GI Infections Flashcards
Define Gastroenteritis
Rapid onset diarrhoeal illness, lasting <2 weeks with diarrhoea (loose or unformed stool) ≥3/day or ≥200g of stool which is either viral or bacterial in aetiology
Define diarrhoea.
loose or watery stool, ≥3 times in 24 hours, acute/chronic/persistent
What is the difference between acute, persistent and chronic diarrhoea?
- Acute <14 days (may be viral or bacterial)
- Persistent 14-29 days
- Chronic >30 days (may be due to parasites and non-infectious aetiology)
What is small and large bowel diarrhoea?
- Small bowel diarrhoea = watery, crampy abdominal pain, bloating and gas; inflammatory cells rare
- Large bowel diarrhoea = small volume, painful, occur with blood/mucous; inflammatory cells common
What are the RFs for gastroenteritis?
- Food borne
- Exposure-related
- Host-related
What are the exposure-related RFs for gastroenteritis?
- Outbreak situation (>2 cases of common food source or exposure)
- Travel history (exposure to poor settings and water facilities)
- Occupational exposure / Health-care related exposure (recent ABx c. diff)
- Animal contacts (pets, farms, zoos)
- Reptile contact (specifically)
- Institution/childcare facility
What are the host-related RFs for gastroenteritis?
- Young children and elderly
- Immunosuppressed patients
- MSM (men who have sex with men)
- Anal-genital, oral-anal, or digital-anal contact
- Haemochromatosis or haemoglobinopathy
Describe the epidemiology of GI infections.
- There is an underreporting of GI infections (most are self-limiting <24 hours, patients do not seek healthcare)
- Viral (i.e. norovirus) >>> bacterial
- Developing countries have outbreaks (especially cholera in war torn countries)
What is the mechanism of disease?
- (1) Secretory diarrhoea (from toxin production):
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Cholera toxin:
- Subunit production
- cAMP opens Cl- channels at the apical membrane of the enterocytes causing an efflux of Cl- to lumen with loss of water and electrolytes → profoundly dehydrated
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Superantigens:
- Superantigens bind directly to TCRs and MHC molecules; outside the peptide binding site: there is massive cytokine production by CD4 cells (systemic toxicity and suppression of adaptive response) → secretory diarrhoea
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Cholera toxin:
- (2) Inflammatory diarrhoea
- (3) Enteric fever – host responses in bacteraemia are…
- Inflammatory (exudative) diarrhoea
- Enteric fever: interstitial inflammation
How do we diagnose GI infections?
What are the extra-intestinal manifestations of GI infections? What are the causative organisms?
- Salmonella, Yersinia → aortitis, osteomyelitis, deep tissue infection
- Campylobacter, Yersinia → haemolytic anaemia
- Shigella, Campylobacter, Yersinia → Glomerulonephritis
- STEC, Shigella → HUS
- Yersinia, Campylobacter, Salmonella, Shigella → erythema nodosum
- Salmonella, Shigella, Campylobacter, yersinia, (giardia, Cyclospora cayetanensis) → reactive arthritis
- Listeria, salmonella (infants <3m) (also enteroviruses) → meningitis
Describe staphylococcus aureus?
- 1/3 population chronic carriers, 1/3 transient
- Spread by skin lesions on food handlers
- Appears in tetrads, clusters on gram stain → yellow colonies on blood agar
- SUPERANTIGEN: produces enterotoxin, an exotoxin that can act as a superantigen in the GI tract, releasing IL1 and IL2 causing prominent vomiting and watery, non-bloody diarrhoea
- Mx: self-limiting
What are the gram +ve rods: spore forming bacteria?
Bacillus cereus
Clostridia
Listeria monocytogenes:
Describe bacillus cereus.
- Gram-positive rods: spore forming
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Bacillus cereus: food poisoning
- Spores germinate in reheated fried rice (heat-stable emetic toxin – not destroyed by reheating)
- Gram +ve rod-spores
- Heat-labile diarrhoeal toxin (food is not cooked to a high enough temperature)
- Watery non-bloody diarrhoea; self-limiting
- Rare cause of bacteraemia in vulnerable population
- Can cause cerebral abscesses
What are the types of clostridia? What is the source? What do you ingest? What does it do? How do we treat it?
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Clostridia (gram +ve anaerobe)
- Clostridium botulinum: botulism
- Source: canned or vacuum-packed food (honey in infants)
- Ingestion of preformed toxin (inactivated by cooking)
- Blocks ACh release from peripheral nerve synapses: paralysis
- Treatment with antitoxin
- Clostridium pefringens: food poisoning
- Source: reheated food (meat)
- Normal flora of colon but not small bowel, where the enterotoxin acts (superantigen)
- Incubation is 8-16hrs
- Watery diarrhoea, cramps, vomiting lasting 24hrs
- Clostridium difficile: pseudomembranous colitis
- Produces 2 toxins – Toxin A and Toxin B
- Toxin A = enterotoxin = inflammation
- Toxin B = cytotoxin = virulence factor (more dangerous than A)
- 3% of community, 30% of hospitalised patients
- Antibiotic related colitis (any but mainly cephalosporins, cipro and clindamycin)
- Infection control – isolate and hand-washing
- Treatment: PO vancomycin, stop antibiotics where possible
- Produces 2 toxins – Toxin A and Toxin B
- Clostridium botulinum: botulism
Pseudomembranous colitis - C.diff
Describe listeria monocytogenes infection.
- Bad for pregnant women
- Outbreaks of febrile gastroenteritis
- ß-haemolytic, aesculin positive with tumbling-weed motility
- Source: refrigerated food (“cold-enhancement”), unpasteurized dairy, vegetables (grows at 4ºC)
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Symptoms: Watery diarrhoea, cramps, headache, fever, little vomiting
- At risk: perinatal infection, immunocompromised patients, elderly (confused)
- Treatment: ampicillin, ceftriaxone, cotrimoxazole
- At risk: perinatal infection, immunocompromised patients, elderly (confused)
Describe the enterobacteriaceae, what is the source toxins, types? What should be avoided?
- Facultative anaerobes, glucose/lactose fermenters (LF), oxidase-negative
- Escherichia coli (Traveler’s diarrhoea)
- Source: food/water contaminated with human faeces.
- Enterotoxins:
- Heat labile stimulates adenyl cyclase and cAMP
- Heat stable stimulates guanylate cyclase
- Act on the jejunum/ileum not on colon
- ETEC; toxigenic → main cause of traveller’s diarrhoea
- EPEC; pathogenic → infantile diarrhoea
- EIEC; invasive → dysentery
- EHEC; haemorrhagic → O157:H7 EHEC: shiga-like verocytotoxin causes HUS
- Avoid antibiotics
Describe salmonella infections. What are the antigens, species …
- Non-lactose fermenters, H2S producers (black colonies), TSI agar, XLD agar, selenite F broth
- Antigens:
- Cell wall O (groups A-I)
- Flagellar H
- Capsular VI (virulence, antiphagocytic)
Three species – distinguished by disease caused
- S type
- S. enteritidis
- S cholerasuis
Differentiate between S.typhi and S enteritides.
Describe shigella infection. What are the antigens? How does it spread? What does it cause? How should it be managed?
- Non-lactose fermenters, non H2S producers, non-motile
- Antigens:
- Cell wall O antigens
- Polysaccharide (groups A-D): S. sonnei, S. dysenteriae, S. flexneri (MSM)
- The most effective enteric pathogen (low infectious dose 50)
- No animal reservoir (human → human transmission)
- No carrier states
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Dysentery
- Invading cells of mucosa of distal ileum and colon
- Producing enterotoxin (Shiga toxin)
- Avoid antibiotics (ciprofloxacin if required)