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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
What do Type I toxins interfere with?
→with host cell signaling by inappropriate activation of host cell receptors
26
What do Type I toxins target? (which target receptors)
→Guanylyl cyclase → ↑ intracellular cGMP →Adenyl cyclase → ↑ intracellular cAMP →Rho proteins →Ras proteins
27
What effect does Type I toxins have on cGMP and cAMP?
→ ↑ intracellular cGMP | → ↑ intracellular cAMP
28
What is an important feature of Type I E.coli toxin?
→stable heat toxin
29
What are the effects of increased cGMP signalling because of E.coli toxin?
→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
30
Describe the mechanisms of Type II toxins
Cause damage to host cell membrane by: →Insert channels into host cell membrane- polymerise and insert →Enzymatical damage OR →Receptor mediated →Receptor Independent
31
What are the two components of intracellular toxins III?
→Receptor binding and translocation function – B →Toxigenic (enzymatic) – A →May be single or multiple B units e.g. Cholera toxin AB5
32
What are the different activities of type A component of intracellular toxins?
``` →ADP – ribosyl transferases →Glucosyltransferases →Deamidase →Protease →Adenylcyclase ```
33
What are other Type III toxins?
→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
Give examples of cytokines released by exotoxin activity
→IL1, IL1β, TNF, IL 6, interferon 𝛾, IL18
35
What are the two mechanisms used by exotoxins to release cytokines?
→superantigens | →activation of different inflammasome
36
Describe the superantigen mechanism of inflammatory cytokines
→non specific bridging of the MHC Class II and T- cell receptor leading to cytokine production →leads to cytokine storm or cytotoxic shock
37
How are toxins inactivated?
→formaldehyde or glutaraldehyde
38
What are toxoids?
→inactive proteins but still highly immunogenic
39
Give examples of vaccines which use toxoids
→Tetanus Vaccine →Diphtheria →Pertussis (acellular)
40
What are the antibodies given as treatment?
→Diphtheria antitoxin – horse antibodies →Tetanus – pooled human immunoglobulin and use it to neutralise →Botulism – horse antibodies
41
What type of bacteria is C.difficile?
→gram-positive bacillus
42
What is the mechanism of C.difficile?
→anaerobic →spore-forming →toxin-producing
43
How many toxins does C.difficile release?
→3
44
Describe the epidemiology of C.difficile
→Common hospital acquired | →Coloniser of the human gut
45
How does C.difficile spread?
→ingestion of spores | →spores allow them to remain dormant in environment
46
What are the risk factors of C.difficile?
→antibiotic use, →age, →antacids →prolonged hospital stay
47
How do antibiotics cause C.difficile growth?
→provide a competitive advantage to spore forming anaerobes over non spore forming anaerobes →allow colonisation
48
What are some antibiotics that cause disease?
→2nd and 3rd generation cephalosporins →Quinolones →Clindamycin →Aminoglycosides →Trimethoprim →vancomycin
49
What activity does the Type A component of Type III toxins have?
→glycosylating enzymes
50
What is the binary toxin in C.difficile?
→C. diff transferase (CDT)
51
Describe the C.difficile mechanism of action
→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
What are the cytotoxic effects of inactivated Rho GTPases?
→activation of inflammasome →increased ROS levels →induction of programmed cell death
53
What are the cytopathic effects of inactivated Rho GTPases?
→cytoskeleton breakdown →loss of cell-cell contacts →increases epithelial permeability
54
What are the symptoms of C.difficile?
``` →Watery Diarrhoea →Dysentery →Pseudomembranous Colitis →Toxic Megacolon and Peritonitis ```
55
What are the clinical signs of C.difficile?
→Raised white cell count in blood
56
What is the 2-phase stool test for C.difficile?
→Glutamate dehydrogenase – detects if C. difficile organism present. →Toxin enzyme linked immunosorbent assay (ELISA) for TcdA and TcdB toxins
57
How are the tcdA and tcdB genes detected in C.difficile?
→PCR
58
How is pseudomembranous colitis detected in C.difficile?
→Colonoscopy
59
What are the treatments for C.difficile?
→removal of offending antibiotic →Antibiotics fidaxomicin or metronidazole or vancomycin →Surgery – partial, total colectomy →Recurrent – faecal transplant
60
What is VTEC?
→Shiga-toxin (Stx) producing E. coli (STEC) can cause disease mild to life threatening disease
61
How is Stx detected?
→growth on sorbitol MacConkey agar (SMac) →does not ferment sorbitol and hence is clear
62
Where does E.coli naturally colonise?
→gastrointestinal tracts of cattle who are generally asymptomatic
63
How is E.coli transmitted?
→consumption of contaminated food and water → Person to person →Animal to person →Very low infectious dose
64
Where is the pathogenic toxin in E.coli found?
→lysogenic virus
65
What components does the E.coli toxin havee?
→Type III exotoxin – AB5 →Enzymatic component A = N-Glycosidase →Bound to 5 B subunits
66
Describe the mechanism of the E.coli toxin
→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
What does STEC bind to in the body?
→endothelial cells of kidney →cardiovascular →central nervous system →Areas that well vascularised
68
Why is the kidney most affected by STEC?
→Very high levels of Gb3
69
What are the symptoms of STEC disease?
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
What are the treatments for STEC disease?
→Supportive including: renal dialysis → and blood product transfusion →Antibiotics have little to no role
71
What is the diagnosis of STEC?
Clinical signs and symptoms Haematological and biochemical evidence Stool culture - growth on SMac PCR for Stx genes
72
Who is at greater risk of STEC disease?
Children < 5 years
73
Severity of STEC disease?
Can be severe and life threatening

lolmyi (31 decks)

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