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Microbiology > 4. CPE, TSST & SpeA > Flashcards

4. CPE, TSST & SpeA Flashcards

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1
Q

Is Clostridium perfringens colonising?

A

No, but live organisms must be consumed. The bacteria sporulate in GIT & produce toxin (CPE)

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2
Q

What type of toxin does C. perfringens produce?

A

CPE (Clostridium perfringens enterotoxin) - pore-forming toxin

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3
Q

What disease is associated with Clostridium perfringens?

A

Food poisoning

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4
Q

Are most Clostridia harmless?

A

Yes

Common in gut

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5
Q

Describe C. perf

A

Gram positive, spore-forming, anaerobic rod

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6
Q

What are the symptoms of a C. perf infection?

A

Cramps, diarrhoea, onset 8-12 hrs, duration 24-36 hrs

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7
Q

What are common food sources of C. perf?

A

Large pieces of meat e.g. pork (pig roast), beef
(CPE is sensitive to proteases like trypsin. If you eat lots of protein (i.e. meat) you dilute out the trypsin & it is not longer there to degrade the CPE)

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8
Q

What may be the cause of >1 million cases of food poisoning in US annually?

A

Clostridium perfringens

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9
Q

Why isn’t C. perf a classic intoxication?

A

Since live cells are involved

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10
Q

C. perf can produce up to how many different toxins?

A

16

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11
Q

C. perf is classified into __ different toxinotypes based on the production of __ major toxins (alpha, beta, epsilon, iota)

A

5 different toxinotypes

4 major toxins

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12
Q

How does CPE work?

A

CPE binds to host cell → inserts into membrane → fluid loss (enterotoxin)

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13
Q

What percentage of C. perf strains produce CPE?

A

Only 5%

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14
Q

What strain of C. perf does not produce CPE?

A

Type B

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15
Q

What is alpha toxin (C. perf)?

A

membrane-damaging, hemolysin

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16
Q

What is beta toxin (C. perf)?

A

membrane-disrupting, pore-forming (halos of lysis form around colonies)

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17
Q

Discuss epsilon toxin (C. perf)?

A
  • ETX is the 4th most potent toxin known
  • Pore-forming
  • Causes enterotoxaemia
  • Produced by type B & D strains
  • Highly lethal disease with major impacts on domestic ruminants
  • LD50 = 100 ng/kg
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18
Q

What is special about the iota toxin (C. perf)?

A

It has ADP ribosylation activity

ADP ribosylates actin - will change actin cytoskeleton of target cell

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19
Q

What is a binary toxin?

A
  • It looks like an A-B toxin but is different
  • Has 2 components (A & B)
  • B component involved in binding to host cell & delivering A component to host cell
  • 2 components are produced separately & don’t interact until they find each other on the surface of the host cell
  • They are not linked by a disulphide bridge
  • They are not encoded by the same gene
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20
Q

What is Perfringolysin O, and what does it do?

A

It is a cholesterol-dependent cytolysin

It forms a pore, which leads to cell lysis

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21
Q

Where are most of the C. perf toxin genes found?

A

on plasmids

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22
Q

What is the binding domain?

A

C-terminus

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23
Q

What is the cytotoxic domain?

A

It carries the cytotoxic activity and inserts into the membrane of the target cell, creating a pore.

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24
Q

What is the function of complementation?

A

It controls for rare off-target genetic events that might account for phenotype

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25
Q

What protein does CPE appear to bind to?

A

Claudin (important in tight junctions)

26
Q

Briefly explain the conformational change in claudin (protein) when CPE binds

A

Protein contracts, cytotoxin domain extends to form a needle-like structure & inserts into membrane of target cell. 6 of those proteins form a hexametric ring - D3 domain from all 6 proteins inserts into membrane - get a clear pore in the membrane through which fluid can leak out

27
Q

What human disease is primarily associated with C. perf A toxinotype?

A

Human myonecrosis (gas gangrene) - characterised by its pungent smell of rotting flesh

28
Q

What is the name for gut rot that is associated with C. perf?

A

Human enteritis necroticans - often fatal food poisoning

29
Q

Does human enteritis necroticans most commonly occur in developed or developing countries?

A

Developing countries

30
Q

Which toxinotype is gut rot associated with?

A

Toxinotype C (which has alpha and beta toxins)

31
Q

What is an example of a food that contains protease inhibitors and increases susceptibility to intoxication by alpha and beta toxins?

A

Sweet potato

32
Q

What bacterium is responsible for MRSA?

A

Staphylococcus aureus

33
Q

Features of S. aureus & S. pyogenes

A

Gram positive cocci
Non-spore forming
Aerobic (require oxygen)

34
Q

What bacterium produces the toxin that is responsible for Toxic Shock Syndrome?

A

Staphylococcus aureus

35
Q

Is TSS exclusively a tampon-associated condition?

A

No - more recently associated with blisters due to football boots

36
Q

What happens after colonisation by S. aureus in TSS?

A

Toxin is produced (TSST-1: toxic shock syndrome toxin)

37
Q

What bacterium produces the superantigen that is responsible for Toxic Shock Like Syndrome?

A

Streptococcus pyogenes

38
Q

Which has a higher death rate: TSS or TSLS?

A

TSLS

39
Q

What is produced in TSLS?

A

A superantigen (SpeA: S. pyogenes erythrogenic toxin)

40
Q

Differences between S. aureus & S. pyogenes?

A

S. aureus is non-invasive (bacteraemia is rare)
S. pyogenes is invasive (more severe than S. aureus, bacteraemia common)
S. aureus never gets into the body - do not get sepsis
TSLS - deep site of infection
TSS - superficial site of infection

41
Q

How are TSST and SpeA functionally related?

A

They both interact with MHC and T cell receptors, but are not similar at the primary sequence level

42
Q

What happens in TSS?

A

S. aureus grows in tampon or wound → TSST-1 enters the bloodstream → fever, rash, shock

43
Q

TSS death rate?

A

3-6%

44
Q

TSLS death rate?

A

> 30%

TSLS also termed severe invasive streptococcal disease

45
Q

What happens in TSLS?

A

S. pyogenes grows in wound → bacteria enter bloodstream → produce SpeA → fever, rash, shock

46
Q

What bacterium causes necrotising fasciitis (‘flesh eating disease’)?

A

Streptococcus pyogenes

47
Q

What is necrotising fasciitis characterised by?

A

The rapid spread of inflammation (intoxication spreads v quickly)

48
Q

What is the treatment for necrotising fasciitis?

A

Directly go in and clean the wound (scrape away all dead tissue) or amputate. Antibiotics are too slow

49
Q

What are the 3 different types of necrotising fasciitis?

A

Type 1: polymicrobial
Type 2: GAS
Type 3: gas gangrene

50
Q

What does acquired SlaA gene encode for?

A

A phospholipase (a membrane-disrupting toxin which allows pyogenes to become even more toxic)

51
Q

How does S. pyogenes evade complement?

A

(i) by producing a C5a peptidase

(ii) surface covered with M protein degrades C3b

52
Q

Where is SpeA gene located?

A

On a temperate bacteriophage

53
Q

Staphylococcal food poisoning

A
  • Common
  • Vomiting, pain, rapid onset
  • Foods which are handled, low water activity
  • Classic intoxication (organism grows on food, produces toxin which is ingested)
  • Superantigens can cause food poisoning independent of activating T cells - emetic properties, caused by SEs (Staphylococcus enterotoxins)
54
Q

True or False: Most strains of S. aureus (food poisoning) produce multiple superantigens

A

True

55
Q

What are superantigens?

A

A large family of pyrogenic (fever-inducing) toxins and their roles are variable. All have very similar shapes & interact with MHC & TCRs

56
Q

What is missing in TSST-1 that is responsible for vomiting reaction?

A

Particular cysteine loop

57
Q

Predominant symptoms associated with superantigens?

A

Vomiting (emesis)

58
Q

Examples of intoxications (disease without colonisation)?

A

C. botulinum (A-B toxin), S. aureus (SAg)

59
Q

Example of a toxicoinfection (disease without colonisation, toxin produced in GIT)?

A

C. perfringens - causes food poisoning, have to ingest the bacteria in order for the toxin to be delivered to gut

60
Q

Example of opportunistic (defences breached) pathogens?

A
  • TSS - S. aureus (SAg)
  • TSLS - S. pyogenes (SAg)
  • Tetanus - C. tetani (A-B toxin)

Microbiology (13 decks)

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