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GENUS CAMPYLOBACTER

This genus include zoonotic bacteria ( like Brucella)


General properties
They are gram negative, curved bacilli, which appear comma or S-shaped in diplo
resulting in a seagull wing image.
-termophilic
-microaerophilic
Representants
C.jenuni
C.fetus
Epidemiology
-reservoir: cattle and poultry
-human contamination: fecal-oral route by water and food
Clinical diseases:
C.jejuni: acute gastroenteritis and enterocolitis. It is a major cause of diarrhea in USA.
C.fetus causes gastroenteritis less frequent, but is often involved in systemic febrile
infections in debilitated patients.
The symptoms are:
-watery, foul-smelling diarrhea
-followed by bloody stools
-fever
-severe abdominal pain
Laboratory diagnosis
A. Direct diagnosis
1.Sample collection: stool specimen (feces)
2.Microscopic examination has no utility
3.Inoculation on media: blood agar containing antibiotics (eg. Skirrow medium
which contains vancomycin, trimethoprim, cephalotin, polymyxin, amphotericin B)
4.Identification based on:
-morfological properties: gram negative, comma-shaped rods, arranged in diplo.
-cultural properties: development of colonies at 42C and failure to grow at 25C
-biochemical properties: oxidase positive

-sensitivity to nalidixic acid


Practically the diagnosis is confirmed by Gram stain and isolation in cultures of fecal
material. The finding of blood or neutrophils in feces suggests invasion of the
intestinal wall, which implies a more severe prognosis. A blood culture incubated at
standard temperature and atmospherica conditions will reveal the growth of
characteristic S-shaped, motile, gram-negative rods.
Treatment: Erythromycin or ciprofloxacin and tetracyclines are most commonly used.
Helicobacter pylori (formerly Campylobacter pylori)
General properties:
-Gram neagative, spiral shaped (helical) rod
-capnophilic (grow best in 10% CO2)
-microaerophilic
-urease producing
Pathogenesis and clinical disease
It is believed to be transmitted person-to-person
-infection is associated (not determined) with chronic gastritis, gastric peptic ulcers,
and gastric carcinoma.
H.pylory attaches to the mucus-secreting cells of the gastric mucosa and damage it by
the production of ammonia from urea, together with the inflammatory response at the
presence of the microorganism. The loss of the protective mucus will favor the
gastritis and peptic ulcer.
Symptoms
-recurrent pain in the upper abdomen
-frequent bleeding in the gastrointestinal tract.
Gold standard approach for diagnosis involves: gastric intubation, endoscopy, and
biopsy.
Laboratory diagnosis
1.Sample collection: biopsy specimen of the gastric mucosa
2.Microscopic examination: Gram-stained smear of the biopsy will reveal gram
negative helical rods.
3.Biochemical properties:
-a rapid test that detects H.pylori based on its production of urease can be performed
on the biopsied tissue: test of urease activity

-noninvasive test of urease activity:


Principle of the test: if an infected patients drinks urea-containing solution, the urea
will be broken down in stomach and ammonia and CO2 will be generated. Both
compounds diffuse into the systemic circulation; the lungs eliminate CO2, and
ammonia is eliminated in the urine.
a)Breath test: breakdown of 14C-labeled urea generates

-labeled CO2, which can

be traced in expired air.(20 min.)


b)Urine test: breakdown of 15N-labeled urea generated

-labeled NH3, which can

be traced in voided urine. (2 hours)


Treatment
A combination of antacids (e.g. omeprazol) and one or two broad-spectrum antibiotics
administered for 1-3 weeks (Claritromycin, Doxycycline and Metronidazole) is the
treatment of ulcer or gastritis.
Bismuth subsalicylate is used in association with the former two drugs.