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infection and immunity > Determinants of infectious diseases > Flashcards

Determinants of infectious diseases Flashcards

1
Q

reservoir

A

where pathogens normally live

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2
Q

course of infection

A

[reservoir] colonisation -> invasion -> proliferation -> transmission [host]

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3
Q

pathogenicity

A

ability of organism to cause disease (either does or doesn’t)

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4
Q

virulence

A

degree of harm caused by microorganism

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5
Q

what does virulence depend on?

A

infectivity, invasiveness and degree of damage

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6
Q

virulence factors

A

adhesion

invasion

evasion of host defense

obtaining nutrients from host

toxicity

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7
Q

how to measure virulence

A
  1. infectious dose (ID50)
    = dose to infect 50% of hosts
  2. lethal dose (LD50)
    = dose to kill 50% of hosts
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8
Q

what factors determine whether an infection will lead to disease?

A

virulence

no. of bacteria

host resistance

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9
Q

direct transmission

A

host-to-host transmission

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10
Q

indirect transmission

A

host-to-host transmission - facilitated by living or inanimate objects

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11
Q

direct transmission routes

A

[respiratory route]

e.g. mycobacterium tuberculosis

[body contract]

-direct contact or body fluids
-HIV, STDs, skin infections

[faecal/oral]

  • GIT pathogens

[vertical transmission]

-prenatal/perinatal/postnatal
-germline

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12
Q

indirect transmission routes

A

soil

contaminated water

contaminated food

inanimate objects (beddings, toys, surgical instruments)

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13
Q

adhesion

A

adhere to host cells or tissues to colonise

survive in host environment

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14
Q

bacterial adhesins

A

[type of virulence factor]

cell surface components

interact with receptors on cell surface of host
-> protein-protein interactions
-> protein-carbohydrate interactions

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15
Q

adhesins receptors

A

membrane proteins

glycolipids

extracellular matrix proteins (collagen, fibronectin)

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16
Q

extracellular invasions

A

barriers of tissues broken down

production of enzymes attack extracellular matrix, degrade carbohydrate-protein complexes between cells and disrupt cell surface

disrupts fibrin meshwork (degrades blood clot + helps pathogens spread)

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17
Q

what type of enzymes are involved in extracellular invasion?

A

digestive enzymes

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18
Q

intracellular invasions

A

microbes penetrate cells + survive intracellularly

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19
Q

facultative intracellular

A

[proliferation/spreading]

phagocytic cells invaded through phagocytosis

non-phagocytic cells invaded using systems that induce phagocytic-like process
-> inject proteins into cells + control cytoskeleton = host cells behaves like a phagocyte

20
Q

surviving phagocytosis

A

phagocytic - survive lysosome conditions

reside in phagolysosome
reside in unfused phagosome.

destroy or escape from phagosome + live in cytosol

21
Q

invading non-phagocytic cells

A

bacterial proteins recruit host proteins to induce phagocytosis

e.g. via secretion system used by gram -ve bacteria

invasion proteins injected

activate host signalling and recruit actin

22
Q

growth and colonisation

A

in blood (septicaemia), tissues or intracellularly

often involves formation of biofilms -> found frequently on medical implements

23
Q

biofilms

A

[provide survival sites for bacteria]

bacteria attach to surface, grow and become enveloped in matrix

protects from phagocytosis, antibiotics + disinfectants

24
Q

microbial nutrition

A

main limiting nutrient = IRON

in aerobic conditions, iron is oxidised in ferric form (FeIII) - v. low solubility

most iron is complexed to proteins

25
Q

acquiring iron

A

uptake of iron or iron complexes

direct contact using cell surface proteins (TBP) and haemoglobin binding protein (HBP)

secreting small compounds (siderophores) with v. high affinity for iron that capture from host proteins or insoluble ferric salts

26
Q

siderophores

A

produced when iron conc. = low

low Mr = high affinity for iron

compete for free or bound iron

transport iron into cell

27
Q

evading host defence - defence mechanisms

A

physical barriers

innate immune system

adaptive immune system

28
Q

avoidance strategies - evade complement

A

[capsules]

thick polysaccharide layer around cells

prevents complement activation

[LPS O-antigen]

elongated O changes prevent complement activation

28
Q

avoidance strategies - resisting phagocytosis

A
  1. prevent effective contact with phagocyte
  2. affect phagocyte migration
  3. destroy phagocytes - using toxins such as leukocidins
29
Q

avoidance strategies - survival inside cells

A

-> survive phagolysosome
-> prevent formation of phagolysosome
-> destroy or escape from phagosome + live in cytosol

some pathogens invade non-phagocytic cells

30
Q

avoidance strategies - evade host-antibody response

A

bind host proteins -> not detected as foreign

produce surface proteins which bond antibodies backwards

31
Q

what do toxins do?

A

[products of bacteria]

cause immediate host damage

induce inflammation

32
Q

exotoxin

A

actively secreted during growth

33
Q

endotoxin

A

structural part of bacteria - only released during bacterial lysis

34
Q

toxoid

A

inactive or very low activity

used for vaccination

35
Q

transmission of exotoxins

A

ingestion of pre-formed exotoxin
-> food poisoning
-> no adherence/colonisation/growth of pathogen in host

colonisation followed by exotoxin production
-> infection of tissue followed by toxin production
-> damage can be local or toxin can spread through blood

36
Q

what are exotoxins?

A

usually proteins (heat-labile)

can be v. powerful

37
Q

types of exotoxins

A
  1. host-site specific exotoxins - affect specific cells (neurotoxins, enterotoxins)
  2. membrane-disrupting toxins (leukocidins, haemolysins, phospholipases)
  3. super-antigen type (stimulate T cells to release cytokines)
38
Q

membrane-disrupting toxins - mechanism of action

A
  1. exotoxin forms pore in membrane
  2. cell lysis - uncontrolled entry of water causes cell to swell and burst
39
Q

superantigens

A

produced by straphylococci/streptococci

staphylococcal toxic shock syndrome toxin (TSST) + 7 other enterotoxins

strep - 6 pyrogenic exotoxins

causes massive non-specific inflammatory response

leads to endothelial damage, circulatory shock + multi-organ failure

40
Q

endotoxin - lipid A component of LPS

A

heat stable

in outer membrane of gram -ve bacteria

released only when bacteria burst open (=lyse)

induces fever (pyrogenic), initiates complement + clotting cascades; toxic shock

antibiotic treatment may lead to release of LPS -> can lead to septic shock in patients treated for severe infections

41
Q

iron regulation - fur protein

A

HIGH IRON - repression of genes (expression switched off)

LOW IRON - de-repression of genes (expression switched on)

42
Q

quorum sensing

A

many pathogenic bacteria only produce virulence factors until quorum (min. number) of cells is present

43
Q

cell-cell communication with 2 components

A
  1. autoinducer (AI) - small diffusable molecule
  2. R-protein - activates transcription of genes when R protein binds to AI; binding only occurs at high concentration AI = only at high cell density
44
Q

biofilms + cell density

A

= high

biofilm formation leads to expression of virulence factors through quorum sensing

infection and immunity (17 decks)

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