VL16b: E.coli pathogenicity Flashcards
How many e.coli pathovars exist?
8 e.coli variants associated with certain types of infections (classifications that don’t necessarily mean anything)
EHEC- enterohemorragic
EPEC- enteropathogenic
UPEC- uropathogenic
What are important e.coli virulence factors?
adhesion:
-type1 pili (adhesion to mucosal epthelium, biofilm formation)
Invasion: (facilitate growth and spread of pathogen
alpha-Hemolysin
Flagella important for UPEC ascension from bladder to kidney
Toxins
What sites can be infected?
Intraintestinal: diarrhoea
Small bowel
large bowel
small and large bowel
Extraintestinal
Urinary tract, bladder kidney
Bloodstream-septicemea
central nervous system- meningitis
What e.coli toxins exist?
Toxins
Heat-labile enterotoxin (LT)
Heat-stabile enterotoxin (ST), secreted
Shiga-like toxin, inhibits protein synthesis by cleaving rRNA in ribosome
How do EPEC and EHEC cause infection?
EPEC and EHEC attach to microvilli, use T3SS to secrete effectors to subvert host cell actin to form pedestals at attachment sites
EPEC attaches to small bowel, EHEC large bowel, with pili
they use many of the sam effectors to manipulate host processes + Shiga-like toxin is released contributing to disease
What kinds of molecules are needed for infection? EPEC
T3SS (to translocate effectors
Intimin + Tir for intimate attachment
Map regulates actin dznamis, disrupts mitochondiral function
EspF triggers mitochondrial death pathway
Why is it dangerous to use the wrong antibiotics to treat EHEC?
causes SOS response in EHEC
promotes release of Shiga toxin,
toxin causes morbidity and mortality of EHEC infection
currently no treatment for EHEC
What about cattle?
major EHEC reservoir (asymptomatic)
colonizes in recto-anal junction where it has no effect, cant attach to intestines
(AHL present in rumen of cattle ) QS -> gene expression (activation of gad genes) -> B become resistant to acid in the stomach of cow and represses LEE genes to prevent colonization within rumen
environment matters ( ecoli not bad, only bad for us)
How works the pathogenesis of Shigella?
Pathogenesis od Shigella, enteroinvasive e.coli
infection begins in the colon
bacteria pass through M cells
Shigella are taken into macrophages
use T3SS effectors to escape from phagosome
released from dead macrophages into submucosa
invade basolateral side of colonocytes (T3SS effectors)
Effectors induce actin polymerization and ruffle formation for bacterial entrz
What is ETEC?
enterotoxigenic E.coli
causes diarrhoea
What’s the big picture?
There are many different varieties, e.coli because of severall common features but hard to say, many indentifying genes are pathogenicity islands, allows them to cause certain types of damage.
imagine original e.coli + all diverged relatives
What about NMEC?
Neonatal meningitis e.coli
extraintestinal
fatalitz rates 40%, and survivors have brain damage
bacteria enters bloodstream through intestine, must cross blood-brain barrier into CNS,
What is the most common type of pathogenic e.coli infection?
UPEC (uropathogenic)
How many e.coli genes are there?
core genome 2000 genes
pan genome >10 000genes
each strain 4800 genes (core + horizontally acquired genetic material, determines specific pathotype)
How does e.coli adapt to different environments?
metabolic flexibility allows E.coli to successfully comp9ete with other bacteria and live as a commensal in the intestine
When UPEC transitions to urinary tract (nutrient poor environment) use virulence properties to cause invasive disease and survive host defences
