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MD3002 GI/GU/Renal > Bacterial and Viral Infections of the GI Tract > Flashcards

Bacterial and Viral Infections of the GI Tract Flashcards

1
Q

How does our GI tract help prevent infection?

A

Barriers:

  • strong stomach acid that kills bacteria
  • peristaltic mechanisms to stop bacteria from sitting in one part of the GI tract for a long period of time
  • gut flora which has a symbiotic relationship with us and fights off pathogenic mechanisms by out-competing them
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2
Q

What is intoxication?

A

ingestion of food containing biologically active toxins which cause disease

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3
Q

What is infection

A

ingestion of live microbes:

  • can multiply readily on food prior to consumption
  • use food only as a vector
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4
Q

What are some methods of transmission of infection?

A
  • faecal-oral
  • food
  • fluids
  • fingers
  • person-person
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5
Q

What are some personal and public health measures to prevent GI infection?

A

Personal:

  • hand hygiene
  • cook foods properly
  • avoid cross contamination
  • wash it, peel it, cook it or forget it

Public health:

  • pasteurisation of milk and dairy products
  • proper sewage disposal
  • provision of safe, clean drinking water
  • vaccination
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6
Q

What are some viruses that cause GI infection?

A
  • norovirus
  • adenovirus
  • rotavirus
    (causes most infections)
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7
Q

What is the clinical presentation of norovirus and the population affected?

A
  • projectile vomiting
  • diarrhoea
  • abdominal cramps
  • headache
  • muscle ache
    (infectious period from onset till 48hrs after symptoms stop)
  • can affect anyone (young-adults, sick-healthy)
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8
Q

What is the clinical presentation of rotavirus and the population affected?

A
  • watery diarrhoea
  • vomiting
  • abdominal cramps
  • fever
  • mainly affects young children, elderly and immunocompromised
  • there is access to live attenuated vaccine
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9
Q

What is the clinical presentation of adenovirus and the population affected?

A
  • mild prolonged diarrhoea

* affects mainly young children, elderly and immunocompromised

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10
Q

What is the level of immunity after GI infection caused by these viruses?

A
  • norovirus immunity only lasts a year after infection

- adenovirus and rotavirus have lifelong immunity after infection

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11
Q

What are the gram-negative bacteria that can cause infection in the GI tract?

A
  • campylobacter
  • vibrio cholerae
  • salmonella
  • shigella
  • E.coli
  • yersinia enterocolitica
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12
Q

How is campylobacter spread, its pathogenesis and clinical presentation?

A

Transmission:

  • animals
  • contaminated food

Pathogenesis:
- invasion of bowel leading to inflammation and ulceration

Presentation:

  • bloody diarrhoea
  • abdominal pain
  • fever
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13
Q

What is the transmission, pathogenesis and clinical presentation of vibrio cholerae?

A

Transmission:
- contaminated food or water

Pathogenesis:

  • polar flagella with mucinase facilitate penetration of intestinal mucus
  • disease caused by exotoxin

Symptoms:

  • severe, profuse watery diarrhoea
  • profound fluid and electrolyte loss
  • hypovolaemic shock
  • cardiac failure
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14
Q

What is the pathogenesis and clinical presentation of salmonella?

A

Pathogenesis:

  • invasion and inflammation of the bowel
  • absorbed at terminal ileum and multiplies in Peyer’s patches
  • inflammatory response mediates release of prostaglandins that stimulate cyclic AMP

Symptoms:

  • watery diarrhoea
  • vomiting
  • fever
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15
Q

Give detail on the pathogenesis of the salmonella infection

A
  • ingestion of large number of bacteria
  • absorption into the terminal ileum
  • bacteria multiply in Peyer’s patches
  • inflammatory response mediates release of prostaglandins
  • stimulates cyclic AMP
  • release of fluid and electrolytes causing watery diarrhoea
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16
Q

What are the other forms of salmonella and its presentation?

A
  • enteric fevers: typhoid and paratyphoid
  • systemic infections in the GI tract
  • malaise
  • headache
  • cough
  • rose spot rash (significant)
  • fever
  • bradycardia (significant)
    lethargy
  • constipation etc
17
Q

What is the pathogenesis and clinical presentation of shigella?

A

Pathogenesis:

  • production of shiga toxin which damages intestinal epithelium
  • toxin can cause haemolytic uremic syndrome

Symptoms:

  • watery followed by bloody diarrhoea
  • crampy abdo pain
  • fever
18
Q

Why would you not want to give antibiotics to a shigella infection?

A
  • causes a burst of the bacteria which causes a big release of the shiga toxin
  • increases risk of haemolytic uremic syndrome
19
Q

What is the pathogenesis and clinical presentation of ETEC?

A

Pathogenesis:

  • heat-labile (structural and functional analogue of cholera toxin)
  • heat-stable (produced in addition to or instead of LT)

Presentation:

  • watery diarrhoea
  • abdominal pain
  • vomiting
  • no associated fever
20
Q

Describe the mode of action of the ETEC enterotoxins

A
  • heat-labile toxin works in same way as cholera toxin by activating adenylate cyclase
  • heat-stable toxin activates guanylase cyclase increases which acts as an on switch for secretory mechanisms
21
Q

What is the pathogenesis and clinical presentation of EHEC?

A

Pathogenesis:
- production of shiga like toxins which target the glomerular endothelium causing haemolytic uremic syndrome

Presentation:

  • bloody diarrhoea
  • abdo pain
  • vomiting
22
Q

What is the pathogenesis and clinical presentation of yersinia enterocolitica?

A

Pathogenesis:
- invasion of terminal ileum with inflammation of mesenteric lymph nodes

Presentation:

  • bloody diarrhoea
  • abdo pain
  • fever
23
Q

What are the gram-positive bacteria that can cause infection in the GI tract?

A
  • staphylococcus aureus
  • clostridium botulinum
  • clostridium difficile
  • listeria monocytogenes
24
Q

What is the pathogenesis and clinical presentation of S. aureus?

A

Pathogenesis:
- heat stable and acid-resistant protein toxins resulting in emetic disease

Presentation:

  • profuse comiting
  • abdo cramps
  • no diarrhoea or fever
25
Q

What is a unique feature of the adenovirus?

A
  • only first infection symptomatic (except in the vulnerable)
  • asymptomatic infection common
26
Q

Describe how the cholera toxin works

A
  • subunit B binds to receptor on surface of cells
  • subunit A refolds and becomes active to promote activity of adenylate cyclase
  • activates cAMP which pushes chloride ions out of the cell
  • positive Na follows and water follows due to osmosis
27
Q

What is haemolytic uremic syndrome?

A
  • group of blood disorders characterised by low RBC, acute kidney failure, and low platelets
28
Q

What is the pathogenesis and clinical presentation of C. botulinium?

A

Pathogenesis:

  • produces heat powerful heat-labile protein neurotoxin
  • absorbed toxins spread by bloodstream and enter peripheral nerves where they cause neuromuscular block

Symptoms:

  • flaccid paralysis
  • progressive muscle weakness ( can cause resp failure)
29
Q

What is the pathogenesis and clinical presentation of C. difficile?

A

Pathogenesis:

  • disruption of normal protective gut flora due to antibiotics, chemo or antacids
  • release of toxins A and B

Presentation:

  • mild to severe diarrhoea
  • pseudomembranous colitis
  • toxic colon dilation or perforation
30
Q

What is the pathogenesis and clinical presentation of listeria monocytes?

A

Pathogenesis:
- invasive infection

Presention:

  • initial flu-like illness with or without diarrhoea
  • can cause severe systemic infection
  • IV antibiotics needed
31
Q

What is the pathogenesis and clinical presentation of helicobacter pylori?

A

Pathogenesis:

  • cytotoxin production and range or factors to promote adhesion and colonisation
  • produces urease to generate ammonia from urea and elevates pH

Presentation:
- asymptomatic unless ulceration develops

MD3002 GI/GU/Renal (64 decks)

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