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Micbi > Enteric Infections > Flashcards

Enteric Infections Flashcards

1
Q

Diarrhea definition

A

Passage of >3 loose stools per day

May be acute (<2 wks) or persistent (>2 wks)
Watery or bloody

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2
Q

Gastroenteritis definition

A

Syndrome characterised by GI symptoms e.g. nausea, vomiting, diarrhoea, abdominal discomfort

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3
Q

Food poisoning definition

A

GE caused by chemical or pathogens in food

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4
Q

Dysentery definition

A

Inflammation of GI tract associated with blood and pus in faeces, with abdominal pain

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5
Q

Causative agents of GE

A

Bacteria - MOST COMMON
Virus - Rotavirus, Norovirus
Protozoa - Giardiasis, Amoebiasis
Non-infective - small bowel malabsorption, drugs etc.

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6
Q

Host factors

A

Age, immunity, gastric acidity (PPI), GI (normal flora, mucosal integrity, motility)

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7
Q

Normal enteric microflora

A

ANAEROBES
- bacteroides, clostridia, peptostreptococcus

Aerobes (mostly gram -ve)

  • E. coli
  • Klebsiella, Proteus, Enterococcus

Small Bowel: lactobacillus, proteobacteria
Large Bowel: bacteroides, clostridia

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8
Q

Effects of antibiotics

A

Disruption/ Depletion of normal flora and commensals

==> overgrowth of pathobionts –> epithelial damage –> systemic dissemination of pathogens and commensals

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9
Q

Infectious doses of pathogens

A

E.coli and Vibrio (10^8)
Salmonella (10^5)
Campylobacter (10^2-6)
Shigella, Giardia, Entamoeba (10^1-2)

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10
Q

Transmission

A

Faecal-Oral route
Person-to-person
Waterborne, food borne, animal reservoir

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11
Q

Storage of food

A

Room temperature, unpreserved increases risk of GE

more cases and outbreaks in summer

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12
Q

Sources for food contamination

A 
Food handlers
Polluted water
Dirty cooking utensils
Contaminated food ingredients
Infected food animals
Human or animal excrete
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13
Q

Pathogenic Mechanisms of different organisms

A

Exotoxins causing profuse water diarrhoea —
Neurotoxins preformed in food
- act directly on CNS, ENS
- S. aureus, B. cereus (short incubation), C. botulinum (adults)

Enterotoxins formed in vivo:

  • fluid secretion without mucosal damage
  • C. perfringens, B cereus (long incubation), C. difficile, ETEC, V. cholerae, V parahaemolyticus, C. botulinum (infants)
  • enterotoxin from ETEC and V. parahaemolyticus can be heat stable (resist 100 degrees for 15 min, susceptible to alkali) or heat labile (denature at 60 degrees for 15 min)

Mucosal invasion/ cytotoxin causing bloody diarrhoea

  • penetration and destruction of mucosa
  • CHESS org. : Campylobacter, EHEC, Entamoeba, Shigella, Salmonella + V parahaemolyticus

Mucosal adherence causing moderate watery diarrhoea

  • effacement of intestinal mucosa
  • EPEC
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14
Q

Food poisoning

A

S. aureus

  • protein rich foods
  • skin or nasal carriage
  • onset 1-6 hrs, nausea and vomiting

B. cereus

  • spore bearer in soil
  • early onset vomiting (6 hrs) due to neurotoxin
  • late onset diarrhoea due to heat labile toxin

C. perfringens

  • anaerobic spore bearer
  • re-heated, pre-cooked meat dishes
  • onset 8-12 hrs
  • abdominal cramps and diarrhoea
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15
Q

Clostridium botulinum: source, pathogenesis, treatment

A

Anaerobic spore bearer in soil
In home preserved or defectively canned foods

Neurotoxin blocked Ach release at NMJ –> flaccid paralysis and respiratory arrest

(preformed toxins in adult, formed in vivo on infants)

Treatment:
- Antitoxins and supportive care

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16
Q

Salmonellosis: pathogen, source, disease, pathogenesis, treatment

A

Salmonella Gastroenteritis Group
- Salmonella Enteritidis

Large animal reservoir (undercooked poultry, eggs, raw milk or food handlers)

Disease:

  • incubation 1-7 days
  • fever, headache, abdominal pain, diarrhoea

Varying mechanisms: enterotoxin-like, invasive or cytotoxin

Treatment:
- Quinolones only if systemic involvement (may extend duration of carriage)

17
Q

Campylobacter GE: pathogen, source, disease, complications, treatment

A

C. jejune and C. coli
- MC cause in western world

Zoonotic infection from undercooked poultry and raw milk

Disease:

  • incubation 1-5 days
  • fever, nausea, severe abdominal cramps, diarrhoea
  • reactive arthritis and neurological complications in minority

Treatment:

  • self-limiting
  • Erythromycin and quinolone reduce duration of symptoms
18
Q

Vibrio parahaemolyticus: source, disease, mechanism, treatment

A

Halophilic

Found in contaminated seafood

Disease:

  • incubation 8hrs - 2 days
  • explosive diarrhoea, abdominal pain, nausea, vomiting

Heat labile and heat stable enterotoxins Cytotoxins

Self-Limiting

19
Q

Traveller’s diarrhoea: high risk areas, causative organisms, prevention, treatment

A

High risk: Poor sanitation, contaminated water

Causative organisms:

  • ETEC most common bacterial cause
  • Giardia lamblia most common parasite

Prevention:
- “cook it, peel it or leave it”

Treatment:

  • oral rehydration
  • Quinolones if dysenteric or fever (but resistance common)
20
Q

Clostridium difficile-associated disease (CDAD): risk factors, pathogenesis, disease manifestations

A

Normal flora in 3-5% of healthy population (carriers, no toxin production, no symptoms)
Accounts for >25% antibiotic associated diarrhoea

Risk factors:

  • prolonged hospitalisation
  • GI surgery
  • immunocompromised
  • advanced age

Pathogenesis:

  • faecal-oral transmission as vegetative form or hardy spores
  • spores germinate in small bowel
  • disruption of normal colonic flora by antibiotics e.g. clindamycin = C. difficile disease can arise
  • C difficile reproduces in intestinal crypts, releasing toxins A (recruit neutrophils) and B (degrade colonic epithelial cells) –> inflammation
  • expelled mucus and cellular debris formed layer of pseudomembrane

Disease:

  • watery diarrhoea
  • toxic megacolon
  • pseudomembranous colitis
  • perforation of colon and sepsis
21
Q

Clostridium difficile infection criteria

A

Definition -
- clinical presentation of diarrhoea
AND
- laboratory test confirmation (presence of toxins)
- STOOL +ve for C. difficile toxins by PCR/ ELISA; detection of toxigenic C. difficile
OR
- colonoscopic/ histopathological findings of pseudomembranous colitis (i.e. pseudomembrane, exudate, bleeding, oedema, local inflammation)
- toxic megacolon (minority of patients)

22
Q

Diagnostic methods for C. difficile infection

A

Targeting C. difficile:

  • direct culture, enrichment culture
  • detects colonisation but not presence of toxins

Target GDH (enzyme in C. dfficile)

  • GDH EIA
  • presence of GDH doesn’t mean toxigenic

Target toxigenic C. difficile

  • toxigenic culture
  • usually for research (culture on anaerobic agar, identify colonisation, then do CTA)

Target tcdA, tcdB, binary toxin genes

  • PCR assay of toxin genes
  • can’t use alone due to false +ve rates

Target Toxins A and B

  • Toxin A/B EIA
  • doesn’t detect colonisation

Target Toxins B

  • Cytotoxicity assay (CTA) – observing for cytopathic effect of toxins in Vero cell
  • doesn’t detect colonisation
  • very tedious, not routine done

Recommendations:

  • need multiple tests to prove presence of org first then presence of toxins
  • GDH EIA first (high NPV to exclude CDI) followed by EIA Toxin A/B or PCR (high specificity)
23
Q

CDAD management

A

Discontinue antimicrobial agent if possible
Supportive therapy (IV fluids)
Antibiotic treatment:
- Oral metronidazole 10-14 days or
- Oral vancomycin 10-14 days
- IV metronidazole (IV vancomycin ineffective)
Surgery (severe cases)
Relapse common: may require tapering course of vancomycin to eradicate spores; faecal microbiota transplant

24
Q

Investigation of Diarrhoea: Hx

A

Incubation period/ onset
Food history
TOCC (travel, occupation, cluster, contact)
Appearance of stool

25
Q

Investigation of Diarrhoea: Physical Examination

A

Hydration status/ Fluid balance

Urine output

26
Q

Investigation of Diarrhoea: Laboratory

A

STOOL

  • bacterial: culture on selective media (DCA for shigella/salmonella, TCBS for Vibrio, Skirrow’s for campylobacter)
  • parasites: microscopy of ova/ cysts x3, modified acid-fast stain for cryptosporidium
  • viral: Ag detection by EIA (rotavirus), PCR (norovirus)
  • C. diff: toxin A/ B detection by EIA/PCR

BLOOD
- culture in severe cases

Outbreak situation:

  • culture suspected food (quantitative culture needed for bacteria; heat stable toxins without viable bacteria; enterotoxins detection)
  • faecal samples of kitchen staff
  • EM of stool for viruses
27
Q

Treatment of Diarrhoea

A

Fluid and Electrolyte replacement

  • Oral Rehydration Therapy (subtotal of 245 mM electrolytes; hypo-osmolar)
  • IV if severe

New ORT better efficacy in children with acute diarrhoea, may cause hypoNa without any clinical signs
(old ORT hyperosmolar, a/w hyperNa and increase stool output)

No antibiotics use unless systemic infection

  • risk of carrier potential in salmonella
  • required in shigella?
28
Q

Prevention, contact precautions

A 
Clean water supply
Avoid undercooked meat, poultry and seafood
Proper handling and storage of food
Handwashing and personal hygiene
Sanitation and public health 
Educational activities

Contact precautions:

  • enteric isolation
  • -> isolation room if strict adherence to perronal hygiene not guaranteed
  • -> cohort
  • -> PPE and decontamination

Micbi (32 decks)

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