L23 Diarrhoea and Acute Gastro-intestinal illness Flashcards

1
Q

Define Gastroenteritis, the time frames for acute, persistent and chronic, and two places of origination

A

Syndrome that has diarrhoea and vomiting

  • Acute <14 days
  • Persistent 14-30 days
  • Chronic 30days +

Two types is

  • Nosocomial (hospital)
  • Community
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2
Q

What are the natural features of the gut that protect against microbial infection (5) and what are the functions of the gut

A

Role: absorption of fluid and nutrients

  • Gastric acidity protects against
  • Intestinal motility can help to move bacteria out
  • intestinal microflora help to compete with bad bacteria for growth

Local and systemic immune responses:
- M cells that sample luminal microbes for immune surveillance

  • IgA non inflammatory antibodies which provide neutralisation and mucosal protection
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3
Q

Compare and contrast the site, presentation and causes of Non-inflammatory diarrhoea and Inflammatory diarrhoea

A

NI: Small Bowel

  • Caused by enterotoxin/producing organism ingestion, viruses that adhere to mucosa.
  • Mucosal disruption that directly affects movement of ions/water without causing acute inflammation/destruction
  • Presents: large volume of watery diarrhoea without blood/pus
  • May have nausea, vomiting or cramps

ID: Distal Ileum and Colon

  • Caused by secretion of cytotoxins, or invasion of intestinal epithelium.
  • Acute mucosal inflammation/ ulceration, neuropeptides cause loss of absorptive surface.
  • Presents: Blood, mucus and WBC in stool. Pain in lower left quadrant, fever,
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4
Q

Compare the pros and cons of the two methods of diagnosing a pathogen from diarrhoea: Culture and Molecular multiplex PCR.

(microscopy is good for parasites mainly)

A
  1. Stool Culture
    Cons:
    - Labour intensive: Have to differentiate pathogenic bacteria from commensal through selective agar, differential agar and chromogenic agar often require
    - Culture is slow: 48-72 hours to grow and identify which isn’t very useful with self limiting acute cases
    -Only bacteria is culturable
  2. Syndromic panel molecular testing
    Pros:
    - Single sample, single test for Viral, bacterial and parasitic pathogens
    -Rapid results within an hour

Cons:

  • more expensive
  • It only detects what primers bind to, so there is potential for missing out pathogens present that are not being tested for
  • more sensitive than culture therefore can be difficult to interpret as DNA/RNA can remain positive after resolution/treatment.
  • doesn’t have an organism for antibiotic susceptibility testing
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5
Q

How does chromogenic agar work

A

Targets an organism that grow as coloured colony due to metabolism/hydrolysis of one or more chromogenic enzyme substrate. Or make something that changes pH.

eg. Salmonella produces H2S - black streaks

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6
Q

What is the general management of diarrhoea

A
  1. Symptomatic relief
  2. Rehydration as morbidity/mortality comes from dehydration
  3. Preventing transmission
  4. Identifying those at risk of severe disease / disease that requires treatment
  5. Antibiotics if appropriate: in cases of shiga toxin ecoli and nontyphoid salmonella it doesn’t confirm benefit.
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7
Q

What type of diarrhoea does Food poisoning cause and what is the main pathogens, presentation

A

Non inflammatory
- Toxin from Staphylococci spp. or B. cereus which are able to multiply at wide range of temperatures

-Rapid onset less than 24hrs usually resolving within 24 hrs. Often at group settings

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8
Q

Describe the pathogenesis of viral gastro-enteritis - what type of diarrhoea and common features

Has a PCR diagnosis.

A

Non-I diarrhoea.

P: infection of enterocyte epithelium with adherence to mucosa disrupt absorption/secretion

Common features
-Primary malabsorption: viral replication causes necrosis in epithelial cells and loss of carb and protein enzymes.

  • Reduces absorptive capacity: Localised responses causing ischaemia of villi and villous atrophy
  • Increased motility of Sm I : Autonomic dysfunction
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9
Q

Compare the presentation of Rotavirus vs Norovirus

3rd most common is Enteric adenovirus

A

N: common and spreads rapidly due to v low infectious dose so needs contact isolation to prevent ward outbreaks which are managed by ward closures.

  • vomiting is common feature due to delayed gastric emptying

R: affects almost all children during infancy/early childhood. Severe disease 3mo -2yrs.

  • Fever and vomiting followed by diarrhoea.
  • Has live attenuated oral vaccine: 6wks , 3 mo.
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10
Q

What is the transmission, presentation, of Shigella spp. bacteria induced inflam diarrhoea

A
  1. Human to human transmission- faecal oral, sexual (MSM). Low infectious dose. Can withstand low pH
  2. Presents with initially watery diarrhoea, fever and abdo pain. Then blood, mucus, pus in diarrhoea.
    - Bacteremia is rare bc invasion is superficial above the lamina propria
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11
Q

What is the transmission, presentation, of Campylobacter induced inflam diarrhoea

A
  1. Mainly faecal-oral, contaminated food/water (chicken), sometimes human human.
  2. Causes self limiting inflammatory colitis of J, I and colon. Post infectious complications include Guillan barre syndrome
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12
Q

What is the transmission, time course of incubation Salmonella induced inflam diarrhoea
- 2 types

A
  1. Person to person spread or via contaminated food/water. Low infectious dose.
  2. Long and variable incubation period (1-6 weeks)
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13
Q

What is the transmission, presentation of Giardia induced non-inflam diarrhoea

A
  1. Faecal-oral transmission via ingestion of cysts in contaminated food/water. Low infectious dose
  2. Acute/chronic diarrhoea, abdo pain and malabsorption
    - Trophozoites adherence to damages mucosal brush border without invasion reducing absorptive surface
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14
Q

What is the class, action, targeted pathogens, effectiveness as a drug and SE/cautions of using Metronidazole

A
  1. Class is Nitroimidazole
  2. Enters organism via passive diffusion and is activated by electron transport protein found in anaerobes.

Inhibits DNA synthesis and induces DNA damage -> DNA degradation and cell death.

  1. Targets Anaerobes and some parasites as aerobic bacteria can’t activate it.
  2. high oral bioavailability, moderate to large volume of distribution, penetrating CNS.
  3. Well tolerated but has
    Nausea, diarrhoea, metallic taste.
    - prolonged use can cause irreversible peripheral neuropathy
    - have to avoid alcohol for 3 days otherwise vomiting, nausea, flushing, tachycardia and dyspnea.
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15
Q

What are differential diagnoses for infectious diarrhoea

A
  1. Intra-abdominal infection/systemic infection

2. Non infectious diarrhoea: IBD, Coeliac disease, new meds, IBS

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16
Q

What is the incubation time course and use of antibiotics as treatment of Shigella spp. bacteria induced inflam diarrhoea

A
  1. incubates 1-4 days, shed days-wks after illness.
  2. Antimicrobials useful to reduce shedding, duration and severity.
    However increasing antibiotic resistance
17
Q

What is the time course of culture and treatment/prevention of Campylobacter induced inflam diarrhoea

A
  1. Grow more slowly than other enteric flora so requires selective culture
  2. Susceptible to gastric acid, freezing, drying, pasteurisation or chlorination.

Generally self limiting, but Use antibiotics in - ppl with severe or prolonged symptoms,

  • high risk complications
  • high risk 4 transmission
18
Q

What is the presentation and treatment of Salmonella induced inflam diarrhoea
- 2 types

A

2a. Typhoidal salmonella
- high fever, headache, bacteremia WITHOUT diarrhoea
4a. Needs antibiotic treatment

2b. Non-typhoidal salmonella.
- ilieum + colon infection, fever, diarrhoea and occasional extra-intestinal infections.

4b) Antibiotic treatment only required for infants <3 mo. Adults with severe disease, immunocompromised or with prosthetic valve grafts.

Intrinsically resistant to cephalosporin and aminoglycosides. Increasing resistance to others with plasmids.

19
Q

What is the time course, diagnosis and treatment of Giardia induced non-inflam diarrhoea

A
  1. Often slow onset, can be present for months
  2. Diagnosed via stool microscopy for cysts/trophozoites + antigen detection/pcr.

Treatment with metronidazole/ornidazole