L2 Host Defences Flashcards

1
Q

What is disease?

A

The result of a host interaction with a pathogen (bacterial in this module)

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2
Q

Is disease a rare or common outcome of host-pathogen interaction?

A

Very rare

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3
Q

What 3 factors are taken into account for disease?

A

Host (human), pathogen (bacterium), environment/circumstances

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4
Q

Examples of ways the host can interact with the pathogen

A

Vectors (insects), food, sexually transmitted

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5
Q

If a pathogen affects a host, it is more virulent if…

A

it is transmitted to the host directly

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6
Q

What is responsible for 70-80% of infections?

A

Zoonosis

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7
Q

What must be overcome in order for disease to occur?

A

Host defences

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8
Q

What part of the immune system is responsible for non-specific defence mechanisms?

A

Innate

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9
Q

What part of the immune system is responsible for specific defence mechanisms?

A

Adaptive

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10
Q

What is the first line of the defence (innate)?

A

Constitutive - skin, mucous membrane, secretions of skin & mucous membrane

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11
Q

What is the second line of defence (innate)?

A

Inducible - phagocytosis, antimicrobial proteins, inflammatory response

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12
Q

What is the third line of defence (adaptive)?

A

Lymphocytes, antibodies

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13
Q

The innate immune system deals with __ infections.

A

acute

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14
Q

The adaptive immune system deals with…

A

reinfection

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15
Q

What are constitutive defences?

A
  • Provide general protection against invasion by normal flora, or colonisation/ infection/ infectious disease caused by pathogens
  • ‘Natural resistance’
  • Skin, mucosal surfaces, tears, saliva, sweat, urine, stomach acid etc.
  • Non-specific
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16
Q

What are inducible defences?

A
  • Must be induced by host exposure to a pathogen
  • Only triggered after host is appropriately exposed to pathogen
  • Immune responses
  • Usually specifically directed against an invading pathogen
  • Can be part of innate or acquired immune system e.g. cytokines, antibodies
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17
Q

What are components of non-specific defences?

A
  1. Anatomical defences
  2. Microbial antagonism
  3. Phagocytosis
  4. Tissue bactericides (incl. complement)
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18
Q

What is the largest organ?

A

The skin (surface area of 1.8 m²)

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19
Q

What are the conditions of the skin that bacteria do not like?

A
  • Dry
  • Acidic (pH 5.0)
  • Low temp.
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20
Q

Are resident microflora in the skin mainly Gram positive or negative?

A

Gram positive

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21
Q

What connects the skin to the immune system of the host?

A

SALT = skin associated lymphoid tissue

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22
Q

Where in the body would you find mucous membranes?

A

GIT, respiratory tract, urogenital tract

23
Q

What is the main function of epithelial cells?

A

Absorption of nutrients

24
Q

What are M cells?

A

Naturally phagocytic specialised epithelia that are continuously sampling the bacterial population in gut & transferring that info to immune cells

25
Q

Why do many pathogens target M cells?

A

Because they know they will get across the gut barrier naturally

26
Q

What epithelia is found mainly in the lungs & GIT?

A

Simple columnar epithelia

27
Q

What facilitates the joining together of epithelial cells to form a barrier?

A

Tight junctions

28
Q

What happens when pathogens target tight junctions?

A

Pathogen destabilises the tight junctions → get water & sometimes blood in the inside moving between cells and into the gut lumen. This causes bloody diarrhoea e.g. Clostridium perfringens

29
Q

Where are M cells located?

A

In the follicle-associated epithelium, that covers Peyer’s patches

30
Q

M cells stimulate the production of which antibody?

A

sIgA

31
Q

What do Goblet cells secrete?

A

Mucus

32
Q

What do entero-endocrine cells secrete?

A

NA and other gut-localised hormones

33
Q

What do Paneth cells secrete, and where do they stay localised?

A

Secrete antimicrobial peptides

Paneth cells stay localised in the crypt at the base of the villus

34
Q

What are Defensins?

A

Antimicrobial peptides that form pores in bacterial membranes

35
Q

What is another term for microbial antagonism?

A

Colonisation resistance

36
Q

What is microbial antagonism?

A

Protection of the surfaces afforded by an intact normal flora (commensal flora) in a healthy host

37
Q

Name 3 ways that the normal flora can protect mucosal surfaces

A
  1. Competition for binding (colonisation) sites
  2. Antagonism against non-indigenous species - highly specific proteins called bacteriocins produced by normal flora to kill/inhibit other species
  3. Immunomodulation - normal flora interact with immune system to stop pathogen growth/survival
38
Q

What are the first to arrive at a site of infection in response to chemokine signals produced in that locality?

A

Neutrophils, followed by monocytes which will develop into macrophages in tissue

39
Q

What is neutropenia and what are sufferers very prone to?

A

Neutropenia is depressed polymorphonuclear leukocyte levels (low neutrophil levels) - sufferers very prone to infection

40
Q

What is an example of a bacterium that lives in macrophages and hijacks the normal macrophage function?

A

Salmonella - uses macrophages as a privileged niche for its replication because they are a great source of nutrients

41
Q

What are examples of tissue bactericides?

A

Transferrin
Interferon
Lysozyme antimicrobial molecule
Complement

42
Q

What is the role of transferrin?

A

Transferrin has a high affinity for iron, so it is released by the body during bacterial infection to reduce the iron available to invading bacterial cells. Its concentration increases during systemic infection.

43
Q

What is the Red Queen Hypothesis?

A

Bacteria produce their own iron-binding molecules, called siderophores, that compete with the body for iron.

44
Q

What does Interferon do?

A

It inhibits viral replication and activates other cells which kill pathogens

45
Q

Where would you find lysozyme and what does it do?

A

Lysozyme is an antimicrobial molecule that is found in serum and tears. It breaks down the bacterial cell wall (peptidoglycan).

46
Q

What is complement?

A

A set of serum (blood) proteins (C1-C9) which provide a form of constitutive defence

47
Q

Where would you find complement, and what does it do?

A

In the blood.
Serum proteins which cause destruction of microorganisms directly or with the help of phagocytic cells. Complement opsonises microorganisms, which makes them more susceptible to phagocytosis.

48
Q

Briefly describe the complement cascade, that eventually leads to phagocytosis

A
  • Ab binds bacteria in blood → activation of C1/2/4 complex → creates an active enzyme (C3 convertase) → cascade
  • C3 convertase cleaves C3 into 2 active subunits (C3a & C3b)
  • C3b binds bacterial cell wall → opsonisation
  • C3b also cleaves C5 into 2 subunits (C5a & C5b)
  • C5a attaches to macrophages & increases their activation
  • C3a & C5a attract & activate macrophages → engulf & destroy opsonised bacteria
49
Q

What is the Classical Pathway?

A

When the complement cascade is triggered by an antibody

50
Q

What is the Alternative Pathway?

A

If the body has never seen the bacteria before, complement can also function to attack that bacteria using the Alternative Pathway

51
Q

What makes up the membrane attack complex (MAC), and what does it do?

A

MAC = C5b, 6, 7, 8, 9

Forms pores in Gram negative cells

52
Q

What immune functions does complement trigger?

A
  • Phagocytosis
  • Inflammation
  • Membrane attack
53
Q

Which complement protein has the most important opsonising activity?

A

C3b

54
Q

What is the main aim of complement?

A

To keep the blood sterile and free of microorganisms