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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
C. tetani incubation period?
4 days to weeks
26
in C. tetani spasms, which muscles are predominant?
flexors
27
will those with C. tetani have a fever?
no
28
will those with C. tetani have sensory deficit?
no
29
what is often the cause of death in tetanus?
- involvement of respiratory muscles leads to respiratory failure, aspiration, dysphagia, with oral pharyngeal involvement - potential for pulmonary infections and respiratory problems
30
diagnosis of tetanus:
- mostly clinical - not likely to find organism in wound - culture positive in 39%
31
how is tetanus generally treated?
- human tetanus immunoglobulin - penicillin (or metronidazole if allergic) plus wound debridement - respiratory support - immunization with tetanus toxin
32
what is the fatality rate with tetanus?
60%
33
describe the tetanus immunization
- 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
34
tetanus prophylaxis
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
35
describe the spores of C. botulinum:
- subterminal oval | - non-diagnostic
36
shape of C. botulinum
rod/bacilli
37
C. botulinum gram + or -?
+
38
C. botulinum spores heat labile?
no
39
botulism toxin heat labile?
yes
40
what happens to C. botulinum spores in canned foods?
They grow in anaerobic conditions and produce botulism toxin within 2-3 days.
41
what does wound associated botulism require?
requires spore germination in the wound
42
what does infant botulism require?
- ingestion of spore by infant (in honey) | - germination and intestinal colonization
43
how potent is botulism toxin?
very. 1mg killed 200,000 mice.
44
is botulism toxin destroyed by stomach?
no
45
how many types of botulism toxin are there and which three are most common?
A to G, but A, B, and E are most common.
46
what are the subunits of the botulism toxin?
A and B
47
is C. botulinum invasive or toxin mediated?
toxin mediated
48
what type of toxin is botulism toxin?
- neurotoxin - absorbed by intestine and carried by blood to peripheral nerve synapses - protease - interferes with proteolytic processing
49
the release of which NT is inhibited by botulism toxin?
acetylcholine
50
what is the mental status of someone with botulism?
normal
51
is there a fever with botulism?
no
52
incubation period for botulism toxin?
18-36 hours
53
which nerves does botulism affect?
peripheral nerves
54
symptoms of botulism
- flaccid paralysis - dysphagia (trouble swallowing) - diplopia (double vision) - dry throat - dilated pupils
55
is there is a sensory deficit with botulism?
no
56
botulism diagnosis:
- usually clinical - detect toxin in serum, vomit, feces - detect toxin in food - EMG (electromyography) - diminished action potential of the peripheral nerves
57
why aren't cultures useful for botulism?
toxin matters much more than organism
58
diseases on differential diagnosis with botulism:
- myasthenia gravis | - Guillain-Barre syndrome
59
botulism fatality rate
12%
60
botulism therapy
- removal of toxin from stomach (lavage) - antitoxin, horse serum, A, B, E - respiratory support
61
what ages usually get infant botulism?
1-8 months
62
why is infant botulism different?
- immature immune system allows colonization in gut.
63
symptoms of infant botulism:
- more subtle than adult botulism - constipation - weak head control - cranial nerve deficit common
64
diagnosis of infant botulism
toxin or organism in stool
65
C. difficile gram + or -?
+
66
C. difficile invasive or toxin mediated?
toxin mediated
67
what percent of the population has C difficile in GI tract?
3%
68
what percent of hospital acquired C. difficile likely comes from hospital personnel?
30%
69
pathogenesis of C. difficile
- 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
what are the two C. difficile exotoxins?
A and B
71
what does C. difficile exotoxin A do?
binds to gut receptor
72
what does C. difficult exotoxin B do? chemical mechanism?
- cytotoxin - damages colonic mucosa | - ADP-ribosylating Rho (GTP-binding protein)
73
what is the appearance of the C. difficile pseudomembrane?
- yellow-white plaque on colonoscopy/sigmoidoscopy | - usually not bloody but can be
74
diagnosis of C. difficile
- history of antibiotic use - exotoxin B in stool - ELISA for toxins - stool culture for C. difficile (not useful alone) - sigmoidoscopy for pseudomembranes
75
C. difficile treatment
- stop offending antibiotics | - treat with metronidazole, vancomycin, or fidazomicin
76
is C. perfringens invasive or toxin mediated?
invasive and highly progressive
77
Clostridium species other than perfringens that can cause gas gangrene?
septicum, bifermentans, ramosum (hallmark is tissue necrosis)
78
what is lecithinase?
alpha toxin - from C. perfringens - damages host cell membrane including capillary and host erythrocytes
79
what is collagenase?
- from C. perfringens - breaks down collagen supporting tissue underlying host cells
80
what is hyaluronidase?
- from C. perfringens - breaks down hyaluronic acid in the host matrix
81
what gases are referred to in "gas gangrene"
H2 and CO2 - byproducts of anaerobic growth in wound or dead tissue
82
clinical syndromes with gas gangrene:
1) cellulitis (superficial) 2) necrotizing cellulitis (dermis and underlying capillaries) 3) necrotizing faciitis (fascia around muscle) 4) myositis or myonecrosis (into muscle)
83
diagnostic tools for gas gangrene:
- 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
diagnosis of C. perfringens food poisoning
ELISA for enterotoxin in feces or implicated food
85
treatment for gas gangrene
- surgical wound debridement - penicillin - hyperbaric oxygen

Microbiology (bacteria) (16 decks)

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