Clostridium spp..ppt
- 1. C L O S T R I D I U M
- 2. Many are saprophytes in soil, water. Some are pathogens : Tetanus, Gas gangrene, Food poisoning. Anaerobes,Microaerophilic. Gram positive, spore bearing bacilli Spores :Central, sub terminal or terminal
- 3. Named so because of their Swollen spindle (Kloster) appearance. Motile except Cl. perfringenes Cl. tetani type VI Non capsulated except Cl. perfringenes. Cl. butyricum.
- 5. Vegetative forms : Sensitive to heat & Disinfecting agents. Spores : Autoclaving (10mts) Formaldehyde solution 1% solution of iodine. 2 % glutaraldehyde solution. Resistance : Phenols. Invasive properties are low. Exotoxin.
- 6. Classification: 1. Morphological features,shape & position of spore. 2. Biochemical features. 3. Clinical conditions: 1. Gas gangrene group. A. Highly pathogens Cl. perfringens Cl. septicum Cl. novyi
- 7. B. Less pathogenic Cl. histolyticum Cl. fallax. C. Doubtful pathogens. Cl. bifermentans Cl. sporgenes.
- 8. II. Tetanus group : Cl. tetani III. Food poisoning : (a) Gastroenteritis: Cl. perfringens. ( b) Botulism : Cl. botulinum. IV. Acute colitis : Cl. difficile.
- 9. Clostridium perfringens: Achalme : Cultivated Welch & Nuttal : Described. Normal inhabitant : Large intestine Morphology : Gram positive bacilli with rounded ends. 4 – 6 μm x 1 μm. Spores are terminal / sub terminal. Capsulated & non motile.
- 11. . Cultural characteristics: Anaerobe, micro aerophilic. pH : 5.5 – 8.0 Temperature: 200 – 500C ( 450 C optimum ). Nutrient Agar. RCM : Meat particles pink Absence of spores in culture.
- 12. Biochemical reactions : Glu, Lac, Suc Acid & Gas. Indole : Negative VP: Negative MR : Positive H2 S ++ . Nitrate reduction: positive.
- 14. Litmus Milk Fermentation Acid Lactose Coagulates Casein Disrupted by vigorous gas Gas Paraffin plug is pushed up and shreds of clots are seen on the sides of tube. Stormy fermentation.
- 15. Classification : Five types based on toxins produced A to E At least 12 verities of toxins are produced. Major : Alfa, Beta, Gamma Epsilon Iota Necrotizing property.
- 16. Alpha toxin : Phospholipidase ( Lecithinase ) Type A. Splits lecithin in serum or egg yolk. Heat stable Responsible for toxemia. Nagler reaction: Purpose : Demonstrate lecithinase effect of ɑ - toxin Use : Rapid test to detect Cl. perfringenes.
- 17. Medium : 5% Filde’s peptic digest sheep blood + 6% agar + Egg yolk + Neomycin sulphate. Half of the plate: Anti toxin Opacity around the colony. Anti toxin Lecithinase effect
- 19. Soluble substances : Neuraminidase : Pan agglutination of RBC. Fibrinolysins, Hemolysins and Histamine. A circulating factor : Adrenaline sensitivity to tissue.
- 20. Predisposing factors : Accidental injuries : Crushing & severing. Surgical wounds : Rough handling. Over zealous clamping. Shock waves : Gunshot injuries. Debility, old age, Diabetes mellitus. Source of infection : Exogenous : Animal / Human excreta. Soil. Road dust. Endogenous: Perineum
- 21. Pathogenicity : 1. Wound contamination. 2. Anaerobic cellulitis. 3. Gas gangrene (anaerobic myositis). 4. Food poisoning. Type A strains. Enterotoxin Cold or warmed up meat dish. I.P is 8 – 24 hrs. Spontaneous recovery (24 – 48 hrs). Symptomatic treatment.
- 22. 5. Gangrenous appendicitis. 6. Necrotizing enteritis : Type C strains . toxin 7. Necrotizing colitis. Elderly people Sporadic diarrhea. 8. Acute Emphysematous cholecystitis. 9. Intra abdominal gas gangrene is rare. Following surgery.
- 23. 10. Panophthalmitis Following penetrating injury. 11. Thoracic infections 12. Urogenital infections Following nephrectomy Septic abortions uterine gangrene Serious septicemia.
- 24. Cl. septicum : Vibrion septique. Soil, animal intestine. Gasgangrene “ Braxy” in sheep. Malignant edema - in cattle. Cl. novyi (Cl. edematiens ): Strict anaerobe. Gas gangrene - With large amounts of edema. Highly mortality.
- 25. Gas gangrene : Rapidly spreading edema, myositis, necrosis of tissues, gas production & profound toxemia. Etiological agents : Clostridial group : Cl. perfringens. Cl. septicum Cl. novyi Others: Anaerobic streptococci Staphylococci, E.coli, Proteus.
- 26. Events in Gas gangrene formation: Tissue damage Contamination with spores. Presence of soil, Ca++ & silicic acid. Inflammation & tissue necrosis Extravasation of fluid (Edema) Impaired tissue perfusion Tissue anoxia (Anaerobic condition) Impaired phagocytosis & leucocytic bactericidal mechanism. Germination of spores
- 27. Multiplication. Toxins & Gas. Further impairment of local blood supply Tissue damage. Profound toxemia & shock Severe hypotension Decreased Tissue perfusion Multiple organ failure Coma and Death.
- 28. S/S : Pain. Tenderness. Edema. Serous discharge. Crepitus - in adjacent tissues.
- 33. Lab. Diagnosis : 1.Necrotic tissue from wound. 2.Exudates from deeper parts. Grams staining : Typical bacilli Culture & confirmation.
- 34. Treatment : 1.Prompt surgical attention. Suture removal. Excision of necrotic & devitalized tissue. Release tension. Remove foreign body if any. 2. Antibiotics : Penicillin, Metronidazole, Amikacin 3. Hyperbaric oxygen : Not universally.
- 35. Prophylaxis : Pre - operative skin preparation. Foreign body removal. Anti gas gangrene serum: 10,000 U IM.
- 36. Cl.tetani : Street & Hospital dust Cotton, bandages, Catguts POP, Plaster, Clothing.
- 37. Morphology : Gram positive, slender 4 – 8 x 0.5 um. Terminal spore - “drumstick”. Non capsulated & motile
- 38. Cultural characteristics: Obligate anaerobe. 370 C 7.4 Grows on ordinary medium. Improved with blood & serum Growth: Swarming. Filde’s technique: Water of condensation in NA slope inoculated . Pure growth on slope.
- 39. In gelatin stab cultures : A fir tree type In Robertson’s cooked meat broth: Turbidity, Gas Meat particles turned black but not digested. On BA : Incomplete hemolysis Complete hemolysis,
- 40. Biochemical reactions : Feeble proteolytic. Not saccharolytic . Greenish fluorescence : On Mac Conkey. Sensitivity : Autoclaving : Best. 1% iodine solution Effective. Hydrogen peroxide
- 41. Toxins : Heat & 02 labile Tetanolysin Leucotoxin Tetanospasmin ( Neurotoxin ) Protein , O2 Stable, heat labile,. Production is plasmid coded. Can be toxoided. Antigenic, Neutralized by antitoxin Birds, reptiles highly resistant MLD - Mouse - 0.1 ng MLD - human - 130 ng.
- 42. Toxicity determined by route of administration. No effect : Ingestion. SC,IM, IV: Equally effective Intraneural :More lethal. Resembles Strychnine Tetanospasmin acts pre synoptically.
- 43. Mode of action: 1. Inhibits motor impulses exercised by UMN. 2. Interferes with synthesis of acetyl choline at presynaptic levels & cause for critical feedback control.
- 44. Pathogenesis : Little invasive power. Under anaerobic conditions Implanted spores germinates TOXIN Absorbed by motor nerve endings (NMJ) CNS Fixed by gangliosides of grey matter.
- 45. Tetanus : Following Injury. Surgery Septic abortion Tooth extraction Ear boring Oral sepsis. Circumcision Application of cow dung to umbilical stump.
- 46. Incubation Period : 1 - 2 weeks. (2 days - weeks) Depends on site of infection, Load of infection Nature of wound. Immune status. Prognosis depends on I.P
- 47. First symptom : Trismus. with onset of spasms. Difficulty in Chewing Swallowing Occlusion of teeth Edentulous patient complain of inability to insert dentures.
- 48. Types of Tetanus : 1.Generalised tetanus: Risus sardonicus. Dysphasia. Stiffness & pain in neck shoulders, abdominal muscles Hands & feet spared. Mild stimulation : Generalized spasms Laryngospasm.
- 50. Risus sardonicus
- 51. Opisthotonus
- 52. Opisthotonus
- 53. Artist’s expression on Opisthotonus.
- 54. 2. Tetanus neonatorum : Following home deliveries. High fatality 50 – 60%
- 55. 3. Autonomic dysfunction : Sustained HTN, Tachycardia. Arrhythmias, hyperpyrexia, Profuse sweating, peripheral vasoconstriction. 4. Post operative tetanus.
- 56. 5. Uterine tetanus : Fatality rate 10 – 100% 6. Otogenic tetanus 7. Cephalic tetanus :Head injury Ear infection Oral sepsis.
- 57. Epidemiology : More common in developing countries. Warm climates, Rural areas. Close association with animal populations Poor wound management. Walking on bear foot. Mortality depends on handling of case Usually 10% USA - 2%
- 58. Lab. Diagnosis : 1. Microscopy : Unreliable Cl. tetanomorphum & Cl. sphenoides 2. Culture : Tissue bits (from depth of wounds) Swabs Blood agar with polymyxin
- 59. 3. Toxigenicity test : A. Horse blood agar to demonstrate tetanolysin B. Experimental animal : Tetanospasmin Material : Pure culture from RCM Animal : mice Test animal : 0.2 ml of culture into root of tail Control animal (1000 U of antitoxin 1 hour before): 0.2 ml of culture into root of tail
- 60. Observation: After 12 - 24 hours. Stiffness in the tail and proceeds to Generalized Tetanus in test animal.
- 61. MANAGEMENT : 1.Surgery : wound debridement. 2.General measures : admit in a quit room 3.Antibiotics : ? Benzathine pencillin is the choice. Clindamycin, Erythromycin, Metronidazole. 4.Antitoxin : TIG 3000 - 6000 U. IM. in divided doses.
- 62. 5. Control of spasms : Diazepam 250mg / day. Lorazepam. 6. Respiratory care : By intubation 7. Autonomic dysfunction By giving ɑ and adrenergic blocking agents. Ex : Labetalol Esmolol.
- 63. IMMUNISATION : Active immunization 1.Monovalent vaccines. Plain toxoid Toxoid with Aluminum hydroxide. 2.Combined vaccines : DPT 3 doses (starting at 6 wks of age) at 4-8 wks interval
- 64. 1st Booster : 18 months age. 2nd Booster DT : 5 - 6 yrs. 3rd Booster TT : After 10 yrs.
- 65. Passive Immunization : Horse 1. ATS Bovine 2. ATG or TIG:: Human origin. ATS : 1500 IU SC / 1M Half life is 7 days Protection for 7 – 10 days
- 66. Complications : Hypersensitivity Serum sickness Immune elimination. TIG : 250 – 500 I.U SC / IM Half life: 6 – 8 wks Protection for 30 days Reduces incidence of tetanus & prolongs I.P
- 67. WOUND MANAGEMENT GUIDE LINES. SIMPLE WOUNDS COMPLICATED WOUNDS (DEEP / LACIRATED / CONTAMINATED) SURGICAL ATTENTION EARLY STAGES DELAYED Clean & close wound Don’t close Do suitable Dressings. Surgical attention Apply simple dressings
- 68. If Patient has had TT Course With in 5yrs : No TT More than 5 yrs : TT Booster If Patient has had no TT course Advice a TT course. HTIG. COMPLICATED WOUNDS REQUIRED REGULAR INSPECTION
- 69. Cl.botulinum : Saprophyte. Non capsulated, Motile. Sub terminal spores. Strict anaerobe. Classified into 8 types: A B C1 C2 D E F G.
- 71. Toxin : Responsible for pathogenecity. Powerful Exotoxin. Phage mediated. Released on autolysis of cell. Pro toxin Toxin absorbed in Small intestine. Trypsin Relatively stable. Can be Toxoided. Neutralized by antitoxin.
- 72. Mode of action : Blocking the production / release of Acetyl choline at synapses & NMJ. Probably most toxic substance. Lethal dose : Mice : 33 pg Human : 1-2 μg. May be isolated as pure crystalline protein.
- 73. Shows signs of spoilage if produced by proteolytic Cl. botulinum. Leave food unchanged if Non proteolytic Cl. botulinum. Pathogenicity : Non invasive. Noninfectious.
- 74. BOTULISM 1. Food borne botulism. 2. Wound botulism. 3. Infant botulism.
- 75. Food borne botulism : Severe. Often fatal. Ingestion of preformed toxin Source : Preserved hams, Sausages Preserved meat Canned foods Liver paste. Hazelnut puree. Fish & other seafood.
- 76. Incubation Period : 12 – 36 hrs. S/S. : Starts with diplopia, Blurred vision with drooping of eyelids, Dysarthria Nausea, vomiting, constipation, Abdominal pain, Urinary retention. Progresses to descending motor loss with flaccid paralysis. Patient is alert & oriented. Drowsy Death due to respiratory failure. Mortality : 25 - 70%
- 77. Infant botulism : Floppy child syndrome. Sudden infant death syndrome. Infants < 6 months Toxico -infection Honey. S/S: Poor feeding, lethargy. Constipation Weakness, weak cry, Floppiness & loss of head control.
- 78. Infant botulism
- 79. Infant botulism
- 80. Wound botulism : Type A strains. Rare. Seen in chronic drug abusers, After cesarean sections. Toxin is produced at the site of wound infection & absorbed. I.P : Longer (10 days). S/S: Same as food borne botulism without GI symptoms.
- 81. Wound botulism : Wound botulism
- 82. Laboratory diagnosis : 1. Demonstration of toxin / bacilli in food or feces: Grams stain, Culture . 2. Animal inoculation. Saline filtrate of macerated food. Intra peritoneal. Mice or Guinea pig. Succumbed to disease. Control animal with polyvalent antitoxin escapes.
- 83. CARE & PROPHYLAXIS OF BOTULISM. Saprophyte : Soil, Vegetables, Fruits, leaves, manure. Insufficient heating : Preservation of foods. Great care must be taken in canning factories to ensure adequate heating in all parts of the can contents. Foods responsible for botulism may not exhibit signs of spoilage. “Home canning” should be avoided. Amateur preservation of meat & vegetables (Beans, Peas, Root vegetables ) highly dangerous.
- 84. Acid fruits safely bottled : Low pH inhibits the growth of Cl. botulinum. Prophylactic dose of antitoxin. Active immunization : Toxoid. 2 doses. 10 Weeks Interval. Booster dose one year later.
- 85. ANTIBIOTIC ASSOCIATED ACUTE COLITIS Clostridium difficile. Long, slender, Gram positive. Terminal spore. Not considered as pathogenic till 1977.
- 86. Pathogenecity : Acute colitis with dysentery with or without membrane formation. Following an oral antibiotics Ampicillin, Tetracycline, Chloramphenicol Cephalosporins. Lincomycin, Clindamycin (Pseudo membranous colitis)
- 87. Lab. Diagnosis : 1. Feces. Culture on selective medium. 2.Demonstration of toxin : By testing in A. Cell monolayer of human embryonic fibroblasts. B. ELISA.
- 88. Treatment : Vancomycin, Bacitracin is drug of choice Prevention : Clinical awareness. Stop the indiscriminate usage of oral antibiotics.