Dr.Rouchelle Tellis

1. Campylobacter & Helicobacter Dr.Rouchelle Tellis

2. Objectives • To discuss the morphology, epidemiology and pathogenesis of H. pylori and campylobacter • Diagnostic tests • Treatment practice guidelines

3. General Characteristics and morphology of H.pylori • Helicobacter pylori - major human pathogen of gastric antral epithelium causing active chronic gastritis • Gram-negative; Helical (spiral or curved) • Cells become coccoid on prolonged culture • Produce urease and catalase • Tuft of 4-6 flagella at one pole

5. Epidemiology • Approx 50-60% of the world population is infected • Person to Person Transmission : fecal-oral • Increased risk of infection

6. Most adults infected but no disease - Protective immunity from multiple childhood infection History of H. pylori: • 1983: Warren and Marshall characterize H. pylori • 2005 Nobel prize in 2005

7. Pathogenesis of Helicobacter Infections • Colonize mucosal lining of stomach & duodenum in man & animals • Adherent to gastric surface epithelium -deep within the mucosal crypts adjacent to gastric mucosal cells • Mucus protects Helicobacter from immune response • Gastric adeno-carcinoma and lymphoma- assoc with infection with H. pylori

8. Virulence Factors of Helicobacter

9. Virulence Factors of Helicobacter(cont.) • Tissue damage: • Vacuolating cytotoxin: Epithelial cell damage • Invasin(s)(??): (e.g., hemolysins; phospholipases • Protection from phagocytosis & intracellular killing: • Superoxide dismutase • Catalase

11. Immune and Inflammatory Response to H. pylori Gastric ulcer H. pylori Adhesion of bacteria Mucosa Inflammatory Mediators Tissue damage Activation Activated T cell Recruitment Immune Response Inflammatory Response

14. CLINICAL FEATURES • H. pylori-positive patients -10-20% life time risk of developing gastritis • 1 to 2% risk of - distal gastric cancer • Various forms of presentations are • Acute / Chronic gastritis • Peptic ulcer disease – gastric/ duodenal ulcer • Non-ulcer dyspepsia • Gastric carcinoma • MALT lymphoma

17. Invasive methods (endoscopy) • Rapid urease test: Urea urease NH3 + CO2 • Rapid, Specificity- 95 -100%, sensitivity- 90 -95%

18. Staining methods of impression smears • Gram stain • Dilute carbol fuchsin • Giemsa stain • Staining methods for tissue biopsies • Hematoxylin and eosin • Modified Giemsa stain

19. Culture : • Gold standard for diagnosis of infection • Very difficult to grow • Commonly used media: • Brain Heart Infusion medium with horse serum • Skirrows medium • Brucella broth base with 10% glycerol

20. Urea breath test: Patient ingests a solution containing a labelled carbon atom, Detection of carbon labelled CO2 in breath indicates presence of infection • sensitivity and • specificity > 95%

22. Serology: • Elevation of specific IgG and IgA levels in serum • Elevated levels of secretoryIgA and IgM in the stomach, • ELISA using commercial kit sensitivity 100% and specificity upto 95%.

23. After eradication - specific IgG and IgA levels tend to decrease, within 6 months • Stool antigen enzyme immunoassay- recently available

26. TREATEMENT

29. Conclusion • H. pylori is the major cause of DU and it should be eradicated in all patients testing positive • H. pylori relationship with the development of MALT and gastric cancer • High eradication rate of H. pylori when triple therapy is used 1 O’Morain C et al. Aliment Pharmacol Ther 2003;17:415-20

30. CAMPYLOBACTER

31. Morphology & Physiologyof Campylobacter • Small, thin, helical (spiral or curved) cells with typical gram-negative cell wall; • “Gull-winged” appearance • Tendency to form coccoid & elongated forms on prolonged culture or when exposed to O2 • Distinctive rapid darting motility • Long sheathed polar flagellum at one (polar) or both (bipolar) ends of the cell

32. Microaerophilic & capnophilic 5%O2,10%CO2,85%N2 • Thermophilic (42-43C) • Cause diarrhea –C.jejuni • Extraintestinal disease: C.fetus

33. Epidemiology of Campylobacteriosis • Zoonotic infections particularly birds –reservoirs • Humans acquire via ingestion of contaminated food, unpasteurized milk, or improperly treated water • Infectious dose is reduced by foods that neutralize gastric acidity, e.g., milk. • Fecal-oral transmission also occurs

34. Pathogenesis • The infection by oral route from food, drink, or contact with infected animals or animal products(Milk,meat products ). • Susceptible to gastric acid • Multiply in the small intestine- invade the epithium produce inflammation - cause bloody stools • Occasionally, the blood stream is invaded

36. Putative Virulence Factors • Cellular components: • Endotoxin • Flagellum: Motility • Adhesins: Mediate attachment to mucosa • Invasins • GBS is associated with C. jejuni serogroup O19 • S-layer protein “microcapsule” in C. fetus: • Extracellular components: • Enterotoxins • Cytopathic toxins

37. Campylobacter - symptoms • Incubation: 4-8d • Acute enteritis: 1wk, • Acute colitis • Acute abdominal pain • Bacteremia: <1% C. jejuni • Septic abortion • Reactive arthritis

38. Diagnostic Laboratory Tests • Specimens: Diarrheal stools/ rectal swabs • Transport medium: Cary Blair • Microscopy: • Small curved rods in gram stain • Darting motility in fresh stool • Fecal leukocytes are commonly present • Culture: • Enrichment broth & selective media • Skirrow’s medium -Two types of colonies: • Spreading colonies • Round and convex colonies

39. Treatment, Prevention & Control • Gastroenteritis: Self-limiting; Replace fluids and electrolytes • Antibiotic treatment can shorten the excretion period -Erythromycin is drug of choice • Ciprofloxacin, Azithromycin • Control should be directed at domestic animal reservoirs and interrupting transmission to humans