Enteric Infections Flashcards
Diarrhea definition
Passage of >3 loose stools per day
May be acute (<2 wks) or persistent (>2 wks)
Watery or bloody
Gastroenteritis definition
Syndrome characterised by GI symptoms e.g. nausea, vomiting, diarrhoea, abdominal discomfort
Food poisoning definition
GE caused by chemical or pathogens in food
Dysentery definition
Inflammation of GI tract associated with blood and pus in faeces, with abdominal pain
Causative agents of GE
Bacteria - MOST COMMON
Virus - Rotavirus, Norovirus
Protozoa - Giardiasis, Amoebiasis
Non-infective - small bowel malabsorption, drugs etc.
Host factors
Age, immunity, gastric acidity (PPI), GI (normal flora, mucosal integrity, motility)
Normal enteric microflora
ANAEROBES
- bacteroides, clostridia, peptostreptococcus
Aerobes (mostly gram -ve)
- E. coli
- Klebsiella, Proteus, Enterococcus
Small Bowel: lactobacillus, proteobacteria
Large Bowel: bacteroides, clostridia
Effects of antibiotics
Disruption/ Depletion of normal flora and commensals
==> overgrowth of pathobionts –> epithelial damage –> systemic dissemination of pathogens and commensals
Infectious doses of pathogens
E.coli and Vibrio (10^8)
Salmonella (10^5)
Campylobacter (10^2-6)
Shigella, Giardia, Entamoeba (10^1-2)
Transmission
Faecal-Oral route
Person-to-person
Waterborne, food borne, animal reservoir
Storage of food
Room temperature, unpreserved increases risk of GE
more cases and outbreaks in summer
Sources for food contamination
Food handlers Polluted water Dirty cooking utensils Contaminated food ingredients Infected food animals Human or animal excrete
Pathogenic Mechanisms of different organisms
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
Food poisoning
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
Clostridium botulinum: source, pathogenesis, treatment
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
Salmonellosis: pathogen, source, disease, pathogenesis, treatment
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)
Campylobacter GE: pathogen, source, disease, complications, treatment
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
Vibrio parahaemolyticus: source, disease, mechanism, treatment
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
Traveller’s diarrhoea: high risk areas, causative organisms, prevention, treatment
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)
Clostridium difficile-associated disease (CDAD): risk factors, pathogenesis, disease manifestations
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
Clostridium difficile infection criteria
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)
Diagnostic methods for C. difficile infection
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)
CDAD management
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
Investigation of Diarrhoea: Hx
Incubation period/ onset
Food history
TOCC (travel, occupation, cluster, contact)
Appearance of stool
Investigation of Diarrhoea: Physical Examination
Hydration status/ Fluid balance
Urine output
Investigation of Diarrhoea: Laboratory
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
Treatment of Diarrhoea
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?
Prevention, contact precautions
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
