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Medical Studies 2B > 6.2 Infections of the Gastrointestinal Tract > Flashcards

6.2 Infections of the Gastrointestinal Tract Flashcards

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USMLE® Step 1 flashcards
1
Q

What are the four types of immune barriers of the gastrointestinal tract?

A
  • Mechanical (e.g. peristalsis)
  • Physical (physically blocking invasion of pathogens (e.g. mucous layer)
  • Enzymatic (using enzymes to break down pathogens)
  • Chemical (altering the chemical environment to kill pathogens)
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2
Q

List two reasons why it might be difficult to record the number of gastroenteritis cases in the community

A
  1. Acute, self-limiting disease (gone quickly)
  2. Many patients w/ viral gastroenteritis won’t present
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3
Q

During which months in Australia are salmonellosis rates higher? Why might that be?

A
  • Summer months
  • Undercooked chicken on barbecues
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4
Q

How long is the incubation period for campylobacter jejuni? How long does it last?

A
  • 2-4 day incubation period
  • Symptoms typically resolve within a week
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5
Q

What is a rare disease outcome of bacterial gastroenteritis caused by molecular mimicry?

A
  • Guillain Barre syndrome
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6
Q

Outline the two categories of virulence factors

A
  1. Help establish infection (nutrient scavenging, immunoresistant)
  2. Damage host (toxins, inflammatory mediators)
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7
Q

What is ID50?

A

The number of pathogenic organisms required to cause infection in 50% of the population

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8
Q

What are the 4 steps in the life cycle of a pathogen? What must the pathogen be able to do to allow this to occur?

A
  1. Transferred to previously-uninfected host
  2. Colonisation (adherence/invasion; settling into the niche)
  3. Proliferation (cranking the adspend)
  4. Transmission to new host (shiny object)

Pathogen must be able to escape host immune system to allow this to occur.

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9
Q

What are three routes of transmission for bacteria that cause gastroenteritis?

A
  1. Faecal oral (E. Coli)
  2. Zoonotic (cows on the ag farm)
  3. Food-borne self inoculation (dodgy chicken)
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10
Q

What is the name of the bacterial projections that are important for attachment vs propulsion? A longer version of the attachment one is called…

A

Attachment: fimbriae
Propulsion: flagellum

Longer version of a fimbriae is a pillus

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11
Q

What is the shape of H Pylori? Is it gram neg or gram pos? How many flagella does it have?

A
  • Helix shaped
  • Gram negative
  • 4-6 flagella
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12
Q

__ to __ percent of peptic/duodenal ulcers are associated with H Pylori. The mechanism of this is…

A
  • 80 to 90 percent of ulcers are caused by this
  • H Pylori uses urease to produce ammonia, neutralising acid and allowing it to survive
  • It can then secrete cytotoxins to destroy the layers of the stomach (also increases the ability of the stomach to produce acid, worsening damage, and increases gastrin, causing inc. risk of gastric carcinoma)
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13
Q

Why does H Pylori specifically bind in the stomach. Link this to a universal aspect of the bacterial pathogenic life cycle

A
  • It is in the nature of H Pylori’s adhesion molecules to bind to stomach cells
  • Just like tissue-specific steroid activation, we see tissue-specific bacterial adhesion
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14
Q

True or false: bacterial exotoxins can be shared between bacteria, and are crucial for growth and proliferation

A
  • False
  • Yes, they can be shared via DNA sharing…
  • But no, they are not required for normal growth
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15
Q

What are the two types of exotoxins that bacteria can secrete?

A
  • Cytolysin (what might they do?)
  • Two-component toxins: B component Binds, and A component is translocated into the cell, where it’s Actively toxic
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16
Q

Describe the pathophysiology of cholera. Causative organism?

A
  • Influences CFTR channel, causing large chloride efflux
  • Creates osmotic gradient, pulls other ions into lumen, massive water loss
  • Causative organism is vibrio cholerae
17
Q

Which demographic is particularly susceptible to E. Coli infection?

A

Children under 5

18
Q

How does shiga toxin cause bleeding/thrombi? Why does it affect the kidneys more than other tissues?

A
  • Inhibits endothelial protein synthesis, in dying cells
  • Causes bleeding (cell falls away) or microthrombi (in response to cellular injury)
  • Receptor for STX is Gb3; expressed highly in kidney vasculature
19
Q

Why does it benefit bacteria to enter host cells? How do they do it?

A
  • Benefit: access to nutrients, evasion of immune system
  • Mechanism: inject proteins called invasins to cell to promote endocytosis in cells with no killing abilities (e.g. mucosal epithelium)
20
Q

What are four ways a bacteria can evade apoptosis by host cells once inside a phagosome?

A
  1. Induce apoptosis
  2. Escape from phagosome
  3. Prevent phagosome fusing w/ lysosome
  4. Inactivate host killing mechanisms
21
Q

What is the leading cause of hospital-acquired infectious diarrhoea? What % of people have it in the general population?

A
  • Leading cause is clostridioides difficile
  • 2-6% of people in the general population carry it
22
Q

Why does antibiotic use predispose to C Diff? What are the clinical features of C Diff?

A
  • C Diff is more resistant than regular microbiota (this explains why it’s common in hospitals)
  • Clinical features range from asymptomatic, to mild diarrhoea, to pancoliits, to toxic megacolon
23
Q

List 3 ways we can diagnose C. Diff

A
  1. Culture
  2. Cytotoxicity assay (detect cytotoxins from C Diff)
  3. PCR
24
Q

How do C Diff endospores work? How long can they live?

A
  • Provide durable escape pods for cellular components
  • Can live for over 20 years (!!!!!!!!!!)
25
Q

C Diff pathogenesis

A
  • Comes out of endospores
  • Releases cytokines to recruit immune cells
  • Produce yellow, suppurative pseudomembrane
26
Q

Which is more common: bacterial or viral gastro

A

Viral (by a wide margin)

27
Q

What are 3 features of viruses that can cause gastroenteritis?

A
  • Small but tough
  • Rapid disease course
  • Extremely good replication
28
Q

List two important viruses that can cause gastroenteritis

A
  • Rotavirus
  • Calicivirus
29
Q

Where, geographically, are the majority of rotavirus deaths concentrated? Why?

A
  • Less developed countries (mostly Africa)
  • Lack of other vaccines, rehydration therapy etc.
30
Q

How is Rotavirus transmitted?

A

Faecal-oral (checks out; young kids)

31
Q

How does rotavirus replicate during its lifecycle?

A
  • Enteres enterocytes
  • Hijacks cell mcahinery to replicate itself (bringing its own polymerase, since it’s dsRNA)
32
Q

How does rotavirus cause a secretory diarrhoea?

A
  • Enters enterocytes, and released non-structural protein 4 (NSP4)
  • Triggers increased release of Ca2+ and water, causing secretory diarrhoea
33
Q

True or false: the innate immune system is our best defense against rotavirus, highlighting the importance of lifestyle changes

A
  • False
  • Rotavirus suppresses the innate immune system
34
Q

Epidemiology of norovirus: which environments is it common in, and where does it usually come from?

A
  • Common in schools, nursing homes, planes, cruises etc.
  • usually comes from contaminated food or water
35
Q

Norovirus is a type of _____virus

A

Calicivirus

36
Q

Describe replication of norovirus

A
  • Positive sense ssRNA; can use host machinery
  • Encodes polypeptide that is cleaved into structural components for more viruses
37
Q

List 5 types of investigations that can be used to diagnose intestinal infections

A
  1. Faecal microscopy
  2. Cytotoxic assays
  3. PCR
  4. Histology
  5. Serology (antibodies)
38
Q

How do we treat bacterial vs viral vs parasitic gastro?

A

Bacterial: ?antibiotics (sparing)
Viral: Primarily rehydration + antidiarrhoeal agents/antiemetics
Parasitic: antiparasitic agents

39
Q

List 3 emerging approaches for the treatment of gastroenteritis

A
  1. Faecal transplant
  2. Probiotics
  3. Weaponised bacteriophages (not in use)

Medical Studies 2B (57 decks)

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