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Flashcards in illustrations of bacterial pathogenicity - GI tract Deck (23):

give 3 examples of food poisinings

1 - clostridium botulinum toxin from anaerobic growth in food
2 - staphylococcus aureus, enterotoxins, bacteria ingested but not colonised
3 - clostridium perfringens - germinates from spores in food and toxins produced in intestine.

all 3 caused without host colonisation


cause of botulinism

clostridium botulinum - toxin during anaerobic growth in food ie home canned foods. toxin absorbed from stomach. cleaves the neuronal snare synaptobrevin. acts at NMJ so flaccid paralysis.
Rare but deadly.


describe staphylococcus aureus poisining

grows in custard and processed meats at room temp from human carrier contamination.
heat and acid stable enterotoxinsinteract with gastric mucosa. could be superantigens in blood.
no colonisation.


describe clostridium perfringens poisining

germinates form spores in preheated food. ingested produces toxins that interact with mucosa and may be superantigens


characteristics of gastroenteritis

nausea, vomiting, diarrhoea, abdominal pain


what's dysentry?

inflammatory GI disorder. blood and pus in feces, pain , fever and cramps. usually disease of colon


cause of cholera

vibrio cholerae colonizing the intestinal epithelium.
spread fecal-oral
acute infection, 50% mortality but electrolyte replacement reduces to 1%.


how does vibrio cholerae colonize?

fimbrial adhesin
cholera toxin genes carried on a bacteriophage in the chromosome and coregulated with adhesin and other genes by a HAP signal (global).


how does cholera toxin act

AB5 structure
B binds receptor GM1-ganglioside
receptor mediated endocytosis and retrograde to ER.
Active A into cytosol.
ADP ribosylates Gs, stuck on, uncontrolled high cAMP.
disturbance of NA and CL CFTR membrane pump.
increase CL out, decrease NA in.
leads to water and electrolyte loss of 12-20 L per day into lumen.
'rice water' diarrhoea, shock, collapse, sometimes cardiac failure.


cause of dysentry

shigella species
locally invasive, inflammatory disease of the large intestine (Colon)


result of dysentry

mucosal ulcers, vascular damage. low vol diarrhoea with blood, mucus and PMNs.
v infectious, only need 100 bacteria vs millions for cholera. person to person or food transmission.


pathogenesis of dysentry

resist stomach acid by outer membrane proteins
travers colon mucosa via phagocytic M (microfold) cells (antigenic sampler cells with no mucus)
force across BM into mucosal cells by needle complex injecting invasion proteins and interacting with actin.
cytoskeletal changes, bacteria in vacuole.
escape vacuole, inflammation
multiply in cytosol,
actin based motility
spread into adjacent cells via protrusion of membrane then lysis of vacuole.
taken up by macrophages inducing more inflammation but triggers its apoptosis.
host inflammation accentuated by shiga toxin (glycosidase - kills cells by blocking protein synth).
Bacteria killed by PMNs but LPS release therefore more inflamm.


what can circulating shiga toxin cause

kidney failure - haemolytic uraemia syndrome, particularly in young children where the AB response is poor.


cause of salmonellosis

salmonella, an invasive intracellular pathogen


cause of food bourne gastroenteritis

salmonella enteritidis, S. typhimurium. large animal reservoirs ie chicken eggs


pathogenesis of salmonellosis

1 - needle and effectors to host cytoskeletal rearrangement. enter apical surface of epithelia of distal ileum and proximal colon.
2 - remain in membrane bound vacuole
3 - released from epithelial cells possibly by lysis. inflammation mainly by LPS lipid A.
4 - taken up by macrophages, replicate. switches on up to 200 genes to inhibit phagolysosome, defensins and oxidative burst (ie superoxide dismutase)
5 - host response activates cAMP and fluid secretion. hence diarrhoea.


cause of typhoid fever

salmonella typhi
no animal reservoir.
replicate in macrophages, travel via blood to liver and spleen etc.
severe symptoms due to LPS lipid A.
shed into the bile to intestine and out.
carriers ie typhoid mary where it is quiescent then recurrent reemergence.


types of E.coli capable of diarrhoeal diseases

1 - ETEC - enterotoxic - fimbrial adhesins. produces cholera-like enterotoxin. common cause of travellers diarrhoea. contaminated water.

2 - EPEC- enteropathic - pilus adhesin, retracts to pull bacterium in. deliver effectors via needle inc Tir which binds EPEC's intimin. generates pedestal. inflammation.

3 - EHEC - enterohaemorrhagic - pili and pedestal like EPEC. inflam accentuated by shiga-like toxin, can also cause renal failure. predom serotype = 0157, often from beef.

other types cause neonatal meningitis and UTI (UPEC). some are harmless flora. consequence of pathogenicity islands.


sources of gastroenteritis other than salmonella?

campylobacter (analogous behaviour to shigella).


danger with listeria?

normally harmless but can invade like shigella, go systemic, cross the placenta to damage fetus or BB to cause meningitis. inflammation and tissue damage.
danger in immunocompromised


cause of antibiotic associated diarrhoea

clostridium difficile
toxin producing, anaerobic, spore forming.
colonises colon following antibiotic eradication of flora. isue in hospitals.
diarrhoea and inflam primarly through 2 toxins that glycosylate small GTPases.
subvert actin cytoskeleton, disrupt tight juncitons, leaky epithelium, tissue damage.
can also be indirect with a pseudomembrane and inflamm


a cause of gastric ulcers?

helicobacter pylori - causes about 90% of gastric and duodenal ulcers. up to half of human pop colonised but few experience illness.
infects the antrum


pathogenesis of H. pylori

colonize mucin near gastric mucosal cells. v motile with flagella. adhesins. urease to neutralise acid. pH change also reduces mucus viscosity.
- intense mucosal inflam and ulceration. pylori induces IL8 from epithelia to recruit PMNs.
- destruciton by vacuolating cytotoxin VacA.
progression of ulcer by more inflamm, more PMNs, tissue destruction.
- correlation with gastric cancer poss by chronic inflam of bacterial protein CagA which increase epithelial proliferation.