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ESA 2 SEMESTER 2 TK > Infection - Innate Immunity > Flashcards

Infection - Innate Immunity Flashcards

1
Q

What is the difference between infectivity and virulence?

A

Infectivity is the capacity of a pathogen to establish itself within a host. Virulence is the capacity of a microbe to damage the host

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2
Q

Define immune system

A

Cells and organs that contribute to immune defences against infectious and non-infectious conditions

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3
Q

Define infectious disease

A

When the pathogen succeeds in evading and/or overwhelming the host’s immune defences

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4
Q

What are the four main roles of the immune system?

A
  • pathogen recognition
  • containing/eliminating the infection
  • regulating itself
  • remembering pathogens
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5
Q

Describe some key differences between innate and adaptive immunity

A

Innate immunity:

  • fast (seconds)
  • lack of specificity and memory
  • no change in intensity

Adaptive immunity:

  • slow (days)
  • specific
  • has immunologic memory
  • changes in intensity
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6
Q

What are ‘barriers’ in immunity?

A

Factors that prevent entry and limit growth of pathogens

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7
Q

Give some examples of physical barriers in innate immunity

A
  • skin
  • mucous membranes (mouth, respiratory tract, GI tract, urinary tract)
  • bronchial cilia
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8
Q

Give some examples of physiological barriers in the innate immune system

A
  • diarrhoea
  • vomiting
  • coughing
  • sneezing
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9
Q

Give some examples of chemical barriers in the innate immune system

A
  • low pH (skin is 5.5, stomach is 1-3, vagina is 4.4)

- antimicrobial molecules

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10
Q

Give some examples of antimicrobial molecules that form part of the innate immune system

A
  • IgA (tears, saliva, mucous membrane)
  • lysozyme (sebum, perspiration, urine)
  • mucus (mucous membranes)
  • beta-defensins (epithelium)
  • gastric acid and pepsin
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11
Q

What are ‘biological barriers’?

A

Non-pathogenic normal flora found in strategic locations, eg. nasopharynx, mouth/throat, skin, GI tract, vagina. They are not found within internal organs/tissues

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12
Q

Give some benefits of the body having ‘normal flora’ (non-pathogenic microbes)

A
  • compete with pathogens for attachment sites and resources
  • produce antimicrobial chemicals
  • synthesise vitamins (K, B12, other B vitamins)
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13
Q

Give some examples of normal flora that inhabit the skin

A
  • staphylococcus aureus
  • staphylococcus epidermidis
  • streptococcus pyogenes
  • Candida albicans
  • clostridium perfringens
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14
Q

Give some examples of normal flora that inhabit the nasopharynx

A
  • streptococcus pneumoniae
  • neisseria meningitidis
  • haemophilus species
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15
Q

How could normal flora be displaced from its normal location to a sterile location?

A
  • breaching skin integrity (skin loss, surgery, injected drugs, IV lines)
  • faecal-oral route (foodborne infection)
  • fecal-perineal-urethral route (UTI infection)
  • poor dental hygiene/dental work
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16
Q

Which groups of patients are seen as high risk for infections from normal flora?

A

Patients who are/have:

  • asplenic/hyposplenic
  • damaged or prosthetic valves
  • previous infective endocarditis
17
Q

Give some examples of conditions that may cause a host to become immunocompromised, allowing overgrowth of normal flora

A
  • diabetes
  • AIDS
  • malignant diseases
  • chemotherapy
18
Q

What is thrush caused by?

A

Vaginal yeast infection (candida albicans) that can occur when normal flora is depleted by antibiotics

19
Q

What are macrophages?

A

Phagocytes which are present in all organs. They ingest and destroy microbes via phagocytosis, and present microbial antigens to T cells (part of adaptive immunity). They produce cytokines/chemokines

20
Q

What are monocytes?

A

Phagocytes which are present in the blood. They are recruited at the infection site where they differentiate into macrophages

21
Q

What are neutrophils?

A

Phagocytes which make up 60% of blood leukocytes. They are increased during infection, when they are recruited by chemokines. They ingest and destroy pyogenic bacteria

22
Q

What is the function of basophils/mast cells?

A

Early actors of inflammation (vasomodulation) which are important in allergic responses

23
Q

What are eosinophils used for?

A

Defence against multi-cellular parasites (worms)

24
Q

What are natural killer cells for?

A

They kill all abnormal host cells (either infected with virus or malignant)

25
Q

What are dendritic cells for?

A

Present microbial antigens to T cells (in acquired/adaptive immunity)

26
Q

How does the phagocyte recognise the pathogen to be consumed?

A

Pathogen will have microbial structures (pathogen-associated molecular patterns or ‘PAMPs’) and phagocyte has pathogen recognition receptors

27
Q

What is opsonisation of microbes?

A

Coating proteins called opsonins bind to the microbial surfaces, leading to enhanced attachment of phagocytes

28
Q

Give some examples of opsonins

A
  • complement proteins (C3b, C4b)
  • antibodies (IgG, IgM)
  • acute phase proteins (C-reactive protein and mannose-binding lectin)

These are all essential in clearing encapsulated bacteria

29
Q

What are the two phagocyte intracellular killing mechanisms?

A
  • oxygen dependent pathway

- oxygen independent pathway

30
Q

What is the oxygen-dependent killing pathway?

A

Reactive oxygen-containing molecules are produced by the phagocyte which are anti-microbial

31
Q

What are the different methods of oxygen-independent destruction of pathogens?

A
  • production of lysozymes which break down bacterial cell wall
  • production of lactoferrins which are present in neutrophil granules and remove the essential iron from bacteria
  • electrically charged cationic proteins damage the bacterium’s membrane
  • proteolytic/hydrolytic enzymes digest the proteins of destroyed bacteria
32
Q

What is the difference between the alternative pathway and the MBL pathway of complement activation?

A
  • alternative pathway is initiated by cell surface microbial constituents (endotoxins on E.coli)
  • MBL pathway is initiated when MBL binds to mannose containing residues of proteins found on many microbes
33
Q

What are complement proteins C3a and C5a responsible for?

A

Recruitment of phagocytes

34
Q

What are complement proteins C3b-C4b responsible for?

A

Opsonisation of pathogens

35
Q

What are complement proteins C5-C9 responsible for?

A

Killing of pathogens, membrane attack complex

36
Q

What are the antimicrobial actions of macrophage-derived TNF-alpha (and where do they take place)?

A
  • liver (CRP and MBL activate complement/opsonisation)
  • bone marrow (neutrophil mobilisation)
  • inflammatory actions (vasodilation, vascular permeability, adhesion molecules lead to attraction of neutrophils)
  • hypothalamus (increased body temperature)
37
Q

What three things can lead to reduced phagocytosis?

A
  • decreased spleen function (asplenic/hypersplenic patients)
  • decreased neutrophil number (chemotherapy, certain drugs, leukaemia and lymphoma)
  • decreased neutrophil function (chronic granulomatous disease, Chediak-Higashi syndrome)

ESA 2 SEMESTER 2 TK (87 decks)

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