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Y2 GI block > Enteric Infections > Flashcards

Enteric Infections Flashcards

1
Q

What bacteria cause diarrhoea/ Gastroenteritis (GE)

A

bacteria (examples);

  • campylobacter (most common)
  • salmonella
  • shigella
  • E.coli
  • clostridium difficile
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2
Q

What virus’ cause diarrhoea/ Gastroenteritis (GE)

A

Norovirus (no.1)
sapovirus
rotavirus
adenovirus

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3
Q

What parasites cause diarrhoea/ Gastroenteritis (GE)

A 
cryptosporidium (very common in UK, especially during lambing season)
Giardia
Entamoeba histolytica
cyclospora
isospora
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4
Q

What are the symptoms of enteric infection

A
  • vomiting/nausea (nausea is more common than vomiting)
  • Diarrhoea (small + large intestine)
  • non intestinal manifestations (Botulism, campylobacter can cause Gullian barre syndrome)
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5
Q

What does vomiting as a symptom suggest regarding the aetiology

A

ingestion of pre-formed toxin in food
S. aureus, B.cereus
norovirus (viral aetiology)

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6
Q

what is the definition of diarrhoea

A

3 or more watery/loose stool per day

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7
Q

what type of diarrhoea is produced if there is too fluid and enzyme secretion in the SMALL INTESTINE

A

large volume watery diarrhoea
cramps, bloating, wind, weight loss due to malabsorption.
fever and blood in stool is rare

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8
Q

what type of diarrhoea is produced if there is absorption of fluid and salt in the LARGE INTESTINE

A

frequent small volume, painful stool

fever and blood in stool is common

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9
Q

Describe the pathogenic mechanism of diarrhoea

A
  • Toxin mediated
    (toxin produced prior to consumption in S.aureus and B.cereus)
    (toxin produced after consumption in C.dificile and E.coli)
  • damage to intestinal epithelial lining
  • invasion across the intestinal epithelial barrier (enterocytes)
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10
Q

Describe the investigation of infectious diarrhoea

A

History (GOOD history is very important)
Stool examination
Endoscopy

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11
Q

What key aspects would be covered in the history taking of a patient

A

food history
onset and nature of symptoms (small/large stools)
residence- more common in nursing homes
occupation- more risk in sewer/livestock workers
travel history
pets/hobbies- lizards or snakes covered in salmonella
recent hospitalisations
co-morbidity (heart failure or diabetes)

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12
Q

Why are majority of the stools not cultured for examination

A

because most pathogens are fastidious (only grows when specific nutrients are available)

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13
Q

describe the role of stool examination

A

low rate of positive stool cultures (1.5-5.6%)

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14
Q

describe the role of endoscopy for GE

A

rarely needed for GE
used to look for non-infection causes like IBD
However, occasionally the diagnosis of some pathogens requires biopsy like CMV in immunocomprimised

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15
Q

What are the treatments available for GE

A

Oral rehydration solution

May require i.v fluid replacement if vomiting

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16
Q

Why are antibiotics not that useful to treat GE

A
  • Antibiotics reduce duration of diarrhoea by 1 day (not a significant difference)
  • Antibiotics can worsen the outcome in some(E.coli)
  • Antibiotic resistance
17
Q

When should patients be given antibiotics

A
  • very ill patients (sepsis)
  • consider if signifcant comorbidity (little reduction in diarrhoea be clinically meaningful)
  • certain causes (c.dificile associated diarrhoea- vancomycin/metronidazole)
18
Q

what is the advice for symptomatic treatment like imodium

A

Do not use them

19
Q

describe how campylobacter causes GE

A
  • infecting dose is of 9000 organisms
  • sensitive to stomach acidity
  • attaches and invades intestinal epithelial cells (small +large intestine)
  • incubation period is of 3 days (1-7 days)
    incubation period is the time from the moment of exposure to until symptoms of the disease appear
20
Q

what are the clinical features of campylobacter

A
  • Diarrhoea (frequent and high volume, blood in stool common)
  • abdominal pain (often severe)
  • nausea is common (vomiting is rare)
  • fever
  • self limiting (organism that limits its own growth by its actions)
  • antibiotics are rarely given (risk of resistance)
21
Q

What are the late complications of campylobacter

A

reactive arthritis

Gullain-Barre syndrome

22
Q

describe how salmonella causes GE

A 
numerous serotypes
- typhoidal (causes typhoid fever)
- non-typhoidal (causes GE)
infectious dose of 10,000 organisms
interactions with host
- increased risk if decreased stomach acid
- increased risk if diminished gut flora
invasion of enterocytes with subsequent inflammatory response
23
Q

what are the clinical features of salmonella

A
  • illness within 72 hrs of ingestion
  • nausea, diarrhoea, abdominal cramps, fever
  • antibiotics dont reduce duration
  • common in food handlers
24
Q

What are the complications of salmonella

A
  • bacteraemia (bacteria in blood)

- secondary infection (endocarditis, osteomyelitis, mycotic aneurysm)

25
Q

describe how E.coli causes GE

A
  • attachment
  • shiga toxin production (enterocyte death, enters sytemic circulation- can cause problems with kidneys)
  • infectious dose of 10 organisms
  • sporadic outbreaks
  • can catch it from animals that haven’t been butchered properly
26
Q

what are the clinical features of E.coli

A
  • incubation period is 3-4 days
  • bloody diarrhoea and abdominal tenderness
  • fever is rare
27
Q

describe a complication of E.coli

A

Haemolytic uraemic syndrome
- systemic effect of shiga toxin
triad of:
- microangiopathic haemolytic anaemia (reduces RBC count)
- acute renal failure
- thrombocytopenia (this more than renal failure in older people)

  • develops 5-10 days after onset diarrhoea
  • 50% require diarrhoea
  • low mortality
  • avoid antibiotics
28
Q

what is the management and prevention of E.coli

A 
management- supportive
prevention
- strict infection control for heath workers
- screening of contacts
- appropriate butchering of meat
- public health measures in outbreaks
29
Q

what are the risk factors of Clostridioides Difficile infection

A
  • chemotherapy (destroys gut flora)
  • antibiotic exposure (broad spectrum destroy gut flora)
  • older age (>65 years)
  • PPI use (increased risk of colonisation)
  • hospitilisation
30
Q

what are the pathogenesis of Clostridioides Difficile

A
  • decreased colonisation resistance
  • colonic colonisation
  • toxin production
    (ulceration of the gut)
31
Q

what are the clinical features of Clostridioides Difficile

A
  • loose stool and colic (severe pain in the abdomen, especially seen in babies)
  • fever
  • leukocytosis (increased WBC in blood)
  • protein losing enteropathy
32
Q

what is the diagnosis of Clostridioides Difficile infection

A
  • presence of organism and toxin in stool

check if CD is present in stool, if it is present then check if it is PRODUCING the toxin- i.e causing diarrhoea

33
Q

what antibiotics are used for treatment of Clostridioides Difficile

A

broad spectrum

  • vancomycin
  • metronidazole
34
Q

what is the treatment for Clostridioides Difficile

A
  • aim is to recolonise normal flora
  • stop causative antibiotics (broad spectrum)
  • take narrow spectrum antibiotics
35
Q

what is the treatment advised for patients with recurrent Clostridioides Difficile

A

Faecal Transplant

36
Q

what is the most common viral cause of gastroenteritis

A

norovirus
present all year round
causes epidemics

37
Q

describe the transmission of norovirus

A
  • faecal oral route
  • infectious dose of 10-100 viruses
  • can grow in stable environment (cant grow in bleach, up to 60 C)
  • occurs in all seasons (peak in winter)
38
Q

what are the clinical features of norovirus

A

acute diarrhoea and vomiting
24-48 hrs
no lasting immunity
(ppl feel like they are dying) LoL

Y2 GI block (25 decks)

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