lecture 4 bacterial pathogenicity Flashcards

1
Q

what are the events involved in the establishment of bacterial infaction

A
|  > reservoir v
|  >  transport to host v
| adhrence&colonisation v
^tissue damage  <  invasion
                              of tissues
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2
Q

what are some key bacterial factors involved in host colonisation and tissue damage

A

competition for nutrients
surface attachment sites

(in)direct effects of bacterial pathogens
induction of autoimmune response

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3
Q

pathogen

A

organism that causes disease by impairing or interfering with the normal physiological activities of the host

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4
Q

what are oppertunistic pathogens

A

only cause serious disease when host defenses are impared

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5
Q

what are reservoirs

A

where the pathogen lives and reproduces before it is in a host for example humans animals environment like soil

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6
Q

how are pathogens transferred between hosts

A

direct
indirect
vehicles

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7
Q

host

A

organism which supports the growth of viruses, bacteria and other parasites

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8
Q

infection

A

bacteria persist in host without nessisarily causing damage

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9
Q

what is colonisation

A

establishment of a stable population in the host

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10
Q

what is adherence

A

to overcome flushing mechanisms bacteria must adhere to host cell surfaces(or other sufaces)

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11
Q

what is the role of iron

A

essential for growth
tissues don’t have enough, more must be acquired
bacteria have high affinity iron uptake systems eg siderophores n direct binding

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12
Q

barriers to infection in the body

A
flora competes
eyes (lysosomes)
skin antimicrobials n flora
mucus in lungs trachea
stomach pH
flushing of urinary tract
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13
Q

what is invasion

A

penetrate into, through or between cells = invasion of host cells & tissues

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14
Q

what are antibodies

A

they are produced by b cells and complement the microbe. they attract phagocytes and aid engulfment. they neutralise toxins

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15
Q

how do pathogens avoid antibodies and avoid complement

A
capsules
antigenic variation
degredation of antibodies
capsules
lipopolysaccharides (gram negatives)
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16
Q

how do bacteria resist phagocytes and macrophages

A

producing structures that prevent effective contact eg capsules, proteins

survival inside engulfed phagocytic cells

17
Q

how do bacteria resist phagocytes and macrophages

A

producing structures that prevent effective contact eg capsules, proteins

survival inside engulfed phagocytic cells. can kill from inside

18
Q

what are endotoxins

A

action is indirect: activates many host systems that cause damage
gram -ve only

19
Q

what are exotoxins

A

act on specific target eg protein synthesis

gram +ve and -ve

20
Q

adhesins example

A

pili
slime capsules
flagella
lipotechioic acids

21
Q

host receptors include

A

blood group antigens

extracellular matrix proteins eg collagen, fibroconnectin

22
Q

advantages of invasion

A

aid in survival
spread to other body sites
required for colonisation

23
Q

how how is invasion accomplishes

A

lytic compounds that attack host tissue

24
Q

invasivness determined by

A

evasion of host defenses

25
Q

protein exo or endo

A

exo

26
Q

lipopolysaccharide exo or endo

A

endo

27
Q

toxin secreted by living bacteria exo or endo

A

exo

28
Q

toxin part of call membrane released on cell lysis exo or endo

A

endo

29
Q

toxin heat labile (easy to change) endo or exo

A

exo

30
Q

toxin heat stable endo or exo

A

ENDO

31
Q

toxin highly immunogenic and potentially lethal endo or exo

A

exo

32
Q

toxin weakly immunogenic and lethal at high concs. only

A

endo

33
Q

how can one become exposed to toxins

A

ingestion
colonisation of mucosal surface
colonisation of wound followed by toxin production

34
Q

exotoxin examples

A

tetanus toxin synapse function

diphtheria toxin inhibits mammalian protein synthesis

35
Q

exotoxin examples

A

tetanus toxin synapse function

diphtheria toxin inhibits mammalian protein synthesis

36
Q

endotoxin specificity

A

Generally considered less potent/specific than exotoxins

37
Q

what is the toxic part of endotoxins

A

Lipid A is the toxic part but the O-polysaccharide part affects the immunogenicity and hence the virulence.Lipid A binds to immune system receptors and stimulates the immune system leading to the physical effects

38
Q

exit routes

A

passive

faeces, urine, saliva,