Lecture 7 - Bacterial diarrhoea Flashcards

1
Q

what are the symptoms of acute gastrointestinal illness?

A
  • vomiting
  • diarrhoea
  • abdominal pain
  • fever
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2
Q

what is dysentery?

A

bloody diarrhoea

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3
Q

what bacteria causes can lead to AGI?

A
  • campylobacter
  • cholera
  • clostridioides difficile
  • salmonella
  • E coli
  • etc
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4
Q

what causes lead to AGI in total?

A
  • bacteria (common)
  • viral
  • protozoal
  • toxin (staph aureus, non-microbial)
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5
Q

what are the sources or routes of transmission?

A

contaminated food, water or direct or indirect contact with feces

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6
Q

what is the most common microbial cause of diarrhoeal disease in NZ?

A

campylobacteriosis (~6000 cases per year)

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7
Q

how many children get diarrhoea disease each year?

A

1.7 billion, and 500,000 die

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8
Q

how many cases are there of cholera worldwide each year?

A

between 1.7-4 million, and 20,000 to 143,000 deaths

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9
Q

what is cholera rice water stool?

A

when profuse diarrhoea is so watery it looks like water rice had been boiled in

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9
Q

is cholera prevalent in new zealand?

A

no, there is hardly any cholera cases in NZ

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10
Q

what does vomiting and diarrhoea due to cholera lead to?

A

dehydration, often severe

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11
Q

where is cholera’s resevior?

A

in shellfish in waters and human carriers

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12
Q

how does transmission of cholera occur?

A

human carriers (feces into water - contamination)
- can be asymptomatic
or eat the shellfish of course

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13
Q

describe the colonisation of cholera

A
  • survives passage through stomach
  • colonises intestine, aided by a pilus for attachment
  • produces toxin AB5
  • stimulates Cl- secretion: secretory diarrhoea
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14
Q

what is the incubation period of cholera?

A

anywhere between 12h and 5 days

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15
Q

what is an infectious dose of cholera?

A

an infectious dose is between 10^5 and 10^8 CFU, but may be lower if stomach acid is not produced (food scarcity)

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16
Q

symptoms of cholera?

A
  • vomiting
  • rice water stools
  • dehydration
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17
Q

how do we diagnose cholera?

A
  • rice water stools very telltale symptom
  • selective agar
  • PCR tests (quicker)
  • rapid diagnostic tests (quickest)
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18
Q

how does the selective agar select for cholera?

A
  • high concentrations of thiosulphate and citrate inhibit enteric bacteria
  • bile salts inhibit gram +ve bacteria
  • TCBs select for vibrios such as cholera
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19
Q

how does the selective agar differentiate cholera?

A
  • the agar plate contains sucrose and an indicator. when cholera ferments the sucrose, the pH drops and the green turns to yellow
  • results overnight
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20
Q

how can a gram stain be used to diagnose cholera?

A

gram staining the rice water stools shows red curved rods
- gram negative bacilli

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21
Q

what are rapid diagnostic tests for vibrio cholerae and why are they not very reliable?

A
  • dipstick which changes colour in presence of cholera
  • high rate of false negatives
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22
Q

what are the treatment aims?

A
  • oral rehydration therapy (or IV drip if severe)
  • prevent the spread with good hygiene and sanitation
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23
Q

role of antibiotics in cholera?

A

recommended in severe cases
also in moderate cases if an epidemic
(cheap and bacteriocidic, but must be used after vomiting phase to retain)

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24
Q

which antibiotic is commonly used against cholera and why?

A

doxycycline
- it is cheap and bacteriocidal

25
Q

how to prevent cholera?

A
  • safe water
  • good sanitation
  • good personal hygiene
    not essential but good:
  • nutrition
  • vaccine?
26
Q

what effect does doxycyline have on a patient with cholera?

A
  • reduction in duration of symptoms (reduces the need for ORT/clean water)
  • reduces shedding (reduces transmission routes)
27
Q

gastroenteritis is often ____ _________

A

self limiting
- GP will say come back if your symptoms worsen or dont improve

28
Q

how long does it take to get over gastroenteritis?

A

approx 10 days

29
Q

why aren’t anti diarrhoeal drugs recommended when there is blood in the feces?

A
  • stop the ‘flow’
  • bacteria become more concentrated have more time in contact with the intestinal mucosa
30
Q

when are anti diarrhoeal drugs okay to use?

A

when the diarrhea is only watery

31
Q

why don’t we use antibiotics for campylobacter infections?

A
  • they reduce the severity and duration of the diarrhoea, but it also damages the good gut flora/bacteria
  • only recommended if severe or prolonged or spread infection
32
Q

if antibiotics are administered for campylobacter, what antibiotics will be used?

A

macrolides
- but campylobacter resistance levels are increasing

33
Q

what does stool microscopy of campylobacter show?

A
  • not highly definitive due to many other bacteria in stool
  • can see campylobacter (thin gram negative bacteria, looks like a skinny crinkle cut chip)
34
Q

what other tests can we do for campylobacter?

A
  • PCR tests
  • cultures
35
Q

what cultures can we use to test for campylobacter

A
  • blood agar containing ABs that reduce emergence of other enteric bacteria
  • microaerophilic
  • other pathogens come back negative
36
Q

sources of campylobacter?

A
  • chicken
  • heavy rainfall causes animal feces into water supply
37
Q

transmission of campylobacter?

A

via the fecal oral route, and ingestion of contaminated food/water
- microorganism is ingested.

38
Q

what is the course and symptoms of campylobacter?

A

incubation is 2-11 days
- vomiting
- diarrhoea
- fever
- sometimes bacteremia
duration is 3 days to 3 weeks

39
Q

how often do people die from campylobacter?

A

not often, only about 1 in 8,000 cases
- infants or immunocompromised
- cross reactions

40
Q

colonisation of campylobacter?

A
  • has a flagella
  • adhesins
  • pili
  • lipopolysaccharide for immune evasion (difficult to recognise - camouflage effect)
41
Q

how does campylobacter cause damage?

A

toxins CLT (cholera like toxin - increases water secretion) and CDT (cytolethal distending toxin - leads to cell death)

42
Q

what is a nosocomical diarrhoea?

A

hospital acquired

43
Q

source of clostridioides difficile?

A
  • part of the normal flora of the GI tract
  • 5% carriers
  • 20% in hospital (contamination from diarrhoea of another infected person)
44
Q

who is most at risk with clostridioides difficile?

A

hospital patients receiving antibiotics (beta lactams and clindamycin and fluroquinolones)
- longer than 1 week in hospital
- other treatments that disrupt the colonic flora (removes competition)

45
Q

colonisation of clostridioides difficile?

A
  • other broad spectrum ABs reduce numbers of other competing colonic flora
  • clostridioides difficile grows to high numbers
  • may be sensitive to antibiotics but forms an endospore and survives them
46
Q

what is an endospore?

A
  • dormant survival structure, not used by many bacterium
  • allows it to survive in hospital
47
Q

how are endospores/clostridioides difficile killed?

A

heated to 121 degrees
sporicidal chemicals

48
Q

what kind of aerobes are clostridioides difficile?

A

obligate anaerobes, which means they can’t survive in oxygen.
however the endospores can survive in oxygen

49
Q

what are the bacterial virulence factors of clostridioides difficile?

A
  • toxin A and toxin B of clostridioides difficile.
50
Q

how does clostridioides difficile move into the cell?

A
  1. attachment
  2. RME
  3. pH increases and clostridioides difficile is released
  4. causes collapse of the actin cytoskeleton
51
Q

how does clostridioides difficile effect the epithelia of the gut?

A
  • rounding of epithelial cells cause loss of protection, allows toxin B and other bacteria to enter into the submucosa
  • leads to epithelial cell death which forms a pseudomembrane (ulceration), and the submucosa underneath becomes inflamed.
  • as this worsens, we get toxic megacolon
52
Q

what diagnostic tests can we use for clostridioides difficile?

A
  • early diagnosis is important for effective treatment
  • antibody based assays
53
Q

what antibody based assays do we use to diagnose clostridioides difficile?

A

for toxins and for GDH, a cell associated antigen

54
Q

what diagnostic tests do we do if the antibody based assays come back negative?

A
  • PCR for toxin genes
  • gram stain for a gram positive bacilli
  • patients will very likely have a raised WBC count
55
Q

why don’t we use microscopy or cultures very often for clostridioides difficile diagnosis?

A

because many people carry this bacterium, so it could come back as present but not be what is causing the issue

56
Q

how do we treat clostridioides difficile?

A
  • discontinue implicated AB
  • kill with an AB (metronidazole or vancomycin if resistant)
  • support fluid loss and pain
  • restoration of microflora/probiotics (fecal transplants to outcompete CD)
57
Q

what must the ward do if there is a clostridioides difficile case?

A
  • attention to hygiene and cleanliness, there is potential for an outbreak
  • limit use of predisposing AB
  • there is a 20% relapse rate
58
Q

if clostridioides difficile became more serious e.g toxic megacolon, how would we treat it?

A

stronger antibiotic such as vancomycin
support fluid loss and pain

59
Q

if clostridioides difficile looks to be getting better what do we do?

A

restoration of gut flora via fecal transplant or probiotics