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Helicobacter pylori
infection and its
consequences
We pathologists
knew squat
about gastritis
before H pylori
was discovered.
H pylori infects the
whole stomach, but
it induces a chronic
gastritis that is most
intense in the antal
mucosa
Classic H pylori gastritis:
the great blue biopsy
Plasmacytosis
(superficial) in
the lamina propria
Induced lymphoid follicles
at the base of the mucosa
Activity with
PMNs in the necks
In most cases, the bacteria
can be found in the H and E
stained section, on the
surface epithelium, often over
the intecellular junctions and
beneath the surface mucus
coat. They appear as tiny thin
rods often with a bend in the
center, like a set of wings.
Bugs on the surface of the epithelium
Often they hide in the detached mucus
Not all H pylori gastritis is the same.
There may be
 population differences
 individual differences
 minimal disease with tons of bugs
 intense disease with few bugs
 variable eosinophils
 variable activity
H pylori identification when they
are difficult to find on H&E;
other stains have been used.
Silver
Diff-quick
H pylori identification when
they are difficult to find on H&E
Immunostain, our current method
Active H pylori
antral gastritis
H pylori Gastritis
Untreated
Plasmacytosis
 Activity
 Bugs
 Lymphoid hyperplasia

Treated
Bugs disappear
 Activity stops
 Plasmacytosis recedes
 Lymphoid follicles atrophy

H pylori
killer
H pylori
killer
Biopsies that
look like
treated H pylori
gastritis are
common
Superficial
Plasmacytosis
No activity.
No bugs on
the surface.
Usually, this inactive
chronic gastritis has
no H pylori
In the pits
In the glands
These days, a few biopsies of inactive chronic
gastritis have bugs on immunostain, often deep in
the pits and even in the glands and not on the
surface. Thid may result from chronic PPI use
Otherwise, this common inactive
chronic gastritis without H pylori
has no name and no literature.
But we keep seeing it.
Chronic inactive gastritis,
with no bugs: WHY?

Biopsy missed bugs

different cause
proton pump inhibitors
 antibiotics

Approach to patients with
heartburn and dyspepsia
First, acid suppression,
commonly Proton Pump
Inhibitors (PPIs)
If no response, then upper
endoscopy and potential
biopsies
Protein pump inhibitor effects
Parietal cell acid secretion
antral pH
Hypergastrinemia
 Parietal cell hypertrophy: snouts
 ?Parietal cell hyperplasia
 ?Polyps containing fundic glands
 ECL cell stimulation in humans
unclear
Protein pump inhibitor effects
Parietal cell acid secretion
antral pH
Treats antral H pylori:
Bugs migrate proximally
or deeply
 activity disappears
 Plasmacytosis recedes
 lymphoid follicles atrophy
H pylori
Causes:
 peptic ulcers ( mechanism
unknown), a clinical disease
 chronic active gastritis,
mostly antral, not a clinical
disease
Complications of H pylori infection
Peptic ulcers, mainly in the duodenum
Adenocarcinoma, secondary to
dysplasias that develop in atrophic
gastritis (see atrophic gastritis module
for definitions and diagnostic criteria)
B cell lymphomas, both low and high
grade, probably developing in the
induced lymphoid follicles at the base
of the mucosa
There is a second
bacterium that causes an
active chronic gastritis,
similar to, but less
intense than, H pylori
gastritis.
Helicobacter heilmannii
Helicobacter heilmannii is
really rare around here.
The bugs:
7-10 microns
 Urease +
 Dog and cat transmitted

The disease:

39 cases in 15,180 antral bxs
(Heilmann & Borchard, Gut 32:137, 1991
Antrum 100%; body 20%
 Chronic active -it is, less than H pylori

H heilmannii comes from household
pets, so don’t share eating utensiles with
your cats and dogs unless you eat first.