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Bacterial Pathogens Flashcards

1
Q

what is the function of bacterial toxins?

A

to cause symptoms of disease that are beneficial to the pathogen and toxic to human cells.

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2
Q

what is a cytotoxin?

A

toxin that affects a range of cell types

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3
Q

what type of bacteria has lipopolysaccharide?

A

Gram negative

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4
Q

what are the main structural components of lipopolysaccharide?

A

lipid A, core polysaccharide, up to 40 O antigen repeats

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5
Q

what part of lipopolysaccharide structure is associated with toxicity?

A

Lipid A

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6
Q

what part of lipopolysaccharide structure is associated with immunogenicity?

A

polysaccharide components

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7
Q

what illness does lipopolysaccharide cause?

A

septic shock

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8
Q

what is the cause of death in septic shock patients?

A

failure of organs such as the heart, lungs, brain and kidneys

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9
Q

what is the first stage of septic shock?

A

systemic inflammatory response syndrome - temperature over 38 or under 36ºC and higher than normal heart and respiratory rate, unnaturally high or low neutrophil count

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10
Q

what disease does Bordatella pertussis cause?

A

Whooping cough

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11
Q

during what stage of growth can pathogens shed part of their cell wall?

A

logarithmic phase

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12
Q

what is the main toxin in whooping cough and what kind of molecule is it?

A

Bordatella tracheal cytotoxin (TCT). low molecular weight glycopeptide from the cell wall peptidoglycan

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13
Q

what is the impact of bordatella tracheal cytotoxin (TCT) on the body?

A

ciliostasis - cilliary movement is stopped, removal of ciliated cells, causing violent coughing episodes as this becomes the only way to remove inflammatory debris, mucus and bacteria. release of IL-1.

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14
Q

what is the main toxin in Mycobacterium ulcerans infection and what kind of molecule is it?

A

mycolactone, polyketide derived macrolites produced as secondary metabolites.

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15
Q

what is the disease caused by Mycobacterium ulcerans?

A

Buruli ulcer - progressive necrotic lesions that can cover 15% of the body

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16
Q

how are mycolactones encoded in the bacterial dna?

A

they are encoded on a 174kb plasmid which encodes 3 polyketide synthases (MLSA1, MLSA2, MLSB) and 3 polyketide modifying enzymes. The MLSA domains encode the core of the molecule and the MLSB domain encodes the side chain.

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17
Q

what is the histopathology of a buruli ulcer?

A

a tissue punch biopsy will show an intact dermis and necrotic subcutis with fat cell ghosts and edema. the epidermis will show epidermal hyperplasia and a band of extracellular ZN positive acid-fast bacteria is present in the deep layer of the necrotic subcutis.

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18
Q

how does mycolactone suppress the host immune response?

A

prevents protein translocation into the ER, therefore blocking production of secretory proteins like TNFa as they then get degraded in the cytosol by the ubiquitin:proteasome system.

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19
Q

how does mycolactone produce an analgesic effect?

A

it targets type 2 angiotensin II receptors, disrupting neuronal cells

20
Q

how does mycolactone impact actin assembly and the cell matrix?

A

it binds to cytosolic WASP/N-WASP complexes after diffusion through the plasma membrane, causing uncontrolled actin assembly and defective cell-matrix adhesion

21
Q

what is the definition of a type I toxin?

A

a toxin that does not enter the cell.

22
Q

what bacterium produces toxic shock syndrome toxin?

A

Staphylococcus aureus

23
Q

what type of toxin is toxic shock syndrome toxin?

A

type I superantigen

24
Q

how do superantigens cause disease?

A

it binds to MHC-II in macrophages and T cell receptors which bind to MHC. as they are not processed by proteolytic digestion and bind directly to MHC-II. this causes many more macrophage-T helper cell pairs to form than normal, causing overproduction of inflammatory cytokines and symptoms of nausea, malaise, vomiting and fever

25
what is the function of type II toxins?
disrupt the plasma membrane, lysing the host cell to destroy it or escape the phagosome by entering the host cell cytoplasm
26
what are a-pore forming toxins?
highly a-helical toxins that form pores via helices eg the colicin family
27
what are b-pore forming toxins?
from a b-barrel in the membrane eg the haemolysin family
28
how do pore-forming toxins enter the membrane and create pores?
they bind to the membrane by interacting with protein receptors or specific interactions with lipids, then undergo the oligomerisation process either at the membrane surface, forming a pre-pore which undergoes conformational change leading to membrane insertion, or by insertion occurring concomitantly with an oligomerisation mechanism, leading to a partially formed but active pore or a complete pore
29
what is the function of phospholipases?
to destroy the integrity of host cell lipid membranes by removing the the lipid head group or cleaving at another site, destabilising the membrane and causing cell lysis
30
what is an example of an infection that uses phopholipase and what is the impact on the host tissue?
gangrene, caused by Clostridium perfringens causes host tissue damage by hydrolysing the lipid lecithin in mammalian cell membranes
31
what are type III toxins?
toxins containing an enzymatic (A) and binding (B) domain, where the A domain is translocated to the host cell cytoplasm, often being cleaved from the B subunit by proteolytic cleavage
32
what toxins are produced by Clostridium tetani and what disease does it cause
Tetanospasmin (TeNT) - a potent neurotoxin and tetanolysin - a haemolysin. Tetanus
33
how does TeNT travel though the body and enter the nervous system?
spreads through tissue spaces into lymphatic and vascular systems, targeting and entering motor nerve terminals at neuromuscular junctions then migrating through nerve trunks and entering the central nervous system by retrograde axonal transport using dyneins
34
what is the impact of TeNT at the neuromuscular junction?
it interferes with the release of inhibitory neurotransmitters across the synapse, causing uninhibited excitation of the neuroaxon, causing muscles to remain in a contracted state
35
what are the 6 main steps of the TeNT mechanism of action?
specific binding in periphery neurons, retrograde axonal transport to the CNS inhibitory interneurons, transcytosis from the axon into the inhibitory interneurons, temperature and pH mediated translocation of the light chain into the cytosol, reduction of the disulphide bond between the light and heavy chain, cleavage of synaptobrevin
36
what is the impact of TeNT cleavage of synaptobrevin?
blockage of inhibitory transmitter release causing constant muscle stimulation
37
what toxin is produced by Clostridium botulinum and what disease does it cause?
BoNT, botulism
38
what is the basic structure of BoNT and how is it activated?
contains a light chain catalytic domain, heavy chain translocation domain, and a receptor binding domain containing an N-terminal and C-terminal
39
how does BoNT move through the body and enter the nervous system?
travels through the blood and lymphatic system and fixes on cranial or periphery nerves and binds to receptor sites at the neuromuscular junction of the parasympathetic nerves
40
what is the BoNT mechanism of action?
binds to receptor sites at the neuromuscular junctions of the parasympathetic nerves and inhibits the release of acetylcholine at peripheral cholinergic synapses
41
what is the impact of BoNT on the host?
causes flaccid muscular paralysis
42
what toxins are produced by Vibrio cholerae and what disease does it cause?
cholera toxin (CTX), Zot, Ace. Cholera
43
what is the structure of cholera toxin?
5 subunit AB type exotoxin with and A subunit and 5 B monomer subunits arranged in a ring like conformation
44
what is the mechanism of action of cholera toxin?
colonises the small intestine by binding to the plasma membrane receptor of the jejunal intestinal epithelial cells, increases cAMP by activating adenylate cyclase, causing secretion of Cl-, HCO3- and water
45
what is the impact of cholera toxin on the host?
dehydration, electrolyte loss and watery diarrhea
46
what is a toxoid vaccine?
bacterial toxins inactivated with heat or chemicals which are no longer toxic but able to induce protective antibodies
47
what are some common toxoid vaccines?
diptheria and tetanus vaccines, and part of the DPT vaccine

cell signalling (11 decks)

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