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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
benefits fo normal flora
o Compete with pathogens for attachment sites and resource o Produce antimicrobial chemicals o Synthesise vitamins (K, B12 etc) o Immune maturation
26
examples of normal flora that inhabit the skin
- Staphylococcus aureus- cellulitis - Staphylococcus epidermidis- implants - Streptococcus pyogenes - Candida albicans - Clostridium perfringens- gas gangrene
27
examples of normal flora that inhabit the nasopharynx
- Streptococcus pneumoniae - Neisseria meningitidis - Haemophilus species
28
clinical problems with normal flora start when
Normal flora is displaced from its normal location into sterile locations
29
how may skin flora breach the skin
``` o Skin loss o Surgery o IV lines o Skin diseases o Injection drug users  HIV  HEP B/C o Tattooing/ body piercing ```
30
fecal-oral route
food born infection
31
fecal-perineal-urethral route
UTI
32
poor dental hygiene
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
clinical problems also begin when normal flora overgrows and becomes pathogenic in immunocompromised host
o Diabetes o AIDs o Malignant disease o Chemotherapy (mucositis)
34
When normal flora in mucosal surfaces is depleted by antibiotic therapy
o Intestine severe colitis (clostridium difficile) | o Vagina  thrush (Candida albicans)
35
main phagocytes
macrophages monocytes neutrophils
36
macrophages
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
monocyte
o Present in the blood (5-7%) | o Recruited at infection site and differentiate into macrophages
38
neutrophils
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
phagocytes recognise what on microbe
pathogen associated molecular pattern (PAMPs
40
PAMPs include
LPS, peptidoglycan, flagellin, bacterial and viral DNA etc
41
how do phagocytes recognise pathogens PAMPS
Pathogen recognition receptors e.g. Toll-like receptors, nod-like receptors
42
TLR4 recognises
lipoteichoic acids (+ve) and LPS (-ve)
43
LPS is found only on
gram negative bacteria
44
TLr2
peptidoglycan - gram positive bacteria
45
opsonisation microbes
Coating proteins called opsonins that bind to microbial surfaces leading to enhanced attachment of phagocytes and clearance of microbes
46
examples of opsonins
Complement antibodies acute phase proteins
47
antibodies
IgG | IgM
48
acute phase protein
CRP | Mannose-binding lectin (MBL)
49
opsonins are essential for
learning encapsulated batcria
50
encapsulated bacteria
e. g. Neisseria meningitidis e. g. Streptococcus pneumoniae e. g. Haemophilus influenzae
51
phagocytosis
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
phagocyte intracellular killing mechanisms
- 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
other key cells of innate immunity
basophils/mast cells eosinophils NK cells dendritic cells
54
basophils/ mast cell
o Early actors of inflammation (vasodilation) | o Important in allergic responses
55
eosinophils
o Defence against multi-cellular parasites (worms)
56
NK cells
o Kill all abnormal host cells (virus/cancer)
57
dendritic cells
o Present microbial antigens to T cells (acquired immunity)
58
inflammation mediated by
complement system cytokines and chemokine
59
Anti-microbial actions of macrophage-derived cytokines such as TNAalpha/IL-1/IL-6
systemic local
60
systemic actions caused by cytokines such as TNFa, IL-1 and IL-6
liver --> CRP, MBL bone marrow --> neutrophil mobilisation hypothalamus --> increased body temp
61
local inflammatory actions caused by cytokines such as TNFa, IL-1 and IL-6
``` o Blood vessels  Vasodilation  Vascular permeability  Expression of adhesion molecules  attraction of neutrophils ```
62
complement summary
20 serum proteins (C1-C9 most important) - 2 activating pathways o Alternative pathway o MBL pathway
63
Alternative pathway
Initiated by cell surface microbial constituents (endotoxins on E.coli)
64
MBL pathway
Initiated by MBL binds to mannose containing residues of proteins found on many microbes (salmonella spp. Candida albicans)
65
C3a and C5a
recruitment of phagocytes
66
C3b-C4b
opsonisation of pathogen
67
C5-C9
killing of pathogens | - Membrane attack complex
68
when may phagocytosis be reduced and start causing clinical problems
- decreased spleen function - decreased neutrophil number - decreased neutrophil function
69
decreased spleen function
- Asplenic patients | - Hyposplenic patients
70
decreased neutrophil number
- Cancer chemotherapy - Certain drugs (phenytoin) - Leukaemia and lymphoma
71
decreased neutrophil function
- Chronic granulomatous disease (no resp burst) | - Chediak- higashi syndrome (no phagolysosome formation)
72
hypothalamus triggered bt cytokines TNF, IL-8 to cause
a fever
73
acute phase protein
CRP
74
CRP
acute phase protein produced by the liver during inflammation - opsonin that helps enhance phagocytosis

Infection (36 decks)

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