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Microbiology and immunology > Exotoxins > Flashcards

Exotoxins Flashcards

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Biology 101 flashcards
1
Q

What is a pathogen

A

A microorganism capable of causing

disease.

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2
Q

what does pathogenicity mean

A

The ability of an infectious agent

to cause disease.

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3
Q

what does virulence mean

A

The quantitative ability of an agent

to cause disease.

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4
Q

what does toxigenicity mean

A

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

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5
Q

What are exotoxins

A

–Heterogeneous group of proteins produced
and secreted by living bacterial cells.
–Produced by both gram negative and gram
positive bacteria.
–Cause disease symptoms in host during
disease.
–Act via a variety of diverse mechanisms.

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6
Q

difference between gram positive and gram negative

A

gram positive: thick peptidoglycan layer and no outer lipid membrane
gram negative: thin peptidoglycan layer and have a lipid membrane

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7
Q

some activities of exotoxins

A
  • Evade immune response
  • Enable biofilm formation
  • Enable attachment to host cells.
  • Escape from phagosomes
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8
Q

in staphylococcus aureus what does haemolytic toxins cause

A

cause cells to lyse by forming pores

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9
Q

in staphylococcus aureus what does phenol soluble modulins (PSM) cause

A

aggregate the lipid bilayer of host cell causing lysis

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10
Q

Genetics of exotoxins

A

• Can be encoded by chromosomal genes e.g. Shiga toxin in Shigella dysenteriae, TcdA & TcdB in C. difficile
• Many toxins coded by extrachromosomal genes
—• Plasmids — Bacillus anthracis toxin, tetanus toxin
—• Lysogenic bacteriophage — e.g. streptococcal pyrogenic exotoxins in Scarlet Fever, Diphtheria toxin.

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11
Q

What are the 3 classification of exotoxins

A
  1. Membrane Acting Toxins — Type I
  2. Membrane Damaging Toxins — Type Il
  3. Intracellular Toxins —Type Ill
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12
Q

How does type 1 exotoxins acts, interfere and target

A

-Act from without the cell.
-Interfere with host cell signaling by inappropriate activation of host cell receptors.
-Target receptors include
• Guanylyl cyclase which increase intracellular cGMP
• Adenyl cyclase which increase intracellular cAMP
• Rho proteins
• Ras proteins

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13
Q

ways type 2 exotoxins work

A

–Insert channels into host cell membrane.
• ß sheet toxins e.g. S.aureus a — toxin, y toxin, PVL
• a helix toxins — e.g. diphtheria toxin
–Enzymatical damage e.g. S. aureus ß- haemolysin, PSM
–Receptor mediated
–Receptor Independent

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14
Q

what are the 2 usual components of type 3 exotoxins

A

AB toxins :
B= receptor binding and translocation function
A= toxigenic(enzymatic)
there can be single or multiple B units shown as AB subscript n

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15
Q

what are the 4 common enzymatic component A of type 3 exotoxins

A
  • ADP — ribosyl transferases - e.g. Exotoxin A of Pseudomonas aeruginosa, pertussis toxin.
  • Glucosyltransferases — e.g. TcdA and TcdB of Clostridium difficile
  • Deamidase — e.g. dermonecrotic toxin of Bordetella pertussis.
  • Protease — e.g. Clostridial neurotoxins: botulism & tetanus
  • Adenylcyclase - e.g. EF toxin of Bacillus anthracis
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16
Q

how does superantigen induce inflammatory cytokine release

A

non specific bridging of the MHC Class Il and T- cell receptor leading to cytokine production. E.g.
Staphylococcal Exfoliative Toxin A, Toxic
Shock Syndrome Toxin 1 (T SST 1)

17
Q

what 2 things can you use to inactivate toxins to create toxoids

A

formaldehyde or glutaraldehyde

18
Q

what are toxoids

A

inactive proteins but still highly immunogenic -form the basis for vaccines

19
Q

Microbiology of clostridium difficile (6 points)

A 
• gram-positive bacillus. 
• anaerobic. 
• spore-forming. 
• toxin-producing. 
• can be carried 
asymptomatically in the 
gut. 
• 3 toxins.
20
Q

Epidemiology of clostridium difficile (4 points)

A

• Common hospital acquired infection
worldwide.
• Spread by ingestion of spores — remain
dormant in environment.
• Coloniser of the human gut up to 5% in
adults. (commensal)
• Risk factors— antibiotic use, age, antacids
& prolonged hospital stay.

21
Q

how does antibiotic worsen Clostridium difficile

A

• Thought to act by disrupting the microbial ecosystem within the gut.
• Antibiotics provide a competitive advantage to spore
forming anaerobes over non spore forming anaerobes.
• Allows C. difficile colonisation and growth.
• All antibiotics have potential for causing disease.

22
Q

C. difficile Pathogenesis

A

–Cytotoxin A - TcdA coded by tcdA gene
–Cytotoxin B — TcdB coded by tcdB gene
–Binary toxin — C. diff transferase (CDT) — minor role in disease
–Tcd A and Tcd B — Type Ill AB toxins.
The A component of toxins are glycosylating enzymes.

23
Q

What are the cytopathic and cytotoxic effects of C. difficile

A
  • Patchy necrosis with neutrophil infiltration
  • Epithelial ulcers
  • Pseudomembranes— leucocytes, fibrin, mucous, cell debris.
24
Q

Diagnosis of C.difficile

A

• Clinical signs and symptoms
• Raised white cell count in blood.
• Detection of organisms and toxins in stool
–• 2 phase test :
I. Glutamate dehydrogenase — detects if C. difficile
organism present.
2. Toxin enzyme linked immunosorbentassay
(ELISA) for TcdA and TcdB toxins.
• Detection of tcdA and tcdb genes — PCR
• Colonoscopy — pseudomembranous colitis

25
Q

C. difficile treatment

A

• Treatment dependent on severity and presence of surgical
complications
• Ideally removal of offending antibiotic — not always possible
• Antibiotics fidaxomicin or metronidazole or vancomycin
• Surgery — partial, total colectomy
• Recurrent — faecal transplant.

26
Q

what is Verocytotoxin Escherichia

coli (VTEC) disease

A 
• VTEC, or Shiga-toxin (Stx) producing E. 
coli (STEC) can cause disease mild to 
life threatening disease. 
• Stx carried by some E. coli — most 
commonly 0157:H7 
• Identified usually by growth on 
sorbitol MacConkey agar (SMac) 
— does not ferment sorbitol and 
hence is clear. 
• Other less common types not 
identified using SMac.
27
Q

Epidemiology of VTEC

A

• E. coli 0157:H7 naturally colonizes the gastrointestinal tracts of cattle
who are generally asymptomatic.
• Transmission
• Predominantly via consumption of contaminated food and water
• Person to person, particularly in child day-care facilities, and from
• Animal to person. E.g. in petting zoos, dairy farms, or camp grounds.
• Very low infectious dose

28
Q

Pathogenesis Toxin of VTEC

A 
• Toxin — Shiga like toxin (SLT) = shigatoxin (Stx) = 
verocytotoxin (VTEC) 
• Stx, Stxl, Stxla, lc, Id Stx2a, 2c, 2d — variations in a.a. 
sequence 
• Gene carried on lysogenic bacteria. 
• Type Ill exotoxin — AB5
• Enzymatic component A = N-Glycosidase 
• Bound to 5 B subunits
29
Q

Mechanism of VTEC

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
• Once in the cytoplasm Al and A2 disassociate
• Al binds to 28S RNA subunit— blocks protein
synthesis

30
Q

STEC Pathogenesis

A

• STEC closely adheres to the epithelial cells of the gut mucosa.
• The route by which Stx is transported from the intestine to the kidney
and other tissues is debated, possibly polymorphonuclear
neutrophils (PMNs)
• Bind to glomerular endothelial cells of kidney, cardiovascular and
central nervous system.
• Very high levels of Gb3 in kidney so kidneys most affected.
• Thought that Stx favours inflammation resulting in microvascular
thrombosis and inhibition of fibrinolysis.

31
Q

STEC Disease

A 
• Can be severe and life threatening 
• Children < 5 years greatest risk 
• Abdominal cramps, watery or bloody diarrhoea — may not be present 
• Haemolytic uraemic syndrome 
    • Anaemia 
    • Renal Failure 
    • Thrombocytopaenia 
• Less common are neurological symptoms 
    . lethargy, 
    • severe headache, 
    • convulsions, 
    • encephalopathy.
32
Q

STEC Diagnosis and Treatment

A 
• Diagnosis 
  • Clinical signs and symptoms 
  • Haematological and biochemical evidence. 
  • Stool culture — Growth on SMac 
  • PCR for Stx genes 
• Treatment 
  • Supportive including renal dialysis and blood 
    product transfusion 
  • Antibiotics have little to no role

Microbiology and immunology (3 decks)

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