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HELICOBACTER PYLORI
Background
Human stomach long considered inhospitable for
bacteria
Spiral shaped organisms occasionally visualized in
gastric mucous layer, but no evidence of disease
association
Organism classified first as Campylobacter pylori
Now Helicobacter pylori
Other species of Helicobacter isolated from
stomach, intestine of other animals
Marshall and Warren culture organism from human
gastric mucosa and show association with gastric
inflammation
MICROBIOLOGY
1. Gram negative, spiral, flagellated
(motile) bacilli
2. Slow growing, requires complex
media, microaerophilic
3. Oxidase and catalase positive
4. Produces urease
5. Noninvasive; proliferates in
mucus overlying gastric type
mucosa
6. Not cleared by host immune
response
TRANSMISSION
1. Humans are major - if not only - reservoir
2. Transmission believed to be by fecal-oral
route
organism can be cultured from feces
family members often carry same strain
prevalence of infection likely related to
inferior hygienic conditions and poor
sanitation
infection from environment or from animals
cannot be totally excluded
EPIDEMIOLOGY
1. Gastric colonization rate in developing countries is
about 80%
Very high from early childhood
2. Gastric colonization rate in US and other
developed countries is about 30%
3. Prevalence of infection increases with age
Age 10 = ~5%
Age 30 = ~ 25%
Age 60 = ~ 50%
4. In US, prevalence rates are higher in AfricanAmericans and Hispanics
5. Age and low income = main risk factors for H.
pylori infection
PATHOGENESIS
Colonization
1. Most bacteria killed in hostile environment of gastric
lumen
2. H. pylori proliferates in mucus layer over epithelium
and is not cleared by host immune response
3. H. pylori survives and grows there because of a
variety of virulence factors that contribute to gastric
inflammation, alter gastric acid production, and cause
tissue destruction.
VIRULENCE FACTORS
Initial colonization facilitated by:
Acid inhibitory protein - blocks acid
secretion from parietal cells during acute
infection
Urease - neutralizes gastric acids due to
ammonia production, also stimulates
monocytes and neutrophil chemotaxis,
stimulates production of inflammatory
cytokines
Heat shock protein - enhances urease
expression; co-expressed with urease on
bacterial surface
Nonendoscopic Testing
1. Antibody testing (quantitative and qualitative)
Advantages : Inexpensive, widely available, very good NPV
PPV dependent upon background H. pylori prevalence.
Disadvantages : Not recommended after H. pylori therapy