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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
Exfoliatin B toxic effect
epidermal cleavage
26
Streptolysin O toxic effect
Destruction of cholesterol
27
Streptococcal pyrogenic exotoxin E toxic effect
Superantigen formation
28
Streptococcal pyrogenic exotoxin B toxic effect
Cysteine protease
29
Mortality rate of necrotizing fasciitis in adults
24%
30
Mortality rate of necrotizing fasciitis in pediatric
10%
31
Mortality rate of necrotizing fasciitis in neonates
50%
32
Necrotizing fasciitis how many organisms in adults?
most are polymicrobial infections
33
Necrotizing fasciitis how many organisms in pediatrics?
Most are monomicrobial Group A Strep
34
Necrotizing fasciitis is commonly associated with the development of?
Toxic Shock Syndrome
35
Treatment of Necrotizing Fasciitis
* QUICK to surgery for debriding * Also antibiotics
36
Question
37
Why does Necrotizing Fasciitis present the way it does?
38
The most important thing in treating Necortizing Fasciitis
Time to surgery (GET THERE QUICK)
39
Empiric Antibiotics to treat Necrotizing Fasciitis
40
Clinical case
Toxic Shock syndrome
41
What is this depicting?
palm & sole involvement
42
Toxin mediated disease NOT associated with a single organism
* Necrotizing fasciitis * Toxic Shock Syndrome
43
What is toxic shock syndrome?
* 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
Describe TSST toxic effect
* 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
Diagnostic criteria of TSS
* 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 **G**ABHS isolated and cultures **R**enal/rash **P**latelets **A**RDS **B**leeding/Blood pressure **H**epatic **S**oft tissue necrosis
46
Streptococcal Toxic-Shock Syndrome Diagnostic criteria Acronym
**G**ABHS isolated and cultures **R**enal/rash (renal impairment) **P**latelets (low) **A**RDS (Acute respiratory distress syndrome) **B**leeding/Blood pressure (low blood pressure and coagulopathy) **H**epatic (dysfunction) **S**oft tissue necrosis
47
GABHS AKA
Group A Beta Hemolytic Strep
48
Treatment of Streptococcal Toxic-Shock Syndrome
* 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
Staphylococcal Toxic-Shock Syndrome Diagnostic criteria
**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
Staphylococcal Toxic-Shock Syndrome Diagnostic Criteria Acronym
* **S**kin (rash, desquamation) * **T**emperature elevation * **A**bsence of alternative dx (eg RMSF, lepto, measles) * **P**oly-system involvement (\>=3) * **H**ypotension
51
Staphylococcal Toxic-Shock Syndrome Treatment
* IVIG (bind toxin) * Antibiotic for staph * Clindamycin to reduce toxic production * Supportive care
52
RMSF AKA
Rocky Mountain Spotted Fever
53
Question
D. only about 20% of Staph carry the gene for TSST
54
Most common cause of TSS
ear-piercings (breaking the skin)
55
Which is the worst form of TSS
Streptococcal Toxic-Shock Syndrome
56
Diptheria toxin produced by?
Corynebacterium
57
Question
58
How does Diptheria present
* 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
Diptheria diagnosis
Culture (culture membrane and underlying exudate)
60
Treatment of Diptheria
* 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
Story about Bordatell Pertussis
Benjamin Franklin didn't vaccinate
62
Pertussis presentation in infants
* 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
Typical WBC in septic
Almost never see any WBC above 40K except in pertussis or leukemia and a few other things
64
Pertussis toxin
* Important but not essential for disease * Exotoxin * ADP-ribosylation of G proteins, with resultant alterations in signal transduction (lymphocytosis, secondary pulmonary hypertension, etc)
65
Tracheal cytotoxin
* Kills ciliated respiratory epithelial cells via complex intracellular mechanisms * Exotoxin
66
Pertussis deaths by age
67
Treatment for Pertussis
* 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
Question
E.
69
Clinical Case
70
Tetanus toxin is produced by?
Clostridium tetani
71
Presentation of Tetanus
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
Opisthtotonus AKA
73
Tetanospasmin tropism
neuro exotoxin
74
Tetanospasmin toxic effect
* 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
Tetanus treatment
* Tetanus immune globulin (single-dose) * IV penicillin for 10-14 days or metronidazole
76
Botulinum toxin is produced by
Clostridium spp.
77
Types of botulism 3 listed
* Infantile botulism * Food-borne botulism * Wound botulism
78
Infantile botulism is spread by?
spores from dust or dirt or honey Gardening is common
79
Food-borne botulism spread by?
ingesting preformed toxin
80
Wound Botulism is spread by?
Spores
81
What protects us from eating honey and getting botulism
intestinal flora protect us
82
Babies breastfed botulism
less bowel flora and more likely to get botulism
83
Infantile Botulism pattern
Descending symmetrical paralysis
84
Food-borne botulism pattern
Descending symmetrical paralysis (cranial nerves down)
85
Wound botulism pattern
Descending symmetrical paralysis (cranial nerves down)
86
Mechanism of botulism
Botulinum toxin causes irreversible binding to pre-synaptic nerve endings with internalization and cleavage of neuroexocytosis apparatus; prevents release of stimulatory (Ach) signals
87
Botulism vs Tetanus
88
Question
D. $45K
89
Treatment for Botulism
Baby big (botulism immunoglobulin) pooled Ig from donors who have had botulism
90
Efficacy of Baby BiG
91
Anthrax caused by?
Bacillus anthracis
92
Question
93
ARS question
94
Clinical distribution of human anthrax cases
95
Anthracis toxins mechanisms
* 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
Bacillus anthracis shape
Gram positive rod

Infectious Disease (82 decks)

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