MICR

HELICOBACTER
O

TREATMENT,
BACTERIA EPIDEMIOLOGY PATHOGENESIS IMMUNE RESPONSE LABORATORY IDENTIFICATION PREVENTION AND
CONTROL
History and Taxonomy Developed Countries Pathpgenesis • Activation of neutrophils, • Recovered from or detected Goal of Treatment:
• Family not yet  United States:  Colonize mucosal lining of stomach & monocytes and in endoscopic antral gastric Eradication of
named (17 30% of total duodenum in man & animals macrophages biopsy material; Multiple Helicobacter pylori –
species by rRNA population infected • Adherent to gastric surface epithelium or • Production of serum biopsies are taken absence of the
sequencing) • Of those, ~1% pit epithelial cells deep within the mucosal antibody IgG and secretory • Many different transport organism 4 or more
• First observed in per year crypts adjacent to gastric mucosal cells antibody IgA weeks after
media
develop • Mucosa protects the stomach wall from its • T cells proliferate eradication therapy
1983 as
• Intensity of the host • Culture media containing - Highest
Campylobacter- duodenal ulcer own gastric milleu of digestive enzymes
immune responses can whole or lysed blood eradication
like organisms • ~1/3 and hydrochloric acid
culminate in one of several • Microaerophilic rate achieved
(formerly eventually • Mucosa also protects Helicobacter from
Campylobacter have peptic immune response
ways • Grow well at 37oC, but not using 3
1. Chronic superficial at 25 nor 42oC antibiotics:
pyloridis) in the ulcer  Most gastric adenocarcinomas and gastritis – most bismuth,
stomachs of disease(PUD) lymphomas are concurrent with or preceded common result • Like Campylobacter, does not metronidazol
patients with  70% gastric ulcer by an infection with H. pylori use carbohydrates, neither
• inflammation of the e and
type B gastritis cases colonized fermentatively nor oxidatively
stomach lining due tetracycline
• Nomenclature of with H. pylori Virulence Factor to the infiltration of - Drawbacks
Helicobacter was  Low socioeconomic • Multiple polar, sheathed flagella Non-invasive Techniques with such
lymphocytes,
first established in status predicts H.  Corkscrew motility enables penetration 1. Breath Test multidrug
plasma cells,
1989, but only pylori infection into viscous environment (mucus) - detection of urease therapy:
eosinophils, and
three species are activity
• Adhesins: Hemagglutinins; Sialic acid monocytes into the
- radioactively
many
currently Developing Countries mucocal lining of adverse
binding adhesin; Lewis blood group adhesin labeled urea with
considered to be  Hyperendemic the stomach. reactions –
human pathogens • Mucinase: Degrades gastric mucus;
Intensity of the carbon 13 and diarrhea,
 About 10%
Localized tissue damage carbon 14 is nausea and
acquisition rate per host immune
Important Human • Urease converts urea (abundant in saliva and ingested vomiting
year for children response can
Pathogens gastric juices) into bicarbonate (to CO2) and - bacterial urease (20% of all
between 2 and 8 culminate in one of
• Helicobacter ammonia splits off labeled patients)
years of age several ways:
CO2 – detected in Triple
pylori (human;  Most adults infected  Neutralize the local acid environment 2. Benefit H. pylori by the breath
no animal but no disease  Localized tissue damage releasing nutrients Chemotherapy
- reflects only current (synergism):
reservoir) • Protective • Acid-inhibitory protein locally for the organism infection  Proton pump
• H. cinaedi immunity from 3. Host could be - disadvantage: small
multiple inhibitor (e.g.,
(male Urea Hydrolysis harmed due to the amount of exposure
childhood omeprazole =
homosexuals; Urease direct damage of to radiation
infections Prilosec(R))
rodents) C=O(NH2)2 + H+ + 2H2O  HCO3- + 2 (NH4+) epithelial cells which
affects their function.  One or more
• H. fenneliae Urea Bicarbonate Ammonium 2. Detection of IgG
antibiotics
(male ions The host then antibody
downregulates its (e.g.,
homosexuals; And then… - immediate immune
immune response clarithromycin
rodents) HCO3-  CO2 + OH- response to H.
making it even more ; amoxicillin;
pylori is IgG and
...Remember that happiness is a way of travel, not a destination. ^_^ shar ^_^
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MICR
HELICOBACTER
O

Tissue Damage difficult to completely secretory antibody metronidazole

General Characteristics  Vacuolating cytotoxin: Epithelial cell eliminate the organism IgA production )
• Helicobacter damage 4. Can lead to duodenal - serologic test using  Bismuth
pylori is major ulcers ELISA – detects IgG compound
 Invasin(s)(??): Poorly defined (e.g., - elevated antibody
human pathogen hemolysins; phospholipases; alcohol 5. Atrophic gastritis –
associated with titer indicates Inadequate treatment
dehydrogenase) nonspecific
gastric antral current infection results in recurrence
inflammation of the
epithelium in - also detects decline of symptoms
Protection from Phagocytosis and entire lining of the
patients with in antibody titer
Intracellular Killing stomach as a result of
active chronic after removal of the
 Superoxide dismutase the infiltration of
gastritis organism
 Catalase lymphocytes into the
• Stomach of many stomach
animal species 6. MALT-type and other
also colonized lymphomas
• Urease (gastric
strains only),
mucinase, and
catalase
positive highly
motile
microorganisms
• Other
Helicobacters:
H. cinnaedi and
H. fenneliae
• Colonize
human
intestinal tract
• Isolated from
homosexual
men with
proctitis,
proctocolitis,
enteritis, and
bacteremia
and are often
transmitted
through
sexual
practices

Morphology and

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MICR
HELICOBACTER
O

Physiology
• Gram-negative;
Helical (spiral or
curved) (0.5-1.0
um X 2.5-5.0 um);
Blunted/rounded
ends in gastric
biopsy specimens;
Cells become rod-
like and coccoid
on prolonged
culture
• Produce urease,
mucinase, and
catalase
• H. pylori tuft
(lophotrichous)
of 4-6 sheathed
flagella (30um X
2.5nm) attached
at one pole
• Single polar
flagellum on H.
fennellae & H.
cinaedi
• Smooth cell wall
with unusual fatty
acids

...Remember that happiness is a way of travel, not a destination. ^_^ shar ^_^
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