Helicobacter pylori

What Does The Scientific Name

Describe?

Called “Helico”bacter

because of its helix shape.

bacter” means bacteria

What Is The Morphology?

It’s shaped like a helix or

Spiral

What Are The Oxygen

Requirements?

Needs Oxygen to live Inside of a human,

it lives in the stomach lining, so H. Pylori

is able to live within those oxygen

requirements.

In What Temperature And pH Does It

Grow Best?

Temperature

37 degrees Celsius

pH

4.5 and lower

H. Pylori is able to live with

the amount of acid in the

stomach’s lining

How Does A Person Contract It?

How people become

affected

Unknown

How people pass it on to

other people

Unknown

Been found in

Saliva

Dental Plaque

Stools of Children

Microbiology of Helicobacter pylori

• Microorganism discovered two decades

ago.

• Helicobacter pylori is specific for humans

& other primates.

• other species, e.g. H. felis, infect other

animals.

Gastric ulcer ->

Duodenal ulcer

l

Pre-1983: Are ulcers caused by an infectious agent? Experts: That’s

ridiculous! Everyone knows that ulcers are caused by stress.

Barry Marshall,

M.D.

• Helicobacter pylori is specific for humans & other primates.

Other mammals have their own Helicobacter species.

• Route of transmission is primarily person-to-person rather than

water contamination. Gastric-oral, oral-oral, and fecal-oral routes.

• Infections cluster in families.

Helicobacter pylori transmission

Gastric

Oral

Fecal

• H. pylori infection: 60-70% prevalence overall in the world.

• Higher prevalence in developing than developed countries.

• Within a country there is inverse relationship between infection

and socioeconomic status.

• After childhood, risk of acquiring (or reacquiring) H. pylori

infection is 0.5-1% per year in developed countries

% prevalence of H. pylori infection

Epidemiology

• Main transmission route: person-to-person (fecal-oral, oral oral, gastric-oral); contaminated water a less common route.

• Infections cluster in families.• Overall global prevalence of H. pylori (Hp) infection: 60-

70%.• Higher prevalence & earlier infection in developing

countries.• Developed countries: inverse relationship between

infection & socioeconomic status; after childhood, risk of acquiring (or reacquiring) infection is 0.5-1% per year.

• H. pylori infection: 90% cases of duodenal ulcer, 50-80% ofgastric ulcer, and 70-90% of gastric carcinoma.

• 10% lifetime risk of peptic ulcer disease (PUD) in U.S. overall.

• 20% lifetime risk of peptic ulcer disease (PUD) &/or

stomach cancer in H. pylori colonized.

Lesion Association

Chronic gastritis +

Gastric ulcer +

Duodenal ulcer +

Gastric adenocarcinoma +

Gastric lymphoma +

Pernicious anemia gastritis 0

Acute erosive gastritis 0

Gastroesophageal reflux 0

Association between H. pylori and upper

GI lesions:

• - H. pylori by itself or with other factors

accounts:

- 90% of cases of duodenal ulcer.

- 50-80% of cases of gastric ulcer

- 70-90% of cases of gastric carcinoma

20% life time risk of peptic ulcer disease and/or

gastric cancer in individuals who are infected

with H. pylori.

• Acute disease: nausea, abdominal pain, and malaise for 1-2 weeks.

• Most common symptom of peptic ulcer disease (PUD) is gnawing or burning.

• Epigastric pain that typically occurs between or before meals.

• or in early morning, and is relieved by eating or antacids.

• Hematemes is or protracted vomiting -> urgent care.

Clinical manifestations

Gastritis with

lymphocytic

hypertrophy

Gastric

adenocarcinoma

Endoscopic view

Pathology of infection: a mixture

of lymphocytes and

polymorphonuclear leukocytes in

the gastric epithelium.

H. pylori’s tolerance of the acid conditions (pH

1-2) of the stomach and this attribute to:

(1) Urease: first, urea -> CO2 + NH3, then NH3+ H+ -> NH4

+, which provides buffering.

(2) Residence in mucus and on the epithelial

cells.

(3) Capacity to create an ionic gradient at a

low pH.

(4) Release of factors that decrease acid

secretion by parietal cells during early

infection.

• Bacteria swim to gastric epithelium with flagella.• H. pylori’s tolerance of the acid conditions (pH 1-2) of the

stomach attributable to:• (1) Urease: urea -> CO2 + NH3, then NH3 + H+ -> NH4

+ provides buffering.• (2) Residence in and under mucus on the epithelial cells.• (3) Capacity to create an ionic gradient at a low pH

(proton diffusion potential).• (4) Release of factors that decrease acid secretion by

parietal cells during early infection.• An outer membrane protein is an adhesion for the Lewis b

antigen of blood type O individuals -> higher risk of PUD.

Disease occurrence

• Higher risk of disease with strains with vacuolating toxinVacA and the cagA gene pathogencity island.

• cagA pathogenicity island: induction of pro-inflammatory IL-8

• and secretion of bacterial molecules into host epithelial cells.

• VacA -> induction of apoptosis of host cells• Pathology of infection: a mixture of lymphocytes and• polymorphonuclear leukocytes in the gastric epithelium.• Mucosa-associated lymphoid tissue (MALT).

Bacteria enter the mucus layer and some adhere

specifically to gastric epithelial cells.

• Specific adhesion to Lewisb antigen (blood group

O).

• The mucus layer is depleted, and an inflammatory

response with neutrophils and lymphocytes begins.

• With less mucus, there is lowered protection of the

host cells to acid.

• An ulcer forms or there may continued

inflammation with atrophy and eventually possibly

adenocarcinoma.

• Mucosa-associated lymphoid tissue can progress

to gastric lymphoma.

Possible Mechanism for H. pylori establishes ulcer

Modified from D.S. Merrell & S. Falkow, Frontal and stealth attack strategies in microbial pathogenesis.

Nature 430: 250-6, 2004

How H. pylori establishes persistent infections

• Direct detection: H. pylori can be detected directly by

microscopy or by urease assay from a stomach biopsy,

but this requires endoscopy.

• Cultured: culture for H. pylori (invasive & expensive).

• Urease breath test: Strong but indirect evidence of

infection is a positive : the patient ingests a meal

containing 14C or 13C-urea, and the breath is examined

for the presence of 14CO2 or 13CO2.

• Detection of antibodies to H. pylori is evidence that the

patient has been infected but does not establish

whether the infection is still active.

• Detection of antigen of H. pylori is evidence that the patient has been infected and still active.

Diagnosis of H. pylori infection

How Is It Treated?

Only treat cases with

ulcers

No treatments for acute

cases

Upset stomach

• Acid reduction: through antacids, H2-receptor

antagonists (e.g. ranitidine), or proton pump inhibitors

(e.g. Omeprazole) will reduce ulcer symptoms and

healing, but there is a high relapse rate.

• Only with eradication of H. pylori is the risk of recurrent

ulcer substantially lowered.

• Two or more antimicrobial agents (metronidazole +

either amoxicillin or tetracycline) are more successful

than a single antibiotic in eradicating the infection.

• Bismuth subsalicylate (e.g. Pepto-Bismol) is effective

as an antimicrobial agent and often combined with

antibiotics.•

Treatment

Triple therapy two antimicrobial agents plus either H2

blocker or proton pump inhibitor for 2-4 weeks

(metronidazole, clarithromycin, amoxicillin or

tetracycline, or bismuth) combined with H2 blocker or

proton pump inhibitor.

Triple therapy regime