Anaerobic bacteria spring 2011

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  • Figure Victim of tetanus , a soldier wounded at the battle of Corunna in 1809, is seen in a drawing made by the Scottish surgeon and anatomist Sir Charles Bell and published in 1832 in his book The Anatomy and Philosophy of Expression . The patient's muscles are working against one another, leaving him in a state of spastic paralysis; his jaw is set in the "sardonic smile" of tetanus, or lockjaw.
  •   Ducks displaying the characteristic flaccid paralysis caused by the disease
  • Anaerobic bacteria spring 2011

    1. 1. Anaerobic bacteria 1
    2. 2. Classification• spore-forming anaerobes Clostridium G+• non-spore-forming anaerobes G+, G- cocci, bacilli 2
    3. 3. Section Ⅰ Clostridium 3
    4. 4. General characteristics• gram-positive, spore-forming bacilli• obligate anaerobes• motile -- peritrichous flagella (exception: C. perfringens—nonmotile)• the sporangia– swollen• typical clinical symptoms 4
    5. 5. Clostridium• C. tetani• C. botulinum• C. perfringens• C. difficile 5
    6. 6. C. tetani 6
    7. 7. 7
    8. 8. Characteristics• anaerobic gram- positive rod that forms terminal spores• motile with peritrichous flagella• tetanospasmin 8
    9. 9. Pathogenicity• portal of entry: wound• conditions of infection regional anaerobic environment – deep and narrow wound, contamination of soil or foreign bodies – necrotic tissues – contamination of aerobes or facultative anaerobes 9
    10. 10. Pathogenicity• Virulence factors – Tetanospasmin • Protein (neurotoxin) • Heat-labile (65℃, 30min) • Mechanisms 10
    11. 11. Mechanisms of tetanospasmin toxin → peripheral nerve fibers / lymph andblood → spinal cord and brain stem →inhibitory interneuron → blocks the release ofneurotransmitters from the presynapticmembrane of inhibitory interneurons→ inhibitthe motor neuron → spastic paralysis (rigidparalysis) 麻痹性痉挛excitatory transmitter: acetylcholineinhibitory transmitter: glycine and γ–aminobutyric acid 11
    12. 12. Mechanisms of tetanospasmin spastic paralysis (rigid paralysis) 12
    13. 13. Pathogenicity• Disease-tetanus(neonatal tetanus) latent period: 4-5d ~ several weeks typical symptoms: Opisthotonos 13 Lockjaw, sardonic smile
    14. 14. Pathogenicity• Disease-neonatal tetanus – a frequent cause of death in developing countries – most common causes: cutting the umbilical cord with unsterilized instruments or infection of the umbilical stump – the fatality rate: around 90% – the common death cause: respiratory failure 14
    15. 15. Immunity• Antitoxin immunity• Weak potent exotoxin rapid combination with target cells• Toxoid vaccine 15
    16. 16. Control• Proper care of wounds: surgical debridement• Active immunization: tetanus toxoid for children: basic immunization: DPT(diphtheria toxoid, pertussis vaccine, tetanus toxoid) for a high-risk group : toxoid booster• Passive immunization: tetanus antitoxin urgent prevention (along with toxoid) As soon as possible• Special treatment – administration of antibiotics – supportive measures 16
    17. 17. C. perfringens 17
    18. 18. Characteristics• Shape and structure – Subterminal endospore – Capsule – Nonmotile 18
    19. 19. Characteristics• Classification – five toxigenic types (A through E) – αtoxin: the most potent toxin→exhibits lecithinase activity→destroys erythrocytes, leukocytes, and platelets→ hemolysis, tissue necrosis Type α, Alpha β, Beta ε, Epsilon ι, Iota A + B + + + C + + D + + E + + 19
    20. 20. Characteristics• Cultivation anaerobic double zones of hemolysis carbohydrate fermentation (lactose) Inner zone: θ toxin complete Outer zone: α toxin Incomplete Stormy 20 fermentation
    21. 21. Pathogenicity• Virulence factors – α toxin • produced by all strains • acts as a lecithinase • diagnosis: Nagler reaction--egg yolk agar 21
    22. 22. Pathogenicity• Virulence factors – Enterotoxin • produced by types A(most), C, and D • heat-labile – Others • collagenase, hemolysin, proteinase, DNase (deoxyribonuclease) 22
    23. 23. Pathogenicity• Disease – Gas gangrene • Occurrence • Transmission: trauma • Pathogens: 60 ~ 80 % cases by type A • Manifestation: sudden outset, emphysema, edema, necrotic tissues, foul-smelling, toxemia, shock 23
    24. 24. Pathogenicity• Disease – Food poisoning • transmission: gastrointestinal tract • pathogens: type A • manifestation: short incubation period (10hrs) diarrhea self-limiting – Necrotizing enteritis • pathogens: type C • highly fatal in children 24
    25. 25. Control• Care of trauma: debridement• Antimicrobial therapy• Antitoxin• Hyperbaric oxygen• Symptomatic care for food poisoning 25
    26. 26. C. botulinum 26
    27. 27. Characteristics• Gram positive rod• Subterminal endospore• Noncapsule• Obligate anaerobe 27
    28. 28. Pathogenicity• Virulence factor—botulinum toxin – neurotoxin – relatively heat-labile and resistant to protease – types: A, B, C, D, E, F, G – the most potent toxic material known potassium times 10,000 cyanide(KCN) mechanism of actionToxin → gut → blood → cholinergic synapses → block therelease of exciting neurotransmitter, e.g., acetylcholine →flaccid paralysis 28
    29. 29. Mechanisms of botulinum toxin flaccid paralysis 29
    30. 30. Pathogenicity• Disease—Botulism – from Latin botulus, "sausage" Sausages, seafood products, milk, and  Food poisoning canned vegetables  Infant botulism Honey  Wound botulism 30
    31. 31. Pathogenicity• Disease – Food poisoning • manifestation: flaccid paralysis: double vision, dysphagia, difficulty in breathing and speaking rare gastrointestinal symptoms cause of death: respiratory failure 31
    32. 32. Pathogenicity• Disease – infant botulism • manifestation: constipation, poor feeding, difficulty in sucking and swallowing, weak cry, loss of head control. Floppy baby • prevention: free of honey 32
    33. 33. Pathogenicity• Disease – wound botulism • Rare • Transmission: trauma 33
    34. 34. MedicineBlepharospasm 34
    35. 35. C. difficile 35
    36. 36. Pathogenicity• Virulence factor exotoxin A: enterotoxin exotoxin B: cytotoxin• Disease pseudomembranous colitis antibiotic-associated diarrhea 36
    37. 37. Control• Treatment discontinuation of causative antibiotics administration of sensitive antibiotics• Prevention no vaccine use antibiotics only in necessary 37
    38. 38. non-spore-forming anaerobes 38
    39. 39. Characteristics• include both G+ and G- bacilli and cocci.• members of the normal flora• cause: endogenous infection 39
    40. 40. Non-spore forming anaerobes G am negat i ve r G am posi t i ve r Baci l l us C occus Baci l l us C occus Bact er i odes Vei l l onel l a Pr opi oni bact er i um Pept ost r ept ococus Pr evot el l a Bi f i dobact er i umPor phyr omonas Eubact er i umFusobact er i um Act i nomyces 40
    41. 41. Conditions causing disease• Change of habitat• Decrease of host defense• Dysbacteriosis• Local anaerobic environment formation 41
    42. 42. Characteristics of infections• endogenous infection throughout body, most chronic• nonspecific manifestations, most pyogenic• foul-smelling discharge, sometimes gas formation• direct smear positive, aerobic culture negative• have no response to some antibiotics such as aminoglycisides 42
    43. 43. Diseases• septicemia• infections in central nervous system• dental sepsis• pulmonary infections• intraabdominal infections• infections of the female genital tract 43
    44. 44. occurrence development of anaerobic environments (e.g., deep wound)spores → vegetative cells ↓ tissue destruction and necrosis; carbohydrate fermentation and gas (H2; ,CO2) formation and accumulation in the tissue ↓ restrict the blood supply (flow) → increases the tissue necrosis 44

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