GE: Non-invasive bacteria Flashcards
Types of serotypes for Vibrio cholerae
Serotype O1 with 2 biotypes:
- classical
- El Torr: used to be considered commensal before causing a pandemic
Serotype O139
Living conditions of cholera
Free-living in coastal waters, infected shellfish
Mechanism of cholera toxin
A-B5 toxin. B5 subunit binds to GM1 gangliosides (cell surface receptor on intestinal cells)
A subunit internalised by endocytosis, cleaves into A1 and A2
A1 adds a ADP-ribose onto GTPase (which regulates cyclase activity) > GTPase locked on > increased AC activity > increased cAMP > inhibition of Na absorption and Cl- secretion > NaCl in lumen > osmotic secretion of water
Toxins of Enterotoxigenic E.coli
Heat labile: permanent, same mechanism as cholera
Heat stable: is a peptide, simple so not destroyed by heat, not permanent
changes activity of guanylate cyclase > changes activity of cGMP
Diagnosis of Vibrio. cholerae
Thiosulfate Citrate Bile salts Sucrose agar. V cholerae forms yellow colonies, other vibro’s form green colonies. Then perform biochemical and serological identification
Enterotoxigenic E.coli infectious profile
- very high infectious dose 10^8
- stays in lumen and does not invade the cell
- symptoms: mild, self limiting, watery diarrhoea, abdominal cramping
Type III secretion system for EPEC
For EPEC
1. bundle forming pili mediates loose attachment
2. T3SS secretes Tir receptor into the enterocyte
3. intimin (outer membrane protein) binds Tir and mediates intimate attachment
4. translocated T3SS proteins activate actin polymerisation, causes rearrangements of host cytoskeleton
5. pedestal formation and attaching and effacing lesions
Shiga toxin
- moves through epithelial cells to effect underlying vasculature
- B5 binds to Gb3 receptor on endothelial cells
- A subunit is a N-glycosidase that inactivates the 60s ribosomal RNA by cleaving a N-glycosidic bond in 28S subunit -> stops protein synthesis -> damage in vasculature of intestine
Enterohaemorrhagic E.coli
- bloody diarrhoea
- zoonosis
- industrialised countries
- produces shiga toxin
EHEC serotype O157:H7
non sorbitol fermenting
- Attaching and effacing pathogen, produces toxin but does not invade
- Unknown adhesions > does not have pili to form loose attachments
- Used T3SS > Tir interacts with intimin (afimbrial adhesion)
- Caused actin rearrangement same as EPEC
Cholera pili
- Toxin coregulated pilus (tcp)
Allows the bacteria to colonize by binding together in small clumps (micro-colonies), which binds to enterocytes, but it is unclear how