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2013-11-07 05:58:29

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  1. General information about Clostridia (gram, shape, aeration, major species w/ disease)
    • Gram+
    • Rods
    • Anaerobic
    • C. perfringens: histotoxic (tissue destructive) infections (myonecrosis). Food poisoning.
    • C. botulinum: botulism (flaccid paralysis)
    • C. tetani: tetanus (spastic paralysis)
    • C. difficile: pseudomembranous colitis
  2. What makes Clostridia anaerobic (physiology)?
    • Cannot use free oxygen as terminal electron acceptor (use small organic molecules instead)
    • Inhibited/damaged by O2 due to lack of peroxidase, catalase, and superoxide dismutase enzymes
    • Must be grown on media in presence of reducing agent OR O2 free environment
  3. General information about C. perfringes (shape, motility, gram, capsule, found where, potential disease states?)
    • Large rod
    • nonmotile
    • gram positive
    • encapsulated
    • Ubiquitous in nature.  Spores in soil, normal flora in vagina and GI.
    • Causes gas gangrene (myonecrosis) when introduced into tissues
    • Some strains causes food poisoning (very common in US)
  4. Virulence factors in C. perfringes
    • Exotoxins: 12 exotoxins (α is most important, lyses membranes)
    • grouped A through E based on exotoxins
    • Enterotoxin: causes loss of fluid and intracellular proteins in small intestine.
    • Degadative enzymes: proteases, DNases, hyaluronidase, collagenases help to promote spread of infection
  5. Describe the disease states caused by C. perfringens (more detailed)
    • Myonecrosis (gas gangrene): clostridial spores introduced into tissue
    • exotoxins and degredative enzyme cause tissue necrosis and quick spread of bacteria
    • Fermentation of tissue carbohydrates yields gas which accumulates in subcutaneous spaces
    • Untreated myonecrosis is fatal within days
    • Food poisoning: most common cause of food poisoning in US
    • nausea, abdominal cramps, and diarrhea (no fever or vomiting)
    • Self-limiting
    • Requires very large inoculum (10^8 organisms)
  6. Lab ID of C. perfringens
    • gram stain reveals vegetative clostridial forms
    • Double zone of hemolysis on blood agar
    • Sought in feces of food poisoning cases
  7. Describe the diseases caused by C. botulinum w/ mechanism
    • mechanism: caused by botulinum toxin
    • Cleaves synaptic vesicle peptides
    • Prevents transmission of aceytlcholine, resulting in inability to contract muscle
    • Classic Boltulism (flaccid paralysis): food poisoning w/o fever or sepsis
    • Patient may die from respiratory paralysis
    • Infant botulism: most common
    • Colonizes large bowel of infants and toxin is slowly absorbed
    • May be in honey supplements
    • Wound botulism: rare form of botulism when toxin is absorbed from colonized wound
  8. Describe the epidemiology of C. botulinum (found where, infection occurs how)
    • In soil, aquatic sediments - contaminate vegetables, meat, fish
    • Toxin is produced during vegetative growth
    • Toxin often elaborated in food (organism not required for botulism)
  9. Treatment of C. botulinum
    • Antitoxin which neutralizes botulinum toxin ASAP (horse antiserum)
    • Penicillin for would botulism (doesn't affect toxin)
    • Toxin is destroyed at boiling temperatures, but spores require autoclaving
    • Immunity DOES NOT occur
  10. Describe the epidemiology of C. tetani (where found, typical infection route)
    • Common in barnyard and garden soils
    • Typical infection is puncture wound (eg nail, splinter) that allows spores to germinate
  11. Describe the disease caused by C. tetani w/ mechanism
    • Mechanism: Tetanus toxin (tetanospasmin) transported from infected locus by retrograde neuronal flow
    • Prevents release of glycine, resulting in constant contraction
    • Tetanus (spastic paralysis): early stage presents lockjaw, then more muscles become involved.
    • Death caused by paralysis of chest muscles leading to respiratory failure
  12. Describe the treatment of C. tetani
    • Prompt administration of antitoxin (before confirmation) to neutralize unbound toxin
    • Human tetanus Ig preferred, but horse antitoxin can be used
    • Organism sensitive to penicillin
  13. Describe the prevention of C. tetani
    • Active immunization (DPT aka TDAP)
    • Boosters are required every 10 years
  14. General information about C. difficile (range of outcomes, amount of infection, how frequent is disease)
    • Can range from loose stools to life-threatening pseudomembranous colitis (PMC)
    • Responsible for 1/4 of antibiotic-associated diarrheas
    • Kills 3 times as many people as MRSA in US
  15. Describe the epidemiology of C. difficile
    • Minor component of normal flora
    • Antibiotic treatement suppresses more predominant species, C. difficile proliferates
  16. What are the virulence factors for C. difficile?
    • Toxin A: enterotoxin that causes excessive fluid secretion, stimulates inflammatory response
    • Toxin B: cytotoxin that disrupts protein synthesis and disorganizes cytoskeleton
  17. Describe the Lab ID of C. difficile
    best tests demonstrate toxin production in stool extracts (ELISA for exotoxins A and B)
  18. Describe the treatment for C. difficile
    • Discontinuance of predisposing drug
    • Fluid replacement
    • Relapses are common.