Lecture Campylobacter & Helicobacter
22/05/2014 Prof. Abbas Hayat
•Food poisoning caused by Campylobacter species can be
debilitating, rarely life-threatening.
Linked with subsequent development of
Guillain- Barré syndrome (GBS), usually developing two to
three weeks after the initial illness.
•Contaminated drinking water and unpasteurized
milk provide an efficient means for distribution.
Contaminated food is a major source of isolated
infections, with incorrectly prepared meat and
poultry are normally the source of the bacteria.
Culture : Skirrow's medium is blood agar infused
with a cocktail of antibiotics: vancomycin, and
trimethoprim under microaerophilic conditions at
42 degrees.
Helicobacter pylori
• Bacterial characteristics:
• Morphology: Gram-negative, aerobic or
microaerophilic, spiral-shaped bacilli.
Motile with Flagella .
• Closely related to Helicobacter are species of the
genera Aquaspirillum, Azospirillum, Spirillum, and
Camplyobacter.
• In 1875, German scientists found helical shaped
bacteria in lining of the human stomach. The
bacteria could not be grown in culture and results
forgotten.
• The bacterium was rediscovered in 1979 by
Australian pathologist Robin Warren, who did
further research on it with Barry Marshall beginning
in 1981; they isolated the organisms from mucosal
specimens from human stomachs and the first to
successfully culture them. In their original paper,
Warren and Marshall contended that most stomach
ulcers and gastritis were caused by infection by this
bacterium and not by stress or spicy food as had
been assumed before.
• Medical community slow to recognize role of this bacterium in
stomach ulcers and gastritis, believing that no microorganism could
survive for long in the acidic environment of the stomach.
• Realization after further studies ,
Marshall drank a Petri dish of H. pylori, developed gastritis, bacteria
were recovered from his stomach lining, thereby satisfying three
out of the four Koch's postulates. The fourth satisfied after second
endoscopy ten days after revealed signs of gastritis and the
presence of "H. pylori".
• Marshall able to treat himself using a fourteen day dual therapy
with bismuth salts and metronidazole. Marshall and Warren went
on to show that antibiotics are effective in the treatment of many
cases of gastritis
• In 2005, Warren and Marshall were awarded the Nobel Prize in
Medicine for their work on H. pylori.
Saturday, August 2, 1997
Smug as a bug
• He was so sure he was right and conventional
medical wisdom wrong about the cause of
stomach ulcers that he swallowed bacteria to
prove his point. Now once-skeptical peers are
talking about a possible Nobel prize. MELISSA
SWEET reports.
Nobel Laureate Dr J Robin Warren
• Genetics :
Helicobacter pylori many strains of H . pylori
which are distinguished by the human
disease with which they are associated.
• Habitat:
Helicobacter pylori lives in interface between
the surface of gastric epithelial cells and the
overlying mucus gel.
Also in the gastric epithelium in the
duodenum and esophagus.
• 1983 that H. pylori was recognized
as having any medical importance.
• Now, it has been proven that H.
pylori infection is the main cause of
chronic superficial gastritis
associated with both gastric and
duodenal ulcers.
Human Disease.
• Peptic ulcer disease: An ulcer is now known to
be the result of an imbalance between
aggressive and defensive mechanisms in the
stomach and duodenum. Part of that imbalance
can be attributed to infection by H. pylori.
Humans only known host of
Helicobacter pylori.
Prevalence :
• In healthy people increases with age to over 50% in
people over the age of 60 in the west.
• In Asia 90-100%
• Blacks more susceptible to infection than Whites,
Incidence:
• Increases with decreasing socioeconomic
status.
• Evidence of H. pylori infection in families,
prisons, and nursing homes suggest that H.
pylori is spread by close personal contact.
• Drinking water main source in
underdeveloped countries.
• Helicobacter pylori infection usually persist
for life
• H. pylori produces urease …formation of
ammonia… pH increases.
• Cytotoxins, Toxic proteins, Platelet AF and
Lipopolysaccharides.
Immune Response
• Activation of neutrophils, monocytes and
macrophages, and the production of serum
antibody IgG and secretory antibody IgA.
• T cells proliferate as in a cell mediated
response.
DISEASES
• 1. Chronic superficial gastritis, which is an
inflammation of the stomach lining due to the
infiltration of lymphocytes, plasma cells,
eosinophils, and monocytes into the mucosal
lining of the stomach, which causes injury to the
gastric glands.
• 2.The immune response can also cause
inflammation of the duodenum, leading to
duodenal ulcers.
• 3. Atrophic gastritis, which is a nonspecific
inflammation of the entire lining of the stomach,
may be the result of the infiltration of
lymphocytes into the stomach.
• 4. MALT-type and other lymphomas
Diagnosis of H. pylori Infection
Invasive techniques:
• Culture. Because of fastidious nature of H. pylori,
Culturing tedious and is no more sensitive or specific than
simple Histologic analyses. Culturing H. pylori also
involves the cost of endoscopy, making the method even
less practical.
• Histologic analysis of biopsy. Routine Histologic
analysis of biopsy samples is common and practical.
Helpful also to visualize the mucosa, permitting detection
of Histologic gastritis and lesions such as MALT-type
lymphomas.
Requires endoscopy, diagnosis days after the procedure.
Campylobacter-like organism (CLO) test.
• This test is based on the fact that mucosal biopsy
specimens inoculated into a medium containing
urea and phenol red, a dye that turns pink in a pH
of 6.0 or greater. Inexpensive, Only one-half hour
is required for diagnosis of infection, and the test
has shown 98% sensitivity and 100% specificity.
• Invasive technique of choice for diagnosing H.
pylori infection.
Noninvasive Techniques:
• Helicobacter pylori Urea Breath Test
Urease activity detected by a breath test.
Urea radioactively labeled with carbon 13
and carbon 14 is ingested. Bacterial urease
splits off labeled carbon dioxide, which can
be detected in the breath. 100% sensitivity
and specificity.
• Detection of IgG
and secretory IgA.
• Enzyme-linked immunosorbent assay (ELISA).
Elevated antibody titer indicates current infection.
Accuracy and low cost makes this test an
attractive choice for detecting H. pylori
Treatment of Peptic Ulcer Disease
• Many excellent treatments for peptic
ulcer disease exist.
• In duodenal ulcers and gastric ulcers,
histamine H2-receptors can be blocked
to cause healing in about 90% of cases
within 8 weeks.
• Antibiotics a must.
Triple Therapy
• Eradication of Helicobacter pylori is defined as the
absence of the organism four or more weeks after
eradication therapy.
• Eradication rate for single-drug therapy is only 19%
for double-drug therapy is still only 48% . 82%,
achieved by combining
Bismuth + Metronidazole + Tetracycline.
Prepare well. Don’t be distracted,
during your exams

Campylobacter & Helicobacter

  • 1.
    Lecture Campylobacter &Helicobacter 22/05/2014 Prof. Abbas Hayat
  • 8.
    •Food poisoning causedby Campylobacter species can be debilitating, rarely life-threatening. Linked with subsequent development of Guillain- Barré syndrome (GBS), usually developing two to three weeks after the initial illness. •Contaminated drinking water and unpasteurized milk provide an efficient means for distribution. Contaminated food is a major source of isolated infections, with incorrectly prepared meat and poultry are normally the source of the bacteria. Culture : Skirrow's medium is blood agar infused with a cocktail of antibiotics: vancomycin, and trimethoprim under microaerophilic conditions at 42 degrees.
  • 9.
    Helicobacter pylori • Bacterialcharacteristics: • Morphology: Gram-negative, aerobic or microaerophilic, spiral-shaped bacilli. Motile with Flagella . • Closely related to Helicobacter are species of the genera Aquaspirillum, Azospirillum, Spirillum, and Camplyobacter.
  • 10.
    • In 1875,German scientists found helical shaped bacteria in lining of the human stomach. The bacteria could not be grown in culture and results forgotten. • The bacterium was rediscovered in 1979 by Australian pathologist Robin Warren, who did further research on it with Barry Marshall beginning in 1981; they isolated the organisms from mucosal specimens from human stomachs and the first to successfully culture them. In their original paper, Warren and Marshall contended that most stomach ulcers and gastritis were caused by infection by this bacterium and not by stress or spicy food as had been assumed before.
  • 11.
    • Medical communityslow to recognize role of this bacterium in stomach ulcers and gastritis, believing that no microorganism could survive for long in the acidic environment of the stomach. • Realization after further studies , Marshall drank a Petri dish of H. pylori, developed gastritis, bacteria were recovered from his stomach lining, thereby satisfying three out of the four Koch's postulates. The fourth satisfied after second endoscopy ten days after revealed signs of gastritis and the presence of "H. pylori". • Marshall able to treat himself using a fourteen day dual therapy with bismuth salts and metronidazole. Marshall and Warren went on to show that antibiotics are effective in the treatment of many cases of gastritis • In 2005, Warren and Marshall were awarded the Nobel Prize in Medicine for their work on H. pylori.
  • 12.
    Saturday, August 2,1997 Smug as a bug • He was so sure he was right and conventional medical wisdom wrong about the cause of stomach ulcers that he swallowed bacteria to prove his point. Now once-skeptical peers are talking about a possible Nobel prize. MELISSA SWEET reports.
  • 15.
    Nobel Laureate DrJ Robin Warren
  • 18.
    • Genetics : Helicobacterpylori many strains of H . pylori which are distinguished by the human disease with which they are associated. • Habitat: Helicobacter pylori lives in interface between the surface of gastric epithelial cells and the overlying mucus gel. Also in the gastric epithelium in the duodenum and esophagus.
  • 21.
    • 1983 thatH. pylori was recognized as having any medical importance. • Now, it has been proven that H. pylori infection is the main cause of chronic superficial gastritis associated with both gastric and duodenal ulcers.
  • 22.
    Human Disease. • Pepticulcer disease: An ulcer is now known to be the result of an imbalance between aggressive and defensive mechanisms in the stomach and duodenum. Part of that imbalance can be attributed to infection by H. pylori. Humans only known host of Helicobacter pylori.
  • 23.
    Prevalence : • Inhealthy people increases with age to over 50% in people over the age of 60 in the west. • In Asia 90-100% • Blacks more susceptible to infection than Whites,
  • 25.
    Incidence: • Increases withdecreasing socioeconomic status. • Evidence of H. pylori infection in families, prisons, and nursing homes suggest that H. pylori is spread by close personal contact. • Drinking water main source in underdeveloped countries.
  • 27.
    • Helicobacter pyloriinfection usually persist for life • H. pylori produces urease …formation of ammonia… pH increases. • Cytotoxins, Toxic proteins, Platelet AF and Lipopolysaccharides.
  • 28.
    Immune Response • Activationof neutrophils, monocytes and macrophages, and the production of serum antibody IgG and secretory antibody IgA. • T cells proliferate as in a cell mediated response.
  • 30.
    DISEASES • 1. Chronicsuperficial gastritis, which is an inflammation of the stomach lining due to the infiltration of lymphocytes, plasma cells, eosinophils, and monocytes into the mucosal lining of the stomach, which causes injury to the gastric glands. • 2.The immune response can also cause inflammation of the duodenum, leading to duodenal ulcers. • 3. Atrophic gastritis, which is a nonspecific inflammation of the entire lining of the stomach, may be the result of the infiltration of lymphocytes into the stomach. • 4. MALT-type and other lymphomas
  • 31.
    Diagnosis of H.pylori Infection Invasive techniques: • Culture. Because of fastidious nature of H. pylori, Culturing tedious and is no more sensitive or specific than simple Histologic analyses. Culturing H. pylori also involves the cost of endoscopy, making the method even less practical. • Histologic analysis of biopsy. Routine Histologic analysis of biopsy samples is common and practical. Helpful also to visualize the mucosa, permitting detection of Histologic gastritis and lesions such as MALT-type lymphomas. Requires endoscopy, diagnosis days after the procedure.
  • 33.
    Campylobacter-like organism (CLO)test. • This test is based on the fact that mucosal biopsy specimens inoculated into a medium containing urea and phenol red, a dye that turns pink in a pH of 6.0 or greater. Inexpensive, Only one-half hour is required for diagnosis of infection, and the test has shown 98% sensitivity and 100% specificity. • Invasive technique of choice for diagnosing H. pylori infection.
  • 34.
    Noninvasive Techniques: • Helicobacterpylori Urea Breath Test Urease activity detected by a breath test. Urea radioactively labeled with carbon 13 and carbon 14 is ingested. Bacterial urease splits off labeled carbon dioxide, which can be detected in the breath. 100% sensitivity and specificity. • Detection of IgG and secretory IgA. • Enzyme-linked immunosorbent assay (ELISA). Elevated antibody titer indicates current infection. Accuracy and low cost makes this test an attractive choice for detecting H. pylori
  • 35.
    Treatment of PepticUlcer Disease • Many excellent treatments for peptic ulcer disease exist. • In duodenal ulcers and gastric ulcers, histamine H2-receptors can be blocked to cause healing in about 90% of cases within 8 weeks. • Antibiotics a must.
  • 36.
    Triple Therapy • Eradicationof Helicobacter pylori is defined as the absence of the organism four or more weeks after eradication therapy. • Eradication rate for single-drug therapy is only 19% for double-drug therapy is still only 48% . 82%, achieved by combining Bismuth + Metronidazole + Tetracycline.
  • 37.
    Prepare well. Don’tbe distracted, during your exams

Editor's Notes

  • #2 Now when you have to differentiate between bloody diahorreha and and watery diahorrea, PMNs mucosal invasion., PMN`s and blood …. Invasios along with that is accompanying fWatery diahorreea , ETEC, parasite ever , with shigella and Campylobacter campylobacter, and exception to the rule is EHEC. persistant diahorrea, P parasites, P persistant
  • #3 Buzz word is seagulls , microaerophilic and grows at 42 o centigrade. ,
  • #4 42 o c entigrade, u have a patient , isolate every hing is to grow , campylobecter is to grow at 42.
  • #5 Poultry most common , it can also be feco oral, most likely poultry
  • #6 To isolate them from stool , most common cause of gastrenteritis in the US no not staph as it is a intoxication .
  • #9 The good thing is that it is self limiting 3-4 days, about 30 % of GB is attributed to Campmpylobacter , lit bit of cross reactivity and immunological mimimiclry leadind to ascendind paralysis. . U can also have reactive arthiritis. Rehydration however if someone is lingering on
  • #10 Does not grow at 42 o C , there is only one organism H, Pylori
  • #17 The most important factor is Urease, ther arent many organism which are urease positive
  • #19 Cyto toxin s are also virulent factors
  • #20 Reservoir is humans oral oral feco oral , very easily spreads amongst house holds
  • #21 H pylori is causing duodenal ulcers.
  • #30 You will like to know B cell lymphoma will resolve during treatment About Gastric adeno carcinoma … WHO classified it as type 1 carcinogen , two types of carcinomas
  • #32 Gold standard is biopsy with culture
  • #36 Treatment is complex because it is multiple and prolonged, the example I am given you one example , omenaperozol, amoxacillin plus Clathromycin, keeping in mind there are many other combinations. For 2-3 weeks.