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MICBI - Clinical MICBI > L32 Enteric infections > Flashcards

L32 Enteric infections Flashcards

1
Q

What is the definition of diarrhea?

A

Passage of =/> 3 loose or liquid stools per day

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2
Q

What is acute and chronic diarrhea?

A

Acute: <2 weeks
Persistent: > 2 weeks

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3
Q

Which of the following is incorrect?
A. Diarrheal stool is stool that is conformed to the shape of the container
B. Gastroenteritis is a syndrome characterised by n/v, diarrhea, abdominal discomfort rather than only diarrhea
C. Food poisoning is a type of gastroenteritis (GE)
D. All GE are caused by food poisoning
E. Dysentry is bloody diarrhea with painful defaecation

A

D

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4
Q

Dysentry is caused by either ________ or _________?

A
  1. Bacterial rods (bacillary)

2. Amobebic (Entamoeba histolytica)

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5
Q

Name the 4 groups of causative agents causing gastroenteritis.

A
  1. Bacteria: MC
  2. Viruses: rotavirus, norovirus (causing watery diarrhea rather than dysentery)
  3. Protozoa: Giardiasis (watery), amoebiasis (dysentery)
  4. Non-infective: small bowel malabsorption
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6
Q

List 4 host factors pre-disposing to gastroenteriris.

A
  1. Age
  2. Immunity (humoral and cell-mediated)
  3. GI: normal flora, mucosal integrity, motility
  4. Gastric acidity: use of PPI

Others: motility of gut

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7
Q

What is the transmission method of gastroenteritis?

A
  1. Fecal-oral route
  2. Person-to-person

(waterborne, animal reservoir, sanitation and public hygiene)

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8
Q

How is the storage of food related to gastroenteritis?

A
  1. Room temperature without refrigeration at 4 degrees celcius
  2. un-preserved food
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9
Q

EPEC (enteropathogenic E Coli) main pathogenic mechanism is by mucosal adherence.
Explain the mode of action and clinical presentation.

A

Effacement of intestinal mucosa;

Presented with moderate watery diarrhea

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10
Q

A patient presented with bloody diarrhea. Possible pathogenesis is Mucosal invasion/ cytotoxin.
The mode of action is the penetration and destruction of the mucosa. What are the examples of causative agents?

A

CHESS mneumonics:

  1. Campylobacter jejuni
  2. EHEC (Enterohaemorrhagic E coli)
  3. Entamoeba histolytica
  4. Shigella
  5. Salmonella
  6. V. parahaemolyticus (vibrio)
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11
Q

Exotoxin from ETEC (enterotoxigenic E coli) and V. parahaemolyticus can be heat stable/ heat-labile. What do they mean?

A

Heat-stable toxin (ST): resist 1000 degrees for 15 minutes, acid resistant, alkali susceptible

Heat-labile toxin (LT): denature at 600 degrees for 15 minutes
(activates adenylate cyclase to increase cAMP in intestinal mucosa)

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12
Q

S. aureus, Bacillus cereus, and Clostridium botulinum all work by the production of ________________ that is pre-formed in food, acting directly on ______________, patients presented with _________________.

A

Neurotoxins/enterotoxins;
CNS/ENS;
Profuse watery diarrhea

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13
Q

Other than exotoxin pre-formed in food, ________________ formed in vivo can also cause profuse watery diarrhea causing fluid secretion ___with/without__ mucosal damage.

List 3 causative agents to this type of infection.

A

Enterotoxins; without;

  1. Clostridium perfringens
  2. Clostridium botulinum (infants)
  3. C. difficile
  4. Vibrio cholerae
  5. V. parahaemolyticus
  6. ETEC (enterotoxigenic E.coli)
  7. Bacillus cereus (long incubation)
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14
Q

What important history taking information to be noted in patients who complained of diarrhea? (4)

It is also important to examine the hydration status (skin turgor, peripheral and central pulses) and urine output of the patient.

A
  1. Onset
  2. Food history
  3. TOCC: travel, occupation, cluster, contact
  4. Appearance of stool
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15
Q

Which of the following about laboratory investigations of diarrhea is correct?
A. Stool can be taken for culture or bacteria or microscopy
B. Blood can be taken for culture
C. Food can be taken for culture routinely
D. Food sample is for the detection of bacteria quantitatively
E. Food sample can detect heat-stable toxins and Enterotoxins

A

C is incorrect

B. yes, in severe cases
C. no! only in case of an outbreak

D. >10^5 cfu/g (colony forming unit) food (S.aureus, B.cereus), >10^6 cfu/g food (C.perfringes)

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16
Q

Which of the following about Stool culture is correct?
A. Bacterial culture: TCBS for Shigella and Salmonella
B. Bacterial culture: DCA (Deoxycholate citrate agar) for Vibrio
C. Skirrow’s agar for Campylobacter
D. Single collection of ova and cysts (parasites) for microscopy
E. Gram stain for Cryptosporidium (parasite)

A

C is correct

A: Thiosulfate-citrate-bile salts-sucrose agar - VIbrio!

  • Yellow: Vibrio cholerae
  • Green: Virbio parahaemolyticus

D: requires 3 times! intermittent excretion, amoebae must be examined within 30 minutes after collection
E: Modified acid fast stain for cryptosporidium

17
Q

Stool test:
A. Viral: antigen detection (rotavirus) in infants
B. Viral: PCR (norovirus)
C. Toxin A/B detection by PCR/ELISA in C. difficile colitis

A

All of the above

18
Q

What is the 1st line treatment for diarrhea? (1)

Briefly describe what is that. (1)

A

Oral rehydration therapy

  • Hypo-osmolar (245nM): low glucose and Na
  • improve efficacy in children with acute diarrhea
  • may cause biochemical hypoNa without any clinical signs
19
Q

If there is severe dehydration, what is given?

A

IV fluid

20
Q

The patient presented with early-onset vomiting (<6 hours) after ingestion of food (neurotoxins) as well as delayed onset of diarrhea (enterotoxins).
Possible agent?

A

Bacillus cereus

21
Q

The patient has consumed defectively-canned food and presented with descending flaccid paralysis.
What is the causative agents and specific treatment? (2)

A

Clostridium botulinum
Tx: Antitoxins

  • neurotoxins at NMJ causing descending flaccid paralysis and respiratory arrest
  • toxins are pre-formed in adult, formed in vivo in infants
22
Q

E coli O157:H7 can cause _________________, thus _________ is contraindicated as it increases lysis of bacteria, increases Shiga-like toxin and aggrevate the above situation.

A

HUS - Hemolytic uremic syndrome

antibiotics

23
Q

The patient has taken re-heated and pre-cooked meat dishes and has a relatively late onset of diarrhea (compared to those with pre-formed neurotoxins: 8-12 hours).
Possible agent?

A

Clostridium perifringens.

24
Q

This agent can be found in undercooked poultry (animal reservoir) and has varying mechanisms of infection - enterotoxin, cytotoxic, and invasive.
Name this agent and what can be given if there is systemic involvement (e.g. fever) as a treatment? (2)

A

Salmonella enteritidis;

Quinolones

(inflammatory diarrhoea: 2nd most common after Campylobacter - Sketchy)

Salmonella typhi - another type causing Typhoid/Enteric fever

Salmonella is the most common causal agent of osteomyelitis in sickle cell disease patients

25
Q

_______________ is the MC cause of diarrhea in western world, found in undercooked poultry. It also causes reactive arthritis and neurological complications.

What can be given as treatment?

A

Campylobacter jejuni/coli;

usually self-limiting but
Erythromycin (macrolide)/ Quinolones to reduce the duration of symptoms

26
Q

This patient experienced explosive diarrhea after consuming contaminated seafood (halophilic - salt-loving bacteria).
This bacteria produces enterotoxins and cytotoxins.
Name the possible agent.

A

Vibrio parahaemolyticus

27
Q

Traveler’s diarrhea has risk highest in areas with poor food and water hygiene.
What are the commonest causative organisms (2).

A
  1. ETEC (enterotoxigenic) E.coli (Bacerial)

2. Giardia lamblia (Parasitic)

28
Q

How is Traveler’s diarrhea prevented? (1)

Treatment (2)

A

Prevention: Cook it, peel it, or leave it
Treatment
- Oral rehydration
- Quinolones if dysenteric of fever, but resistance common

29
Q

Clostridium difficile-associated disease (CDAD) is found in 3% of colonic flora of a healthy population.
Which of the following are risk factors of it?
A. Advanced age
B. Immunocompromised
C. GI surgery
D. Prolonged hospitalization

A

all of the above

30
Q

What is the pathogenesis of Clostridium difficile-associated disease (CDAD)?

It spreads via ________________route as vegetative form/hard spores.
When antibiotics like clindamycin is given, there is the destruction of colonic normal flora.
C. difficile then? (2)

A

Fecal oral route;

  • reproduces in intestinal crypts,
  • releasing toxins A (recruit neutrophils) and B (degrade colon epithelial cells)
31
Q

What are the possible presentations of Clostridium difficile-associated disease (CDAD)?

A
  1. Watery diarrhea
  2. Toxic megacolon
  3. Pseudomembranous colitis (PMC): yellowish plaques - a pseudomembrane of necrotic epithelial cells, mucus, fibrin and neutrophils adhering to colonic mucosal surface
  4. Colon perforation and sepsis
32
Q

How can Clostridium difficile-associated disease (CDAD) be diagnosed?

A

Detection of Toxins A and B in stool by PCR, ELISA

33
Q

Treatment of Clostridium difficile-associated disease (CDAD)?

A
  1. Discontinue antibiotics (+PPI) if possible
  2. Antibiotics treatment
    a. Oral metronidazole 500mg Q8h 10-14 days
    b. Oral vancomycin 125-500mg Q6h
  • IV metronidazole and IV vancomycin is INEFFECTIVE
    3. Surgery
  • Relapse common >50%
  • Mx: tapering course of vancomycin over few weeks, or donor faecal transplant
34
Q

Prevention of Clostridium difficile-associated disease (CDAD)? (3)

A

Personal hygiene
- contact precaution - handwashing, gowns, gloves, decontamination

Food hygiene

  • avoid uncooked meat and seafood
  • refrigeration and preservation

Environmental hygiene
- clean water hygiene

(also avoid overprescribing antibiotics - nosocomial! - Clindamycin, cephalosporins, amoxicillin, ampicillin caused)

MICBI - Clinical MICBI (19 decks)

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