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Biology of Disease > Lecture 27 - Bacterial Pathogenicity in the Gastrointestinal Tract > Flashcards

Lecture 27 - Bacterial Pathogenicity in the Gastrointestinal Tract Flashcards

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1
Q

Which toxin does Clostridium botulinum produce? In what circumstances?

A

Botulinum toxin (BoNT) during anaerobic growth in food (e.g. home canned)

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2
Q

Where is BoNT absorbed along the GI tract?

A

From the stomach.

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3
Q

What is BoNT and where does it act?

A

It is a protease that cleaves synaptobrevin, a neuronal SNARE. BoNT acts at the neuromuscular junction, preventing exocytosis of the stimulatory neurotransmitter ACh, causing flaccid paralysis. Rare, but life threatening.

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4
Q

Where does Staphylococcus aureus grow?

A

In custard, processed meats at room temperature.

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5
Q

What happens to stable enterotoxins of staphylococcus aureus in the the stomach?

A

They interact with gastric mucosa and are thought to act as superantigens.

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6
Q

Where does Clostridium perfringens germinate from?

A

Spores that survive in pre-heated food.

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7
Q

Where are clostridium perfringens toxins produced?

A

in the intestine.

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8
Q

What is gastroenteritis characterised by?

A

Nausea, diarrhoea and abdominal pains.

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9
Q

What is cholera characterised by?

A

Vibrio cholerae colonizing the intestinal epithelium.

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10
Q

What is the treatment for a cholera infection?

A

Electrolyte replacement.

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11
Q

How does Vibrio cholerae colonise the GI tract?

A

It colonises the small intestine mucosa by a fimbrial adhesin.

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12
Q

What are the principal disease symptoms of cholera caused by?

A

The secreted cholera toxin (CTX).

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13
Q

Where are CTX genes carried? What are they co-regulated with and by what?

A

On a bacteriophage integrated into the bacterial chromosome and are co-regulated with adhesin and other genes by a HAP signal transduction system (global regulation).

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14
Q

What is the structure of CTX.

A

AB-5

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15
Q

What does the B part of CTX bind to? How is uptake achieved?

A

Host-receptor GM-1-ganglioside. Uptake by receptor mediated endocytosis and retrograde transport to ER.

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16
Q

What is the function of active A subunit of CTX?

A

It translocates into the host cell cytosol.
It then short-circuits control of adenylyl cyclase (AC) activity by ADP-ribosylating stimulatory G (GTP-hydrolysing) protein (G-S) and fixing it in the ‘on’ state. This resuts in uncontrolled high levels of cAMP.

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17
Q

What do the increased cAMP levels caused by CTX lead to?

A

Disturbed activity of Na+ and Cl- (CFTR) membrane pumps. The ion imbalance leads to water/electrolyte loss (12-20 litres/day) into the lumen.

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18
Q

What are the symptoms of a cholera infection?

A

Copious watery diarrhoea (‘rice water’), shock, collapse and sometimes cardiac failure.

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19
Q

What is salmonellosis caused by?

A

Salmonella, mainly S.enterica.

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20
Q

When was the peak of salmonellosis in the UK?

A

1990s, 30,000 cases p.a.

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21
Q

Where do salmonella enter the GI tract and how?

A

They induce host cytoskeleton rearrangement (require SPI-1-encoded needle and effectors e.g. the actin binding SipA, SipC) force entry directly via the apical surface of epithelial cells of the distal ileum and proximal colon.

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22
Q

Where does Salmonella multiply?

A

Within a membrane-bound vacuole in which they remian, a ‘replicative niche’.

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23
Q

How is salmonella released from epithelial cells?

A

By lysis.

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24
Q

What does released salmonella induce?

A

Inflammation (principally via LPS lipid A), gastroenteritis.

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25
Q

What happens to salmonella after it is released from epithelial cells of the distal ileum and proximal colon?

A

It is taken up by macrophages and replicates. Survives intracellularly by switching on up to 200 genes (including SPI-2 genes, encoding needle and effectors) that inhibit maturation of the phagolysosome and confer resistance to defensins and oxidative burst (pumps, superoxide dismutase (SOD), catalase).

26
Q

What is the host response to salmonella?

A

Activation of cAMP production and fluid secretion. Diarrhoea.

27
Q

What causes systemic typhoid fever?

A

S.typhi.

28
Q

Where does S.typhi replicate? How is it spread?

A

In macrophages and is spread systematically via blood stream to the liver and spleen etc.

29
Q

What are the severe symptoms of typhoid fever generally caused by?

A

Typhoid toxin (CDT) and the response to LPS lipid A.

30
Q

Where are bacteria shed?

A

In bile.

31
Q

What do ETEC, EPEC and EHEC stand for?

A

Enterotoxinogenic E. Coli
Enteropathogenic E. Coli
Enterohemorrhagic E.Coli

32
Q

How does ETEC colonise? Which toxin is formed?

A

By fimbrial (pili) adhesins -> cholera like enterotoxin LT (labile toxin).

33
Q

How does EPEC attach to the host GI tract? What else attaches in this manner?

A 
Initially attaches by pilus adhesin.
Delivers efffectors, including its own receptor Tir (which binds intimin on the EPEC surface) into the target cell to facilitate tight adhesion by cytoskeleton rearrangement.
Generates 'pedestals'.
Causes inflammation.
EHEC attaches in the same manner.
34
Q

Why is inflammation accentuated in EHEC?

A

By SLT (Shiga-like toxin), which can also cause renal failure.

35
Q

Which serotype of EHEC is predominant? Where can it commonly be found?

A

O157. In beef.

36
Q

Which strain of E. Coli causes UTIs?

A

UHEC

37
Q

Name some other causes of food-borne infections?

A

Campylobacter (behaves like Salmonella)
Listeria (can cross to the placenta and the blood-brain barrier.
Shigella (causes bacterial dysentry)

38
Q

What is a Shigella infection characterised by?

A

Acute inflammation of the colon and low-volume diarrhoea containing blood mucus and PMNs.

39
Q

How is damage by shigella infection caused?

A

Directly by Shiga toxin (ST) and indirectly by the inflammatory response.

40
Q

What causes antibiotic associated diarrhoea and pseudomembranous colitis?

A

Clostridium difficile

41
Q

How does Clostridium difficile manage to colonise the GI tract? Where does it colonise?

A

It colonises the colon following antibiotic eradication of the normal human gut microflora. Special problem in hospitals.

42
Q

Which other animal does Clostridium difficile affect?

A

Horses.

43
Q

Which toxins does Clostridium difficile secrete?

A

TcdA and TcdB.

44
Q

What effect do the toxins secreted by Clostridium difficile have?

A

They cause diarrhoea and inflammation of the colonic mucosa.

45
Q

What is the biochemical action of the toxins produced by Clostridium difficile?

A

They glycosylate small GTPases in intracellular signalling pathways, resulting in subversion of the actin cytoskeleton and disruption of tight junctions - epithelium becomes ‘leaky’, cell destruction.

46
Q

How does Clostridium difficile produce indirect cell damage?

A

By inflammation and pseudomembrane (comprised of dead cells, polymorphonucleocytes/PMNs and bacteria) being produced.

47
Q

What are the primary treatments for a Clostridium difficile infection?

A

Antibiotics (e.g. vancomycin) and rehydration therapy.

48
Q

How are refractory and recurrent infections by C. difficile treated?

A

Using faecal transplants - liquid suspensions of donor faeces, screened for enteric pathogens (bacteria, viruses and parasites) are introduced into the patient’s colon.

49
Q

What percentage of gastric and duodenal ulcers are caused by Helicobacter pylori?

A

90%

50
Q

What shape is Helicobacter pylori?

A

Spiral shaped

51
Q

Is Helicobacter pylori Gram +ve or -ve?

A

Gram negative.

52
Q

When was Helicobacter pylori discovered and in patients with which disease?

A

1983, in patients with gastritis.

53
Q

What percentage of the human population is infected with Helicobacter pylori at any one time?

A

Up to 50%.

54
Q

Where does Helicobacter pylori colonise?

A

The mucin layer near gastric mucosal cells in the antrum (the lower part) of the stomach.

55
Q

How does Helicobacter pylori move and adhere to cells?

A

Extremely motile by means of flagella, binds using adhesins.

56
Q

What effect does Helicobacter pylori have on gastric mucosa to make it easier for it to swim towards the epithelium?

A

It neutralises acid by urease, which splits urea to ammonia, raising the pH, which makes gastric mucous less viscous, so it is easier for the H. pylori to swim towards the epithelium.

57
Q

How does H. pylori cause intense inflammation and ulceration?

A

1) Helicobacter induced IL-8 (attracts PMNs) production by epithelial cells
2) Destruction of epithelial cells by VacA (a pore forming vacuolating cytotoxin) which is secreted by H.pylori.

58
Q

What is the action of the hexameric VacA toxin?

A

It inserts into the host cell membrane to form anion-selective channels that are endocytosed. VacA pores disturb ion balance of late endosomes and water flows in, swelling endosomes to form characteristic vacuoles.

59
Q

What occurs during progression of the ulcer?

A

It is accompanied by more inflammation, including increased recruitment of PMNs etc, and tissue destruction.

60
Q

Which other disease (apart from gastric ulcers) does H. pylori have a correlation with?

A

Gastric cancer.

61
Q

What is the theory that links the correlation between H. pylori and gastric cancer?

A

That possibly chronic inflammation exposes proliferating mucosal stem cells to dietary carcinogens and generates mutagenic reactive oxygen.
It seems also that the bacterial effector CagA, delivered into the gastric epithelial cells, interferes with signalling pathways, leading to increased cell proliferation.

Biology of Disease (43 decks)

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