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MBD/MI (Wothaya) > Bacterial Pathogens And Disease 1 - Exotoxins > Flashcards

Bacterial Pathogens And Disease 1 - Exotoxins Flashcards

1
Q

What do antibodies do?

A

Opsonise
Activate complement
Neutralise

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2
Q

What is a pathogen?

A

Microorganism capable of causing disease

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3
Q

What is pathogenicity?

A

The ability of an infectious agent to cause disease

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4
Q

What is virulence?

A

Quantitative ability of an agent to cause disease

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5
Q

What is toxigenicity?

A

The ability of a microorganism to produce a toxin that contributes to the development of a disease

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6
Q

What are the mechanisms of virulence?

A

Adherence
Biofilms
Invasion of host cells and tissues
Toxins

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7
Q

What are endotoxins?

A

Heterogeneous group of proteins produced and secreted by lining bacterial cells

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8
Q

What type of bacteria are endotoxins produced by?

A

Both gram positive and negative bacteria

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9
Q

What do endotoxins do?

A

Cause disease symptoms in host during disease

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10
Q

What are the selective advantages of exotoxins to bacteria?

A

Train immune response
Enable biofilm formation
Enable attachment to host cells
Escape from phagosomes

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11
Q

What do the advantages of exotoxins to bacteria allow for?

A

Colonisation, niche establishment and carriage

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12
Q

What do haemolytic toxins do?

A

Cause cells to lyse by forming pores

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13
Q

What do phenol soluable modulins (PSM) do?

A

Aggregate lipid bilayer of host cells causing lysis

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14
Q

What chromosomal genes encode C. Difficile?

A

Ted A and ted B

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15
Q

What toxins are encoded by plasmids?

A

Bacillus anthracis

Tetanus

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16
Q

What toxins are encoded by lysogenic bacteriophages?

A

Scarlett fever and diphtheria

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17
Q

What are the types of toxin classification?

A

Type I, II and III

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18
Q

What are type I toxins?

A

Membrane acting toxins

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19
Q

What are type II toxins?

A

Membrane damaging

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20
Q

What are type III toxins?

A

Intracellular

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21
Q

What are the issues with classifying toxins by activity?

A

Many toxins have more than one type of activity

The better understood the mechanism, the less sense it makes

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22
Q

Where do type I toxins act from?

A

Outside the cell

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23
Q

How do type I toxins work?

A

Interfere with host cell signalling by inappropriate activation of host cell receptors

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24
Q

What do target receptors include?

A

Guanylyl cyclase
Adenyl cyclase
Rho proteins
Ras proteins

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25
Q

What does guanylyl cyclase do?

A

Increase intracellular cGMP

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26
Q

What does adenyl cyclase do?

A

Increase intracellular cAMP

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27
Q

What is the mechanism by which the E. Coli stable heat toxin works?

A 
Increases cGMP
Increases chloride and bicarbonate transporters
Inhibits sodium reuptake
More water out of cells
Diarrhoea
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28
Q

How do type II toxins work?

A

Insert channels into the host cell membrane

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29
Q

What are some examples of beta sheet toxins?

A

S. Aureus alpha toxin, gamma toxin and PVL

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30
Q

What are some examples of alpha helix toxins?

A

Diphtheria

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31
Q

What are some examples of type II enzymal damage toxins?

A

S. Aureus, beta haemolysin and PSM

32
Q

What are the two types of type II toxins?

A

Receptor mediated

Receptor independant

33
Q

What are the two components of type III toxins?

34
Q

What are the B components of toxins responsible for?

A

Receptor binding and translocation

35
Q

What are the A components of type III toxins?

A

The toxigenic (enzymatic) bit

36
Q

What are the types of the A component?

A 
ADP-ribosyl transferases
Glucosyltransferase
Deaminase
Protease
Adenyl cyclase
37
Q

What are type III membrane acting toxins?

A

Intracellular

38
Q

What do type III toxins act like?

39
Q

What do type IV intracellular toxins act like?

A

A pump of toxins in the cell

40
Q

What are exotoxins able to induce?

A

Inflammatory cytokine release

41
Q

What are some examples of inflammatory cytokine release?

A

IL1, IL1 beta, TNF, IL6, interferon gamma and IL18

42
Q

What are the mechanisms of a superantigen?

A

Non-specific bridging or the MHC class 2 and T cell receptor leading to cytokine production

43
Q

How do superantigens cause non-specific bridging of MHCs?

A

Activation of the different inflammasome leading to IL1 beta and IL18 release

44
Q

What are examples of different inflammasomes?

A

S. Aureus toxin A and PVL

45
Q

How do superantigens work?

A

Antigen presenting cells -> lymph node -> T cell that processes the antigen that forms the specific antibody

46
Q

What are toxins inactivated by?

A

Heat, formaldehyde or gluteraldehyde

47
Q

What is an inactivated toxin called?

48
Q

What is a toxoid?

A

Inactive proteins that are still highly immunogenic

49
Q

What vaccines are based on toxoids?

A

Tetanus, diphtheria, pertussis

50
Q

What illnesses are treated by administering preformed antibodies?

A

Diphtheria cuboxin (horse antibodies)
Tetanus (pooled human Ig)
Botulism (human antibodies)

51
Q

What is the microbiology of clostridium difficile?

A 
Gram positive
Anaerobic
Spore forming
Toxin producing
Carried asymptomatically in the gut
52
Q

How many toxins does clostridium difficile produce?

53
Q

Where do you tend to get clostridium difficile?

54
Q

How is clostridium difficile spread?

A

Ingestion of spores that remain dormant in the environment

55
Q

What are the risk factors for clostridium difficile?

A

Antibiotic use
Age
Antacids
Prolonged hospital stay

56
Q

What is the relevance for antibiotics with clostridium difficile?

A

Disrupt the microbial ecosystem in the gut which allows clostridium difficile overgrowth causing disease

57
Q

What do antibiotics provide a competitive advantage to?

A

Spore forming macrobes over non-spore forming macrobes

58
Q

What antibiotics are especially bad at disrupting the microbial ecosystem?

A

Quinolones
Clindamycin
Cephalosporins

59
Q

What are the steps in Clostridium Difficile colonisation?

A

Toxins bind to specific host cell receptors are internalised
Endosome acidification allows for inc CPD activity
Pore formation in the endosome
GTD release from the endosome to the host cell cytoplasm
Rho GTPase inactivation by glucosylation

60
Q

What are the downstream cytopathic effects of Clostridium Difficile colonisation?

A

Cytoskeleton breakdown
Loss of cell-cell contacts
Increased epithelial permeability

61
Q

What are the downstream cytotoxic effects of Clostridium Difficile colonisation?

A

Activation of inflammasome
Increase in reactive oxygen species (ROS) levels
Induction of programmed cell death

62
Q

What are symptoms of Clostridium Difficile disease?

A

Watery diarrhoea
Dysentery
Pseudomembranous colitis
Toxic mega colon and peritonitis

63
Q

What are the cytopathic and cytotoxic effects of Clostridium Difficile disease?

A

Patchy necrosis with neutrophil infiltration
Epithelial ulcers
Pseudomembranous leukocytes, fibrin, mucus and cell debris

64
Q

What are the lab signs and symptoms of Clostridium Difficile disease?

A

Raised WBC count
Detector of organisms and toxins in stool
Defection of IgA/ B genes -> PCR
Colonoscopy shows pseudomembranous colitis

65
Q

How can you treat Clostridium Difficile disease?

A

Removal of offending antibiotic
Give fidaxomicin, metronidazole or vancomycin
Surgery (colectomy)

66
Q

How do you treat recurrent Clostridium Difficile disease?

A

Faecal transplant

67
Q

What causes VTEC disease?

A

Shigatoxin

68
Q

How do you identify shigatoxin?

A

Growth on a sorbitol macconkey agar (SMAC) - doesnt ferment sorbitol so its clear

69
Q

How is VTEC transmitted?

A

Predominantly by consumption of contaminated food and water

Person-person particularly in childcare facilities and animal- person

Low infectious dose

70
Q

Where does VTEC come from?

71
Q

What does low infectious dose mean?

A

Small amount -> outbreak

72
Q

Where is the VTEC gene carried?

A

On a lysogenic virus

73
Q

What are all the variations of the VTEC toxin?

A

Stx, stx1, ta1c, 1d2a, 2c, 2d

74
Q

What type of toxin is the VTEC toxin?

75
Q

What is the mechanism for VTEC binding?

A

Bind to receptor globotriasylceramide Gb3 or globotetraosylceramide Gb4 on host cell membrane
Bound toxin internalised by endocytosis
Carried by retrograde trafficking via the Golgi apparatus-> endoplasmic reticulum
A subunit cleaved off by proteases

76
Q

What happens once VTEC gets into the cytoplasm?

A

A1 and A2 dissociate

77
Q

What does A2 do after it dissociates?

A

Binds to 285 RNA subunit - blocks protein synthesis

MBD/MI (Wothaya) (57 decks)

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