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MIMM 211 > Lecture 23: Bacterial pathogenesis II > Flashcards

Lecture 23: Bacterial pathogenesis II Flashcards

1
Q

What is virulence?

A

The degree of pathogenicity

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2
Q

What are virulence factors?

A

Toxic or destructive substances produced by the pathogen that directly or indirectly enhance invasiveness and host damage by facilitating and promoting infection.

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3
Q

Name 4 ways that virulence factors can increase the ability of a microorganism to cause disease.

A

Could improve:
1. Colonization or invasion of host
2. Ability to multiply and complete life cycles on or in host
3. Ability to evade host defenses
4. Ability to leave host and enter new host

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4
Q

Name Koch’s 6 molecular postulates that define virulence factors.

A
  1. Gene is present in strains of bacteria that cause the disease
  2. Gene not present in avirulent strains
  3. Disrupting the gene reduces virulence
  4. Re-introduction of gene restores virulence
  5. The gene is expressed during infection
  6. Specific immune response to the gene -> protected against disease
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5
Q

How are bacterial virulence factors acquired?

A

Through horizontal gene transfer

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6
Q

E. coli strains that typically don’t cause disease are called…

A

Commensal E. coli

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7
Q

Name 3 ways in which virulence factors can be taken up by a bacterium.

A

By bacteriophage, which injects its bacteria into it, by taking up a plasmid, or by picking up a transposon.

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8
Q

The opposite of a commensal bacterium is a […]

A

Pathogenic bacterium.

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9
Q

Give an example of how different pathogenic E. coli strains can have different properties.

A

One strain can cause urinary tract and kidney infection, while another can cause diarrhea, colitis, and kidney damage

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10
Q

Name 5 types of virulence factors.

A
  1. Adhesins
  2. Nutrient acquisition systems
  3. Capsule
  4. Virulence-associated secretion systems
  5. Toxins
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11
Q

Describe the function of adhesins as virulence factors.

A

These can allow for better binding to host cells. By binding to the host cells via receptors, this can lead to invasion and colonization. This improves the ability of bacteria to colonize a particular area.

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12
Q

Explain how antiviral drugs can target adhesins.

A

The interaction between adhesins and receptors on a host cell can actually be targeted by anti-viral drugs. The drugs create receptor decoys.

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13
Q

Explain how nutrient acquisition systems work as virulence factors, including the specific molecules responsible for this function.

A

Pathogenic bacteria can steal iron from host cells via siderophores, which are proteins secreted by the pathogens. The siderophores bind iron more tighly than host cells.

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14
Q

Describe how siderophores execute their function as nutrient acquisition systems.

A

They can destroy erythrocytes, release iron from hemoglobin, or bind directly to iron-transport proteins and hemoglobin.

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15
Q

Where is the capsule located? What is it made of?

A

It is located outside the cell wall and is usually made of polysaccharides.

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16
Q

What is the function of the capsule?

A

Can protect from phagocytosis by host cells.

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17
Q

Describe the role of the capsule in Streptococcus pneumoniae and how it affects mice.

A

When they have the capsule, they can kill mice. When they don’t have the capsule, they do not cause disease in mice.

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18
Q

Name a virulence-associated secretion system.

A

Type III secretion system (T3SS)

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19
Q

Describe the structure of T3SS. It can be compared to what other structure?

A

It is shaped like a syringe and is composed of a multi-subunit protein complex. Its structure is similar to that of a gram-negative flagellum.

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20
Q

How many bacterial membranes do T3SS have?

A

2

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21
Q

What kind of bacteria have T3SS? Give 3 examples.

A

It is only present in gram-negative pathogens. Examples include Salmonella, Shigella, and Yersinia.

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22
Q

Explain how T3SS works.

A

It injects bacterial proteins directly into host cells

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23
Q

How do the T3SS synringe genes, injected proteins, and cellular effects vary between bacteria and host species?

A

Syringe genes: similar between species
Injected proteins: vary between bacteria
Cellular effects: vary between different bacteria.

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24
Q

The T3SS is related to […] of the target bacteria.

A

The flagellar basal body

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25
Q

Describe how the function of T3SS effectors varies between Salmonella and Yersinia.

A

For salmonella, T3SS induces its uptake into host cells, allowing it to multiply and colonize more easily. For Yersinia, T3SS blocks uptake into host cells, as it multiplies better outside of cells.

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26
Q

What are toxins?

A

Toxins are poisonous substances that are produced by certain microorganisms and which cause damage to host cells.

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27
Q

What are the 2 categories of toxins? Explain the difference between them.

A

Endotoxin: within the bacterial cell (i.e. lipids in the cell wall). Not voluntarily released.
Exotoxin: produced in the bacterial cell but secreted out voluntarily.

28
Q

What types of bacteria typically produce endotoxins? Explain why.

A

Only gram-negatives, as endotoxins are found in the lipid A portion of their LPS.

29
Q

How are endotoxins released?

A

They are only released either when the bacteria lyses or during bacterial multiplication.

30
Q

Does LPS cause its effects directly or indirectly? Explain how.

A

It causes its effects indirectly. It stimulates macrophages to release cytokines at high concentrations, causing a cytokine storm.

31
Q

Name the major effects on the host of endotoxin release.

A

The cytokine storm leads to sepsis, such as fever, increased heart rate, increased breathing rate, and low blood pressure.

32
Q

Are endotoxins heat stable?

A

Yes, they remain largely unaffected by heat.

33
Q

Are exotoxins heat stable?

A

No, they can easily be inactivated by heat.

34
Q

Exotoxins can be used as […]

A

Antiserum

35
Q

What are antitoxins?

A

They are antibodies produced by the body that provide immunity to exotoxins.

36
Q

What types of bacterial typically make exotoxins?

A

Gram - or gram +

37
Q

Name 3 types of exotoxins.

A

AB exotoxins, membrane-disrupting exotoxins, and superantigens.

38
Q

Exotoxins can also be categorized by […]. Give 2 examples.

A

Site of action. For example, neurotoxins affect neurons, while enterotoxins affect the intestine.

39
Q

What are superantigens?

A

They stimulate T cells and cause an exagerrated immune response.

40
Q

Describe the structure of AB toxins.

A

The A subunit has enzyme activity and is responsible for the toxic effect. The B subunit mediates cell binding/entry to the target.

41
Q

How do the following vary between different AB toxins:
a) Receptors on host cells
b) Enzymatic activity
c) Biological effects
d) Overall organization

A

a) Different
b) Different
c) Different
d) Similar

42
Q

Name the 3 steps by which AB toxins have their effect.

A
  1. B binds to host receptor
  2. Endocytosis
  3. A-B components separate. A alters host cell function, while B is released from the host. The target cell receptor gets pushed out and reused.
43
Q

Give an example of important exotoxin.

A

Clostridium botulinum

44
Q

How big of a health risk is clostridium botulinum?

A

It is the most poisonous naturally occurring substance in the world and is one of the greatest threats for biological warfare.

45
Q

How does clostridium botulinum work as an exotoxin?

A

It cleaves a protein involved in the neurotransmission from motor neurons to muscles and/or blocks acetylcholine from binding to receptors.

46
Q

What are the major symptoms of clostridium botulinum?

A

Double vision, blurred vision, droopy eyelids, slurred speech, difficulty swallowing, muscle weakness, localized paralysis

47
Q

What are membrane-disrupting exotoxins?

A

They attack host cell membranes by forming protein channels or disrupt phospholipid portion of the membrane.

48
Q

Membrane-disrupting exotoxins destroy erythrocytes using […]

A

Hemolysins

49
Q

What are the 2 types of membrane-disrupting exotoxins?

A

Pore-forming and phospho-lipases

50
Q

How do pore-forming membrane-disrupting exotoxins work?

A

They make holes in the host cell membrane, which allows the contents of the cell to leak out and causes lysis.

51
Q

How do phospho-lipase membrane-disrupting exotoxins work?

A

They remove the hydrophillic heads from the phospholipid bilayer, causing an unstable membrane and cell lysis.

52
Q

What are intoxications? What is their cause?

A

They occur when toxins cause disease without infection. They are caused by the entry of a specific pre-formed toxin, not by microbial growth or the entry or replication of bacteria.

53
Q

What is the typical onset time for intoxication?

A

Very fast - 30 min - 6 h

54
Q

Give an example of intoxication, including the species involved and context.

A

Bacillus cereus causes improper storage and contamination of food. Their toxin is pre-formed in food, and when it is ingested it causes vomiting. People usually recover within 6-24 hours.

55
Q

What are EHEC? What is it associated with?

A

Enterohemorrhagic E. coli. It is associated with ground beef and manure-contaminated produce.

56
Q

What is the reservoir for EHEC?

A

Cattle.

57
Q

What is the infectious dose for EHEC?

A

As few as 10 E. coli bacterial cells.

58
Q

Name the 5 major symptoms of EHEC and the likelihood of each.

A
  1. Diarrhea which can become bloody (hemorrhagic colitis) - 100%
  2. Hemolytic uremic syndrome (HUS): hemolytic anemia, platelet deficiency, kidney failure - 0-20%
  3. Chronic renal problems - 50% of HUS patients
  4. Neurological symptoms such as seizures, stroke, coma - 25% of HUS patients
  5. Fatality - 3-5% of HUS patients
59
Q

What does EHEC’s T3SS inject (2)? Explain how it works.

A

A TIR (Translocated intimin receptor). It gets inserted into the host cell membrane and becomes a receptor for EHEC on the host cell.

Also inserts 30 other proteins that dissociate tight junctions between intestinal epithelial cells, interfering with the host immune response.

60
Q

Where is EHEC located relative to the host cell?

A

It remains extracellular. T3SS is the main interface with the host cell.

61
Q

EHEC encodes which toxin?

A

Shiga toxin

62
Q

What type of toxin is Shiga? Describe its structure and its associated functions.

A

AB toxin. The A subunit inhibits protein synthesis in the host by modifying the 60S subunit of the ribosome. The B subunit binds specific glycolipids on host cells (G3b)

63
Q

What is repsonsible for encoding Shiga toxin?

A

It is encoded by bacteriophages that have integrated into the bacterial chromosome.

64
Q

What features of disease does the presence of Shiga toxin receptor cause in the following locations?
a) Intestinal epithelium
b) Kidney
c) Neurons
d) Absent in cow intestine

A

a) Bloody diarrhea
b) Kidney problems
c) Neurological complications
d) Asymptomatic carriers

65
Q

What is the treatment for EHEC?

A

There is no specific treatment for EHEC aside from supportive care, meaning watching and waiting for the development of complications, providing fluids, a blood transfusion, and kidney dialysis in anticipation.

66
Q

Can antibiotic therapy be used to treat EHEC? Why?

A

No, because it can increase the risk of HUS.

67
Q

Name 4 ways to prevent EHEC.

A
  1. Handwashing
  2. Thorough cooking of beef
  3. Keep raw/cooked utensils separate
  4. Pasteurization of milk, juice

MIMM 211 (38 decks)

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