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Medsci 202 > Diarrhoeal Disease > Flashcards

Diarrhoeal Disease Flashcards

1
Q

What are the different causes of Diarrhoea?

A

Bacteria

Viral (rotavirus, norovirus)

Protozoa (Giardia, etc)

Fungal (mycotoxins)
non-infectious (Coeliac disease, lactose-intolerance, etc)

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2
Q

What are the three main types of bacteria that cause diarrhoea?

A
  •   Vibrio cholerae
  •   Campylobacter jejuni!
  •   Clostridium difficile!
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3
Q

What are the three types of diarrhoea?

A
  •   acute watery diarrhoea
  •   acute bloody diarrhoea
  •   persistent diarrhoea
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4
Q

Describe the duration and how acute water diarrhoea is caused?

A

lasts several hours or days,

and includes disease caused by Vibrio cholerae, Escherichia coli and Rotavirus

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5
Q

How and by what is acute bloody diarrhoea caused?

A

also called dysentery-
mainly caused by Shigella- often a result of tissue
invasion

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6
Q

Describe the duration and how persistant diarrhoea and what it causes?

A

– lasts 14 days or longer- a

major cause of malnutrition in children

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7
Q

What doeas Vibrio cholerae microbiology?

A
  •   Gram-negative, comma-shaped bacterium

*   Flagellum at one cell pole!

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8
Q

What is the source, reservoir, transmission of V. cholerae?

A

Associated with shellfish

Lack of sanitation when disasters occur i.e. human faeces in water

Need a high dose for infections to occur (10^4 - 10^6)

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9
Q

Is V.cholerae prevelant in nz?

A

no. However there are 5 million cases around the world a year

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10
Q

How does V.cholerae colonize and become virulent? i.e. how does it work to cause the disease?

A

Large doses allow some cholerae to survive the stomach and small intestine using the pilus.

They then secrete the cholera toxin which only the virulent strains can do.

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11
Q

How does the cholera toxin cause the disease?

A

The toxin = A and B = AB5 family toxin
A = 1 subunit
B = 5 subunits only bind to enterocytes
So B binds to enterocytes and the cell endocytoses the whole toxin.
The toxin goes to endosome, Golgi then ER.
ER releases the A subunit which is an enzyme that stimulates the adenylate cyclase converting ATP to cAMP.
cAMP activates Cl- channels causing the efflux of Cl-. Na+ follows the gradient creating an osmotic IMBALANCE causing water to leave the cell and enter the gut lumen resulting in DIARRHOEA.

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12
Q

What are two important characterics of V.cholera disease?

A

It causes deregulation i.e. osmotic imbalance but DOES NOT cause cellular damage.
There is no inflammation
no physical damage to the epithelial cells in the gut.
RECOVERY is quick

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13
Q

What are the symptoms of V.Cholera?

A 
Vomiting (1-2L/day)
Rice water stools (20L/day)
Headache due to thick blood when severe
Dehydration  leading to shock 
NON-BLOODY stools
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14
Q

In moderate dehydration regarding V.cholera what are the symptoms?

A 
tired
thirsty
decreased urine output
dry skin
headache
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15
Q

In severe dehydration regarding V.cholera what are the symptoms?

A
  • Lack of sweating
  • Little or no urination — any urine that is produced will be dark yellow or amber !
  • Sunken eyes
  • Shriveled and dry skin that lacks elasticity and doesn’t “bounce back” when pinched into a fold
  • Low blood pressure
  • Rapid heartbeat
  • Rapid breathing
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16
Q

How do you treat a moderate dehydration due to v.cholera?

A

good hygiene
intravenous fluid
improved sanitation

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17
Q

How do you treat severe dehydration due to v.cholera?

A

intravenous fluid
Oral rehydration salts solution
mixute of clean water, salt and sugar which is absorbed replacing lost water
antibiotics

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18
Q

Which antibiotic should be used for severe and maybe moderate cases?

A

Doxycycline

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19
Q

Why is doxycycline effective?

A
  • Cheap, effective antibiotic against V. cholerae!
  • Kills bacteria
  • Reduces duration of symptoms
  • Reduces shedding
  • In an epidemic this reduces pressure on water for
    rehydration and reduces numbers of bacteria shed into the local environment!
  • Use after vomiting phase has ended
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20
Q

Case Numbers = Campylobacter

A

6708, 153.6

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21
Q

Case Numbers = Salmonella

22
Q

Case Numbers = Shigella

23
Q

Case Numbers = VTEC

24
Q

Case Numbers = Yersinia

25
Q

How do you kill campylobacter on a daily basis?

A

cooking meat well

26
Q

What is the incubation period of campylobacter

27
Q

What is the duration of the disease caused by campylobacter?

A

3 days to 3 weeks

28
Q

What are the symptoms of campylobacter?

A
  • Diarrhoea, sometimes bloody
  • Abdominal cramps
  • Fever
  • Sometimes bacteraemia – particularly in neonates and
    compromised adults
  • death is rare - mainly in infants
29
Q

How does campylobacteriosis work?

A

Small dose, don’t have endospores killed by heat.
BUT
they work by having several virulence factors i.e. lipooligosacchaide which is proinflammatory
Capsule for immune evasion
CDT - cytolethal distending toxin that leads to cell death

30
Q

What do campylobacter look under the microscope?

A
  • darkfield or phase-contrast microscopy of faecal
    specimens demonstrates the characteristic darting
  • Gram stain of the stool show slim, short (0.3-0.6 µm), curved rods.
  • cultured on Selective and discriminative agars. Look like watery drops on agar plates
31
Q

How is gastroenteritis self limiting?

C.jejuni

A

! Recovery in 10 days!

  • Fluid and electrolyte replacement
  • Pain relief
  • Come back if symptoms worsen, do not improve!
  • Emphasise hygiene
    • Faeces contain the pathogen!
32
Q

Why are anti-diarrhoeal drugs not recommended?

C.jejuni

A
  • Stop ‘flow’
  • But concentrate toxins in GIT, increase contact time
    of pathogen/toxin with the intestinal mucosa
    * OK in some cases- control of watery diarrhoea
  • Not recommended for dysentery without
    antimicrobial therapy
33
Q

Why are antibiotics for campylobacteria not recommended?

A
  •  Rarely effective against diarrhoea
    • Duration and severity
  •  Affect good bacteria too
34
Q

When would you recommend antibiotics to cure campylobacteria?

A
  • Recommended if severe, if there is spread (or the

risk of spread) to blood or if a prolonged case

35
Q

When would you recommend antibiotics to cure c.jejuni?

A
  • Recommended if bloody stools
  • MACROLIDES e.g. AZITHROMYCIN or
    ERYTHROMYCIN!
  • Increasing levels of resistance have been observed
36
Q

What food hygiene advice would you give to avoid any stomach disease especially campylobacter?

A

cook properly
reheat thoroughly
storage
utensil change

37
Q

How would you culture campylobacter?

A
  • blood agar, containing antibiotics that reduce the
    emergence of other enteric microorganisms.
    * Microaerophilic: Incubated in 5% O2 and 10% CO2
    at 42°C.
  • Water droplet like colonies. Appear 24-48 hours.
38
Q

What further tests would you do to identify c.jejuni?

A
  • Catalase and oxidase positive!

* There are other Campylobacter and related species, but most probably C. jejuni

39
Q

What are the long term consequence of C.jejuni?

A

Patients develop autoimmune disease due cross reacting antibodies. They affect myelin (Guillian-Barre syndrom (1/1000 cases)) and some structure of cells like glycoproteins. This causes slight paralysis.
Reactive arthritis 1% of cases affecting multiple joints with debilitating pain.

40
Q

What is an example of nosocomial diarrhoea?

A

Clostridium difficile

41
Q

What is the microbiology of Clostridum difficile?

A 
•  Gram-positive, rod-shaped bacterium
•  Obligate anaerobes
•  Produces Endospores!
- Dormant!
- Survival structure!
- Airborne spread!
42
Q

What is the mode of transportation of Clostridium dificile?

A
  • Normal flora in GI tract
  • 5% carriage rate, 20% in hospital
  • Person to person in hospital
    • diarrhoea spread
    • endospores
43
Q

Who are the people most at risk with clostridium difficile?

A
  • Antibiotic recievers
    • beta lactams and clindamycin especially
    • fluoroquinolones (epidemic strain)
  • longer that 1 week patients
    • give time for bacteria to colonize
  • antibiotics disrupts normal flora. decreased competition for bacteria
44
Q

How do clostridium difficle grow in the body?

A

Antibiotics kill competition that are non endosporic. Which means the endospores of C.difficile can grow and out compete other species when treatment is stopped.

45
Q

What are the virulence factors of C.difficle?

A

Two toxins - A and B.
A causes this = depolarise actin cytoskeleton, actin depolymerises, cells round up and lose integrity.
B = gains access to submucosa and causes apoptosis of cells in the sub mucusa. This allows colon bacteria/ LPS to enter the blood.
The loss of epithelial barrier intergrity causes a pseudomembrane to be formed containing bacteria and immune cells like a puss. Inflammation and death occurs of the submucosa.

46
Q

What are the physical altercations due C.difficle?

A

ulceration of the colon
Pseudomembranous colitis - pus
Toxic megacolon - inflammation then sepsis

47
Q

What would you do to diagnose C. difficile?

A 
Early diagnosis good
Antibody assay for toxins
Culture on selective agar or PCR (preferred)
look for hypervirulent ribotype 027
raised WBC count
48
Q

Who is more susceptible to C.difficile?

A

Ederly people get it after antibiotic consumption

49
Q

How do we treat c.difficile?

A

Don’t use broad range antibiotics like pennicilin that kills good bacteria use narrow spectrum antibiotics like METRONIDAZOLE (anaerobic bacteria) or Oral vancomyacin (gram positive bacteria) both are specific to C.difficile
ALSO
support fluid loos and pain
use probiotics (faeces of recovered patient in unrecovered patient) to restore microflora

50
Q

How would you prevent the rest of the hospital from getting infected with c.difficile?

A

be clean
screen patients with stool toxin test
always note 20% relapses
limit use of predisposing antibiotics

Medsci 202 (15 decks)

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