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Infection > Innate immunity > Flashcards

Innate immunity Flashcards

1
Q

factors determining the outcome fo the host pathogen relationship

A

infectivity
host immune response
virulence

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2
Q

infectivity

A

the ability of the microbe toe stablish itself on the host or in the host

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3
Q

host immune response

A

Immunocompromised: elderly, young, pregnancy

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4
Q

virulence

A

capacity of the microbe to do damage to the host

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5
Q

immune system definition

A

cells and organs that contribute to immune defences against infectious and non-infectious conditions (self vs non-self)

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6
Q

infectious disease

A

when the pathogen succeeds in evading and/or overwhelming the hosts immune defences

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7
Q

role of immune system (4)

A

1) Pathogen recognition
2) Containing/eliminating infection
3) regulation itself (e.g. sepsis or autoimmune)
4) Remembering pathogens

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8
Q

two arms of the immune system

A

innate and adaptive

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9
Q

innate immune system overview

A
  • Immediate protection- fast
  • Prevent pathogen from entering e.g. skin
  • Lack of specificity- recognises antigens if a group of pathogens e.g. Lipopolysaccharide (LPS)
  • Lack of memory
  • No change in intensity overtime
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10
Q

adaptive immune system

A
  • Long lasting protection
  • Slow (days)
  • Specificity
  • Immunologic membrane
  • Changes in intensity
  • Needed for human survival
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11
Q

innate system made up of

A

1) first line defences

2) Second line defences

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12
Q

1) first line defences

A
  1. Physical barriers e.g. skin
  2. Physiological barriers
  3. Chemical
  4. Biological
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13
Q

2) second line defences

A
  • Phagocytes
  • Chemicals
  • Inflammation
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14
Q

physical barriers

A
  • Skin
-	Mucous membranes
o	Mouth
o	Respiratory tract
o	GI tract
o	Urinary tract
  • Bronchial cilia
    o Expel pathogens from the lungs e.g. CF
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15
Q

physical barriers do what

A

expel pathogen out of the body - not always caused by infection

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16
Q

physical barrier mechanisms

A
  • Diarrhoea- Food poisoning
  • Vomiting
    o Food poisoning
    o Hepatitis
    o Meningitis
  • Coughing
    o pneumonia
  • Sneezing
    o sinusitis

*also increases spread of microbes into environment

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17
Q

chemical barriers

A

low pH

antimicrobial molecules

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18
Q

pH of the skin

A

5.5

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19
Q

pH of stomach

A

1-3

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20
Q

pH of vagina

A

4.4

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21
Q

antimicrobial molecules

A 
o	IgA (tears, saliva, mucous membrane)
o	Lysosome (sebum, perspiration, urine)
o	Mucus (mucous membranes)
o	Beta-defensins (epithelium)
o	Gastric acid and pepsin
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22
Q

biological barriers

A

normal flora

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23
Q

normal flora

A

non-pathogenic microbes 9as long as they stay where they are

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24
Q

normal flora found in strategic locations

A 
	Nasopharynx
	Mouth/throat
	Skin
	GI tract
	Vagina (lactobacillus- makes it acidic- candidiasis after antibiotics)

Absent in internal organs/tissue

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25
Q

benefits fo normal flora

A

o Compete with pathogens for attachment sites and resource
o Produce antimicrobial chemicals
o Synthesise vitamins (K, B12 etc)
o Immune maturation

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26
Q

examples of normal flora that inhabit the skin

A
  • Staphylococcus aureus- cellulitis
  • Staphylococcus epidermidis- implants
  • Streptococcus pyogenes
  • Candida albicans
  • Clostridium perfringens- gas gangrene
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27
Q

examples of normal flora that inhabit the nasopharynx

A
  • Streptococcus pneumoniae
  • Neisseria meningitidis
  • Haemophilus species
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28
Q

clinical problems with normal flora start when

A

Normal flora is displaced from its normal location into sterile locations

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29
Q

how may skin flora breach the skin

A 
o	Skin loss
o	Surgery
o	IV lines
o	Skin diseases
o	Injection drug users
	HIV
	HEP B/C
o	Tattooing/ body piercing
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30
Q

fecal-oral route

A

food born infection

31
Q

fecal-perineal-urethral route

32
Q

poor dental hygiene

A

o Dental extraction
o Gingivitis
o Brushing/ flossing
 Common cause of harmless bacteraemia (spleen very important)
o Serious infections in high-risk patient
 Asplenic patients
 Patients with damaged prosthetic valves
 Patients with previous infective e endocarditis

33
Q

clinical problems also begin when normal flora overgrows and becomes pathogenic in immunocompromised host

A

o Diabetes
o AIDs
o Malignant disease
o Chemotherapy (mucositis)

34
Q

When normal flora in mucosal surfaces is depleted by antibiotic therapy

A

o Intestine severe colitis (clostridium difficile)

o Vagina  thrush (Candida albicans)

35
Q

main phagocytes

A

macrophages

monocytes

neutrophils

36
Q

macrophages

A

o Present in all organs
o Ingesta and destroy microbes via phagocytosis
o Present microbial antigens to T cells
o Produce cytokines and chemokines

37
Q

monocyte

A

o Present in the blood (5-7%)

o Recruited at infection site and differentiate into macrophages

38
Q

neutrophils

A

o Increased during infection
o Present in the blood (60% of blood leukocytes)
o Recruited by chemokines to the site of infection
o Ingest and destroy pyogenic bacteria: Staph aureus and strep pyogenes

39
Q

phagocytes recognise what on microbe

A

pathogen associated molecular pattern (PAMPs

40
Q

PAMPs include

A

LPS, peptidoglycan, flagellin, bacterial and viral DNA etc

41
Q

how do phagocytes recognise pathogens PAMPS

A

Pathogen recognition receptors e.g. Toll-like receptors, nod-like receptors

42
Q

TLR4 recognises

A

lipoteichoic acids (+ve) and LPS (-ve)

43
Q

LPS is found only on

A

gram negative bacteria

44
Q

TLr2

A

peptidoglycan - gram positive bacteria

45
Q

opsonisation microbes

A

Coating proteins called opsonins that bind to microbial surfaces leading to enhanced attachment of phagocytes and clearance of microbes

46
Q

examples of opsonins

A

Complement

antibodies

acute phase proteins

47
Q

antibodies

48
Q

acute phase protein

A

CRP

Mannose-binding lectin (MBL)

49
Q

opsonins are essential for

A

learning encapsulated batcria

50
Q

encapsulated bacteria

A

e. g. Neisseria meningitidis
e. g. Streptococcus pneumoniae
e. g. Haemophilus influenzae

51
Q

phagocytosis

A
  1. Chemotaxis and adherence of microbe phagocyte
  2. Ingestion of microbe by phagocyte
  3. Formation of phagosome
  4. Fusion of the phagosome with lysosome to form a phagolysosome
  5. digestion of ingested microbe by enzyme
  6. Formation of residual body containing indigestible material
  7. Discharge of waste materia
52
Q

phagocyte intracellular killing mechanisms

A
  • Oxygen dependent pathway (respiratory burst)
    o Toxic O2 products for the pathogens: Hydrogen peroxide, Hydroxyl radical, Nitric oxide, Singlet oxygen, Hypohalite
-	Oxygen -independent pathways
o	Lysosome
o	Lactoferrin
o	Cationic proteins
o	Proteolytic and hydrolytic enzymes
53
Q

other key cells of innate immunity

A

basophils/mast cells

eosinophils

NK cells

dendritic cells

54
Q

basophils/ mast cell

A

o Early actors of inflammation (vasodilation)

o Important in allergic responses

55
Q

eosinophils

A

o Defence against multi-cellular parasites (worms)

56
Q

NK cells

A

o Kill all abnormal host cells (virus/cancer)

57
Q

dendritic cells

A

o Present microbial antigens to T cells (acquired immunity)

58
Q

inflammation mediated by

A

complement system

cytokines and chemokine

59
Q

Anti-microbial actions of macrophage-derived cytokines such as TNAalpha/IL-1/IL-6

A

systemic

local

60
Q

systemic actions caused by cytokines such as TNFa, IL-1 and IL-6

A

liver –> CRP, MBL

bone marrow –> neutrophil mobilisation

hypothalamus –> increased body temp

61
Q

local inflammatory actions caused by cytokines such as TNFa, IL-1 and IL-6

A 
o	Blood vessels
	Vasodilation
	Vascular permeability
	Expression of adhesion molecules 
 attraction of neutrophils
62
Q

complement summary

A

20 serum proteins (C1-C9 most important)
- 2 activating pathways
o Alternative pathway

o MBL pathway

63
Q

Alternative pathway

A

Initiated by cell surface microbial constituents (endotoxins on E.coli)

64
Q

MBL pathway

A

Initiated by MBL binds to mannose containing residues of proteins found on many microbes (salmonella spp. Candida albicans)

65
Q

C3a and C5a

A

recruitment of phagocytes

66
Q

C3b-C4b

A

opsonisation of pathogen

67
Q

C5-C9

A

killing of pathogens

- Membrane attack complex

68
Q

when may phagocytosis be reduced and start causing clinical problems

A
  • decreased spleen function
  • decreased neutrophil number
  • decreased neutrophil function
69
Q

decreased spleen function

A
  • Asplenic patients

- Hyposplenic patients

70
Q

decreased neutrophil number

A
  • Cancer chemotherapy
  • Certain drugs (phenytoin)
  • Leukaemia and lymphoma
71
Q

decreased neutrophil function

A
  • Chronic granulomatous disease (no resp burst)

- Chediak- higashi syndrome (no phagolysosome formation)

72
Q

hypothalamus triggered bt cytokines TNF, IL-8 to cause

73
Q

acute phase protein

74
Q

CRP

A

acute phase protein produced by the liver during inflammation
- opsonin that helps enhance phagocytosis

Infection (36 decks)

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