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ANAEROBIC SPORE FORMING. ANAEROBIC SPORE FORMING THE GENUS CLOSTRIDIUM MORPHOLOGY Gram + rod, club shape oxidase - spore forming, anaerobe catalase - most motile. soil intestinal tract of man and animals most are saprophytic organisms.

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    2. ANAEROBIC SPORE FORMING THE GENUS CLOSTRIDIUM MORPHOLOGY Gram + rod, club shape oxidase - spore forming, anaerobe catalase - most motile

    3. soil intestinal tract of man and animals most are saprophytic organisms HABITAT

    4. DISEASE PRODUCING CLOSTRIDIUM 1. Neurotoxic Clostridia 2. Histotoxic Clostridia 3. Enteropathogenic - producing Clostridia Enterotoxaemia- producing Clostridia

    5. PATHOGENESIS 1. Neurotoxic disease (non-invasive) C. tetani C. botulinum (botulism)

    6. PATHOGENESIS 2. Histotoxic disease (invasive, gas gangrene) trauma of deep muscle tissue inflamme, edema, necrosis degenerative capillaries C. chauvoei(Black leg) C. septicum(Malignant edema) etc. C. perfringenstype A (Gas gangrene)

    7. 3. Enteropathogenic & Enterotoxaemia • C. perfringens (C. welchii) • type A, B, C, D, E

    8. TRANSMISSION Ingestion, Botulism C. botulinum Wound, Gas gangrene C. chauvoei C. septicum C. perfringens etc.

    9. 2. Histotoxic disease PATHOGENICITY C. chauvoei Black leg in cattle * ingestion is the most probable route * skeletal muscles seeded with spore (local muscle anoxia, overexercise, insect) * damage to muscle provide spore germination * subsequent multification & toxin production tissue necrosis, gas gangrene, toxaemia

    10. Toxins released : • α - hemolysin, necrotizing • β - deoxyribonuclease (DNase) • γ - hyaluronidase • δ- hemolysin

    11. myositis

    12. Myocarditis (blackleg)

    13. C. septicum • Malignant edema in horse cattle swine • wound(exogenous infection) • edema, gasin soft tissue • hemorrhage,edema and necrosis • “Braxy” in sheep (winter in Europe) • ingest frozen harbage may cause • wound in abomasum, gangrene, • edema at gastrointestinal wall, toxemia • Toxin released as the same as C. chauvoei

    14. Ovine abomastitis ( Braxy, C. septicum)

    15. C. septicum in cook meat media.

    16. C. novyi (C. oedematiens) Type A :Gas gangrene wound, inflammation man, cattle, sheep mix organisms(C. chauvoei, C. septicum) “big head” in ram toxin α - necrotizing (typeA & B)

    17. Type B Black disease (Infectious Necrotic Hepatitis) sheep in U.S.A. (cattle, horse, pig rarely) - dormant spore germinate in liver tissue often damaged by fluke migration - systemic effects – death - follow dissermination of – αtoxin hepatic efffects produce edema, necrosis

    18. Black disease caused by C. novyi (type B) Dark skin caused by marked subcutaneous venous congestion

    19. C. novyi

    20. C. haemolyticum (C. novyi type D) • Bacillary Hemoglobinuria • Ruminant : cattle, lamb • deposition of type D spores or vegetative cells in the digestive tract & liver follow digestion • immature liver flukemigrate through the liver resulting in tissue damaged • spore germinate & toxigenesis • hemoglobinuria caused by extensive RBCdestruction • death caused by anoxia • hemoglobinuria “Red water”

    21. Toxin released : • β - hemolysin, necrotizing • Lecithinase - act on lecithroproteinof RBC surface hemolysis

    22. C. perfringens (C. welchii) • myonecrosis and gas gangrene • types A Toxin released • α - hemolytic, necrotizing, lecithinase, lethal

    23. Gas gangrene C. perfringens type A

    24. Gas gangrene following leg amputation C. perfringenstype A

    25. Gangrenous dermatitis

    26. Histotoxic clostridia Toxin Species biological activity name Lethal, hemolytic, necrotizing Deoxyribonucleus Hyaluronidase Oxygen-labile haemolysis Same as C. chauvoei toxins Necrotizing, lethal Haemolytic, necrotizing, lethal, lecithinase C. chauvoei C. septicum C. novyi type A C. perfringens typeA     4 toxins  

    27. Species Toxin name biological activity Lecithinase Edema-producing lethal factor Necrotizing, lethal Necrotizing, haemolytic lethal, lecithinase Necrotizing, haemolytic, lethal, lecithinase      C. sordellii C. novyi type B C. haemolyticum

    28. 3. Enteropathogenic & Enterotoxaemia • C. perfringens (C. welchii) • - 5 types A B C D E • Major toxin released : • α - hemolytic, necrotizing, lecithinase, lethal • β - necrotizing, lethal • ε - protoxin(convert to toxin by trypsin, pepsin) • ι- protoxin

    29. Other toxin released : •  Theta - A B C D E, lethal, hemotytic • necrotizing • Lamda - B E D, proteolytic enzyme • Mu - hydrolyzing hyaluronic • Enterotoxin - A, C, cytotoxin

    30. Clostridium perfringens types in animal diseases MAJOR TOXIN PRESENT Type Alpha Beta Epsilon Iota A + - - - B + + + - C + + - - D + - + - E* + - - + Enterotoxin all types * Type E strain often present in cattle and sheep intestine. Rarely implicated in enterotoxemia

    31. Types of C. perfringens and their major toxins Toxin C.perfringens biological activity name Lecithinase Cytotoxin Lecithinase Lethal, necrotizing increase intestinal and capillary permeability, lethal Lecithinase Lethal, necrotizing Cytotoxin * Enterotoxin  *   * Enterotoxin Type A Type B Type C

    32. Types of C. perfringens and their major toxins C.perfringens Toxin biological activity name  *  ι* Lecithinase increase intestinal and capillary permeability, lethal Lecithinase Lethal Type D Type E * Major toxin

    33. A - necrotic enteritis in chicken, pig, dog B - lamb dysentery, hemorrhagic enteritis in calves and foals C - necrotic enteritis in chicken, hemorrhagic enteritis in piglets D - pulpy kidney in sheep, enterotoxemia in calves and goats E - hemorrhagic enteritis in calves enteritis in rabbits

    34. C. perfringens

    35. 1. Neurotoxic Clostridia C. tetani (tetanus) Man, horse are most susceptible Swine & ruminant moderate susceptible Carnivores are comparative resistant Poultry are not susceptible * wound from docking, dehorning castrating, umbilical infection

    36. C. tetani.

    37. Toxin released : • 1. Hemolysin (tetanolysin) released during replicated in the tissue • 2. Neurotoxin (tetanospasmin) • harmless if administered by mouth • highly toxic when injected parenterally

    38. Pathogenesis of C. tetani Tetanospasmin produced at wound site peripheral nerve & blood vessel motor nerve terminal vesicle, travel inside axon nerve cell body and its dendritic process in CNS terminal of inhibitory neurones suppress of release inhibitoryneurotransmitterfrom signaling relaxation (glycine) clonic or tonic spasm(spastic paralysis)

    39. Ascending tetanus * typical of animals not susceptible to toxin e.g. dogs and cats * only nerve trunk near toxigenic site absorb sufficient toxin to produce signs, localizedtetanus Descending tetanus * typical of animals highly susceptible (horse, humans) * toxin disseminated via vascular channels to nerve endings in areas remote from that site * toxin enter CNS producing, generalized tetanus

    40. Tetanus in cat

    41. Muscle spasm can break bone

    42. C. Botulinum (7 types) neurotoxin A, B, (soil) C, D, E, F, G (wet environment) intoxication ingestion spoiled food, animal carcasses contain toxin toxico-infection (uncommon) spore germinate in intestine, wound toxin producing by vegetative cell “infant botulism” – honey, dust muscle weakness, breathing problem

    43. Most commonly in waterfowl, cattle, horse, sheep, poultry (C, D) Pig and dog are relative resistant Rare in domestic cat

    44. Pathogenesis of C. botulinum • toxin (absorbed from gastrointestinal tract) transferred to neurone via blood stream to peripheral nerves act at neuromuscular junction • inhibit release of acetylcholine • synapse degenerate and flaccid paralysis • death from circulartory failure of • respiratory paralysis

    45. Avian botulism (type C)