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Infectious Disease > Week 5: Toxin-mediated infections > Flashcards

Week 5: Toxin-mediated infections Flashcards

1
Q

What is a bacterial toxin?

A

PRotein or lipopolysaccharide toxin secreted by or remaining a component of the bacteria

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2
Q

What is an exotoxin?

A

Toxin secreted by bacteria

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3
Q

What is an endotoxin?

A

Toxin that remains a component of bacteria (eg in the cell membrane)

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4
Q

Examples of exotoxins

A
  • Diptheria toxin
  • Pertussis toxin
  • Shiga toxin
  • Botulinum toxin
  • Tetanus toxin
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5
Q

Examples of endotoxins

A
  • LPS in gram negative bacteria
  • Normally lipopolysaccharide complexes
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6
Q

Tropism of toxins

A

eg

  • neurotoxin indicates nervous system
  • enterotoxin indicates GI tract
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7
Q

Protein toxin components

A
  • protein toxins often have 2 components (A and B units)
  • one bind to a receptor and another with enzymatic capabilities
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8
Q

Examples of toxins involved in invasive infections

A
  • Spe B in necrotizing fasciitis
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9
Q

Toxins that commonly cause problems from a distance WITHOUT invasion

A
  • Botulism
  • Tetanus
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10
Q

Question

What is the most potent toxin?

A. Strychine

B. Rattlesnake Venom

C. Botulinum toxin

D. Tetanus toxin

A

C. Botulinum toxin

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11
Q

Relative toxin potencies

A
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12
Q

Clinical case

A

Necrotizing Fascitis (often associated following varicella)

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13
Q

Toxin mediated disease NOT associated with a single organism

A

Necrotizing fasciitis

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14
Q

How does necrotizing fasciitis present?

A
  • Rapid spread (hours)
  • Initially pain is out of proportion
  • Appear sicker than one might expect
  • As disease progresses pain lessens (nerves destroyed)
  • Progressively worse local perfusion (capillaries destroyed)
  • ‘Brawny’ edema of the affected site (feels like wrestling mat on skin)
  • Frequent sepsis/hypotension
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15
Q

Toxins with a potential role in Necrotizing Fasciitis

A
  • Leukocidin
  • Exfoliatin B
  • Streptolysin O
  • Streptococcal pyrogenic exotoxin E
  • Streptococcal pyrogenic exotocin B
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16
Q

Organisms that produce toxins in necrotizing fasciitis

A
  • S. aureus
  • S. pyogenes
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17
Q

Toxins produced by S. aureus in necrotizing fasciitis

A
  • Leukocidin
  • Exfoliatin B
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18
Q

Toxins produced by S. pyogenes in necrotizing fasciitis

A
  • Streptolysin O
  • Streptococcal pyrogenic exotoxin E
  • Streptococcal pyrogenic exotoxin B
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19
Q

Leukocydin is produced by?

A

S. aureus

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20
Q

Exfoliatin B is produced by?

A

S. aureus

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21
Q

Streptolysin O is produced by?

A

S. pyogenes

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22
Q

Streptococcal pyrogenic exotoxin E is produced by?

A

S. pyogenes

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23
Q

Streptococcal pyrogenic exotoxin B is produced by?

A

S. pyogenes

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24
Q

Leukocidin toxic effect

A

Destruction of phagocyte membranes

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25
Q

Exfoliatin B toxic effect

A

epidermal cleavage

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26
Q

Streptolysin O toxic effect

A

Destruction of cholesterol

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27
Q

Streptococcal pyrogenic exotoxin E toxic effect

A

Superantigen formation

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28
Q

Streptococcal pyrogenic exotoxin B toxic effect

A

Cysteine protease

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29
Q

Mortality rate of necrotizing fasciitis in adults

A

24%

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30
Q

Mortality rate of necrotizing fasciitis in pediatric

A

10%

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31
Q

Mortality rate of necrotizing fasciitis in neonates

A

50%

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32
Q

Necrotizing fasciitis how many organisms in adults?

A

most are polymicrobial infections

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33
Q

Necrotizing fasciitis how many organisms in pediatrics?

A

Most are monomicrobial Group A Strep

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34
Q

Necrotizing fasciitis is commonly associated with the development of?

A

Toxic Shock Syndrome

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35
Q

Treatment of Necrotizing Fasciitis

A
  • QUICK to surgery for debriding
  • Also antibiotics
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36
Q

Question

A
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37
Q

Why does Necrotizing Fasciitis present the way it does?

A
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38
Q

The most important thing in treating Necortizing Fasciitis

A

Time to surgery (GET THERE QUICK)

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39
Q

Empiric Antibiotics to treat Necrotizing Fasciitis

40
Q

Clinical case

A

Toxic Shock syndrome

41
Q

What is this depicting?

A

palm & sole involvement

42
Q

Toxin mediated disease NOT associated with a single organism

A
  • Necrotizing fasciitis
  • Toxic Shock Syndrome
43
Q

What is toxic shock syndrome?

A
  • caused by S. aureus or S. pyogenes
  • S. aureus secretes TSST (Toxic Shock Syndrome Toxin)
  • S. pyogenes secretes pyrogenic exotoxins
  • TSST binds to both MHC II complex and T-cell receptors
  • This binding activates the T-cells 2000 fold more than traditional binding in the cleft leading to a cytokine storm with resultant shock, capillary leak, multi-organ system failure, etc.
44
Q

Describe TSST toxic effect

A
  • Toxins bind to both MHC II complex and T-cell receptors
  • This binding activates the T-cells 2000 fold more than traditional binding in the cleft leading to a cytokine storm with resultant shock, capillary leak, multi-organ system failure, etc.
45
Q

Diagnostic criteria of TSS

A
  • isolation of GABHS (Group A Beta Hemolytic Strep)
  • Hypotension (SBP <= 90 or < 5% for age/height in children)

and 2 or more of the following abnormalities

  • Renal
  • Coagulopathy
  • Liver
  • ARDS
  • Rash
  • Soft tissue necrosis

GABHS isolated and cultures

Renal/rash

Platelets

ARDS

Bleeding/Blood pressure

Hepatic

Soft tissue necrosis

46
Q

Streptococcal Toxic-Shock Syndrome Diagnostic criteria Acronym

A

GABHS isolated and cultures

Renal/rash (renal impairment)

Platelets (low)

ARDS (Acute respiratory distress syndrome)

Bleeding/Blood pressure (low blood pressure and coagulopathy)

Hepatic (dysfunction)

Soft tissue necrosis

47
Q

GABHS AKA

A

Group A Beta Hemolytic Strep

48
Q

Treatment of Streptococcal Toxic-Shock Syndrome

A
  • Debride
  • Antibiotics (IV until afebrile transition to oral)
  • Peniciilin for Strep
  • Clindamycin to reduce toxin production
  • IVIG may be considered (to bind up toxin)
49
Q

Staphylococcal Toxic-Shock Syndrome Diagnostic criteria

A

Clinical Criteria

  • Fever >38.9oC
  • Rash (Macular or erythrodermic)
  • Desquamation 1-2 weeks after onset
  • Hypotension
  • Multiorgan system disease: 3>= (GI, muscular, renal, liver, hematologic, CNS, mucous membranes)

Laboratory criteria

  • Negative evaluation for RMSF, leptospirosis, measles
  • Sterile blood/CSF cultures for organisms other than S. aureus
50
Q

Staphylococcal Toxic-Shock Syndrome Diagnostic Criteria Acronym

A
  • Skin (rash, desquamation)
  • Temperature elevation
  • Absence of alternative dx (eg RMSF, lepto, measles)
  • Poly-system involvement (>=3)
  • Hypotension
51
Q

Staphylococcal Toxic-Shock Syndrome Treatment

A
  • IVIG (bind toxin)
  • Antibiotic for staph
  • Clindamycin to reduce toxic production
  • Supportive care
52
Q

RMSF AKA

A

Rocky Mountain Spotted Fever

53
Q

Question

A

D. only about 20% of Staph carry the gene for TSST

54
Q

Most common cause of TSS

A

ear-piercings (breaking the skin)

55
Q

Which is the worst form of TSS

A

Streptococcal Toxic-Shock Syndrome

56
Q

Diptheria toxin produced by?

A

Corynebacterium

57
Q

Question

58
Q

How does Diptheria present

A
  • Low grade or afebrile
  • Erosive rhinorrhea (discharge will erode ulcers in upper lip)
  • ‘Bull neck’ from soft tissue edema and lymphadenopathy
  • Exudates throughout the poterior oropharynx will spread to uvula, hard and soft palate–starts out whitem will become grey)
  • End-organ damage (toxin-mediated, toxin enters affected tissue and leads to destruction)
59
Q

Diptheria diagnosis

A

Culture (culture membrane and underlying exudate)

60
Q

Treatment of Diptheria

A
  • Antitoxin+penicillin
  • Antitoxin binds free toxin only
  • Antibiotics decrease localized disease and decrease further toxin production
  • Mortality increases 20x if anti-toxin is delayed for 4 days (ineffective once toxin has entered cells)
61
Q

Story about Bordatell Pertussis

A

Benjamin Franklin didn’t vaccinate

62
Q

Pertussis presentation in infants

A
  • Kills babies
  • May be see an extreme leukocytosis (WBC > 100,000)
  • Apnea (whoop)
  • Lack of Fever
  • High mortality rate
  • May see seizures (from pertussis toxin)
63
Q

Typical WBC in septic

A

Almost never see any WBC above 40K except in pertussis or leukemia and a few other things

64
Q

Pertussis toxin

A
  • Important but not essential for disease
  • Exotoxin
  • ADP-ribosylation of G proteins, with resultant alterations in signal transduction (lymphocytosis, secondary pulmonary hypertension, etc)
65
Q

Tracheal cytotoxin

A
  • Kills ciliated respiratory epithelial cells via complex intracellular mechanisms
  • Exotoxin
66
Q

Pertussis deaths by age

67
Q

Treatment for Pertussis

A
  • Vaccinate for prophylaxis
  • Contagious until completion of antibiotic course
  • Treatment (Azithromycin for 5 days) not very effective after the cough begins (used only for infection control measures, not contagious anymore)
68
Q

Question

69
Q

Clinical Case

70
Q

Tetanus toxin is produced by?

A

Clostridium tetani

71
Q

Presentation of Tetanus

A

Tetanospasmin is a neurotoxin produced by all toxigenic strains

Released at the site of infection where it spreads throughout the body

It affects the nerve endings of inhibitory neurons in the central nervous system

  • Inhibits release of inhibitory neurotransmitters (ie GABA and glycine) resulting spasm
  • Functional denervation of lower motor neurons
  • Muscles with the shortest neural pathways are affected first
  • Lockjaw
  • Risus sardonicus (Sarcastic smile)
72
Q

Opisthtotonus AKA

73
Q

Tetanospasmin tropism

A

neuro exotoxin

74
Q

Tetanospasmin toxic effect

A
  • inhibits release of inhibitory neurotransmitters (ie GABA and glycine) resulting in spasm
  • Functional denervation of lower motor neurons
  • Muscles with the shortest neural pathways are affected first
75
Q

Tetanus treatment

A
  • Tetanus immune globulin (single-dose)
  • IV penicillin for 10-14 days or metronidazole
76
Q

Botulinum toxin is produced by

A

Clostridium spp.

77
Q

Types of botulism

3 listed

A
  • Infantile botulism
  • Food-borne botulism
  • Wound botulism
78
Q

Infantile botulism is spread by?

A

spores from dust or dirt or honey Gardening is common

79
Q

Food-borne botulism spread by?

A

ingesting preformed toxin

80
Q

Wound Botulism is spread by?

81
Q

What protects us from eating honey and getting botulism

A

intestinal flora protect us

82
Q

Babies breastfed botulism

A

less bowel flora and more likely to get botulism

83
Q

Infantile Botulism pattern

A

Descending symmetrical paralysis

84
Q

Food-borne botulism pattern

A

Descending symmetrical paralysis (cranial nerves down)

85
Q

Wound botulism pattern

A

Descending symmetrical paralysis (cranial nerves down)

86
Q

Mechanism of botulism

A

Botulinum toxin causes irreversible binding to pre-synaptic nerve endings with internalization and cleavage of neuroexocytosis apparatus; prevents release of stimulatory (Ach) signals

87
Q

Botulism vs Tetanus

88
Q

Question

89
Q

Treatment for Botulism

A

Baby big (botulism immunoglobulin) pooled Ig from donors who have had botulism

90
Q

Efficacy of Baby BiG

91
Q

Anthrax caused by?

A

Bacillus anthracis

92
Q

Question

93
Q

ARS question

94
Q

Clinical distribution of human anthrax cases

95
Q

Anthracis toxins mechanisms

A
  • Two exotoxins
    • Lethal toxin
    • Edema toxin
  • Internalized by cells
  • Lethal toxin inhibits protein-kinase mediated signal transduction in the cell
  • Edema toxin increases cAMP levels causing dysregulation of cellular physiology and edema
96
Q

Bacillus anthracis shape

A

Gram positive rod

Infectious Disease (82 decks)

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