GE: invasive bacteria Flashcards
How does shigella invade cells using M cells?
- Invades M cells using IpA
- released into lamina propria > ingested by macrophages. Shigella causes inflammation and can cause apoptosis of macrophage
- inflammation triggers neutrophils to flood the lamina propria, junctions widen and more shigella can enter
- makes contact with the basal side of epithelial cells and delivers T3SS effector proteins that trigger actin rearrangement > bacterial uptake
- escapes phagosomal vesicle with Ipa proteins that disrupt the membrane > enters cytoplasm
- Makes IcsA (intracellular spread A) protein at one pole, induces polymerisation of host cell actin
- propels bacteria forward, into the neighbouring cell
- og cell lyses
What does the shigella virulence plasmid encode for?
- A T3SS
- Ipa proteins: induces membrane ruffling, helps escape epithelial phagosomal vesicle
- IcsA: recruits host actin
Shigella infectious profile
- human to human spread
- Low ID: 10^2 acid stable bacteria
- lactose non-fermenting
- species grouped by O (cell wall) antigens
> only one to produce shigella toxin is shigella dysenteriae
incubation period: 12-96 hrs - bloody diarrhoea
How does shigella cause damage?
Invasion destroys epithelial cells, causing a focal ulcer in the gut > red blood cells and neutrophils escape into the lumen
shigella toxin causes cell death
> targeting sodium absorptive villus cells leads to excessive fluid in the lumen
How to diagnose shigella
- cannot distinguish from E.coli by DNA hybridisation but can distinguish on MAC agar (does not lactose ferment = yellow colonies)
- agglutination reactions with blood sera with specific antibodies to group antigens of shigella
- does not produce H2S (distinguish from salmonella)
- no H antigens (flagellar)
Shigella treatment
- does not cause severe dehydration
- no vaccine
- antibiotic treatment reduces infectious period and duration of illness
Salmonella infectious profile
- lactose non-fermenting
- two serotypes that cause human GE
> serovar typhimurium and enteritidis - acid labile, high ID
- associated with chickens, eggs, milk
- IP: 12 hrs - 3 days
- symptoms: diarrhoea, cramping
How does salmonella infect the gut?
- Invade M cells or enterocytes from luminal side
> salmonella invasion proteins (sip’s) induces cytoskeleton rearrangements that allow the uptake of bacteria by endocytosis. This is shown by membrane ruffling. The proteins are delivered by a T3SS - bacteria travels to basal membrane and are released into the lamina propria
Pathogenicity islands of salmonella
Salmonella pathogenicity island (SPI) 1
- located on the bacterial chromosome, encodes for T3SS, salmonella invasion proteins
SPI 2
also encodes for a T3SS
encodes for survival inside the host cell (esp the vacuole of macrophages)
Diagnosis of salmonella
lactose non-fermenter = yellow on MAC
produces H2S = black centred colonies on deoxycholate citrate agar
Biochemical tests for O and H antigens
differentiate strains by whole genome sequencing or phage typing
Yersinia enterocolitica infectious profile
Associated with: cattle
Symptoms: diarrhoea
ID: 100+ bacteria
IP: 2-6 days
infects: mesenteric lymph nodes
Yersinia enterocolitica adhesins
an outer membrane protein called invasin
> contains a RGD tri-peptide motif which mimics the ligand that usually binds to beta 1 integrins (a host cell surface receptor)
Yersinia enterocolitica plasmid
- 90 kb
- encodes for:
- T3SS that translocate
- Yersinia Outer Proteins that downregulate the immune response by:
> preventing apoptosis
> being anti-inflammatory
> prevent phagocytosis
Diagnosis of Yersinia enterocolitica
lactose non-fermenter = yellow on MAC
Pyschrotrophs = grow at low temperature
grows on selective CIN agar > bullseyes colonies (not diagnostic, further testing needed)
Campylobacter characteristics
- microaerophilic
- curved rods
- large reservoir in animals (poultry common because of their higher body temp), possibly forms biofilms in water
- Low ID
Long IP: 2-4 days
symptoms: diarrhoea, bloody diarrhoea
