Basic Bacteriology: Toxins Flashcards Preview

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Flashcards in Basic Bacteriology: Toxins Deck (24):
1

What defines an exotoxin?

What is the typical source of exotoxins?

What are exotoxins made of?

 

Exotoxins are secreted from the bacterial cell.

Certain species of gram-positive and gram-negative bacteria produce them.

Exotoxins are polypeptides.

2

What defines an endotoxin?

What produces endotoxins?

What is it made of?

Endotoxins are not secreted from cells.

Located in the outer cell membrane of most gram-negative bacteria.

Lipopolysaccharide (structural part of bacteria; released when lysed)

3

Where are exotoxin genes located?

What is the toxicity of exotoxins?

Exotoxins are encoded by plasmids or bacteriophages.

Toxicity is high (fatal dose on the order of 1 microgram)

4

Where are endotoxin genes located?

What is the toxicity of endotoxin? What are its clinical effects?

How are these clinical effects produced?

Endotoxin genes located on the bacterial chromosome.

Low toxicity (fatal does on order of hundreds of micrograms)

Clinical effects: Fever, shock (hypotension), DIC

Activates TNF, IL-1, and IL-6

5

Are exotoxins highly or poorly antigenic?

Can exotoxins be vaccinated against? If so, what is used as a vaccine?

Are exotoxins heat stable?

Exotoxins are highly antigenic - induce high-titer antibodies called antitoxins.

Toxoids are used as vaccines against exotoxins (inactivated toxin)

Exotoxins are destroyed rapidly at 60°C (except for staphyloccal enterotoxin)

6

Are endotoxins highly or poorly antigenic?

Can endotoxins be vaccinated against? If so, what is used as a vaccine?

Are endotoxins heat stable?

Poorly antigenic

No toxoids formed, no vaccine available.

Stable at 100° for 1 hour.

7

What are typical diseases caused by exotoxins?

Tetanus, botulism, diphtheria.

8

What is a typical disease caused by endotoxin?

.Meningococcemia; sepsis by gram-negative rods.

9

What does each component of an A-B toxin do?

 

B (binding) component binds to host surface receptor, enabling endocytosis

A (active) component attaches ADP-ribosyl to disrupt cell proteins

10

What toxin does Corynebacterium diphtheriae make?

What is its mechanism of action?

What is the clinical manifestation?

Diphtheria toxin, an ADP ribosylating A-B toxin.

Inactivates elongation factor (EF-2), inhibiting protein synthesis

Causes pharyngitis with pseudomembranes in throat and severe lymphadenopathy (bull neck)

11

What toxin does Pseudomonas aeruginosa make?

What is its mechanism of action?

What is the clinical manifestation?

Exotoxin A, an ADP ribosylating A-B toxin.

Inactivates elongation factor (EF-2), inhibiting protein synthesis.

Causes host cell death.

12

What toxin does Shigella spp. make?

What is its mechanism of action?

What is the clinical manifestation?

Shiga toxin, an ADP-ribosylating A-B toxin.

Inactivates 60S ribosome by removing adenine from rRNA

Causes GI mucosal damage -> dysentery. Also enhances cytokine release, causing hemolytic-uremic syndrome.

 

13

What toxin does Enterohemorrhagic E. coli make (O157:H7 strain included)

What is its mechanism of action?

What is the clinical manifestation?

Shiga-like toxin (SLT)

Inactivates the 60S ribosome by removing adenine from rRNA

SLT enhances cytokine release, causing HUS. EHEC does not invade host cells, unlike shigella.

14

What toxins are produced by enterotoxigenic E. Coli (ETEC)?

What is the mechanism of action for each?

Heat-labile toxin (LT): A-B toxin. Overactivates adenylate cyclase, increases cAMP, increases chloride secretion and H2O efflux.

Heat-stable toxin (ST): Overactivates guanylate cyclase, reduces resorption of NaCl and H2O in the gut.

 

Both cause watery diarrhea: Labile in the Air (Adenylate cyclase), stable on the ground (Guanylate cyclase).

15

What toxin is produced by Bacillus anthracis?

What is its mechanism of action?

What is its manifestation?

Edema factor

Mimics the adenylate cyclase enzyme (increases cAMP)

Likely responsible for edematous borders of black eschar in cutaneous anthrax.

16

What toxin is produced by Vibrio cholerae?

What is its mechanism of action?

What is its manifestation?

Cholera toxin, an A-B toxin.

Overactivates adenylate cyclase (increase cAMP) permanently activating Gs. This induces chloride secretion in the gut and H2O efflux.

Causes voluminous "rice-water" diarrhea.

17

What toxin does Bordetella pertussis make?

What is its mechanism of action?

What is the clinical manifestation?

Pertussis toxin, an A-B toxin.

Overactivates adenylate cyclase (increases cAMP) by disabling Gi, this impairs phagocytosis to permit survival of the organism.

Whooping cough: Child coughs in expiration and "woops" in inspiration. 100-day cough in adults. Toxin may not be a cause of cough.

18

What toxin does Clostridium tetani make?

What is its mechanism of action?

What is the clinical manifestation?

 

Tetanospasmin.

A protease that cleaves SNARE proteins required for neurotransmitter release.

Causes spasticity, risus sardonicus, and "lockjaw". Toxin prevents release of inhibitory (GABA and glycine) neurotransmitters from Renshaw cells in spinal cord.

19

What toxin does Clostridium botulinum make?

What is its mechanism of action?

What is the clinical manifestation?

 

Botulinum toxin

Protease that cleaves SNARE proteins required for neurotransmitter release.

Causes flaccid paralysis, floppy baby. Toxin prevents release of stimulatory (ACh) signals at neuromuscular junctions -> flaccid paralysis.

20

What toxin does Clostridium perfringens make?

What is its mechanism of action?

What is the clinical manifestation?

 

Alpha toxin

Phospholipase (lecithinase) that degrades tissue and cell membranes

Degrades phospholipids -> myonecrosis ("gas gangrene") and hemolysis ("double zone" of hemolysis on blood agar).

21

What cell-lysing toxin does Streptococcus pyogenes make?

What is its mechanism of action?

What is the clinical manifestation?

 

Streptolysin O

Protein that degrades cell membrane

Lyses RBCs; contributes to beta-hemolysis; host antibodies against toxin (ASO) used to diagnose rheumatic fever (do not confuse with immune complexes of poststreptococcal glomerulonephritis).

22

What toxin does Staphylococcus aureus make?

What is its mechanism of action?

What is the clinical manifestation?

 

Toxic shock syndrome toxin (TSST-1)

Bring MHC II and TCR in proximity to outside of antigen binding site to cause overwhelmin release of INF-gamma and IL-2 -> shock.

Toxic shock syndrome: Fever, rash, shock; other toxins cause scalded skin syndrome (exfoliative toxin) and food poisoning (enterotoxin)

23

What superantigen toxin does Streptococcus pyogenes make?

What is its mechanism of action?

What is the clinical manifestation?

Exotoxin A

Bring MHC II and TCR in proximity to outside of antigen binding site to cause overwhelmin release of INF-gamma and IL-2 -> shock.

Toxic shock syndrome: Fever, rash, shock.

24

What organisms produce endotoxin?

What are the effects of ENDOTOXIN?

A lipopolysaccharide found on otuer membrane of gram-negative bacterial, both cocci and rods. Lipid A most antigenic. See page 127 for important flowchart of effects mentioned in acronym.

ENDOTOXIN: Activates macrophages, complement, and tissue factor.

Edema (C3a activates hypotension and edema)

Nitric oxide (from macrophage activation)

DIC (from tissue factor -> coagulation cascade activation)/Death

Outer membrane

TNF-alpha (from macrophage activation. Fever + hypotension)

O-antigen

eXtremely heat stable

IL-1 (from macrophage activation, fever)

Neutophil chemotaxis (C5a)