CAMPYLOBACTER and

HELICOBACTER
 Objectives
At the end of the lecture the students should be
able to:
 Recall the general characteristics of C & H
 Understand their pathogenesis
 Recall the clinical manifestations
 Enumerate the infections they cause
 Recall their laboratory diagnosis
 Enumerate how to treat the infections
 CAMPYLOBACTER
 Contains 13 species:
 Clinically important: C. jejuni and C. coli
– Small, slender, spirally shaped Gram-negative
bacilli with single flagellum
– Rapidly motile
– Microaerophilic and sensitive to superoxides
– Grow best at 42-43oC.
– Strongly oxidase-positive, non-fermentative
 CAMPYLOBACTER
 C. jejuni hydrolyses hippurate while C. coli
does not
 C. jejuni causes 90-95% of infections and
are associated with poultry.
Close up view of C. jejuni on
blood agar illustrating raised,
gray-white and somewhat
mucoid colonies.
Gram stain of C. jejuni
illustrating pleomorphic
gram-negative bacilli, some
short and curved, others
forming spirals.
 Pathogenesis
 Infection is acquired by ingestion
 Infective dose ≥ 10,000 (103cfu/ml)
 Initial colonized site – jejunum and ileum
 Usually extends to the colon and rectum
 The organisms are invasive
– transient bacteraemia.
 Clinical manifestation
 IP:1-7 days; av. 3days
 Abdominal pain
 Diarrhoea
 Fever
 Nausea is common but vomiting is rare
 WBC - stool ± frank blood
 Self-limiting but carrier state continues
 Developed countries- 15-40yr
 Developing countries - <3years are infected
 Complications
 Intestinal
haemorrhage
 Toxic megacolon
 Haemolytic uraemic syndrome (HUS)
 Bacteremia
 Laboratory diagnosis
 Directmicroscopy (wet preparation)
 Culture - on selective agar
– Skirrow’s medium
– Preston medium
 Incubation - ↓O2 tension + 5-10% CO2 in
sealed anaerobic jar without catalysts
 Incubation temperature - 42oC
 Treatment
 Campylobacter enteritis (CE) is self-
limiting
 Fluid and electrolyte replacement
 Erythromycin - drug of choice
 In septicaemic patients - ciprofloxacin or
gentamicin can be added
 Sources and transmission
 Animals are the main source of infection
 Person-to-person spread plays a minor role
 Adapted to life in the gut of birds
 Present in surface water; lakes, rivers and streams
 Colonize domestic poultry in counts > 107
cfu/ml.
 Mass processing - contamination of final product.
 Salad and bread contaminated by raw poultry
Food (shellfish, poultry, raw eggs, homemade mayonnaise)
implicated in food poisoning
 Control
 Purification of water
 Pasteurization of milk
 Gamma irradiation of broiler carcasses
 Public education on basic food handling
 Proper hand washing between handling raw
meat and other foods.
 Case presentation
Ahmad, a 32-year old computer engineer, is seen in the
A&E complaining of fever, nausea, diarrhoea and crampy
abdominal pain. He had attended a birthday party a day
earlier where chicken salad and milk were served.

 What is the most likely diagnosis in this patient?

 How relevant might the birthday party be?
 Which particular organisms are associated with this type
food?
 When, if ever, are antibiotics indicated? If indicated,
which ones?
 What other findings may be seen in this case?
 HELICOBACTER
H. pylori
 Gram-negative, spiral, non-capsulated rod
 Strictly microaerophilic; needs CO2
 Motile
 Biochemically inactive
 Produces a very powerful urease
 It is susceptible to penicillin, most other
types of β-lactams, macrolides,
metronidazole and bismuth compounds
 Site of infection
 Gastric antrum and any part of the stomach

 Gastric glands

 Duodenum
 Pathogenesis
 Survives in the mucus layer
– Chemotactic factor – attracted to urea & hemin
in the mucosal crypts

 Causes chronic inflammation of mucosa

 Non-invasive

 Recruits and activates inflammatory cells

 Pathogenesis
 Releases urease  Urea = NH3 and CO2

 NH3 - neutralizes stomach acid

- cause injury
- potentate the effect of cytotoxin

 Hemin – stimulates growth

 Enzyme & mediator release cause chronic
inflammation
 Little immunity develops, relapse is frequent
 Diseases/Infections
 Type B gastritis

 Non-peptic ulcer dyspepsia

 Duodenal ulcer (DU)

 Most of gastric ulcers (GU)

 Gastric and duodenal carcinoma

 Laboratory Diagnosis
 Histological examination
 Culture of antrum biopsy
 Grows on Skirrow’s medium and on
Chocolate and Blood Agar
 It forms discrete colonies unlike the diffuse
colonies of Campylobacter.
 Non-cultural diagnosis
Biopsy Urease test
 Biopsy tissue in urea solution containing a
pH indicator.
– positive within 2 min to 2 hours if H. pylori is
present.

Urea Breath test

 Urea C13 or C14.
 If positive the isotope gives high reading in
the CO2 emitted in the breath.
 Treatment

 Colloidalbismuth + amoxicillin +
metronidazole

 Omeprazone (Proton pump) +

clarithromycin + metronidazole

 Prone to relapse
 Epidemiology
 Infection rate increases with age.
 Onset of infection is different in the
developed and developing countries
 Close contact
 Found only in humans
 Case presentation
A 40-year old woman complains of epigastric pain
which radiates to the back and wakes her up at night.
It is worsened by spicy food, alcohol and recumbent
position.
 What is the likely diagnosis?
 Is this an infective process? If yes, which organism
is responsible?
 What is the pathogenesis?
 What are the complications of this disease?
 How can it be treated?