GI Infections Flashcards
(54 cards)
What groups are most vulnerable to GI infections
Infants
Elderly
What are the reportable GI infections of note
Campylobacter Salmonella Shigella E.coli O157 Listeria Norovirus
No fever or low grade fever
No white blood cells in stool sample
Secondary diarrhoea
E.g. vibrio cholerae, ETEC, EAggEC, EPEC, EHEC
Fever
White blood cells in the stool sample (neutrophilia)
Inflammatory diarrhoea
E.g. campylobacter jejuni, shigella spp, non-typhoid salmonella serotypes, EIEC
Fever
White blood cells in stool sample (mononuclear cells)
Enteric fever
E.g. typhoidal salmonella serotypes
Enteropathogenic yersinia spp
Brucella spp
Incubation period for campylobacter
1-10 days
Disease duration of campylobacter
2-20 days
Most common source of campylobacter
Poultry
Incubation period for E.coli O157
1-5 days
Disease duration of e.coli O157
1-4 days
Incubation period of shigella
12-96 hours
Disease duration of shigella
5-7 days
Incubation period of salmonella
8-48 hours
Disease duration of salmonella
4-7 days
Incubation period of vibrio parahaemolyticus
24-72 hours
Disease duration of vibrio parahaemolyticus
2-10 days
Most common source of vibrio parahaemolyticus
Shellfish
Mechanism of disease of cholera toxins
It is a secretory diarrhoea toxin production
cAMP: opens Cl channel at the apical membrane of enterocytes
Efflux of Cl to lumen: loss of H2O and electrolytes
Mechanism of disease of superantigens
They are secretory diarrhoea-toxin production
Superantigens bind directly to T cell receptors and MHC class II molecules OUTSIDE the peptide binding site.
This leads to a massive cytokine production by CD4 cells (i.e. systemic toxicity and suppression of adaptive responses)
Host responses in enteric fever
Intestinal inflammation –> bacteraemia (in an immunocompromised patient) –> weak stimulation of acute phase responses (monocytes) –> no septic shock and no neutrophilia
Host responses in inflammatory (exudative) diarrhoea
Exudative inflammation –> bacteraemia (immunocompromised patient) –> detection of LPS by monocytes expressing TLR4 –> TNFa, IFNg, IL1B –> neutrophilia and septic shock
Features of staphylococcus aureus food poisoning
1/3 population chronic carriers, 1/3 transient
Spread by skin lesions on food handlers
Catalase, coagulase positive Gram positive coccus
Appears in tetrads, clusters on Gram stain
Yellow colonies on blood agar
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
Don’t treat, self limited
Bacillus cereus
Causes food poisoning
Gram positive rod: spore forming
Spores germinate in reheated fried rice (e.g. chinease fried rice)
Heat stable emetic toxin - not destroyed by reheating
Heat labile diarrhoeal toxin - food is not cooked to a high enough temperature
Causes: water non-bloody diarrhoea which is self-limited
Rare cause of bacteraemia in vulnerable population
Can cause cerebral abscesses
Clostridium botulinum
Gram positive anaerobe
Causes botulism
Source : canned or vacuum packed food (honey / infants)
Ingestion of preformed toxin (inactivated by cooking)
Blocks Ach release from peripheral nerve synapses
Treatment with antitoxin