Requirements         Microaerophilic &  capnophilic  5%O2,10%CO2,85%N2 Thermophilic (42-43C)  (except C. fetus) ...
Important Zoonotic    Infection                        Campylobacter remains the                 leading cause worldwide...
C.jejuni carried in …. Although C. jejuni is  not carried by healthy individuals in the United States or Europe, it is o...
Laboratory Diagnosis                             Feces refrigerated & examined within few hours    Rectal swabs in semi...
Laboratory IdentificationMicroscopy:                            Gull-wing appearance in gram stain   Darting motility ...
Culture                     An atmosphere with reduced O2 (5% O2) with added CO2 (10% CO2)At 42 ℃ (for selection)Sever...
Selective Medium                      • Blood-free,                charcoal-based                selective               ...
Characteristics of C.jejuniCharacteristicGrowth at 25 °C                      Result                                     ...
Pathogenesis & Immunity Infectious dose and host immunity determine  whether gastro enteric disease develops    • Some pe...
Putative Virulence FactorsCellular components:     Endotoxin     Flagellum: Motility     Adhesins: Mediate attachment t...
Other Species of Campylobacters C jejuni infections may  also produce serious                                bacteremic ...
Other Species ofCampylobacters        Campylobacter                            upsaliensis may cause                    ...
Treatment, Prevention & Control Gastroenteritis:   •Self-limiting; Replace fluids and electrolytes                       ...
Complication are rare    but occurs occasionally                           Complications are relatively rare, but infect...
Sequelae to Infection             Guillain-Barre syndrome (GBS), a demy elating disorder  resulting in acute neuromuscul...
Complications with          C.jejuni                          Guillain-Barre  Syndrome (GBS)  • Favorable     prognosis ...
Dr.T.V.Rao MD   25
A Tribute to Warren and        Marshallfor Discovery of H.pylori                     Dr.T.V.Rao MD     26
Helicobacter pylori              Helicobacter pylori (H. pylori) is a type of bacteria. Researchers believe that H. pylo...
Helicobacter pylori               Helicobacter pylori is the prototype organism in this                       gastritis,...
Helicobacter pyloriHelicobacter pylori is a spiral gram negative bacteria.It has a multiple polar flagella above the pol...
Beginning of Scientific           understanding                         Peptic ulcers have plagued men throughout the  c...
History of H.pylori                         for short) was first Helicobacter pylori (H.pylori  discovered in the stomac...
Global prevalence of H. Pylori             
Land Mark Changes in           H.pylori The name of the           bacterium was  grammatically  corrected in 1987 to  Ca...
How is it transmitted?                           Believed to be transmitted orally due to tainted food  or water. Also ...
Genes Contribute to    Pathogenicity          CAG – Cytotoxin associated geneVac – Vacuolating cytotoxin gene          ...
Pathogenic Mechanism                          It is well established that urease, Vacuolating  cytotoxic VacA, and the p...
Culturing H.pyloriH.pylori grows on  Skirrow”s medium  with 1Vancomycin,  2 Polymyxin  3 TrimethoprimGrows in 3 -6 days a...
Biochemical CharactersMotileCatalase +Oxidase + Strong producer of     Urease               Dr.T.V.Rao MD   38
Urea Hydrolysis                      UreaseC=O(NH2)2 + H+   + 2H2O  HCO3- + 2 (NH4+)Urea                                B...
Pathology and             Pathogenesis                          H.pylori is found in the deep mucus layer Grows optimal...
Mechanisms inPathogenicity          Dr.T.V.Rao MD   41
Localization of H.pylori                     Dr.T.V.Rao MD    42
Pathogenesis                          The potential character of H.pylori lie with  production of potent Urease activity...
Factors contributing to Peptic            ulceration                             There is a strong  association between ...
H.pylori causes Peptic ulcers in the             Stomach                               Dr.T.V.Rao MD           45
Factors influencing       Pathogenicity               Lipopolysaccharides - damage mucosal cells  and Ammonia produced b...
Clinical Manifestations          Acute infection  Upper Gastrointestinal illness            Nausea            Pain      ...
Consequences of H.pylori Infection                             Dr.T.V.Rao MD          48
Association of Duodenal and     Gastric ulcers in H.pylori                   About 90 % of patients with Duodenal ulcer,...
Mechanism of Cancer in      H.pylori                   Dr.T.V.Rao MD   50
Laboratory Diagnosis           Specimens for histopathology – Gastric biopsy specimens can be used for Histological exam...
Endoscopy – Gastric      Biopsy               Dr.T.V.Rao MD   52
Serology The detection of  Antibodies in active  infection is useful But the tests are limited  utility as antibodies  p...
Special Tests for H.pylori Rapid tests for detection of  Urease activity are widely  used in presumptive  identification ...
Urea Breath Test H. pylori infection can  be detected in the  exhaled breath using  this special test. This  test is posi...
Carbon-14-urea Breath Test                       Dr.T.V.Rao MD     56
Urea Breath TestIn this test 13C or 14C labeled urea is ingested by patientsIf H.pylori is present the urease activity g...
Antigen Detection Test in           StoolDetection of H.pylori antigen in stool is appropriate test in patients with H.py...
H.pylori and Cancer                .If a person has had an H.pylori                infection constantly for 20-30         ...
Treatment                        Triple therapy has prompt response, contain a  combination of following drugs    1 Metr...
Other Drug Combinations                         Other alternatives   Proton pump inhibitor directly inhibit    H.pylori ...
Vaccines trails for H.pylori      are in Progress                         pylori may A vaccination against Helicobacter ...
Epidemiology                         In Developed countries H.pylori are present in <20 %  of the persons below 30 years...
Helicobacter pylori changes the  future of Gastroenterology                           Dr.T.V.Rao MD        64
Barry J. Marshall and J. RobinWarren have been awarded the2005 Nobel Prize in medicine                          Dr.T.V.Ra...
Helicobacter Foundation The "Helicobacter                            Foundation" was  founded by Prof. Barry  J. Marshal...
Created by Dr.T.V.Rao MD for ‘e’learning resources for Microbiologists        in Developing World              Email   ...
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Campylobacter jejuni & Helicobacter pylori

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Campylobacter jejuni & Helicobacter pylori

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Transcript of "Campylobacter jejuni & Helicobacter pylori "

  1. 1. Dr.T.V.Rao MD Dr.T.V.Rao MD 1
  2. 2. Dr.T.V.Rao MD 2
  3. 3. Campylobacters causes Important Zoonotic Infections  Dr.T.V.Rao MD 3
  4. 4. History of Campylobacter First isolated as Vibrio fetus in 1909 from spontaneous abortions in livestock  Campylobacter enteritis was not recognized until the mid-1970s when selective isolation media were developed for culturing campylobacters from human feces Most common form of acute infectious diarrhea in developed countries; Higher incidence than Salmonella & Shigella combined Dr.T.V.Rao MD 4
  5. 5. General Characteristics Common to Superfamily Gram-negative Helical (spiral or curved) morphology; Tend to be pleomorphic Characteristics that facilitate penetration and colonization of mucosal environments (e.g., motile by polar flagella; corkscrew shape) Microaerophilic atmospheric requirements Become coccoid when exposed to oxygen or upon prolonged culture Neither ferment nor oxidize carbohydrates Dr.T.V.Rao MD 5
  6. 6. Campylobacter jejuni Bacteria commonly found in animal feces. It is one of the most common causes of human gastroenteritis in the world. Food poisoning caused by Campylobacter species can be severely debilitating, but is rarely life- threatening. It has been linked with subsequent development of Guillain-Barre syndrome (GBS), which usually develops two to three weeks after the initial illness Dr.T.V.Rao MD 6
  7. 7. Morphology & Physiology of Campylobacter  Small, thin (0.2 - 0.5 um X 0.5 - 5.0 um), helical (spiral or curved) cells with typical  gram-negative cell wall; “Gull-winged” appearance • Tendency to form coccoid & elongated forms on prolonged culture or when exposed to O2 Dr.T.V.Rao MD 7
  8. 8. Motility – A Darting type  Distinctive rapid darting motility • Long sheathed polar flagellum at one (polar) or both (bipolar) ends of the cell • Motility slows quickly in wet mount preparation Dr.T.V.Rao MD 8
  9. 9. Growth Requirements  Microaerophilic & capnophilic 5%O2,10%CO2,85%N2 Thermophilic (42-43C) (except C. fetus) • Body temperature of natural avian reservoir May become nonculturable in nature Dr.T.V.Rao MD 9
  10. 10. Important Zoonotic Infection   Campylobacter remains the leading cause worldwide of zoonotic disease in humans, surpassing Salmonella infections. Moreover, cases are still believed to be underreported. Often causing the same symptoms as Salmonella, such as mild to severe diarrhea, Campylobacter infections can also be an infectious trigger for the more serious Guillain-Barre Syndrome. Dr.T.V.Rao MD 10
  11. 11. C.jejuni carried in …. Although C. jejuni is  not carried by healthy individuals in the United States or Europe, it is often isolated from healthy cattle, chickens, birds and even flies. It is sometimes present in non-chlorinated water sources such as streams and ponds. Dr.T.V.Rao MD 11
  12. 12. Laboratory Diagnosis   Feces refrigerated & examined within few hours  Rectal swabs in semisolid transport medium  Blood drawn for C. fetus  Care to avoid oxygen exposure  Selective isolation by filtration of stool specimen  Enrichment broth & selective media  Filtration: pass through 0.45 μm filters Dr.T.V.Rao MD 12
  13. 13. Laboratory IdentificationMicroscopy:   Gull-wing appearance in gram stain  Darting motility in fresh stool (rarely done in clinical lab)  Fecal leukocytes are commonly presentIdentification:  Growth at 25o, 37o, or 42-43oC  Hippurate hydrolysis (C. jejuni is positive)  Susceptibility to nalidixic acid & cephalothin Dr.T.V.Rao MD 13
  14. 14. Culture An atmosphere with reduced O2 (5% O2) with added CO2 (10% CO2)At 42 ℃ (for selection)Several selective media can be used (eg, Skirrow’s medium)Two types of colonies:  watery and spreading  round and convex Dr.T.V.Rao MD 14
  15. 15. Selective Medium  • Blood-free, charcoal-based selective medium agar (CSM) for isolation of Campylobacter jejuni Dr.T.V.Rao MD 15
  16. 16. Characteristics of C.jejuniCharacteristicGrowth at 25 °C  Result -Growth at 35-37 °C -Growth at 42 °C +Nitrate reduction +Catalase test +Oxidase test +Growth on MacConkey agar +Motility (wet mount) +Glucose utilization -Hippurate hydrolysis +Resistance to nalidixic acid -Resistance to cephalothin + Dr.T.V.Rao MD 16
  17. 17. Pathogenesis & Immunity Infectious dose and host immunity determine whether gastro enteric disease develops • Some people infected with as few as 500 organisms while others need >106 CFU Pathogenesis not fully characterized • No good animal model • Damage (ulcerated, edematous and bloody) to the mucosal surfaces of the jejunum, ileum, colon • Inflammatory process consistent with invasion of the organisms into the intestinal tissue; M-cell (Payers patches) uptake and presentation of antigen to underlying lymphatic system Non-motile & adhesion-lacking strains are a virulent Dr.T.V.Rao MD 17
  18. 18. Putative Virulence FactorsCellular components:  Endotoxin  Flagellum: Motility  Adhesins: Mediate attachment to mucosa  Invasins  GBS is associated with C. jejuni Serogroup O19  S-layer protein “microcapsule” in C. fetus:Extracellular components:  Enterotoxins  Cytopathic toxins Dr.T.V.Rao MD 18
  19. 19. Other Species of Campylobacters C jejuni infections may also produce serious  bacteremic conditions in individuals with AIDS. Most reported bacteremias have been due to Campylobacter fetus fetus infection. Campylobacter lari, which is found in healthy seagulls, has also been reported to produce mild recurrent Dr.T.V.Rao MD 19 diarrhea in children
  20. 20. Other Species ofCampylobacters  Campylobacter  upsaliensis may cause diarrhea or bacteremia, while Campylobacter hyointestinalis, which has biochemical characteristics similar to those of C fetus, causes occasional bacteremia in immunocompromised Dr.T.V.Rao MD individuals. 20
  21. 21. Treatment, Prevention & Control Gastroenteritis: •Self-limiting; Replace fluids and electrolytes  •Antibiotic treatment can shorten the excretion period; Erythromycin is drug of choice for severe or complicated enteritis & bacteremia; Fluoroquinolones are highly active (e.g., ciprofloxacin was becoming drug of choice) but fluoroquinolones resistance has developed rapidly since the mid-1980s apparently related to unrestricted use and the use of enrofloxacin in poultry •Azithromycin was effective in recent human clinical trials •Control should be directed at domestic animal reservoirs and interrupting transmission to humans Dr.T.V.Rao MD 21
  22. 22. Complication are rare but occurs occasionally  Complications are relatively rare, but infections have been associated with reactive arthritis, hemolytic uremic syndrome, and following septicemia, infections of nearly any organ. The estimated case/fatality ratio for all C. jejuni infections is 0.1, meaning one death per 1,000 cases. Fatalities are rare in healthy individuals and usually occur in cancer patients or in the otherwise debilitated. Only 20 reported cases of septic abortion induced by C. jejuni have been recorded in the literature. Dr.T.V.Rao MD 22
  23. 23. Sequelae to Infection  Guillain-Barre syndrome (GBS), a demy elating disorder resulting in acute neuromuscular paralysis, is a serious sequelae of Campylobacter infection . An estimated one case of GBS occurs for every 1,000 cases of Campylobacteriosis Up to 40% of patients with the syndrome have evidence of recent Campylobacter infection . Approximately 20% of patients with GBS are left with some disability, and approximately 5% die despite advances in respiratory care. Campylobacteriosis is also associated with Reiter syndrome, a reactive arthropathy. In approximately 1% of patients with campylobacteriosis, the sterile postinfection process occurs 7 to 10 days after onset of diarrhea . Multiple joints can be affected, particularly the knee joint. Pain and incapacitation can last for months or become chronic. Dr.T.V.Rao MD 23
  24. 24. Complications with C.jejuni  Guillain-Barre Syndrome (GBS) • Favorable prognosis with optimal supportive care Intensive-care unit for 33% of cases Dr.T.V.Rao MD 24
  25. 25. Dr.T.V.Rao MD 25
  26. 26. A Tribute to Warren and Marshallfor Discovery of H.pylori  Dr.T.V.Rao MD 26
  27. 27. Helicobacter pylori 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 per cent 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 Dr.T.V.Rao MD 27
  28. 28. Helicobacter pylori  Helicobacter pylori is the prototype organism in this gastritis, group. It is associated with antral gastric ulcers, and gastric carcinoma. Dr.T.V.Rao MD 28
  29. 29. Helicobacter pyloriHelicobacter pylori is a spiral gram negative bacteria.It has a multiple polar flagella above the pole and motile Dr.T.V.Rao MD 29
  30. 30. Beginning of Scientific understanding  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 laboratory Dr.T.V.Rao MD 30
  31. 31. History of H.pylori  for short) was first Helicobacter pylori (H.pylori 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. Dr.T.V.Rao MD 31
  32. 32. Global prevalence of H. Pylori 
  33. 33. 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. Dr.T.V.Rao MD 33
  34. 34. How is it transmitted?  Believed to be transmitted orally due to tainted food or water. Also believed to be passed through belching, or gastro-esophageal reflux, which is when small amount of stomachs contents is forced up the esophagus. After this process, it’s believed that the H. Pylori is passed orally.
  35. 35. Genes Contribute to Pathogenicity CAG – Cytotoxin associated geneVac – Vacuolating cytotoxin gene Dr.T.V.Rao MD 35
  36. 36. Pathogenic Mechanism  It is well established that urease, Vacuolating cytotoxic VacA, and the pathogenicity island (cag PAI) gene products, are the main factors of virulence of this organism. Thus, individuals infected with strains that express these virulence factors probably develop a severe local inflammation that may induce the development of peptic ulcer and gastric cancer. The way the infection spreads throughout the world suggests the possibility that there are multiple pathways of transmission. Dr.T.V.Rao MD 36
  37. 37. Culturing H.pyloriH.pylori grows on Skirrow”s medium with 1Vancomycin, 2 Polymyxin 3 TrimethoprimGrows in 3 -6 days at 370cColonies appear Translucent 1-2 mm in diameterOptimal growth occurs in Microaerophic environment Dr.T.V.Rao MD 37
  38. 38. Biochemical CharactersMotileCatalase +Oxidase + Strong producer of Urease Dr.T.V.Rao MD 38
  39. 39. Urea Hydrolysis UreaseC=O(NH2)2 + H+ + 2H2O  HCO3- + 2 (NH4+)Urea Bicarbonate Ammonium ions And then… HCO3-  CO2 + OH- Dr.T.V.Rao MD 39
  40. 40. 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 Dr.T.V.Rao MD 40
  41. 41. Mechanisms inPathogenicity  Dr.T.V.Rao MD 41
  42. 42. Localization of H.pylori  Dr.T.V.Rao MD 42
  43. 43. Pathogenesis  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. Dr.T.V.Rao MD 43
  44. 44. 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 Dr.T.V.Rao MD 44
  45. 45. H.pylori causes Peptic ulcers in the Stomach  Dr.T.V.Rao MD 45
  46. 46. Factors influencing Pathogenicity  Lipopolysaccharides - damage mucosal cells and Ammonia produced by Urease activity may directly damage cells. Gastritis – Chronic and active inflammation establishes Polymorph nuclear and Mononuclear cell infiltration within the Epithelial and Lamina propria Events lead to Destruction of epithelium is common. Glandular atrophy is common. Dr.T.V.Rao MD 46
  47. 47. Clinical Manifestations Acute infection Upper Gastrointestinal illness Nausea Pain Fever – very occasionallyAcute symptoms lasts for < 1 week, May extend up to 2 weeksInfection last for years, decades or even lifetime Dr.T.V.Rao MD 47
  48. 48. Consequences of H.pylori Infection  Dr.T.V.Rao MD 48
  49. 49. 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 Dr.T.V.Rao MD 49
  50. 50. Mechanism of Cancer in H.pylori  Dr.T.V.Rao MD 50
  51. 51. Laboratory Diagnosis 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 Dr.T.V.Rao MD 51
  52. 52. Endoscopy – Gastric Biopsy  Dr.T.V.Rao MD 52
  53. 53. Serology 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. Dr.T.V.Rao MD 53
  54. 54. 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 Dr.T.V.Rao MD 54
  55. 55. 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%. Dr.T.V.Rao MD 55
  56. 56. Carbon-14-urea Breath Test  Dr.T.V.Rao MD 56
  57. 57. Urea Breath TestIn this test 13C or 14C labeled urea is ingested by patientsIf H.pylori is present the urease activity generates labeled Co2 that can be detected in the patients exhaled breath Dr.T.V.Rao MD 57
  58. 58. 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. Dr.T.V.Rao MD 58
  59. 59. H.pylori and Cancer .If a person has had an H.pylori infection constantly for 20-30 years, it can lead to cancer of the stomach. This is the reason that the World Health Organizations (WHO) International Agency for Research into Cancer (IARC) has classified H.pylori as a “Class- I- Carcinogen” i.e. in the same category as cigarette smoking is to cancer of the lung & respiratory tract. Dr.T.V.Rao MD 59
  60. 60. Treatment  Triple therapy has prompt response, contain a combination of following drugs 1 Metronidazole 2 Bismuth subsalicylate or Bismuth sub citrate 3 Amoxicillin or Teracycles administered up to 14 days Eradicates H.pylori In 70 – 95 % of patients Acid suppressing agent is supporting Dr.T.V.Rao MD 60
  61. 61. Other Drug Combinations  Other alternatives Proton pump inhibitor directly inhibit H.pylori Combined with Amoxicillin Clarithromycin or Amoxicillin And Metronidazole Dr.T.V.Rao MD 61
  62. 62. Vaccines trails for H.pylori are in Progress  pylori may A vaccination against Helicobacter represent both prophylactic and therapeutic approaches to the control of H. pylori infection. Different protective H. pylori-derived antigens, such as urease, vacuolating cytotoxin A, cytotoxin- associated antigen, neutrophil-activating protein and others can be produced at low cost in prokaryote expression systems and most of these antigens have already been administered to humans and shown to be safe. Dr.T.V.Rao MD 62
  63. 63. Epidemiology  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. Dr.T.V.Rao MD 63
  64. 64. Helicobacter pylori changes the future of Gastroenterology  Dr.T.V.Rao MD 64
  65. 65. Barry J. Marshall and J. RobinWarren have been awarded the2005 Nobel Prize in medicine  Dr.T.V.Rao MD 65
  66. 66. Helicobacter Foundation The "Helicobacter  Foundation" was founded by Prof. Barry J. Marshall in early 1994, and is dedicated to providing you with the latest information about Helicobacter pylori, its diagnosis, treatment and clinical perspectives. Dr.T.V.Rao MD 66
  67. 67. Created by Dr.T.V.Rao MD for ‘e’learning resources for Microbiologists in Developing World Email doctortvrao@gmail.com Dr.T.V.Rao MD 67
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