MMI 301: Lecture 22: Clostridium and other Anaerobes

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  1. Clostridium perfringens morphology
    Large Gram + Rectangular rods
  2. Clostridium perfringens aerobics
    Obligate anaerboic
  3. Clostridium perfringens and spores/capsules
    Makes spores, makes capsules
  4. Clostridium perfringens growth
    Grows fast on BAP, produces lots of gas when growing on carbohydrates
  5. Gas Gangrene
    • Endospores of C. perfringens infect traumatic muscle injuries
    • Results in sever muscle destruction
    • Life-threatening
    • Diseased tissue must be cut out, and patient in hyperbolic chamber: oxygenates tissue and kills anaerobes
  6. Clostridium perfringens food poisoning
    • Caused by Type A enterotoxin, causes fluid loss
    • Later there is nausea, vomiting and abdominal pain
    • Associated with meat dishes, that are not stored properly
    • Third most common food poisoning
  7. Clostridium tetani morphology
    Large gram + rods, frequently stain Gram -
  8. Clostridium tetani location
    Found in soil worldwide
  9. Clostridium tetani motility
    Very motile: peritrichous flagella
  10. Clostridium tetani and spores
    Terminal endospores: "drumstick appearance"
  11. Clostridium tetani growth
    Grows slowly, very oxygen sensitive
  12. Tetanus
    • Aka Jockjaw
    • Infection of break in skin by Clostridium tetani endospores
    • Infected tissue must be low oxidation-reduction area (puncture wound w/ necrosis)
    • Disease from Tetanospasmin exotoxin (A-B type toxin) w/ zinc endopeptidase activity
    •     -rigid paralysis
  13. Clostridial Tet neurotoxin and what are related:
    • BoNT,
    • Amino-terminal portions have zinc-metalloprotease activity
    • C- terminal of the neurotoxins contains domain necessary for binding neuronal cell receptors.
  14. Neonatal Tetanus
    • Disease attacks in first few days of life
    • Occurs from spores being introduced through poor hygiene during birth
  15. Treatment and Prevention of Clostridium tetani
    • Toxin not yet bound to postsynaptic membrane can be neutralized with anti-bodies.
    • Treatment mostly supportive measures (open blocked airway)
    • Drugs that cause flaccid paralysis
    • Immunization with vaccine
    • Active immunization of pregnant women
  16. Clostridium botulinum morphology
    Large Gram + rods
  17. Clostridium botulinum found
    Naturally in soil
  18. Clostridium botulinum aerobics
    Obligate anaerobe
  19. Clostridium botulinum and spores
    Forms subterminal endospores
  20. Clostridium botulinum secretes what toxin
    Botulinum neurotoxins (BoNTs), zinc endopeptidases, cause botulism
  21. Mechanism of botulism toxin
  22. Foodborne botulism
    • -Occurs when foodstuffs contaminated with preformed BoNT are consumed
    • -Seen in home-canned foods
    • -BoNTs are heat labile
    •     -Acid resist
    •     -Germination prevented by acidic environments
  23. Intestinal Botulism
    • Occurs when spore are ingested/germinate in gasto tract
    • Release of toxin in situ (primary infection, secondary intoxication)
    • Most common botulism
    • Hits infants (honey) and people with weak immune
  24. Infant botulism
    Floppy Baby Syndrome
  25. Wound Botulism
    • Occurs mostly in punctures
    • On rise with IV
  26. Clinical/Cosmetic application
    • Blepharospam
    • Cervical dystonia/Spamodic toticollis
    • Hyperhydrosis
    • Glabellar lines
    • Focal spasticity in cerebral palsy patients
    • Migraine headaches
  27. Clostridium difficile morphology
    Gram +
  28. Clostridium difficile aerobics
    Strict anaerobe w/ vegetative cells that are oxyen sensitive
  29. Clostridium difficile causes
    Diarrhea in patients recently undergoing antibiotics
  30. Pseudomembranous colitis disease
    • Colon has thick pseudomembrane (fibrin, leukocytes, and necrotic colonic epithelial cells).
    • Result of overgrowth of C. difficile in colon
    • Only occurs when normal colon biota has been reduced with antibiotics
    • •In general, C. difficile is non-invasive, i.e. the organismdoes not go directly through the intestinal wall into the blood stream.Instead, it stays within the hollow of the intestinal space and causes damageby producing two toxins (A & B) that attack the intestinal wall. •The presence of these two toxins in the stool is the hallmark of this disease.
  31. Pseudomembranous colitis: Ecology
    • Obligate anaerobic gram + bacillus (C. difficile)
    • Found in small number of healthy adults
    • Common hospital contaminant
  32. Pseudomembranous colitis: Toxins
    • TcdA, TcdB
    • TcdA: Enters epithelial cells, causes cytoskeletal protein rearrangements/loss of tight junctions, enables TcdB to enter lamina.
    • TcdB: Along with TcdA, are cytotoxic, elicit strong host inflammatory response including neutrophil influx.
  33. Pseudomebranous colitis: Antibiotics
    • Caused by: Ampicillin and clindamycin
    • Treat with: Vancomycin
  34. Bacteriodes morphology
    Gram - bacilli (most common of this type in intestine
  35. Bacteriodes aerobics
    Obligate anaerobes
  36. Bacteriodes species
    • distasonis and thetaiotaomicron= gut commensal
    • fragilis=infectious
  37. Bacteriodes fragilis disease and physiology
    • Cause most intra-abdominal infections from fecal contamination via ruptured appendix/intestinal surgery
    • Virulence from prominent capsule
    • Increased growth in presence of bile salts
  38. Reducing Bacteriodes fragilis toxicity
    • Penta-acylation of lipid a vrs. hexa-acylation
    • or
    • monophosphorylation of lipid A
  39. Bacteriodes fragilis Antigenic switching
    • Has exceptional capability to use dietary polysaccharides
    • Uses multiple DNA inversion system with multiple operons for polysacc. synthesis/transport along with other membrane proteins
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MMI 301: Lecture 22: Clostridium and other Anaerobes
2013-12-03 15:51:42
MMI 301

MMI 301
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