2. Campylobacter Microbiology properties Curved (comma- or S-shaped)
Gram-negative rods
Microaerophilic (growing in 5% oxygen)
Nonfermenting
Motile(darting motility) with single flagellum
Oxidase positive

5. Important species Campylobacter jejuni : Gastroenteritis
Campylobacter fetus:
An opportunistic organism
Bacteremia in compromised hosts and self-limited diarrhea in previously healthy individuals.
Campylobacter coli:

6. Transmission Source of the organisms:
Domestic animals, such as cattle, chickens and dogs
Person-to-person transmission:
oral-fecal

7. Epidemiology
The major cause of bacterial diarrhea in developed countries (4.6% of patients with diarrhea, compared with 2.3 and 1% for salmonella and Shigella)
Campylobacter jejuni & C. coli are endemic worldwide and hyperendemic in developing countries.
Infant and young adults are most often infected.
The incidence peak in the summer.
Sporadic outbreaks are associated with contaminated animal products or water.

9. Pathogenesis
Invasion to the epithelial cells and colonization the small and large intestines often occurs, accompanied by blood in stool causing inflammatory diarrhea and fever.
Systematic infections, e.g. bacteremia, occur most often in neonates or debilitated adults.

10. Acts in the same manner as cholera toxin
Campylobacter jejuni
Virulence factors
Endotoxin
Flagellum is not only facilitates motility but secretion of Campylobacter invasive antigens (Cia)
Enterotoxin (Cytolethal distending toxin)
Acts in the same manner as cholera toxin

17. Clinical findings Enterocolitis: watery, fuel-smelling diarrhea
bloody stools
fever
severe abdominal pain.
Systemic infections, most commonly bacteremia, are caused by C. fetus showing symptoms of fever and malaise.

18. Detection of C jejuni and related enteric bacteria.

19. Laboratory diagnosis for Campylobacter
A stool specimen
Blood agar culture
Microaerophilic atmosphere (5% O2 and 10% CO2)
Skirrow’s medium (containing vancomycin, trimethoprim, cephalothin, polymyxin, and amphotericin B.)

20. The identification of C. jejuni is confirmed by:
Ability to grow at 42 C
Failure to grow at 25 C
Oxidase positive
Sensitivity to nalidixic acid
The identification of C. fetus is confirmed by:
Failure to grow at 42 C
Ability to grow at 25 C
Resistance to nalidixic acid

21. Treatment Erythromycin in C. jejuni enterocolitis
An aminoglycoside in C. fetus bacteremia

22. Prevention No vaccine Proper sewage disposal
Personal hygiene (Hand washing)

23. Helicobacter pylori
Multiple flagella (lophotrichous): Darting motility
Gram-negative curved (comma- or S-shaped) rods
Microaerophilic (growing in 5% oxygen)
Oxidase & Catalase positive
Nonfermenting
Urease

24. Seventy-two hour culture of H pylori showing typical thin, comma- or S-shaped forms

25. Virulence Factors

27. Pathogenesis
H. pylori is associated with type B gastritis (antral stomach inflammation/ peptic ulcer).
It shelters from gastric acid in the gastric mucous layer and probably is able to adhere to gastric epithelial cells.
Production of urease and cytotoxin is associated with injury to the gastric epithelium.

36. Epidemiology
The prevalence of infection increases with age.
The source and mode of transmission are not known.
H. pylori is in the mucosa of the stomach of 20% people under 30 years but in 40 – 60 % of 60 years old.

37. Detection methods for H pylori

38. Laboratory diagnosis Invasive methods: Histological examination
Culture
PCR (polymerase chain reaction)
A rapid urease test on the sample

40. Skirrow’s medium (containing vancomycin, trimethoprim, polymyxin, and amphotericin B.) A selective blood agar medium

41. Laboratory diagnosis Non-invasive methods:
Serological tests for antibodies on blood or saliva
13C or 14C urea breath tests
Fecal antigen testing

42. The Carbon urea breath test (CUBT)
The breath tests are performed by asking the patient to swallow carbon-labeled urea which is metabolised by H. pylori’s urease to produce labeled carbon dioxide.
Two forms of urea breath tests by using 13C urea or 14C urea is available.
This is absorbed into the blood stream and then exhaled in the breath of infected individuals.

45. 13C or 14C urea breath tests (CUBT) for Helicobacter pylori detection

47. The rapid urease test
Least expensive and can be performed on endoscopic biopsy specimens.
The urease produced by the organism converts urea to ammonia resulting in a PH change detected by phenol red.
The tests usually give a rapid result but typical sensitivity at 1 hour is 71% which increases to 96% at 6 hours.

48. Serology Testing IgG is the most sensitive as seen in 95%.
Testing IgA responses in 68-80%.
Testing IgM responses in only 14% of infected patients.

49. Serological tests for H. pylori
Elisa
Complement fixation
Latex agglutination

50. Control A three drug treatment for 2 weeks:
1. A proton pump inhibitor (such as lansoprazole and omeprazole decreasing stomach's production of acid allowing the ulcer to heal)
2. Metronidazole
3. Tetracycline