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Microbiology (bacteria) > Exotoxin producing clostridia > Flashcards

Exotoxin producing clostridia Flashcards

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1
Q

what are the two major mechanisms with which bacteria cause disease? Examples.

A

1) toxin-mediated - no organisms required for infection, botulism toxin or staph aureus enterotoxin are examples
2) invasion and inflammation - direct tissue invasion and over-reactive immune response, clostridium perfringens is an example

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2
Q

two pathogenic possibilities for ingesting toxin

A

1) toxin already in food

2) ingestion of microorganisms, colonization, toxin formed in gut

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3
Q

what is the metabolic nature of clostridium?

A

obligate anaerobe

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4
Q

clostridium gram + or -?

A

+

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5
Q

shape of clostridium?

A

rod/bacilli

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6
Q

does clostridium form spores?

A

yes

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7
Q

what type of clostridium is indicated by terminal spores?

A

clostridium tetani

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8
Q

clostridium catalase + or -?

A

-

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9
Q

clostridium oxidase + or -?

A

-

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10
Q

which clostridium species causes botulism?

A

C. botulinum

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11
Q

which clostridium species causes tetanus?

A

C. tetani

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12
Q

which clostridium species causes pseudomembranous enterocolitis?

A

C. difficile

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13
Q

which clostridium species causes gas gangrene?

A

C. perfringens

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14
Q

which clostridium species is invasive in malignancy?

A

C. septicum

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15
Q

major symptom of botulism toxin:

A

flaccid paralysis

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16
Q

major symptom of tetanus toxin:

A

tetanus - spastic paralysis (locked jaw)

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17
Q

major symptoms of exotoxins A and B:

A

cause diarrhea in pseudomembranous enterocolitis due to C. difficile

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18
Q

major symptoms of alpha toxin:

A

gas gangrene - in combination with other degradative enzymes

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19
Q

what does a tennis racket shape indicate?

A

terminal spore - must be C. tetani which causes tetanus

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20
Q

symptom of tetanus in developing countries:

A

infected umbilical stump

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21
Q

is C. tetani invasive or toxin mediated?

A

toxin mediated

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22
Q

how many serological types of C. tetani are there?

A

only one

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23
Q

what type of toxin is tetanus toxin?

A
  • it’s a neurotoxin - goes from site of infection to peripheral and CNS nerves
  • two subunits A and B
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24
Q

what does tetanus toxin do exactly?

A

binds to neuronal gangliosides and prevents release of GABA and glycine resulting in convulsive contractions (locked jaw)

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25
Q

C. tetani incubation period?

A

4 days to weeks

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26
Q

in C. tetani spasms, which muscles are predominant?

A

flexors

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27
Q

will those with C. tetani have a fever?

A

no

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28
Q

will those with C. tetani have sensory deficit?

A

no

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29
Q

what is often the cause of death in tetanus?

A
  • involvement of respiratory muscles leads to respiratory failure, aspiration, dysphagia, with oral pharyngeal involvement
  • potential for pulmonary infections and respiratory problems
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30
Q

diagnosis of tetanus:

A
  • mostly clinical
  • not likely to find organism in wound
  • culture positive in 39%
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31
Q

how is tetanus generally treated?

A
  • human tetanus immunoglobulin
  • penicillin (or metronidazole if allergic) plus wound debridement
  • respiratory support
  • immunization with tetanus toxin
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32
Q

what is the fatality rate with tetanus?

A

60%

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33
Q

describe the tetanus immunization

A
  • three doses in first six months of life (toxin inactivated by formaldehyde)
  • given as part of DPT
  • booster at one year, before school entry, and every ten years after
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34
Q

tetanus prophylaxis

A

1) immunized - just clean the wound and keep getting booster every 10 years
2) dirty wound in uncertain immunization - anti-tetanus immunglobulin and complete immunization
3) unimmunized - complete immunization

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35
Q

describe the spores of C. botulinum:

A
  • subterminal oval

- non-diagnostic

36
Q

shape of C. botulinum

A

rod/bacilli

37
Q

C. botulinum gram + or -?

A

+

38
Q

C. botulinum spores heat labile?

A

no

39
Q

botulism toxin heat labile?

A

yes

40
Q

what happens to C. botulinum spores in canned foods?

A

They grow in anaerobic conditions and produce botulism toxin within 2-3 days.

41
Q

what does wound associated botulism require?

A

requires spore germination in the wound

42
Q

what does infant botulism require?

A
  • ingestion of spore by infant (in honey)

- germination and intestinal colonization

43
Q

how potent is botulism toxin?

A

very. 1mg killed 200,000 mice.

44
Q

is botulism toxin destroyed by stomach?

A

no

45
Q

how many types of botulism toxin are there and which three are most common?

A

A to G, but A, B, and E are most common.

46
Q

what are the subunits of the botulism toxin?

A

A and B

47
Q

is C. botulinum invasive or toxin mediated?

A

toxin mediated

48
Q

what type of toxin is botulism toxin?

A
  • neurotoxin - absorbed by intestine and carried by blood to peripheral nerve synapses
  • protease - interferes with proteolytic processing
49
Q

the release of which NT is inhibited by botulism toxin?

A

acetylcholine

50
Q

what is the mental status of someone with botulism?

A

normal

51
Q

is there a fever with botulism?

A

no

52
Q

incubation period for botulism toxin?

A

18-36 hours

53
Q

which nerves does botulism affect?

A

peripheral nerves

54
Q

symptoms of botulism

A
  • flaccid paralysis
  • dysphagia (trouble swallowing)
  • diplopia (double vision)
  • dry throat
  • dilated pupils
55
Q

is there is a sensory deficit with botulism?

A

no

56
Q

botulism diagnosis:

A
  • usually clinical
  • detect toxin in serum, vomit, feces
  • detect toxin in food
  • EMG (electromyography) - diminished action potential of the peripheral nerves
57
Q

why aren’t cultures useful for botulism?

A

toxin matters much more than organism

58
Q

diseases on differential diagnosis with botulism:

A
  • myasthenia gravis

- Guillain-Barre syndrome

59
Q

botulism fatality rate

A

12%

60
Q

botulism therapy

A
  • removal of toxin from stomach (lavage)
  • antitoxin, horse serum, A, B, E
  • respiratory support
61
Q

what ages usually get infant botulism?

A

1-8 months

62
Q

why is infant botulism different?

A
  • immature immune system allows colonization in gut.
63
Q

symptoms of infant botulism:

A
  • more subtle than adult botulism
  • constipation
  • weak head control
  • cranial nerve deficit common
64
Q

diagnosis of infant botulism

A

toxin or organism in stool

65
Q

C. difficile gram + or -?

A

+

66
Q

C. difficile invasive or toxin mediated?

A

toxin mediated

67
Q

what percent of the population has C difficile in GI tract?

A

3%

68
Q

what percent of hospital acquired C. difficile likely comes from hospital personnel?

A

30%

69
Q

pathogenesis of C. difficile

A
  • proliferates under antibiotic induced suppression of normal flora
  • exotoxins bind and damage colonic mucosa (bloody diarrhea)
  • damage to colon by exotoxin B leads to pseudomembrane formation
70
Q

what are the two C. difficile exotoxins?

A

A and B

71
Q

what does C. difficile exotoxin A do?

A

binds to gut receptor

72
Q

what does C. difficult exotoxin B do? chemical mechanism?

A
  • cytotoxin - damages colonic mucosa

- ADP-ribosylating Rho (GTP-binding protein)

73
Q

what is the appearance of the C. difficile pseudomembrane?

A
  • yellow-white plaque on colonoscopy/sigmoidoscopy

- usually not bloody but can be

74
Q

diagnosis of C. difficile

A
  • history of antibiotic use
  • exotoxin B in stool
  • ELISA for toxins
  • stool culture for C. difficile (not useful alone)
  • sigmoidoscopy for pseudomembranes
75
Q

C. difficile treatment

A
  • stop offending antibiotics

- treat with metronidazole, vancomycin, or fidazomicin

76
Q

is C. perfringens invasive or toxin mediated?

A

invasive and highly progressive

77
Q

Clostridium species other than perfringens that can cause gas gangrene?

A

septicum, bifermentans, ramosum (hallmark is tissue necrosis)

78
Q

what is lecithinase?

A

alpha toxin - from C. perfringens - damages host cell membrane including capillary and host erythrocytes

79
Q

what is collagenase?

A
  • from C. perfringens - breaks down collagen supporting tissue underlying host cells
80
Q

what is hyaluronidase?

A
  • from C. perfringens - breaks down hyaluronic acid in the host matrix
81
Q

what gases are referred to in “gas gangrene”

A

H2 and CO2 - byproducts of anaerobic growth in wound or dead tissue

82
Q

clinical syndromes with gas gangrene:

A

1) cellulitis (superficial)
2) necrotizing cellulitis (dermis and underlying capillaries)
3) necrotizing faciitis (fascia around muscle)
4) myositis or myonecrosis (into muscle)

83
Q

diagnostic tools for gas gangrene:

A
  • crepitus upon pressing skin
  • discoloration and edema of skin
  • serous dark exudates (maybe)
  • gram stain of fluid
  • culture of wound (anaerobic media)
  • x-ray
84
Q

diagnosis of C. perfringens food poisoning

A

ELISA for enterotoxin in feces or implicated food

85
Q

treatment for gas gangrene

A
  • surgical wound debridement
  • penicillin
  • hyperbaric oxygen

Microbiology (bacteria) (16 decks)

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