Campylobacter & Helicobacter.ppt

Campylobacter
Dr. Rakesh Prasad Sah
Associate Professor, Microbiology

Introduction
Compylobacter
Gram negative, Curved bacilli
Microaerophilic
Nonsporing
Motile (Polar flagellum 
Monotrichate/amphitrichate flagella)

Campylobacter
• 0.2-0.5 µ thick and 0.5-5 µ long.
• Gram –ve bacilli & pleomorphic.
• Non sporing
• Motile [darting / tumbling]  single polar flagella.
• Resemble vibrio but differ
– Microaerophilic
– Not fermenting sugars
– Lower G+C content of DNA.

Campylobacter
Species Habitat
Intestinal flora
Diseases produced
C. jejuni Domestic animals,
poultry & birds
Diarrhea
C. coli Pigs Diarrhea
C. laridis Animals & birds Diarrhea
C. fetus Cattle & sheep Septicemia
C. sputorum Man Nonpathogenic

Human Pathogen
Primarily diarrheal disease Extraintestinal infection
Caused by C. jejuni Caused by C. fetus
80-90% of total cases

Epidemiology
• Source
– Zoonotic
– Found in the intestine of many animals (Poultry, cattle, sheep and
swine) and household pets (including birds, dogs and cats)
• Mode of transmission
 By raw or undercooked food products
 Ingestion of contaminated poultry (most common), raw (unpasteurized)
milk or untreated water
 Direct contact with the infected household pets
 Oral-anal sexual contact
• Infective dose
 Small; <500 organisms can cause disease

Pathogenesis
All the campylobacter to be inhabitants of the GIT of animals
Ingestion of contaminated food (raw milk, partly cooked poultry)
Produce diarrhoea by
Producing a heat-labile enterotoxin resembling cholera toxin (CT)
Like Shigella & Salmonella, It penetrates gut epithelium  C.
jejuni produces a heat-labile enterotoxin (CJT) and a cytotoxin.
Invasive property of the organism contribute to the production of damage.

Clinical Manifestations
• Incubation period:- 2-4 days.
• Manifestation are
– Inflammatory diarrhoea
– Abdominal pain
– Fever
– Diarrhea (several loose stools to grossly bloody stools)
– Self-liminting
• Complication
– Mainly due to C. fetus  developed in immunocomprised hosts and at
the extremes of age.
– Common manifestionations (include bacteremia, sepsis, meningitis,
vascular infections (endocarditis, aneurysm and thrombophlebitis)

• Campylobacter can precipitate the pathogenesis of various
other diseases such as:
 Guillain–Barre syndrome (mainly by C. jejuni serotype O19)
 Irritable bowel syndrome
 Alpha chain disease, a form of lymphoma that originates in small
intestinal mucosa-associated lymphoid tissue.
 Reactive arthritis and other rheumatologic manifestations, in
persons with the HLA-B27 phenotype.

Laboratory Diagnosis
• Freshly collected stool specimen and rectal swab are the
preferred specimens.
• Direct Microscopy
– Gram stained smear of feces - curved gram negative bacilli, comma or S-
shaped or spiral (gull wing) shaped.
– Dark ground microscopy demonstrates the darting motility of the bacilli.

Culture
• Transport medium: If delay is
expected - Cary-Blair medium can be
used.
• Selective media: Feces or rectal
swabs are plated onto selective media
such as:
 Skirrow’s selective medium - figure
 Butzler’s selective medium
 Campy BAP selective medium.

Lab diagnosis
• Campy BAP (lysed blood agar, vancomycin, polymyxin B,
trimethoprim, cephalothin and amphotericin B.)
• Incubation at 420C in +ce of 5% O2, 10% CO2 and 85% N2
• Serotyping

• Culture conditions: Incubated at - Microaerophilic condition (5%
oxygen)
• Growth at 42°C: Thermophilic Campylobacter species (C. jejuni, C.
coli and C. lari) – differentiated from C. fetus, which is
nonthermophilic.

After 2–5 days of incubation, characteristic effuse droplet-like
colonies are produced - further subjected to conventional
biochemical tests or automated systems such as MALDI-TOF or
VITEK for species identification.

Biochemical reactions
• Catalse +
• Oxidase +
• Nitrate reduction test +
• Hippurate hydrolysis test +
• Inactive (do not utilize sugars or produce indole).

Species other than jejuni
• C. coli
• Diarrhea
• C.concicus
• Gingivitis &
periodontal disease
• C.fetus (370C)
• Abortion in cattle &
sheep
• Septicemia
• C. hyointetinalis
• Diarrhea & proctitis
[homosexuals]
• C.lari
• Diarrhea
• C.sputorum
• Diarrhea &
septicemia

Introduction
• In 1983, Warren and Marshall  described a spiral
Campylobacter-like organism  colonizing human stomach.
• Initially named Campylobacter pyloridis  C. pylori.
• Now assigned to a new genus Helicobacter and called H.
pylori.
• Distinguished from Campylobacter
– Multiple sheathed flagella
– Strong hydrolysis of Urea.

Campylobacter & Helicobacter.ppt

Introduction
• Strict microaerophilies with a spiral morphology.
• Three species
– H. pylori
– H. cinnaedi
– H. fennelliae
• Helicobacter pylori - curved gram-negative rod that colonizes
stomach and is associated with
– peptic ulcer disease and
– gastric carcinoma.

Morphology
• Gram negative.
• Curved, Spiral or S shaped bacteria.
• Motile by a tuft of unipolar flagella (lophotrichate). While
Campylobacter have a single unsheathed flagella.

Pathogenesis
• Colonization of the Gastric Mucosa (Gastric
antrum) - 50% of the world’s population (30%
in developed & nearly 80% in developing
countries)
• Colonization favoured by :
 Acid-resistance
Urease enzyme: urea hydrolysis 
ammonia  turns buffers the gastric
acid.
Amidase and arginase: contributes to
the production of ammonia.

 Adhesins
 Resistance to oxidative stress
produces many detoxifying enzymes
 protect organism against the
effects of oxygen-derived free radicals
 generated from the bacterium’s own
metabolism and the inflammatory
defense of the host.

Induces Pathological Changes
 Vacuolating cytotoxin (VacA)  secretes VacA  induces
formation of vacuoles in the cytoplasm of epithelial cells.
 Cytotoxin-associated gene A (CagA) helps the bacterium to
modulate certain aspects of the host cell’s metabolism including:
 Cytoskeleton rearrangements (structure that helps cells maintain their shape
and internal organization)
 Host-cell morphological changes
 Expression of proto-oncogenes
 Release of proinflammatory cytokines from gastric epithelial cells.

 Molecular mimicry
 Lipopolysaccharides of H. pylori (glycoprotein moiety) is identical
to the lewis blood group Ag  expressed on gastrical parietal
cells which may result in:
 Immune tolerance by downregulating T cells
 Induction of autoantibodies that cross-react with mucosal epitopes and
contribute to the development of chronic active gastritis.
 Alteration in gastric mucus
 Inhibits glycosylation and sulfation of gastric mucus, which may
impede its protective function and increase the vulnerability of the
epithelial surface to gastric acidity.

 Host factors
 People with polymorphisms in cytokine genes (e.g. interleukin-1) or
genes coding Toll-like receptors  increased risk of gastric
adenocarcinoma.
 Environmental risk factors
– Smoking increases the risk of ulcers and cancer in H. pylori colonized
individuals.
– Diets high in salts and preserved foods  increases cancer risk,
whereas diets high in antioxidants and vitamins C are protective.

• Acute gastritis
– Antrum (most common site involved)
– Candiac end is not involved.
– Antral gastitis: duodenal ulcers
– Pangastritis: adenocarcinoma of stomach

Peptic ulcer disease
70% of duodenal ulcers 50% of gastric ulcers
Mechanism of Action
H. Pylori induced inflammation
Inhibits somatostatin producing D cells
Increase gastrin release
Increase meal-stimulated acid secretion
Induces duodenal ulcer and gastric metaplasia of duodenal mucosa

Peptic ulcer disease
• Though it is not clear.
• However it is believed, there is hypochondria despited increased
gastrin release.
• Epigastric Pain with burning sensation
– Most common presentation;
– Develops either following a meal (as in duodenal ulcer) or in empty stomach
(as in gastric ulcer.)
50% of gastric ulcers
Mechanism of Action

• Chronic atrophic gastritis
• Autoimmune gastritis
• Pernicious anemia
• Adenocarcinoma of stomach
• Gastric mucosa associated
lymphoid tissue (MALT)
lymphomas.

Lab Diagnosis
• Endoscopy-guided multiple biopsies (antrum)
• Histopathology with Warthin Starry silver staining -
immunostaining to improve sensitivity

Microbiological methods
• Gram-staining: Curved gram-negative bacilli
with seagull-shaped morphology.
• Culture: Most specific test for H. pylori - it is
not sensitive
 Skirrow’s media and chocolate agar
 Plates are incubated at 37°C under
microaerophilic condition (5% oxygen).
 High humidity and 5-10% CO2 required
for growth.

Biochemical reactions
• Catalase
• Oxidase
• Urease (100 times more powerful than Pr. vulgaris)
• Phosphatase
• H2S

Biopsy urease test (also called rapid urease test)
• Detects the presence of urease activity in gastric biopsies by
using a broth that contains urea and a pH indicator.
• Rapid, sensitive and cheap.

Urea breath test
 Most consistent and accurate test.
 Most sensitive, quick and simple.
 Used to monitor treatment response.

Fecal antigen (coproantigen) assay
 Used to monitor treatment response.
 Useful for screening of children.

• Antibody (IgG) detection by ELISA:
 Screening before endoscopy,
 Seroepidemiological study.

Campylobacter & Helicobacter.ppt

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