More Related Content
Recently uploaded (20)
Featured (20)
Vibrio species in medical microbiology and immunology
- 1. GRAM NEGATIVE RODS Dr Marianne Mureithi marianne@uonbi.ac.ke
- 2. 2
- 4. LEARNING OBJECTIVES Discuss the disease produced by Vibrio cholerae with emphasis on its prevention and diagnosis Describe characteristics and importance of microaerophilic members of group Campylobacter and Helicobacter.
- 5. VIBRIOS Belong to the Family Vibrionaceae Gram-negative curved or comma shaped bacilli Highly motile by a single polar flagellum Non spore formers Non capsulated Facultative anaerobes Possess both H & O antigens
- 6. Identification Vibrios are highly motile, gram-negative, curved or comma- shaped rods with a single polar flagellum
- 7. IDENTIFICATION 2 Grow on variety of simple media including: 揃MacConkeys agar 揃TCBS (Thiosulfate Citrate Bile salts Sucrose) agar V. cholerae grow without salt 揃Most other vibrios are halophilic-salt loving
- 8. Pathogenic strains V. cholerae V. parahaemolyticus V. vulnificus
- 9. All Vibrio spp. can survive and replicate in contaminated waters with increased salinity and at temperatures of 10-30o C Pathogenic Vibrio spp. appear to form symbiotic (?) associations with chitinous shellfish which serve as an important and only recently recognized reservoir Asymptomatically infected humans also serve as an important reservoir in regions where Epidemiology of Vibrio spp.
- 10. What is Cholera? Intestinal infection Severe diarrhea Caused by Cholera Toxin of bacterium, Vibrio cholera
- 11. Introduction Causes cholera Classified as category B bioterrorism agent- water supply threat (CDC) Transmitted by ingestion of contaminated water (sewage contaminated water is the primary source) Poor sanitation practices are the source of outbreaks
- 12. Epidemiology Responsible for seven global pandemics over the past two centuries Common in India, Sub-Saharan Africa, Southern Asia Very rare in industrialized countries
- 13. Figure 1 The Lancet 2018 391, 1908-1915DOI: (10.1016/S0140-6736(17)33050-7) Copyright 息 2018 The Author(s). Published by Elsevier Ltd. This is an Open Access article under the CC BY 4.0 license Terms and Conditions
- 14. Strains Causing Epidemics 2 main serogroups carry set of virulence genes necessary for pathogenesis O1 Classical: 1 case per 30-100 infections El Tor: 1 case per 2-4 infections O139 Contained in India, Bangladesh
- 15. Transmission Contaminated food or water Inadequate sewage treatment Lack of water treatment Improperly cooked shellfish Wash fruits/vegetables with untreated water Transmission by casual contact unlikely
- 17. Pathogenesis Virulence factors Bacteria adheres to the epithelia cells of gastric intestinal mucosa via pilli survive the acidic conditions of the human stomach Production of proteases (mucinase) which dissolves protective glycoprotein coating cells High motility Ability to produce an enterotoxin-cholera toxin (CT)
- 18. Inactivates GTPase function of G-protein coupled receptors in intestinal cells G proteins stuck in On position 100 fold increase in cAMP Activation of ion channels Ions flow out and water follows How Does Cholera Toxin Work?
- 19. Mechanism of Action of Cholera Toxin
- 20. Symptoms of V.cholerae Incubation period: 2-3 days High infectious dose: >108 CFU 揃 103 - 105 CFU with achlorhydria or hypochlorhydria (lack of or reduced stomach acid) Abrupt onset of vomiting and life-threatening watery diarrhea (15-20 liters/day) As more fluid is lost, feces-streaked stool changes to rice-water stools: 揃 Colorless 揃 Odorless 揃 No protein 揃 Speckled with mucus
- 21. People with low gastric acid levels Children: 10x more susceptible than adults Elderly Blood types O>> B > A > AB (O more susceptible allows bacteria to adhere to gut lining???) People Most at Risk
- 22. Diagnosis: Visible Symptoms Decreased skin turgor Sunken eyes, cheeks Almost no urine production Dry mucous membranes Watery diarrhea consists of: fluid without RBC, proteins electrolytes enormous numbers of vibrio cholera (107 vibrios/mL)
- 23. Outline of laboratory isolation and identification Specimen; ?????? Cary-Blair transport medium Microscopy; Wet preparation -darting motility Enrichment medium - Alkaline peptone water for 4-6hrs SubCulture on TCBS (thiosulphate citrate bile salt sucrose) in air, at 37属C, for 18-24hrs Colonial morphology; yellow colonies Gram stain of colony; ???? Biochemical test; Oxidase positive
- 25. Other tests Toxin assays Dipstick PCR
- 26. Treatment *Even before identifying cause of disease, rehydration therapy must begin Immediately because death can occur within hours* Oral rehydration Intravenous rehydration Antimicrobial therapy
- 27. Boil or treat water with chlorine or iodine No ice Cook everything Rule of thumb: Boil it, cook it, peel it, or forget it. Wash hands frequently VACCINES Traveling Precautions
- 28. REVIEW Antibiotic Resistance in Vibrio cholerae Cholera vaccine
- 29. Campylobacter
- 30. Campylobacter Gram negative curved rods Often attached in pairs giving a seagull appearance Motile by polar flagella; darting motility in corkscrew fashion Facilitate penetration and colonization of mucosal environment Species; Campylobacter jejuni causes 80- 90% of all illnesses
- 32. Source C. jejuni commonly associated with poultry, naturally colonises the digestive tract of many bird species Transmission Raw or undercooked food products Through direct contact with infected animals
- 33. Laboratory diagnosis Specimen- stool, blood, etc Wet preparation of stool: dark-field microscopy observe darting motility Culture on Skirrows medium Incubate in microaerophilic conditions at 42属C, for up to 48 hours Gram stain Gram negative comma- or S- shaped rods Oxidase positive 35
- 34. Treatment Rehydration - usually self-limiting Severe dysentry erythromycin, ciprofloxacin Antimotility agents not recommended 36
- 35. Helicobacter
- 37. Helicobacter Colonizes stomach 50% of world population H. pylori is contagious, although the exact route of transmission is not known. Main risk factor for; Gastric & duodenal ulceration Stomach cancer Gastric MALT (mucosa-associated lymphoid tissue) lymphoma 39
- 38. Characteristics Gram negative curved rod Microaerophilic: requires oxygen to survive, but requires environments containing lower levels of oxygen than are present in the atmosphere Motile Produces oxidase, mucinase and urease enzymes 40
- 39. Virulence Factors Corkscrew motility enables penetration into mucosal layer Adhesins: which help it adhere to epithelial cells Mucinase: Degrades gastric mucus; Localized tissue damage Urease converts urea into ammonia Neutralize the local acid environment Localized tissue damage Vacuolating cytotoxin (VacA) apoptosis in eukaryotic cells generating large cytoplasmic vacuoles epithelial cell damage
- 41. Pathogenesis 43
- 43. Laboratory diagnosis Non-invasive Blood antibody test- IgG detection Stool antigen test- detection of specific antigens in the stools carbon urea breath test 45
- 44. Invasive - most reliable Gastric biopsy Urease positive Culture on Helicobacter Agar- takes 3-5days Oxidase, urease positive 46
- 45. Treatment 47
- 48. Characteristics and Epidemiology of Aeromonas (Family Aeromonadaceae) Gram-negative facultatively anaerobic bacillus resembling members of the Enterobacteriaceae Motile species have single polar flagellum (nonmotile species apparently not associated with human disease) 16 phenospecies: Most significant human pathogens A. hydrophila, A. caviae, A. veronii biovar sobria Ubiquitous in fresh and brackish water Acquired by ingestion of or exposure to contaminated water or food
- 49. Associated with gastrointestinal disease 揃 Chronic diarrhea in adults 揃 Self-limited acute, severe disease in children resembling shigellosis with blood and leukocytes in the stool 揃 3% carriage rate Wound infections Opportunistic systemic disease in immunocompromised Putative virulence factors include: endotoxin; hemolysins; eneterotoxin; proteases; siderophores; adhesins Clinical Syndromes of Aeromonas
- 50. CONCLUSIONS
Editor's Notes
- #12: 1)Endemic regions a)attack rate low in adults b)common in children
- #13: Mean annual cholera incidence (A) Mean annual cholera incidence per 100000 people in sub-Saharan Africa between 2010 and 2016, and (B) locations with mean annual incidence of more than one per 1000 people, (C) more than one per 10000 people, or (D) more than one per 100000 people.
- #14: Serogroup- group of microorg serotype having 1/more antigens in common O1-two major biotypes O39 restricted to Bangladesh, India O1-South America --what does O MEAN??? two biotypesclassicla and E1 Tordist based on biochem prop and susceptibility to bacteriophages 1993 outbreak in Bangladesh and India E1TOR prod hemolysins 9) O39 genetically derived from E1 tor, but antigenic structure different enoughno existing immunityall agues susceptible
- #15: 1)inadequte sewage treatmentunsafe drinking water 2)Preparation of food/beverages with contaminated water 3)Unsafe domestic storage of freshwater 4)Commercial bottled water 5)Wash fruits/vegetables with untreated water 6)shellfishundercooked
- #19: 1)Bact prod toxin that. 2)Prevents hydrolysis of GTP to GDP
- #22: Not sure why O more susceptibleallows bacteria to adhere to gut liningguess a)e1tor and 0139cholera gravismostly O blood type endemic regions a)bangladeshlow attack rates in adults b) Antibodies resistance--- intestinal IgA prevent attachment to mucosal surface, neutralize cholera toxin b)Cmmon in children
- #27: 1) Treatment depends on severity of dehydration
- #43: H. pylori produces large amounts of the enzyme urease which breaks down urea to carbon dioxide and ammonia The ammonia is converted to ammonium which neutralizes gastric acid. The ammonia produced is toxic to the epithelial cells, and, along with the other products of H. pyloriincluding proteases, cytotoxin A and certain phospholipases damages the cells Colonization of the stomach by H. pylori results in chronic gastritis, an inflammation of the stomach lining. Duodenal and stomach ulcers result when the consequences of inflammation allow the acid and pepsin in the stomach lumen to overwhelm the mechanisms that protect the stomach and duodenal mucosa from these caustic substances.