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Microbiology- HLSC 124 🦠 > Microbio Chapter 15- Mechanisms of Pathogenicity > Flashcards

Microbio Chapter 15- Mechanisms of Pathogenicity Flashcards

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Biology 101 flashcards
1
Q

What are portals of entry?

A

Places where microbes can enter a host

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2
Q

What are types of portals of entry?

A
  1. Mucous membrane
  2. Skin
  3. Parenteral route
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3
Q

Examples of mucous membrane portals of entry?

A

Repiratory tract e.g Pneumonia
GI tract e.g, E. coli
Genitourinary (GU) tract e.g, HIV
Conjunctiva e.g Pink eye

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4
Q

Example of bacteria that invades through the skin?

A

Staphylococcus aureus

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5
Q

How does bacteria enter a host through parenteral routes?

A

(Punctured skin)
Insect bite, wound, broken tissue

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6
Q

What is adherence?

A

How bacteria attaches to establish a colony and invade a host

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7
Q

How does a pathogen and host bond?

A

The host has receptors which the pathogen’s adhesions/ligand’s bind to

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8
Q

What are host receptors made from?

A

Complex sugars
-Mannose, fucose

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9
Q

What are pathogen’s ligands made from?

A

Glycoproteins or lipoproteins

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10
Q

What structures (5) on a pathogens help to attach?

A
  1. Capsule
  2. Fimbrae
  3. M-protein
  4. Mycolic acid
  5. Opa protein
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11
Q

Example of a bacteria with a capsule?

A

Streptococcus mutans (teeth decay)

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12
Q

How does Streptococcus mutans invade?

A

Enzyme called glucosyltransferase

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13
Q

S. mutans breaks down what kind of sugar present on teeth?

A

Sucrose
-from dietary sugar

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14
Q

What is sucrose broken down into?

A

Glucose and fructose

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15
Q

What does glucosyltransferase break down?

A

Glucose and fructose

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16
Q

What does glucosyltransferase turn Glucose into?

A

Glucan

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17
Q

What does glucosyltransferase turn Fructose into?

A

Acid

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18
Q

What does Glucan cause on the surface of teeth?

A

Plaque (leads to tooth decay)

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19
Q

What does the broken down fructose acid do to teeth?

A

degeneration on teeth and loosing of teeth

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20
Q

Example of bacteria with M-protein?

A

Streptococcus pyogenes

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21
Q

What is the purpose of M-protein?

A

Heat and acid resistance
Attachment
Evade phagocytosis

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22
Q

What species of bacteria has Mycolic acid?

A

Mycobacterium sp.

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23
Q

What is an exoenzyme?

A

enzyme that is secreted by a bacterial cell and functions outside that cell

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24
Q

Examples of exoenzymes?

A
  1. Coagulase
  2. Kinase
  3. Hyaluronidase
  4. Collagenase
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25
Q

What does Coagulase do?

A

Coagulate blood (form a clot)
Converts fibrinogen to fibrin threads

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26
Q

Example of a bacteria with Coagulase?

A

Staphylococcus aureus

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27
Q

What does kinase do?

A

Digest fibrin clots

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28
Q

Example of a bacteria with Kinase?

A

Streptococcus pyogenes

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29
Q

What does hyaluronidase do?

A

Hydrolyses hyaluronic acid

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30
Q

Examples of bacteria with hyalyronidase?

A
  1. Clostridium perfringens (gangrene: blackening of the skin)
  2. Streptococcus pyogenes
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31
Q

What does Collagenase do?

A

Hydrolyses (breaks down) collagen

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32
Q

Example of bacteria with Collagenase?

A

Clostridium perfringens

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33
Q

What is a toxoid?

A

Inactivated toxin used in a vaccine

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34
Q

What is toxemia?

A

Presence of toxin used in a vaccine

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35
Q

What is an antitoxin?

A

Antibody against a specific toxin

36
Q

What is an Exotoxin?

A

Proteins produced inside pathogenic bacteria

37
Q

What kind of bacteria produce exotoxins?

A

Gram positive and a few gram negative

38
Q

How are exotoxins produced?

A

As a part of metabolism (not on the cell wall)
-They circulate

39
Q

What do exotoxins produce?

A

Specific signs and symptoms

***Don’t cause fever

40
Q

How are exotoxins neutralised?

A

The body produces antitoxins called Ig molecules

41
Q

What are exotoxins chemically change into to use in vaccines?

A

Toxoids
e.g; DTAP vaccine

42
Q

What are the 3 classes of exotoxins?

A
  1. Classic A-B
  2. Membrane disrupting
  3. Superantigens
43
Q

What are classic A-B exotoxins?

A

-Have two polypeptide chains
Chain #1- A
Chain #2- B

44
Q

What is the A polypeptide’s function?

A

the Active part
-Causes cell damage
-Creates signs and symptoms

45
Q

What is the B polypeptide’s function?

A

the Binding part (binds to host cell)
-Used for entry
-Brings A into the cell so it can cause damage

46
Q

examples of bacteria classic A-B exotoxins?

A

A. C. diphtheriae (Diphtheriotoxin)
B. Botulinum toxin
C. Tetanospasmin
D. Vibriotoxin

47
Q

What does A and B do in Diphtheriotoxin?

A

B- binds to host cell
A- Inactivates protein synthesis

48
Q

How does Diphtheriotoxin damage a cell?

A

After protein synthesis is deactivated, cell death occurs, a pseudomembrane forms
—> leads to suffocation/ blocks resp. tract

49
Q

What does A and B do in Botulinum toxin?

A

B- binds to host cell
A- becomes a neurotoxin.

50
Q

What does A in Botulinum toxin inhibit?

A

Acetylcholine in neuromuscular junction
-No action potential/nerve movement
-muscles freeze

51
Q

What does botulinum toxin cause?

A

Flaccid paralysis

52
Q

What does A and B do in Tetanospasmin?

A

B- Binds to host cell
A- becomes a neurotoxin

53
Q

What does A in Tetanospasmin inhibit?

A

GABA (neurotransmitter that allows muscles to relax)

54
Q

what does Tetanospasmin cause?

A

Severe spasms
Stages
1- Lock jaw
2- Opisthosomas (spinal fracture; end stage tetanus)
3- CV and respiratory affected

55
Q

What does A and B do in Vibriotoxin?

A

B- binds to host INTESTINAL cells
A- Converts cells into little pumps (secondary cyclic AMP system) and pumps out water

56
Q

What does Vibriotoxin cause?

A

Rice water stools

57
Q

What are membrane-disrupting toxins?

A

Disrupt plasma membrane by forming holes in it (cell content leave)
-2 ways

58
Q

What are 2 ways a membrane-disrupting toxin can form a hole in the plasma membrane?

A
  1. Disrupting the phosphilipid bilayer
  2. Creating protein channels
59
Q

Example of membrane-disrupting toxins?

A

Hemolysins
leukocidin
Erythrogenic toxin

60
Q

What does hemolysis disrupt?

A

Red blood cells
e.g blood agar —> clear zone

61
Q

What does Leukocidin disrupt?

A

Leucocytes (white blood cells)

62
Q

What does erythrogenic disrupt?

A

Membrane of skin and blood vessels

63
Q

What does erythrogenic toxin cause?

A

Scarlet fever
-Red skin rash

64
Q

What bacteria has hemolysis, leucocidin and erythrogenic?

A

Streptococcus pyogenes

65
Q

What are superantigens?

A

provoke an intense immune response

66
Q

How do superantigens function?

A

trigger T-cells to activate and over release cytokines (Interleukins) which circulate in the blood to vital organs (especially GI tract)

67
Q

What symptoms do superantigens cause?

A

Nausea, vomitting, diarrhoea and shock

68
Q

Example of bacteria with a superantigen?

A

Staphylococcus aureus

69
Q

What does staphylococcus aureus cause?

A
  1. TSS
  2. Food poisoning
70
Q

What is an endotoxin?

A

Lipid portion of LPS is released when cell dies and cell wall lyses

71
Q

What is the name of the lipid that is an endotoxin?

A

Lipid A

72
Q

What kind of bacteria can have an endotoxin?

A

only Gram- negative

73
Q

What symptoms does endotoxins cause?

A

Fever
GI tract (nausea, vomiting, diarrhoea and dysentry)
Shock

74
Q

Do endotoxins promote the formation of antitoxins (Immunoglobulins Ig)

A

No they don’t
-Antibodies can be produced but won’t counter the effect of the toxin

75
Q

What triggers a fever?

A

When Gram negative bacteria is digested by a macrophage

76
Q

What do lysosomes do to trigger a fever?

A

Lysosomes degrade (w/ enzymes) the bacteria cause the LPS (lipid A) to be released

77
Q

When LPS is released what does it trigger in a fever?

A

Triggers the release of interleukin-1(a cytokine)
-IL-1 is over released therefore is toxic

78
Q

Where does IL-1 in the blood travel to during a fever?

A

The brain and specifically the Hypothalamus

79
Q

What does the hypothalamus secrete during a fever?

A

Prostaglandins
-Which tell the body to reset its temperature to a high temperature
Causing a fever

80
Q

What are the two stages of fevers?

A
  1. Chills stage
  2. Crisis stage
    (stages work in a cycle)
81
Q

What is the Chills stage?

A

Lots of IL-1 in blood
Leads to shivering

82
Q

What is the Crisis stage?

A

IL-1 decreases in the blood
-Sweating

83
Q

How is septic shock triggered?

A

Gram-negative bacteria is digested by a macrophage causing LPS to be released

84
Q

What does the release of LPS trigger in shock?

A

TNF (tumor necrosis factor) or Cachetin

85
Q

What does TNF/Cachetin do?

A

Travels to vital organs via blood and changes the permeability of their blood vessels (BP drops drastically)

Microbiology- HLSC 124 🦠 (18 decks)

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