Determinant of Pathogenicity Flashcards

1
Q

what are the important stages for pathogens

A

maintain reservoir, transport/entry into host, adhere and invade cells/tissues, multiply in host, evade host defence, damage host, return to reservoir

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2
Q

what is the definition of pathogenicity

A

the ability of an organism to cause disease

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3
Q

what is the definition of virulence

A

the degree of harm caused by a microorganism

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4
Q

what does virulence depend on

A

infectivity, invasiveness and degree of damage

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5
Q

what are some virulence factors

A

adhesion, invasion, evasion of host defence, obtaining nutrients from the host, toxicity

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6
Q

what is ID50

A

infectious dose;

ID50 is dose required to infect 50% of hosts

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7
Q

what is LD50

A

lethal dose; LD50 is dose required to kill 50% of hosts

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8
Q

what is direct transmission

A

host-to-host transmission of disease

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9
Q

what is indirect transmission

A

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

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10
Q

what are some direct transmission routes

A

respiratory, body contact, faecal-oral, body fluids, vertical transmission

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11
Q

what pathogen uses respiratory direct transmission route

A

myobacterium tuberculosis

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12
Q

what pathogens use body contact direct transmission route

A

STDs, skin infections, staph.aureus through damaged skin

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13
Q

what pathogens use the faecal-oral route of direct transmission

A

GIT pathogens like salmonella enterica

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14
Q

what pathogens use the body fluid route of direct transmission

A

hepatitis, HIV

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15
Q

what pathogens use the vertical direct transmission route

A

parenteral/perinatal/postnatal

germline (through viral DNA, like certain types of leukemia)

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16
Q

what are some vehicles for indirect transmission

A

soil, contaminated water, contaminated food, fomites

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17
Q

what are fomites

A

inanimate objects that act as vehicles for indirect transmission

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18
Q

what are some vectors for indirect transmission

A

plasmodium, warm-blooded animals, rat flea

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19
Q

what are some portals of entry

A

skin, mucosal surfaces

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20
Q

what are some bacterial adhesins

A

proteins, polysaccharides

they help the bacteria adhere to the host’s target site

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21
Q

what are the host factors for adhesion

A

protein-protein interactions
protein-carbohydrate interactions
receptors like membrane protiens, glycolipids, extracellular matrix proteins (collagen, fibronectin)

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22
Q

how do e.coli cells cause UTIs

A

P-pili or type 1 pili bind to sugar moieties (globobiose mannose) of glycolipids on epithelial cells lining urinary tract
e.coli bind to epithelial cells in the bladder

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23
Q

what is extracellular invasion

A

when barriers of tissues are broken down

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24
Q

what is intracellular invasion

A

when microbes penetrate cells and survive intracellularly

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25
Q

what is meant by vertical transmission routes

A

from mother to child

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26
Q

what is the flagellum used for

A

motility in bacterial adhesion

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27
Q

what is the fimbrium used for

A

attachment/binding during adhesion

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28
Q

where can obligate intracellular bacteria survive

A

only inside cells

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29
Q

what is an advantage of extracellular invasion

A

allows access to niches in tissue that aid in proliferation and spreading

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30
Q

how is extracellular invasion achieved

A

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

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31
Q

what is the action of the hyaluronidase enzyme

A

hydrolyses hyaluronan

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32
Q

which organisms utilise the hyaluronidase enzyme

A

streptococci, staphylococci, clostridia

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33
Q

what is the action of the enzyme collagenase

A

degrades collagen

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34
Q

which organisms utilise the collagenase enzyme

A

clostridium perfringens

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35
Q

what is the action of the enzyme haemolysin

A

lyses erythrocytes and other cells

36
Q

which organisms utilise the enzyme haemolysin

A

staphylococci, streptococci, e.coli

37
Q

what is the action of the enzyme streptokinase

A

digests fibrin clots

38
Q

which organisms utilise the enzyme streptokinase

A

staphylococci, streptococci

39
Q

how do bacteria utilise intracellular invasion

A

some use it to survive, others use it as a means of proliferation or spreading

40
Q

what are some methods of intracellular invasion

A

phagocytic cells invading through phagocytosis

non-phagocytic cells invaded using systems that induce a phagocytosis-like process

41
Q

what are the five steps of phagocytosis

A
  1. phagocyte encounters bacterium that binds to cell membrane
  2. phagocyte uses cytoskeleton to push its cell membrane around the bacterium, creating a large vesicle (phagosome)
  3. phagosome containing bacterium separates from the cell membrane and moves into the cytoplasm
  4. phagosome fuses with lysosomes containing digestive enzymes
  5. bacterium is killed and digested within the vesicle
42
Q

what happens to bacteria that survive phagocytosis

A

they reside in the phagolysosome
they reside in an unfused phagosome
they destroy or escape from the phagosome and live in the cytosol

43
Q

what happens during invasion of non-phagocytic cells

A
  1. bacterial proteins recruit host proteins to induce pagocytosis
    similar to gram-negative secretion system used by salmonella or pseudonomas
  2. invasion proteins injected
  3. activate host signalling and recruit actin
44
Q

what happens during invasion - extracellular summary

A

adhered bacterial pathogen combines with proteases and glycanases to extracellularly invade host cells

45
Q

what happens during invasion - intracellular summary

A

adhered bacterial pathogen invades host using phagocytosis or induced uptake
intracellular residence in phagolysosome, unfused phagosome or host-cell cytosol

46
Q

how are biofilms formed

A

bacteria attach to a surface, grow and become enveloped in a matrix

47
Q

what is high bacterial density

A

production of virulence factors through quorum sensing

48
Q

what is the function of a biofilm

A

to protect from phagocytosis, antibiotcs and disinfectants

49
Q

what is the main nutrient that is limiting for bacteria in the host

A

iron

in aerobic conditions, it is oxidised in ferric form and has low solubility

50
Q

what proteins include iron complexes and are found in the body

A

transferrin, lactoferrin, ferritin, haemoglobin

51
Q

how do bacteria take in iron

A

direct contact using cell surface proteins
by secreting small compounds (siderophores) with high affinity for iron that capture iron from host proteins or insoluble ferric salts

52
Q

what cell surface proteins are used in bacterial uptake of iron

A

transferrin binding protein, haemoglobin binding protein

53
Q

what are siderophores

A

they are produced when iron concentration is low, high affinity for iron, compete for free or bound iron, transport iron into cell

54
Q

what are defence mechanisms used to evade host defence

A

physical barriers, innate immune system, adaptive immune system

55
Q

what avoidance strategies are used by bacteria to evade host defence

A

evade complement, resist phagocytosis, intracellular survival, evade host antibody response

56
Q

how do bacterial capsules help them evade complement

A

they have thick polysaccharide layers around the cells which prevents complete activation by host cells

57
Q

how to LPS O-antigens on bacterial cells help them evade complement

A

the elongated O chains prevent complement activation

58
Q

how do bacteria prevent effective contact with phagocytes

A

using biofilms, capsules or specific proteins

59
Q

how do bacteria affect phagocyte migration

A

s. pyogenes peptidase cleaves complement factor C5a

60
Q

how do bacteria destroy phagocytes

A

using toxins such as leukocidins

61
Q

what is a phagolysosome

A

a phagocyte fused with a lysosome

62
Q

how do phagocytosed bacteria survive

A

they prevent formation of phagolysosomes and destroy or escape from the phagosome and live in cytosol

63
Q

how do bacteria evade the host-antibody response

A

by binding to host proteins like fibronectin or albumin
this means the body will not detect them as foreign
they also produce surface proteins which bind antibodies ‘backwards’ staph aureus reverses protein A to prevent opsonisation

64
Q

what is opsonisation

A

the attachment of antibodies to a foreign body

65
Q

what is anti-opsonisation

A

antibodies are bound with the antigen binding site facing outwards, the bacteria is not identified as foreign

66
Q

what is the body response to bacterial toxins

A

immediate host damage and induced inflammation

67
Q

what are exotoxins

A

actively secreted during growth

68
Q

what are endotoxins

A

structural parts of bacteria only released during bacterial lysis

69
Q

what are toxoids

A

inactive or low activity and used for vaccinations

70
Q

how are exotoxins ingested

A

food poisoning

no adherance/growth/colonisation of the pathogen in the host

71
Q

how are exotoxins produced

A

colonised after infection

damage can be local or toxin can spread through blood

72
Q

what cells do host-sit specific exotoxins target

A

neurotoxins, enterotoxins, cytotoxin

73
Q

what do membrane disrupting toxins target

A

leukicidins, haemolysins, phospholipidases

74
Q

what do superantigen type exotoxins do

A

stimulate T cells to release cytokines

75
Q

how does a pore forming toxin work

A

exotoxin forms a pore in the cell membrane, an uncontrollable entry of water then causes the cell to lyse

76
Q

how does bilayer disruption work

A

phospholipase exotoxin causes disruption of the bilayer which causes cell lysis

77
Q

what is the effect of superantigens

A

massive non-specific inflammatory response

leads to epitelial damage, circulatory shock, multi-organ failure

78
Q

what bacteria produce superantigens

A

staphalococci and steptacocci

79
Q

what are features of the lipid A component of LPS in endotoxins

A

heat stable, only released when bacteria lyse, induces fever, initiates complement and clotting cascades, toxic shock
antibiotic treatment may lead to release of LPS

80
Q

where are lipid A components of LPS in endotoxins found

A

in the outer membrane of gram-negative bacteria

81
Q

what does the bacterial Fur protein regulate

A

iron

82
Q

what is the Fur protein response to high levels of iron

A

repression or ‘switching off’ of genes

83
Q

what is the Fur protein response to low levels of iron

A

de-repression or ‘switching on’ of genes

84
Q

what is a quorum

A

minimal number of cells before virulence factors are produced

85
Q

what does quorum sensing involve

A

two components:

  1. autoinducer - small diffusable molecule
  2. R protein - activates transcription of genes when R protein binds to autoinducer; binding only occurs at high concentrations; high concentration of autoinducer only at high cell density
86
Q

can quorum sensing be effective for biofilms

A

biofilms have high cell density; biofilm formation often leads to expression of virulence factors through quorum sensing