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Determinant of Pathogenicity Flashcards

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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
what is meant by vertical transmission routes
from mother to child
26
what is the flagellum used for
motility in bacterial adhesion
27
what is the fimbrium used for
attachment/binding during adhesion
28
where can obligate intracellular bacteria survive
only inside cells
29
what is an advantage of extracellular invasion
allows access to niches in tissue that aid in proliferation and spreading
30
how is extracellular invasion achieved
through production of enzymes that attack the extracellular matrix, degrade carbohydrate-protein complexes between cells and disrupt cell surface
31
what is the action of the hyaluronidase enzyme
hydrolyses hyaluronan
32
which organisms utilise the hyaluronidase enzyme
streptococci, staphylococci, clostridia
33
what is the action of the enzyme collagenase
degrades collagen
34
which organisms utilise the collagenase enzyme
clostridium perfringens
35
what is the action of the enzyme haemolysin
lyses erythrocytes and other cells
36
which organisms utilise the enzyme haemolysin
staphylococci, streptococci, e.coli
37
what is the action of the enzyme streptokinase
digests fibrin clots
38
which organisms utilise the enzyme streptokinase
staphylococci, streptococci
39
how do bacteria utilise intracellular invasion
some use it to survive, others use it as a means of proliferation or spreading
40
what are some methods of intracellular invasion
phagocytic cells invading through phagocytosis | non-phagocytic cells invaded using systems that induce a phagocytosis-like process
41
what are the five steps of phagocytosis
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
what happens to bacteria that survive phagocytosis
they reside in the phagolysosome they reside in an unfused phagosome they destroy or escape from the phagosome and live in the cytosol
43
what happens during invasion of non-phagocytic cells
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
what happens during invasion - extracellular summary
adhered bacterial pathogen combines with proteases and glycanases to extracellularly invade host cells
45
what happens during invasion - intracellular summary
adhered bacterial pathogen invades host using phagocytosis or induced uptake intracellular residence in phagolysosome, unfused phagosome or host-cell cytosol
46
how are biofilms formed
bacteria attach to a surface, grow and become enveloped in a matrix
47
what is high bacterial density
production of virulence factors through quorum sensing
48
what is the function of a biofilm
to protect from phagocytosis, antibiotcs and disinfectants
49
what is the main nutrient that is limiting for bacteria in the host
iron | in aerobic conditions, it is oxidised in ferric form and has low solubility
50
what proteins include iron complexes and are found in the body
transferrin, lactoferrin, ferritin, haemoglobin
51
how do bacteria take in iron
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
what cell surface proteins are used in bacterial uptake of iron
transferrin binding protein, haemoglobin binding protein
53
what are siderophores
they are produced when iron concentration is low, high affinity for iron, compete for free or bound iron, transport iron into cell
54
what are defence mechanisms used to evade host defence
physical barriers, innate immune system, adaptive immune system
55
what avoidance strategies are used by bacteria to evade host defence
evade complement, resist phagocytosis, intracellular survival, evade host antibody response
56
how do bacterial capsules help them evade complement
they have thick polysaccharide layers around the cells which prevents complete activation by host cells
57
how to LPS O-antigens on bacterial cells help them evade complement
the elongated O chains prevent complement activation
58
how do bacteria prevent effective contact with phagocytes
using biofilms, capsules or specific proteins
59
how do bacteria affect phagocyte migration
s. pyogenes peptidase cleaves complement factor C5a
60
how do bacteria destroy phagocytes
using toxins such as leukocidins
61
what is a phagolysosome
a phagocyte fused with a lysosome
62
how do phagocytosed bacteria survive
they prevent formation of phagolysosomes and destroy or escape from the phagosome and live in cytosol
63
how do bacteria evade the host-antibody response
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
what is opsonisation
the attachment of antibodies to a foreign body
65
what is anti-opsonisation
antibodies are bound with the antigen binding site facing outwards, the bacteria is not identified as foreign
66
what is the body response to bacterial toxins
immediate host damage and induced inflammation
67
what are exotoxins
actively secreted during growth
68
what are endotoxins
structural parts of bacteria only released during bacterial lysis
69
what are toxoids
inactive or low activity and used for vaccinations
70
how are exotoxins ingested
food poisoning | no adherance/growth/colonisation of the pathogen in the host
71
how are exotoxins produced
colonised after infection | damage can be local or toxin can spread through blood
72
what cells do host-sit specific exotoxins target
neurotoxins, enterotoxins, cytotoxin
73
what do membrane disrupting toxins target
leukicidins, haemolysins, phospholipidases
74
what do superantigen type exotoxins do
stimulate T cells to release cytokines
75
how does a pore forming toxin work
exotoxin forms a pore in the cell membrane, an uncontrollable entry of water then causes the cell to lyse
76
how does bilayer disruption work
phospholipase exotoxin causes disruption of the bilayer which causes cell lysis
77
what is the effect of superantigens
massive non-specific inflammatory response | leads to epitelial damage, circulatory shock, multi-organ failure
78
what bacteria produce superantigens
staphalococci and steptacocci
79
what are features of the lipid A component of LPS in endotoxins
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
where are lipid A components of LPS in endotoxins found
in the outer membrane of gram-negative bacteria
81
what does the bacterial Fur protein regulate
iron
82
what is the Fur protein response to high levels of iron
repression or 'switching off' of genes
83
what is the Fur protein response to low levels of iron
de-repression or 'switching on' of genes
84
what is a quorum
minimal number of cells before virulence factors are produced
85
what does quorum sensing involve
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
can quorum sensing be effective for biofilms
biofilms have high cell density; biofilm formation often leads to expression of virulence factors through quorum sensing

Infection & Immunity (22 decks)

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