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lolmyi > L1: Bacterial pathogens & disease- EXOTOXINS > Flashcards

L1: Bacterial pathogens & disease- EXOTOXINS Flashcards

1
Q

Define pathogen

A

→microorganism capable of causing disease

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2
Q

Define pathogenicity

A

→ability of an infectious agent to cause disease

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3
Q

Define virulence

A

→The quantitative ability of an agent to cause disease.

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4
Q

Define toxigenicity

A

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

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5
Q

What are the 4 virulence mechanisms of bacteria?

A

→Adherence Factors
→Biofilms
→Invasion of Host Cells and Tissues
→Toxins – endotoxins and exotoxins

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6
Q

What are exotoxins and how do they act by?

A

→Heterogeneous group of proteins produced and secreted by living bacterial cells

Act by variety of diverse mechanisms

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7
Q

What are exotoxins produced by?

A

→both gram negative and gram-positive bacteria

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8
Q

What do exotoxins cause?

A

→symptoms in host during disease

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9
Q

What selective advantages do exotoxins give to the bacteria?

A 
→help transmission of disease
→ in severe disease, host may be a dead end
→Evade immune response
→Enable biofilm formation 
→Enable attachment to host cells. 
→Escape from phagosomes

remember: bacteria do not want to cause disease they want to survive so although they cause disease in host tissue, severe disease will kill them

ALL ALLOW FOR:
→colonisation,
→niche establishment
→carriage

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10
Q

What other activities in which exotoxins give a selective advantage to bacteria?

A

→Evade immune response
→Enable biofilm formation
→Enable attachment to host cells.
→Escape from phagosomes

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11
Q

What do all of the exotoxins activity allow?

A

→colonisation,
→niche establishment
→carriage

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12
Q

What are haemolytic toxins?

A

→cause cells to lyse by forming pores

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13
Q

What type toxins does Staphylococcus aureus have?

A

→haemolytic toxins

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14
Q

What are the types of haemolytic toxins?

A

→α,β,𝛾, toxins ,
→Panton Valentine Leukocidin (PVL),
→LukAB, LukED, LukMF

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15
Q

What are PSMs?

A

→Phenol soluble modulins

→Aggregate the lipid bilayer of host cells - causing lysis

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16
Q

Where in the body are majority of S.aureus aymptomatic carriage?

A

→in the nose

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17
Q

What do alpha and beta toxins allow in S.Aureus?

A

→allow for attachment
alpha - initial attachement
beta- accumulation

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18
Q

What do PSMs allow in S.Aureus?

A

→allows bacteria to escape phagosome

→kills other bacteria

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19
Q

What are exotoxins encoded by?

A

→chromosomal genes: Shiga toxin in Shigella dysenteriae,

→TcdA & TcdB in C. difficile

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20
Q

Give 2 examples of a plasmid with toxins encoded by extrachromosomal genes

A

→Bacillus anthracis toxin,

→tetanus toxin

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21
Q

Give examples of lysogenic bacteriophage with toxins encoded by extrachromosomal genes

A

→streptococcal pyrogenic exotoxins in
→Scarlet Fever,
→Diphtheria toxin

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22
Q

What are the classifications of exotoxins?

Classification by the toxins activity (hint: 3)

A

→Membrane Acting Toxins – Type I

→Membrane Damaging Toxins – Type II

→Intracellular Toxins – Type III

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23
Q

What are the problems of toxin activity classification of toxins?

A

→Many toxins may have more than one type activity

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24
Q

Where do Type I membrane acting toxins act from?

A

→Act from without the cell

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25
Q

What do Type I toxins interfere with?

A

→with host cell signaling by inappropriate activation of host cell receptors

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26
Q

What do Type I toxins target? (which target receptors)

A

→Guanylyl cyclase → ↑ intracellular cGMP

→Adenyl cyclase → ↑ intracellular cAMP

→Rho proteins
→Ras proteins

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27
Q

What effect does Type I toxins have on cGMP and cAMP?

A

→ ↑ intracellular cGMP

→ ↑ intracellular cAMP

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28
Q

What is an important feature of Type I E.coli toxin?

A

→stable heat toxin

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29
Q

What are the effects of increased cGMP signalling because of E.coli toxin?

A

→Dysregulated secretion of Cl and bicarbonate ions (cGMP -> + PKGII -> +-> Cl- HCO3)

→Effect on Na/K pump so increased Na secretion

→ if in colon then diarrhoea

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30
Q

Describe the mechanisms of Type II toxins

A

Cause damage to host cell membrane by:

→Insert channels into host cell membrane- polymerise and insert
→Enzymatical damage

OR
→Receptor mediated

→Receptor Independent

31
Q

What are the two components of intracellular toxins III?

A

→Receptor binding and translocation function – B

→Toxigenic (enzymatic) – A

→May be single or multiple B units e.g. Cholera toxin AB5

32
Q

What are the different activities of type A component of intracellular toxins?

A 
→ADP – ribosyl transferases 
→Glucosyltransferases
→Deamidase
→Protease
→Adenylcyclase
33
Q

What are other Type III toxins?

A

→Type III secretion and toxin injection
E.g. YopE in Yersinia species
→Type IV secretion and toxin injection- multimeric
E.g. CagA in Helicobacter pylori

34
Q

Give examples of cytokines released by exotoxin activity

A

→IL1, IL1β, TNF, IL 6, interferon 𝛾, IL18

35
Q

What are the two mechanisms used by exotoxins to release cytokines?

A

→superantigens

→activation of different inflammasome

36
Q

Describe the superantigen mechanism of inflammatory cytokines

A

→non specific bridging of the MHC Class II and T- cell receptor leading to cytokine production
→leads to cytokine storm or cytotoxic shock

37
Q

How are toxins inactivated?

A

→formaldehyde or glutaraldehyde

38
Q

What are toxoids?

A

→inactive proteins but still highly immunogenic

39
Q

Give examples of vaccines which use toxoids

A

→Tetanus Vaccine
→Diphtheria
→Pertussis (acellular)

40
Q

What are the antibodies given as treatment?

A

→Diphtheria antitoxin – horse antibodies

→Tetanus – pooled human immunoglobulin and use it to neutralise

→Botulism – horse antibodies

41
Q

What type of bacteria is C.difficile?

A

→gram-positive bacillus

42
Q

What is the mechanism of C.difficile?

A

→anaerobic

→spore-forming

→toxin-producing

43
Q

How many toxins does C.difficile release?

A

→3

44
Q

Describe the epidemiology of C.difficile

A

→Common hospital acquired

→Coloniser of the human gut

45
Q

How does C.difficile spread?

A

→ingestion of spores

→spores allow them to remain dormant in environment

46
Q

What are the risk factors of C.difficile?

A

→antibiotic use,
→age,
→antacids
→prolonged hospital stay

47
Q

How do antibiotics cause C.difficile growth?

A

→provide a competitive advantage to spore forming anaerobes over non spore forming anaerobes
→allow colonisation

48
Q

What are some antibiotics that cause disease?

A

→2nd and 3rd generation cephalosporins

→Quinolones

→Clindamycin
→Aminoglycosides

→Trimethoprim

→vancomycin

49
Q

What activity does the Type A component of Type III toxins have?

A

→glycosylating enzymes

50
Q

What is the binary toxin in C.difficile?

A

→C. diff transferase (CDT)

51
Q

Describe the C.difficile mechanism of action

A

→toxins bind to specific host cell receptor
→toxins internalised
→endosome is acidified via ATP
→pore is formed in the endosome
→GTD is released from the endosome to host cell cytoplasm
→Rho GTPases inactivation by glucosylation by GTD

52
Q

What are the cytotoxic effects of inactivated Rho GTPases?

A

→activation of inflammasome
→increased ROS levels
→induction of programmed cell death

53
Q

What are the cytopathic effects of inactivated Rho GTPases?

A

→cytoskeleton breakdown
→loss of cell-cell contacts
→increases epithelial permeability

54
Q

What are the symptoms of C.difficile?

A 
→Watery Diarrhoea
→Dysentery
→Pseudomembranous Colitis
→Toxic Megacolon and 
Peritonitis
55
Q

What are the clinical signs of C.difficile?

A

→Raised white cell count in blood

56
Q

What is the 2-phase stool test for C.difficile?

A

→Glutamate dehydrogenase – detects if C. difficile organism present.

→Toxin enzyme linked immunosorbent assay (ELISA) for TcdA and TcdB toxins

57
Q

How are the tcdA and tcdB genes detected in C.difficile?

A

→PCR

58
Q

How is pseudomembranous colitis detected in C.difficile?

A

→Colonoscopy

59
Q

What are the treatments for C.difficile?

A

→removal of offending antibiotic
→Antibiotics fidaxomicin or metronidazole or vancomycin
→Surgery – partial, total colectomy
→Recurrent – faecal transplant

60
Q

What is VTEC?

A

→Shiga-toxin (Stx) producing E. coli (STEC) can cause disease mild to life threatening disease

61
Q

How is Stx detected?

A

→growth on sorbitol MacConkey agar (SMac)

→does not ferment sorbitol and hence is clear

62
Q

Where does E.coli naturally colonise?

A

→gastrointestinal tracts of cattle who are generally asymptomatic

63
Q

How is E.coli transmitted?

A

→consumption of contaminated food and water
→ Person to person
→Animal to person
→Very low infectious dose

64
Q

Where is the pathogenic toxin in E.coli found?

A

→lysogenic virus

65
Q

What components does the E.coli toxin havee?

A

→Type III exotoxin – AB5
→Enzymatic component A = N-Glycosidase

→Bound to 5 B subunits

66
Q

Describe the mechanism of the E.coli toxin

A

→Bind to receptor globotriaosylceramide Gb3 or globotetraosylceramide (Gb4) on host cell membrane

→Bound toxin internalised by receptor mediated endocytosis.

→Carried by retrograde trafficking via the Golgi apparatus to the endoplasmic reticulum.

→The A subunit is cleaved off by membrane bound proteases

vOnce in the cytoplasm A1 and A2 disassociate

→A1 binds to 28S RNA subunit – blocks protein synthesis

67
Q

What does STEC bind to in the body?

A

→endothelial cells of kidney
→cardiovascular
→central nervous system
→Areas that well vascularised

68
Q

Why is the kidney most affected by STEC?

A

→Very high levels of Gb3

69
Q

What are the symptoms of STEC disease?

A

May not be present:
→Abdominal cramps,
→watery or bloody diarrhoea

Haemolytic uraemia syndrome:
→Anaemia
→Renal Failure
→Thrombocytopaenia

Less common are neurological symptoms:
→lethargy, 
→severe headache, 
→convulsions,
→encephalopathy
70
Q

What are the treatments for STEC disease?

A

→Supportive including: renal dialysis
→ and blood product transfusion

→Antibiotics have little to no role

71
Q

What is the diagnosis of STEC?

A

Clinical signs and symptoms
Haematological and biochemical evidence
Stool culture - growth on SMac
PCR for Stx genes

72
Q

Who is at greater risk of STEC disease?

A

Children < 5 years

73
Q

Severity of STEC disease?

A

Can be severe and life threatening

lolmyi (31 decks)

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