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30 Cards in this Set

  • Front
  • Back
C.difficile transmission
spore former
Microbio of C. difficile
Gram+ rod, spore former, part of human microflora, use an A-B toxin
Air usage of C. difficile
Anaerobic
Why is C. difficile important in industrialized countries?
-Can survive as spores
-Antibiotics drive this
-Most common diarrheal disease require specific antimicrobial interventions
In which age range is C. difficile most prevalent?
>65yo
What has driven re-emergence of C. difficile?
-Improved lab diagnosis
-Aging population
-Inc use of antimicrobials, especially fluoroquinolones w/anti-anaerobic activity, to which Cdiff is resistant
Keys to pathogenesis of Cdiff
When anaerobic gut flora are present, Cdiff resistant.
Altered gut flora creates permissive environment.
Spores present or obtained can start colony
-susceptible for up to 6 weeks after antimicrobials
Grows and produces toxin A and B
Toxins bind and come in via receptor mediated endocytosis
Toxins inactivate small GTPase
C.difficile intestinal response
pseudomembranous colitis
Spectrum of disease of Cdiff
asymptomatic
mild diarrhea
profuse diarrhea w/non-specific colitis
pseudomembranous colitis
toxic megacolon
New pandemic of Cdiff?
NAP1
-has mutation in specific gene which down-regulates toxin production during log phase (growth)
-results in 20-fold inc of toxin production (during stationary phase)
Lab dx of Cdiff
-Stool screen for glutamate dehydrogenase, if positive, screen for gene with PCR (GDH test is sensitive, but modest specificity, good screen)
-Run PCR for toxin genes
Rules for Cdiff testing.
-If stick stands, the test is banned.
-If stick falls, test them all.
Tx for Cdiff
Vancomycin po, tapered dosing to kill spores may be used
Metronidazole was drug of choice, concerns of high relapse.
Fidaxomicin is new, but very expensive
Hand cleaning for Cdiff patients
soap and water, not alcohol
Difference in botulism and tetanus paralysis
Flaccid in botulism, spastic in tetanus
Cause of botulism and tetanus
Activity of protein exotoxins produced by C. botulinum and C. tetani
Sources of botulism toxins
honey, canned foods, black tar heroin, bioterrorism
Most common form of botulism
infant botulism
Why is honey associated disease much more common in US?
Recommendations by AAP
How is toxin transported to infants?
Time of weaning, toxin absorbed from gut into bloodstream; presents with constipation, poor suck, weak cry
Describe presentation of wound botulism
-Skin popping
-Organism enters and produces toxin
-Cosmetic Botox
Describe presentation of food-borne botulism.
Ingestion of pre-formed toxin, outbreaks limited to family members
What makes botulism a good weapon?
High lethality, isolated easily from soil, released as aerosol, inhalation botulism
Botulism pathogenesis
Inactivates SNARE proteins, necessary for acetylcholine
Presentation of botulism
Blurred, muscle weakness, drooping eyelids, slurred speech, difficulty swallowing, patient is afebrile and alert
When is botulism antitoxin actually administered?
Early, effects are irreversible
Why is tetanus pretty much eliminated?
Tetanus vaccine (every 10 years)
Common population of tetanus
Between 25-59 without boosters
Concerns for tetanus
Following trauma/catastrophic events
Childbirth
Pathogenesis of tetanus
Inactivates synaptobrevin, which inhibits normal post synaptic inhibition