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Clinical Micro > Toxins > Flashcards

Toxins Flashcards

1
Q

What is the definition of a toxin?

A

A bacterial product that either causes direct harm or triggers a destructive process

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2
Q

Compare and contrast endotoxins vs. exotoxins (3 points)

A

Exotoxin

  • Produced by gram neg & pos bacteria
  • Proteins, released by the bacteria
  • Heat labile

Endotoxin

  • Cell wall components of gram neg bacteria
  • LPS of outer membrane
  • Heat stable
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3
Q

Exotoxins can appear in 2 forms, what are they?

A

A-B toxins of cytolytic toxins

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4
Q

what are exotoxins classified by?

A

Their site of action

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5
Q

what are the 4 types of exotoxins?

A
  1. Enterotoxins
  2. Neurotoxins
  3. Cytotoxins
  4. Pyrogenic toxins
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6
Q

For AB toxins, how many types are there? which subunit does what? specific or non-specific binding?

A

B subunit binds, A subunit has the active action

can be AB or AB5

Binding is specific

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7
Q

What are superantigens able to do?

A

able to stimulate non specific T cell proliferation leading to a significant immune response regardless of antigenic specificity

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8
Q

what are two examples of superantigens?

A
  1. Staphylococcus aureus TSST-1

2. Streptococcal pyrogenic exotoxins

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9
Q

What kinds of symptoms does LPS induce at low concentrations? At high concentrations?

A

Low concentration: Fever, Vasodilation, Inflammatory response

High concentration: Fever, vasodilation, DIC, hypotension, shock/death

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10
Q

What kind of bacteria are Clostridium species?

A

gram positive (although can stain gram variable), spore forming, anaerobic rods

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11
Q

What are the 4 Clostridium sp. we discussed and what do each of them cause?

A
  1. C. tetani: tetanus
  2. C. botulinum: botulism (ingestion or wound)
  3. C. perfringens: gangrene, food poisoning
  4. C. difficile: CDAD
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12
Q

Tetanus is most often associated with what kind of wound?

A

A puncture wound

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13
Q

What two toxins are involved in tetanus infections?

A
  1. Tetanolysin

2. Tetanospasmin

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14
Q

What is tetanolysin? what does it do?

A

Oxygen labile hemolysin

- RBC lysis

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15
Q

What is tetanospasmin?

A

Heat labile neurotoxin

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16
Q

What form of toxin is tetanospasmin? what is it encoded on?

A

plasmid encoded AB toxin

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17
Q

Where does tetanospasmin bind? how does it exert its effects?

A
  1. Binds to specific sialic acid receptors/glycoproteins of motor neurons
  2. Internalized in endosome
  3. Travels by retrograde axonal transport to CNS
  4. Blocks inhibitory impulse to motor neurons by blocking neurotransmitter release
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18
Q

How does tetanospasmin block the inhibitory impulse/neurotransmitters?

A

Inactivates proteins that regulate release of inhibitory neurotransmitters glycine & gamma-aminobutryic acid (GABA)

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19
Q

Is binding of the tetanus toxin reversible or irreversible?

A

Irreversible

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20
Q

What kind of paralysis does tetanus cause?

A

Spastic paralysis

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21
Q

Botulism is what kind of disease?

A

Neuroparalytic

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22
Q

What are 3 main types of botulism?

A
  1. Foodborne
  2. Wound botulism
  3. Infant botulism
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23
Q

How do people normally get foodborne botulism ?

A

ingestion of preformed botulinal toxin in contaminated food (classically associated with home canned foods that were not prepared sterilely)

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24
Q

What is occurring at the site of infection when people get wound botulism?

A

elaboration of botulinal toxin in vivo after the growth of C. botulinum in an infected wound

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25
Q

What is happening in the infant with botulism ?

A

botulinal toxin is elaborated in vivo in the gastrointestinal tract of an infant colonized with C. botulinum…after ingestion of spores from honey, soil…

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26
Q

What kind of toxin is botulinum toxin?

A

AB exotoxin

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27
Q

How many different types of botulinum toxins are there? which cause disease in humans?

A

7 (A-G)

only A,B, E and F cause disease in humans

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28
Q

Where does the botulinum toxin bind? How is the progression similar or different to tetanus?

A
  1. Also binds specific sialic acid receptors + glycoproteins (different ones from tetanus)
  2. Brought in via endosome
  3. Remains at neuromuscular junction
  4. Toxin prevents release of acetylcholine at the peripheral nerve endings leading to acute flaccid paralysis
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29
Q

Clostridium perfringens is the causative agent of which 3 things?

A
  1. gas gangrene
  2. food poisoning
  3. Enteritis necroticans
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30
Q

What is enteritis necroticans?

A

Ischemic necrosis of the jejunum, associated with pig feasts, Alpha & Beta toxin (mainly)

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31
Q

What kinds of toxins does C. perfringens have?

A

Alpha, Beta, and Theta toxins

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32
Q

What kind of injury do you need to be infected with C. perfringens?

A

Need a fairly significant injury to occur where the open wounds are exposed to dirt contaminated with spores

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33
Q

Which two toxins are the causative agents in gas gangrene?

A
  1. Alpha/Lecithinase toxin

2. Theta/perfringolysin

34
Q

What is the alpha/lecithinase toxin in gas gangrene? how does it work?

A

has both phospholipase C and sphingomyelinase activities

causes intravascular activation of platelets and clot formation

blocks of the arterioles/venules/capilaries and leads to an anaerobic environment where the bacteria can flourish

35
Q

How do people normally get food poisoning from C. perfringens?

A

Contaminated meat not cooked properly - spores survive

Spores germinate and the vegetative cells proliferate and are ingested

Enterotoxin produced by vegetative cells in the individual

36
Q

What kind of symptoms are caused by C. perfringens food poisoning?

A

generally mild, self limiting diarrhea

37
Q

What is the most common cause of infectious diarrhea in hospitals?

A

C. difficile

38
Q

What is the clinical spectrum of CDAD?

A

colonized to mild disease to severe disease to severe with toxic megacolon

39
Q

What two toxins does C. difficile produce? where do they act on? which one is needed to be pathogenic?

A 
Toxin A (TcdA), enterotoxin
Toxin B (TcdB), cytotoxin
- toxin B is needed to be pathogenic
40
Q

How does C. difficile establish an infection?

A
  1. Vegetative cells and spores are ingested
  2. Cells die in stomach but spores survive
  3. spores germinate in the small bowel when exposed to bile salts
  4. Cells release toxins and adhere to the mucosa in the colon and then multiply
    - will often proliferate following disruption of normal microflora
41
Q

Which bacteria shares a high degree of relation with Shigella but has distinctive pathogenesis?

A

E. coli

42
Q

What kind of bacteria are E.coli?

A

Gram negative, facultative, mobile rods

43
Q

Most strains of E.coli cause?

A

Intestinal/Diarrheal disease; Diarrheagenic E.coli

44
Q

Other strains of E. coli can cause?

A

Urinary tract infection
Neonatal meningitis
Septicemia

45
Q

How many types of diarrhea producing E.coli are there? How many are toxigenic?

A

6, 2 are toxigenic

46
Q

Which of the diarrhea causing strains of E.coli are toxigenic?

A

ETEC: Enterotoxigenic
EHEC: Enterohemorrhagic

47
Q

What does ETEC cause? How is it acquired?

A

Contaminated food/water
- fecal oral

Causes traveller’s diarrhea and watery diarrhea in children in developing countries

48
Q

How many organisms of ETEC E.coli do you need to cause disease?

A

10^8-10^10 in a healthy individual

49
Q

What two toxins do ETEC E. coli produce? What other pathogenic mechanism does it use?

A

LT(heat labile) / ST(heat stabile)

also uses fimbriae to attach to the intestine

50
Q

What is the LT toxin? How does it work? what is it similar to?

A

Heat labile, AB5 toxin
Similar to cholera

Stimulates adenylate cyclase, increases cAMP, leading to electrolytes & water excretion in intestinal lumen (watery diarrhea)

51
Q

What is the ST toxin? How does it work?

A

Heat-stabile, STA and STB forms

Activates guanylate cyclase,↑cyclic guanosine monophosphate, ↑ fluid & electrolyte excretion (watery diarrhea)

52
Q

What is another name for EHEC ?

A

Also called Shiga toxin producing E.coli or Verotoxogenic E.coli

53
Q

What does EHEC cause?

A

hemorrhagic colitis (bloody diarrhea) & may lead to hemolytic urea syndrome

54
Q

How do people become infected with EHEC?

A

contaminated food: undercooked ground beef, raw milk, unpasteurized apple juice, vegetables

55
Q

What is the most common serotype of EHEC E.coli?

A

O157:H7 most common

56
Q

Where is the shiga like toxin gene encoded?

A

on a bacteriophage

57
Q

What type of toxin is the shiga like toxin?

A

AB5

58
Q

Where does the shiga-like toxin bind?

A

glycolipid receptors (gb3), found in varying degrees in membranes of eukaryotic cells

59
Q

What does shiga like toxin target while in systemic circulation? what does this cause?

A

endothelial cells, causing vascular damage, bloody diarrhea, and, in some patients, a prothrombotic state that precedes the hemolytic uremic syndrome

60
Q

What type of bacteria is Shigella?

A

gram negative non motile rod

61
Q

What is the reservoir for Shigella?

A

There is none. human pathogen only

62
Q

How is Shigella spread?

A

more often by fecal oral route and less by contaminated foods

63
Q

What is the infectious dose of Shigella like compared with E. coli?

A

much lower, around 10-100 organisms

64
Q

What kind of bacteria are Vibrio?

A

curved gram negative rods, highly motile, facultative anaerobes

65
Q

Where is Vibrio typically found?

A

in salt water

66
Q

What are the 3 species of Vibrio that were discussed? What do they cause?

A

V. cholerae = cholera
V. parahaemolyticus = gastroenteritis
V. vulnificus = cellulitis, septicemia

67
Q

How is Vibrio cholera usually acquired?

A

from contaminated water and occasionally through contaminated food

68
Q

Where is V. cholera endemic?

A

South East Asia, parts of Africa & S. America

69
Q

What kind of toxin is the V. cholera toxin?

A

An AB5 toxin

70
Q

Where does the cholera toxin bind?

A

Bind ganglioside GM1 receptors on intestinal cells

71
Q

What does the binding of the cholera toxin cause?

A

Increase cAMP, leading to electrolytes & water secretions (watery diarrhea)

72
Q

What kind of bacteria is Staph aureus?

A

non motile, gram positive cocci

73
Q

What 4 kinds of toxins can staph aureus produce?

A
  1. Cytotoxins
  2. Exfoliative toxins
  3. Toxic shock toxins
  4. Enterotoxins
74
Q

What kinds of cytotoxins can S. aureus produce?

A

alpha, beta, delta, gamma and panton-velntine leukociden

75
Q

What are the 2 exfoliative toxins that S. aureus produces? What kind of action do they have ?

A

ETA and ETB

Serine proteases that disrupt cell adhesion structures

76
Q

What is the difference between ETA and ETB?

A

ETA – heat stable, chromosomal

ETB – heat labile, on plasmid

77
Q

How is food poisoning caused by S. aureus?

A

toxins present in food at time of ingestion - not live bacteria

78
Q

What is the source of food contamination in S. aureus food poisoning?

A

the food handler

- 50% are cases of asymptomatic carriage

79
Q

What is the most common enterotoxin associated with S. aureus food poisoning? Why?

A

Enterotoxin A

Heat stable and resistant to gastric enzymes

80
Q

What % of S. aureus strains produce Enterotoxin A?

A

30-50%

81
Q

How quickly is the onset of S. aureus food poisoning?

A

abrupt, about 4 hours after ingestion of food

82
Q

What are some of the symptoms of a S. aureus food poisoning episode? how long do the symptoms last?

A

Should resolve in about 24 hours

severe vomiting
watery non-bloddy diahrrhea
abdominal pain
nausea
no fever!!

Clinical Micro (28 decks)

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