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SA infections > S3) Innate Immune System > Flashcards

S3) Innate Immune System Flashcards

1
Q

What is the immune system?

A

The immune system is a network of cells and organs that contribute to immune defences against infectious and non-infectious conditions (self vs non-self)

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2
Q

Identify 4 roles of the immune system

A
  • Pathogen recognition: cell surface and soluble receptors
  • Containing/eliminating the infection: killing and clearance mechanisms
  • Regulating itself: minimum damage to host (resolution)
  • Remembering pathogens: preventing disease from recurring
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3
Q

Compare and contrast the innate and adaptive immunity

A
  • Innate (immediate protection): fast (seconds), lack of specificity and memory, no change in intensity
  • Adaptive (long lasting protection): slow (days), specificity, immunologic memory, changes in intensity
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4
Q

What is an infectious disease?

A

An infectious disease is when a pathogen succeeds in evading and/or overwhelming the host’s immune defences

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5
Q

Identify and describe the 3 mechanisms by which micro-organisms trigger the inflammatory cascade

A
  • Pilus enhances attachment
  • Lipopolysaccharide endotoxins triggers inflammation
  • Polysaccharide capsule promotes adherence and prevents phagocytosis
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6
Q

The inflammatory cascade is triggered when an endotoxin binds to macrophages.

Outline its following phases:

  • Local
  • Systemic
  • Sepsis
A
  • Local: cytokines, TNFs and interleukins promote wound repair and recruit the reticuloendothelial system
  • Systemic: cytokines released into circulation and stimulate GF, macrophages & platelets (aims to control infection)
  • Sepsis: cytokines lead to activation of humoral cascades, RE System, circulatory insult (infection is not controlled)
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7
Q

Explain the relationship between sepsis and coagulation

A
  • Cytokines released in sepsis initiates production of thrombin
  • Thrombin promotes coagulation and cytokines also inhibit fibrinolysis
  • Coagulation cascade leads to microvascular thrombosis → organ ischaemia, dysfunction and failure (sepsis)
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8
Q

What are the three factors determining the outcome of the host-pathogen relationship?

A
  • Infectivity
  • Host’s immune response
  • Virulence
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9
Q

The first line of defence consists of factors that prevent entry and limit growth of pathogens.

Identify the different innate barriers to infection

A
  • Physical barriers
  • Physiological barriers
  • Chemical barriers
  • Biological barriers
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10
Q

Identify the 3 different physical barriers to infection in the innate immune system

A
  • Skin
  • Mucous membranes: mouth, resp tract, GI tract, urinary tract
  • Bronchial cilia

flaw:

Once this layer has been breeched pathogens can move freely into tissue

takes time to heal eg skin

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11
Q

Identify and describe the 4 physiological barriers to infection in the innate immune system

A
  • Diarrhoea – food poisoning
  • Coughing – pneumonia
  • Sneezing – sinusitis
  • Vomiting – food poisoning, hepatitis, meningitis

lots of these have side effects

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12
Q

Identify and describe the 2 different chemical barriers to infection in the innate immune system

A
  • Low pH – skin (5.5), stomach (1-3), vagina (4.4)
  • Antimicrobial molecules:

I. IgA (tears, saliva, mucous membranes)

II. Lysozyme (sebum, perspiration, urine)

III. Mucus (mucous membranes)

IV. Gastric acid + pepsin

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13
Q

Identify and describe the biological barrier to infection in the innate immune system

A

Normal flora:

  • Non pathogenic microbes
  • Found in nasopharyngeal, mouth/throat, skin, GI tract, vagina
  • Absent in internal organs/tissues

bad when normal flora enter different parts of the body

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14
Q

What are the benefits of normal flora as a biological barrier in the innate immune system?

A
  • Compete with pathogens for attachment sites and resources
  • Produce antimicrobial chemicals
  • Synthesise vitamins (K, B12, other B vitamins)
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15
Q

Describe how the different innate barriers work together to maximise the response against microbes

A

Innate barriers trigger the second lines of defence:

  • Phagocytes
  • Chemicals
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16
Q

What does the second line of defence in the innate immune system do?

A
  • Causes inflammation
  • Contain and clear the infection
  1. phagocytes
  2. basophils (mast cells) , eosinophils, dendritic cells
  3. chemicals - cytokiens
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17
Q

Provide some examples of opsonins

A
  • Complement proteins: C3b, C4b
  • Antibodies: IgG, IgM
  • Acute phase proteins: CRP, MBL
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18
Q

Opsonis are essential in clearing encapsulated bacteria.

Identify three examples of this type of bacteria

A
  • Neisseria meningitidis
  • Streptococcus pneumoniae
  • Haemophilus influenzae b
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19
Q

Identify the 3 main types of phagocytes

A
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20
Q

State the location and functions of macrophages

A
  • Location: present in all organs
  • Functions:

I. Ingest and destroy microbes by phagocytosis

II. Present microbial antigens to T cells

III. Produce cytokines/chemokines

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21
Q

State the location and function of monocytes

A
  • Location: present in the blood (5-7%)
  • Function: recruited at the infection site and differentiate into macrophages
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22
Q

State the location and functions of neutrophils

A
  • Location: present in the blood (60% of blood leukocytes)
  • Functions:

I. Increased during infection

II. Recruited by chemokines to the site of infection

III. Ingest and destroy progenitor bacteria e.g. Staph aureus

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23
Q

State the function of the following key cells in the innate immunity:

  • Basophils/mast cells
  • Eosinophils
  • Natural Killer cells
  • Dendritic cells
A
  • Basophils/ mast cells: early actors of inflammation (vasomodulation) in allergic responses
  • Eosinophils: defence against multicellular parasites (worms)
  • NK cells: kills all abnormal host cells (viral infected/malignant)
  • Dendritic cells: present microbial antigens to T cells (acquired immunity)
24
Q

What is opsonisation?

A

Opsonisation is the process that involves coating microbial surfaces with opsonin proteins leading to enhanced attachment of phagocytes and clearance of microbes and help clumping of microbes

eg igG antibody

25
Q

Identify the structures involved in pathogen recognition

A
  • Microbial structures: pathogen-associated molecular patterns (PAMPS) – carbohydrates eg peptoglycan, lipids, proteins, nucleic acids. This is recognised by the phagocytes
  • Phagocytes: pathogen recogniton receptors (PRRs) interact with the PAMPS
26
Q

In 7 steps, outline the process of phagocytosis

A

⇒ Recognition (PAMPS and opsonins)

⇒ Chemotaxis and adherence of the microbe to the phagocyte

⇒ Ingestion of the microbe by the phagocytes

⇒ Formation of phagosome

⇒ Fusion with lysosome to form a phagolysosome

⇒ Digestion of ingested microbe by enzymes

⇒ Discharge of waste materials

27
Q

Identify and describe the 2 different phagocytic intracellular killing mechanisms

A
  • Oxygen-dependent pathway (respiratory burst): toxic O2 products for pathogens – peroxide, hydroxyl radical, nitric oxide
  • Oxygen-independent pathways: lactoferrin and transferrin, proteolytic and hydrolytic enzymes
28
Q

The complement pathway consist of 20 serum proteins.

Identify and describe the 2 activating pathways

A
  • Alternate pathway – initiated by cell surface microbial constituents e.g. endotoxins on E.coli
  • MBL pathway – initiated when MBL binds to mannose containing residues of proteins found on many microbes e.g. Candida albicans

Classical - antibody-antigen complex

29
Q

Describe the antimicrobial actions in the alternate pathway of the complement system

A
  • C3a and C5a: recruitment of phagocytes
  • C3b-C4b: opsonisation of pathogens
  • C5-C9: killing of pathogens, membrane attack complex
30
Q

Provide 4 examples of normal flora that inhabit the skin

A
  • Staphylococcus aureus (cellulitis)
  • Staphylococcus epidermidis
  • Streptococcus pyogenes (cellulitis)
  • Candida albicans (candida)
31
Q

Provide 3 examples of the normal flora which live in the nasopharynx

A
  • Streptococcus pneumoniae
  • Neisseria meningitidis
  • Haemophilus species
32
Q

CRP

A
  • recognises self and foreign molecules
  • generates pro - iflammatory cytokines to activate complement system and acute phase response (vascular changes)
  • acts on opsonin for pathogens and makes pathogens more suscpetible to phagocytosis
  • produced in the liver
33
Q

cellulitis

A
  • acute inflammation
  • treated with antibiotics
34
Q

candida

A

caused by yeast candida which is normal body flora

infections occur when bacterial flora are eliminated

most HIV positive individuals get it

35
Q

what is the complement system

A
  • second stage of the innate immune response where pathogen slips through physical and chemical barriers

mediates activation of leukocytes attracting them to site of infection where they can directly attack the organism

36
Q

opassification

A

areas on the x ray that are white and should be black

37
Q

acute phase response

A
  • produces CRP
  • vasodialation
38
Q

endothemlium system

A

allows adhesion and migration of stimulated immune cells

becomes porous to large molecules such as proteins resulting in tissue odema

39
Q

coagulation system

A

increase in procoagulant factors

seen as clotting in some sites or bleeding at others

40
Q

multiple organ dysfunction

A
  • relative and absolute hypovolemia compounded due to reduced left ventricular contractility to produce hypotension

-

41
Q

how does odema cause impared tissue 02 delivery

A

o2 has a greater distance to travel due to the odema

42
Q

sepsis 6

A
  1. respiratory rate
  2. o2 saturations
  3. temp
  4. systolic blood pressure
  5. pulse rate
  6. level of consciousness
43
Q

neisseria meningitis

A

gram negative found within neutrophils

surrounded by a polysaccharide capsule

44
Q

clinical features of neisseria meinigitis

A

in meningitis the bacteria attach to the meningeal lining and cause intense inflammation = headache

  • fever
  • sepsis
  • DIC (coagulation, lots of clots form, platelet count becomes low)
  • rash
45
Q

petechiae

A

discerete lesions 1-2mm in diameter due to low platelet and tiny bleed into the skin

rash doesnt blanch when pressure is applied (doesnt go yellow)

46
Q

ECCHYMOSES

A

petechial lesions can clump together and form larger lesions and are secondary to secondary hemmorage

47
Q

necrosis

A

death of tissue

vascular damage and lack of blood and 02 lots of clots in small vessel and haemorrhage

48
Q

treatment of neisseria meningitidis

A
  • early recognition
  • early administration of antibiotics
  • urgent invesitgation
  • supportive care
  • prevention
49
Q

properties of the innate immune system

A

non - specific

pretects body from non-self cells

  1. physical/chemical barriers etc
  2. complement system
  3. inflammation (red, heat, swelling pain) = contains and neutralises threat
50
Q

cytokines

A
  • key link between adaptive and innate immune response
  • TNFa/IL-1/IL-6
  • increase CRP activating complement pathways
  • neutrophil mobilisation
  • vasodialation
  • increase body temp
51
Q

TNFa

A
  • main cytokine
  • triggers inflammatory response (tells liver to release CRP)
  • increase permeability of blood vessel

= more movement of immunoglobins and phagocytes

-activates T/B cells and immunoglobulin production

52
Q

IL-1/IL-6

A
  • IL-1 produced mainly by macrophages and activated T/B cells
  • IL-6 produced by macrophages and monocytes, activates B cells, hepatocyte - stimulating factor => increase inflammatory and immune response
53
Q

problems start to arise when phagocytosis is reduced to

A
  • decrease in spleen function
  • decrease in neutrophil number
  • decrease in neutrophil function
54
Q

summary

A
55
Q

what is the quickest investigation that can be done to test for bacteria?

A

gram stain (within 6 hours)

SA infections (19 decks)

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