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Helicobacter pylori

Briann McGovern
(microbiology spR)
1983-discovered by Warren and Marshall in

Discovery revolutionised the treatment of
duodenal and gastric ulcers

Earned them the Nobel Prize for Medicine in

Formerly known as Campylobacter pyloridis
Nearly 20 species of Helicobacter are now

The gastric helicobacters colonise the stomachs
of animals. The monkey, cat, dog, cheetah all
harbour their own species

H. cinaedi and H. fennelliae are associated with
proctitis in homosexual men

H. pylori are found in the human stomach.
Molecular studies suggest transmission from an
animal source.
Helicobacter pylori
McColl K. N Engl J Med 2010;362:1597-1604
Gram-negative spiral bacillus

Fastidious in terms of growth requirements
:strictly micro-aerophilic
:require C02 for growth
:on charcoal medium

Has a tuft of sheathed unipolar flagella; specially
adapted to colonise mucous membranes
Gram stain of H. pylori recovered from an individual without prior antimicrobial therapy.
Organisms display typical seagull-like appearance.

Hallmark of the species is production of urease
-urease breaks urea down to C02+NH3
-amonia is a strong base
-process helps H. pylori survive
strongly acidic stomach conditions

Very fragile (a point of importance
when referring samples to the lab)

H. pylori infection occurs worldwide

Prevalence varies greatly among countries and
population groups

20 50% prevalence in middle age adults in
industrialised countries

>80% prevalence in middle age adults in
developing countries
:may reflect poorer living conditions

Oral ingestion of bacterium
within families (esp children)
person-person contact
faecal-oral transmission
?role of waterborne transmission

Usually contracted in the first 2 years of life

Site of infection
Highly adapted organism that lives only on
gastric mucosa

Gastric antrum is the most favoured site

Present in the mucus that overlies the mucosa

Gastric-biopsy specimen showing Helicobacter pylori adhering to gastric epithelium and
underlying inflammation
McColl K. N Engl J Med 2010;362:1597-1604
Course of infection
After several days incubation period, patients
suffer mild attack of acute gastritis
-abdominal pain
-bad breath

Symptoms last about 2/52 but hypochlorhydria
can last up to one year
Despite a substantial
ab response, infxn
and chronic gastritis
After decades there
may be progression
to atrophic gastritis
(conditions which are
inhospitable for the
bacteria) and
numbers reduce
The outcome of infection by H. pylori reflects an
interaction between:
Strain virulence
Host genotype
H. pylori infection directly
associated with
-lifetime risk 3% in US, 25% Japan
-eradication provides long-term cure
Gastric carcinoma
-strong evidence of increased risk 0.1-3%
-unclear whether eradication reduces the
risk of gastric cancer
MALT lymphoma
-72% 98% of MALT lymphoma
infected with H. pylori

H. pylori may be implicated in:-

Non-ulcer dyspepsia
-increased prevalence of H. pylori but
data inconsistent (symptomatic improvement
only 9%)
-little evidence that chronic H. pylori
infection in the absence of ulceration causes
upper GI symptoms

-recent meta-analysis : no significant

Laboratory diagnosis:
non-invasive tests
Serology : detect an immune response by
examining a blood sample for abs to the
organism (ELISA)
: poor accuracy

Urea breath test : a urea solution labelled with
C14 isotope is given to pt. The C02 subsequently
exhaled by the pt contains the C14 isotope and
this is measured. A high reading indicates
presence of H. pylori
Faecal antigen test : detect H. pylori antigens in
faecal specimens

Polymerase chain reaction (PCR) : can detect HP
within a few hours. Not routine in clinical use.
Invasive testing
1. Histological examination of biopsy specimens of
gastric/duodenal mucosa take at endoscopy
2. CLO-test : based again on urease-production
by the organism->NH3 production->rise in
pH=>change in the colour indicator of the kit
-High sensitivity and specificity
-Prompt result
Invasive testing
3. Culture :
-no more sensitive than skilled
microscopy of histological sections
-used for antibiotic resistance testing
-requires selective agars and
incubation periods
Tests for Helicobacter pylori Infection
McColl K. N Engl J Med 2010;362:1597-1604
Indications for therapy
Strongly recommended

Duodenal or gastric ulcer

MALT lymphoma

Atrophic gastritis

Recent resection of gastric cancer

Maastricht 2-2000 Consensus Report
Indications for therapy
Treatment advised

Functional dyspepsia

Gastro-oesophageal reflux disease (patients
requiring long-term acid suppressive therapy)

Use of NSAIDs
Maastricht 2-2000 Consensus Report
Goal of treatment to eradicate infection

Triple therapy regimens consist of one anti-
secretory agent and two antimicrobial agents for
7 to 14 days

Triple therapy regimens must
- have cure rate of approximately 80%
- be without major side effects
- minimal induction of resistance
First line treatment
Combination of two or more antimicrobial
agents increases rates of cure and reduces the
risk of selecting for resistant H. pylori

Many factors may result in failure of treatment
microbial factors
patient compliance
geographical differences
First line therapy
PPI b.d. + clarithromycin 500mg b.d.
amoxicillin 1000mg b.d. or metronidazole 400mg BD minimum of 7

In case of failure

Second line therapy
PPI b.d. + bismuth subsalicylate/subcitrate 120mg QDS +
metronidazole 500mg t.d.s. + tetracycline 500mg q.d.s.
for a minimum of 7 days
If bismuth is not available, PPI based triple therapies should be used

Subsequent failures should be handled on a case-case basis. Patients
failing second-line therapy in primary care should be referred

Maastricht 2-2000 Consensus Report
NEJM 2002;347:1175-86
Guidelines for Evaluation and Management of Helicobacter pylori Infection
McColl K. N Engl J Med 2010;362:1597-1604
Reinfection following successful bacterial cure is

Commonly represents recrudescence of the
original bacterial strain

In adults, reacquisition of the bacteria occurs in
<2%/persons/year which is similar to the rate of
primary infection in adults
Failure of treatment
Failure of initial course occurs in 1 in 5

-line Tx :
either an alternative regimen
quadruple Tx (PPI+bismuth+2 antibx)
Key points
-> H. pylori is a flagellated spiral micro-aerobe
-> Infection is a risk factor for gastric cancer
-> Causes PUD and gastritis
-> Produces a cell-damaging toxin
-> Transmission route is unclear
-> Dz rates are falling in industrialised countries
-> Tx is by eradication using combination therapy
The noninvasive test-and-treat strategy for H. pylori infection is
reasonable for younger patients who have upper gastrointestinal
symptoms but not alarm symptoms

Noninvasive testing can be performed with the use of the urea
breath test, fecal antigen test, or serologic test; the serologic test is
the least accurate

Triple therapy with a proton-pump inhibitor, clarithromycin, and
amoxicillin or metronidazole remains an appropriate first-line

Recurrence or persistence of symptoms after eradication therapy
for uninvestigated dyspepsia is much less likely to indicate that
treatment has failed than to indicate that the symptoms are
unrelated to H. pylori infection.
Further eradication therapy should not be considered unless
persistent H. pylori infection is confirmed

Data are lacking to inform the optimal management of
recurrent or persistent dyspepsia after noninvasive testing
and treatment of H. pylori infection

Options include symptomatic acid-inhibitory therapy,
endoscopy to check for underlying ulcer or another cause of
symptoms, and repeat of the H. pylori test-and-treat strategy;
other potential reasons for the symptoms should also be
Clinical Practice
Helicobacter pylori Infection
Kenneth E.L. McColl, M.D.
N Engl J Med
Volume 362(17):1597-1604
April 29, 2010
Thanks for your attention!