Clostridia Flashcards

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0
Q

C. perfringens toxins

A

produces 12 toxins
alpha-toxin (lecithinase): damages cell membranes and causes gas gangrene
phospholipase type C
hydrolyzes phosphatidylcholine and sphingomyelin that leads to cell death
muscle tissue is destroyed

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1
Q

Describe C. perfringens

infection via, type of damage, toxin cause what

A

associated with wounds/damaged tissue
local damage and systemic effects
toxins cause cellulitis which can lead to gas gangrene

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2
Q

C. perfringens infections can lead to what?

A

tissue damage

food poisoning

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3
Q

C. perfringens tissue infections treatment and prevention

A

removal of infected muscle
antibiotics to control infection
prompt care is imperative- restore arterial blood supply
antitoxin from horses has relatively little effect
untreated 100% fatality rate- renal failure and shock usually result

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4
Q

C. perfringens food poisoning

how common, toxin, symptoms, treatment

A

3rd most common type of food poisoning in US
produces enterotoxin in intestines after being consumed
diarrhea in 12-24 hrs
disappears in 1-3 days

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5
Q

Describe C. botulinum

unique features, causative agent of disease

A

heat resistant spores may survive food processing
causative agent of botulism- preformed toxin, organisms don’t need to be present
bioweapon/bioterrorism threat

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6
Q

C. botulinum toxins

how many, structure

A
8 neurotoxin (BoNT) serotypes A-G
very poisonous
900kDa protein complex
150kDa toxic componet
750kDa non-toxic binding component
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7
Q

C. botulinum mechanism of action

type of paralysis, path of paralysis

A

prevents release of acetylcholine
flaccid paralysis in 12-36 hrs
cranial nerves affect first
paralysis desends

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8
Q

Types of botulism

A

3 types
food borne
wound (rare)
infant (floppy baby, no honey, favorable outcome)

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9
Q

C. botulinum treatment

mortality rate, antitoxin, antibiotics, damage

A
mortality rate 25%
administer antitoxin immediately
trivalent antitoxin from horses, administer ASAP
some muscle may be permanently damaged
no antibiotics
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10
Q

Describe C. tetani

infection association, toxin, symptoms

A
infection associated with traumatic wounds (neonatal contamination of umbilical cord at delivery)
toxin: tetanospasmin
lockjaw is first symptom (80% of cases)
rigid/spastic paralysis
opisthotonos: characteristic arc
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11
Q

C. tetani tetanospsmin mechanism of action

A

toxin invades neurons close to site of wound
toxins travel through neurons of periphery to cranial nerves
inhibits release of GABA (spastic paralysis)
paralysis descends down body

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12
Q

C. tetani treatment and prevention and mortality

A

DPT vaccine
11% mortality
antitoxin along with penicillin G
cleaning of wound to prevent new bacteria growth
again antibiotics aren’t very affective and antitoxin must be administered before onset of symptoms

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13
Q

Name the basic features of Clostridium

A

Gram positive rods
strictly anaerobic
produce endospores and toxins

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14
Q

What are the common Clostriduim species we discussed?

A
4 of them
   C. difficile
   C. perfringens
   C. botulinum
   C.tetani
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15
Q

Briefly describe the spore/vegetative cell cycle

A

vegetative cell is active
becomes spore in unfavorable conditions
spore part buds off then cell reuptakes it and peptidoglycan coat forms around spore
spore becomes active in favorable conditions

16
Q

Describe C. difficile

A

PMC
leading cause of nosocomial (antibiotic induced) diarrhea
spores are resistant to antibiotics
invasion of bowel wall doesn’t occur

17
Q

C. difficile: describe symptoms, toxin, toxin affects and toxin detection

A

diarrhea
2 toxins
toxin A: enterotoxin, prevents Na uptake= fluid loss
toxin B: cytotoxin, results in cell death
toxins act in cytoplasm and glycosylate GTP binding proteins-damages cell’s cytoskeleton
ELISA detection of toxin A