Uploaded byDr. Kanwal Deep Singh Lyall
Clostridium
Clostridium are anaerobic, spore-forming bacteria found in soil and the gastrointestinal tract of humans and animals. Certain Clostridium species cause diseases like tetanus, gas gangrene, and food poisoning. They produce potent exotoxins and can be diagnosed through gram staining, culture techniques, and toxin detection assays. Treatment involves surgery, antibiotics, antitoxins, and in some cases hyperbaric oxygen therapy. Vaccination provides protection against tetanus.
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Clostridium
- 1. Clostridium Dr. Kanwal DeepSingh Lyall M.D. Microbiology
- 2. Sporogenous Gram PositiveBacilli Aerobic Bacilli Anaerobic Clostridia Non- bulging spores bulging spores
- 3. General features • Anaerobic,sporing, bulging spores • Kloster = spindle • Saprophytes – soil, water • Or live in GIT – C. tetani, C. perfringens • Cause three major diseases : Tetanus, Gas gangrene and food poisoning • All are motile except C. perfringens & C. tetani type VI
- 4. Classification Tetanus : C.tetani Acute colitis: C. difficile Food poisoning: GE – C. perfringens type A Necrotizing enteritis – C. p. type C Botulism – C. botulinum Gas gangrene: Established pathogens: C. perfringens, C. Septicum, C. novyi Less pathogenic: C. histoliticum, C. fallax Doubtful path: C. bifermentans, C. sporogens PerSeN has HiFi BiSness
- 5. Culture • Macintosh –Fildes jar • CMB (unsat. Free fatty acids consume O2 catalysed by haemetin, and low redox pot d/t sulpjydrl groups) • Gaspacks • All spores die in autoclave • Halogens and 2% glutraldehyde kill spores effectively
- 6. C. Perfringens (welchii) •Capsulated & NM, Subterminal spores • M/I cause of gas gangrene, causes food poisoning & necrotizing enteritis • Commensal in GIT • Soil & dust • Spores rarely seen in cultures or tissues & absent spores characteristic feature • Glucose BA – Target haemolysis Alpha toxin Theta toxin
- 7. Biochemical reactions • SacchrolyticI pink • G/L/S – acid + gas • Abundant H2S • Stormy fermentation reaction: litmus milk – lactose ferm. Leads to acid production – color changes blue to red – acid clots milk – gas disrupts the clot
- 8. Classification • 12 typesof toxins • Alpha, beta, epsilon & iota (αβει) • Type A : α, • Type B : α, β,ε • Type C : α, β • Type D : α, ε • Type E : α, ι • Alpha – m/I : gas gangrene & food poisoning
- 9. Alpha toxin • Phospholipidase(lecithinase C) • Lecithin – part of mammalian cells walls • Heat stable, lethal, dermonecrotic, hemolytic • Hot – cold lysis • Naegler’s reaction • Reverse CAMP test
- 10. Pathogenesis • Gas gangrene6h 6 wks , anaerobic cellulitis, myonecrosis • Food poisoning: type A, 8-12 hrs, meat, poultry – like enterotoxin of V. cholerae • Necrotic enteritis
- 11. Diagnosis = clinical Labdiagnosis Gram stain: GPB without spores, pleomorphic GPB (Citron bodies, leaf or boat shapes) in C. septicum, large GPB & oval subterminal spores – C. novyi Culture: heated BA , CMB Colony morphology, biochemical reactions, reverse CAMP test etc. Animal pathogenicity , RCM i/m GP – death – heart, spleen Food poisoning: RCM inculated - heated @ 100 C x 30 m – cooled – incubated @ 37 C x overnight – s/c on selective media – S. A . above
- 12. Prophylaxis & Treatment •Surgery – debridement, irrigation • Antibiotics – metronidazole, sulphonamides, tetracycline, amoxycillin etc. • Antitoxin • Hyperbaric O2
- 13. Cl. Tetani • Soiland GIT • Terminal spores – drumstick appearance • Non capsulated, motile except type VI • Grows on BA,NA,CMB, Thioglycoslate broth • CMB- Black, BA – Swarming, • Iridescence – greenish fluorescence on MA • No sugars fermented
- 14. • Spores survivein soil for years • Ten serological types based on flagellar (H) Ag • Type VI – non-flagellated • All produce same toxin • Toxins: – Tetanolysin (heat & O2 labile, lysis RBC & WBC), – Tetanospasmin (heat labile, O2 stable, powerful neurotoxin, rapidly destroyed by proteolytic enzymes, plasmid coded, neutralized by AB
- 15. Pathogenesis • Little invasiveness •Toxin – acts presynaptically – blocks synaptic inhibition in spinal cord – continuous spread of spread of impulses – muscles rigidity & spasm • Diagnosis – clinical grounds • Lab diagnosis – GPB with terminal spores • Cl. tetanomorphium & Cl. spheroides – similar apperance on GS – hence GS unreliable
- 18. Lab diagnosis • Onlyfor confirmation • Gram stain – drumstick GPB • Culture: sample – Fresh BA + Poly B – swarming • CMB x 3 tubes – 1st – 80° C X 15 m, 2nd 80° C x 5 m and 3rd unheated (kills vegetative bacteria) – s/c daily x 4 days • 02 ml CMB – mice tail – rigidity in 2 – 4 days – ascending paralysis – death
- 19. Prophylaxis • Surgical debridement– prevent anaerobiasis • Antibiotics – destroy or inhibit bacterial load • Immunization – vaccination with toxoid, ATS or combined • Protect patients from light & noise • Clinical attacks don’t provide protection
- 20. Cl. Botulinum • Botulus= sausages • Soil, manure, vegetables • Strict aerobes grow on ordinary media • Large fimbriate irregular colonies • GPB with sub-terminal highly resistant spores • Classification based on toxin produced – 8 types A (most toxic), B, C 1- 3, D, E, F, G
- 21. Toxin • Exotoxin -Blocks production of Acetylycholine @ synapses & Neuromucular junctions • Protoxin Protease active form • Once bound cant be inactivated
- 22. Pathogenesis (Non-invasive) • Foodbourne botulism: Canned food • Infant: <6mnths – Honey • Wound: rare, toxin is absorbed into blood
- 24. Lab diagnosis • Gramstain • Culture • Animal inoculation Prophylaxis • Proper processing of canned food
- 25. Cl. Difficile • Newborn’sfeces • Difficult to culture • GPB with terminal spores • Toxin: Toxin A (Enterotoxin),Toxin B (Cytotoxic) • AAD & Pseudomembranous colitis • Lincomycin, Clindamycin • Diagnosis: Culture & Toxin detection • Treatment: Metronidazole, Vancomycin
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