Diagnostic laboratory tests
 Specimen
o Spiral –shaped
o Gram –negative rod
o Associated with antral gastritis, duodenal and gastric ulcers,
gastric adenocarcinoma, gastric MALT lymphomas
Morphology
 Typical organisms
o (+) multiple flagella at one pole
o Actively motile
 Culture
o Grows in 3 – 6 d at 37C, microaerophilic environment
o Media for primary isolation: Skirrow’s medium with
vancomycin, polymyxin B, and trimethroprim, chocolate
medium, others with abx (vancomycin, nalidixic acid,
amphotericin)
o Colonies: translucent; 1 -2 mm diameter
 Growth characteristics
o Oxidase (+)
o Catalase (+)
o Motile
o Strong producer of urease
Pathogenesis and pathology
o Grows optimally at pH 6.0 – 7.0
o Killed or not grow at gastric lumen pH (pH 1.0 – 2.0)
o Epithelial side (pH 7.4) – (+) H. pylori deep in mucous layer
near epithelial surface
o Produces proteases – modifies gastric mucus; reducing
ability of acid to diffuse thru mucus
o Potent urease activity – prodxn of ammonia; buffers acid
o Motile – find its way to epithelial surface
Overlies gastric –type epithelial cells but not intestinal –
type cells
o H. pylori infxn – gastritis and hypochlorhydria; strong
association with duodenal ulceration
o Mucosal inflammation and damage >> bacterial and host
factors >> toxins and lipopolysaccharides damage cells as
well as ammonia
o Histologic: (+) polymorphonuclear and mononuclear cell
infiltrates seen – epithelium and lamina propria
Vacuoles – pronounced
Epithelial destruction – common
(+) glandular atrophy
H. pylori is a major risk factor for gastric cancer
Clinical findings
 Acute infection
- UG illness (nausea and pain)
- (+) vomiting and fever
- Last for less than 1 week (2 weeks)
 Colonizes after infection
- Infection may persist for years or decades
- 90% with DU and 50 – 80% GU have H. pylori infxn
- Risk factor for gastric carcinoma and lymphoma
o Gastric biopsy – histologic exam; minced in saline for culture
o Blood – serum abd determination
o Stool – Ag detection
 Smear
o Routine stains – gastritis
o Giemsa/special silver stains – curved or spiral –shaped
organism
o Diagnosis of H. pylori can be made histologically (requires
gastroscopy with biopsy)
 Culture
o Performed when not responding to tx and a need to assess
susceptibility
 Antibodies
o Serum abd persists even after eradication
o Role in diagnosing active infection or after therapy is limited
 Special tests
o Rapid test – urease activity (presumptive ID of H. pylori)
o Gastric biopsy material placed onto urea –containing medium
with color indicator
(+) H. pylori – urease split urea rapidly (1 – 2 h); color change
o Urea breath tests – 13C or 14C-labeled urea is ingested
(+) H. pylori – urease activity forms CO2 (detected in exhaled
breath
o Stool Ag detection – test of cure for pt with H. pylori infxn who
have been treated
Immunity
- Infected: IgM abd response
- Production of IgG and IgA: (chronically infected – persists
systemically and at the mucosa)
- Early abx tx of H. pylori blunts abd response > subject for rpt
infection
Treatment
 Triple therapy
o Metronidazole
- + bismuth subsalicylate/ bismuth subcitrate
+ amoxicillin/ tetracycline
for 14 days (eradicated in 70 – 95% of pts)
 Acid –suppressing agent for 4 – 6 weeks
o Enhances ulcer healing
o PPI – directly inhibit H. pylori; potent urease inhibitor (7 – 10d
alone + amox, clari or quadruple therapy – PPI
metronidazole, tetra, and bismuth for 10 days
Epidemiology and control
o Present in gastric mucosa in less than 20% in <30 yo; 40 – 60
% in 60 yo (including asymptomatic)
o Developing countries – 80% prevalence rate; higher in adults
o Person –person transmission – intrafamilial clustering
o Acute epidemics of gastritis – common source of H. pylori