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Microbio 3 > Clostidium > Flashcards

Clostidium Flashcards

1
Q

2 ways a bacteria causes disease

A

toxins or invasions

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2
Q

two ways to establish infection via ingesting toxin

A

toxins preformed in food (c. botulism, S aureus)

ingestion and toxin formed in gut (infant botulism, v. cholerae)

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3
Q

general properties of clostriudium

A

gram positive rods

spore forming- spore location is diagnostic

obligate anerobes

catalse negative

oxidase negative

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4
Q

clostridium tetani epi

A

soil, puncture wounds

very rare in US. immigrants and developing countries

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5
Q

clostridium tetani pathogenesis

A

toxin mediated- tetanus toxin = neurotoxin. toxin has 2 subunits. one subunit binds neurogangliosides, the other has toxin activity

toxin inhibits release of NTs glycine and GABA, resulting in spastic paralysis

“convulsive contractions”

only 1 serotype

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6
Q

clostridium tetani syndromes

A

violant muscle spasms, clenched teeth, neck and back

no fever or sensory deficits

complications w/ pulmonary infection, aspiration, or respiratory failure

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7
Q

clostridium tetani diagnosis

A

clinical

culture positive in only 40%

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8
Q

clostridium tetani incubation period

A

4 days - weeks. vague

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9
Q

clostridium tetani treatment

A

immunization w/ human tetanus IgG.

penicillin plus wound debridement

resipratory support

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10
Q

clostridium tetani mortality rate

A

60%

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11
Q

clostridium tetani vaccine

A

3 doses in first 6 months of life w/ toxoid in part of DPT

booster every 10 years

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12
Q

clostridium botulism epi

A

very low incidence

soil organism. spores very resistant to chemical/physical agents

found in canned food, wounds. or infant botulsim (honey)

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13
Q

clostridium botulism pathogenesis

A

extremely potent but heat labile

acid resistance

7 types of toxin, A, B, E most common

toxin has A and B subunits. carried to nerves via blood and acts as neurotoxin. enters synapse and blocks release of ACh

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14
Q

clostridium botulism syndrome

A

no fever
normal mental status
no sensory deficits
symmetrical weakness or flaccid paralysis- can affect cranial nerves and respiratory muscles

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15
Q

clostridium botulism incubation period

A

18-36 hr

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16
Q

clostridium botulism diagnosis

A

detect toxin in food or serum/vomit/feces

17
Q

clostridium botulism differential

A

myasthenia gravis or guillan barre syndrome

18
Q

clostridium botulism therapy

A

removal of toxin, antitoxin from horse serum

12% mortality

19
Q

clostridium botulism prevention

A

canned food cooked for 10 min at 100 C

20
Q

infant botulism

A

1-8 months

eat honey- no immune in gut

symptoms- constipation, weak head control, cranial nerve deficits

diagnosis- find toxin

treatment- antitoxin Abs for types A and B, supportive

21
Q

wound-associated botulism

A

spores from soil contaiminate

diagnose via wound culture or toxin in serum

22
Q

clostridium difficile epi

A

Ab associated diarrhea

found in GI tract, espcially in hospital

virulent strain 027 recently emerged

23
Q

clostridium difficile pathogenesis

A

Ab induced suppression of normal flora allows clostridium difficile to proliferate and make 2 toxins

exotoxin A- enterotoxin binding to gut receptors

exotoxin B- cytotoxin, damaging colonic mucosa via ADP ribosulating Rho, a GTP binding protein

damage via exotoxin B leads to pseudomembrane formation

24
Q

clostridium difficile syndromes

A

diarrhea w/ pseudomembranes (plaques on colonoscopy)

25
Q

clostridium difficile diagnosis

A

history of Ab use

exotoxin B in stool

ELISA

visualization of pseudomembranes

26
Q

clostridium difficile treatment

A

stop Abs

treat with metronidazole, vanco, or fidaxomicin

27
Q

clostridium perfiringes epi

A

cause gas gangrene and food poisoning

found in soil organisms and human GI

28
Q

clostridium perfringes gas gangrene pathogenesis

A

many toxins/enzymes cause necrosis in host

lecithinase- alpha toxin- damage host cell membranes

collagenase

hyaluroniase- matrix disruption

grows rapidly in anerobic environment and produces anerobic gases H2 and CO2

29
Q

clostridium perfringes food poisoning pathogenesis

A

ingestion w/ large numbre of spores

enterotoxin released into intestine

30
Q

clostridium perfringes gas gangrene syndromes

A

cellulitis, necrotizing cellulitis, necrotizing fascitits, myositis or myonecrosis

may occur in absence of open wound

31
Q

clostridium perfringes food poisoning

A

cramps and water diarrhea w/in 1 day

common cause of food poisoning

32
Q

clostridium perfringes diagnosis of gas gangrene

A

crepitus upon pressing skin

discoloration/pain in skin

serous dark exudates

culture

33
Q

gas gangrene treatment

A

surgical and penicillin

fatal if not treated

Microbio 3 (7 decks)

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