Week 3: E.coli Infections + Adhesins Flashcards
1
Q
E.coli bacteria fact file
A
- Commensal bacteria
- An abundant facultative anaerobe of colon mucous layer
- Survives in the presence of bile + adapted to redox potential
2
Q
Non-diarrhoeal E. coli disease examples
A
- MNEC neonatal meningitis
- UPEC in the bladder + kidney
- Septicaemia from gut/kidney, followed by septic shock
3
Q
Diarrhoeal E. coli disease examples
A
- Enterotoxigenic E. coli (ETEC)
- Enteropathogenic E. coli (EPEC)
- Enterhaemorraghic E. coli (EHEC)
4
Q
MNEC neonatal meningitis
A
- Multiplies in blood, crossing BBB
- K1 capsule, S fimbriae, OmpA + other attachment factors, Fe acquisition mechanisms are its main virulence factors
5
Q
UPEC in the bladder + kidney
A
- Frequent cause of cystisis
- Can cause kidney failure, but this occasional only if it spreads upwards
- Can cause septicaemia but this is rare
- Possesses fimbriae + Pap pili + Haemolysin-Alpaha (HlyA) toxin
6
Q
ETEC
A
- Adheres to intestinal cells, produce heat latent + stable toxins
- Toxins enter intestinal cell, disrupting water + ion flow
- Symptoms include secretory diarrhoea
7
Q
EPEC
A
- Adheres to intestinal cells + produces toxic proteins
- Toxin proteins introduced directly from EPEC cytoplasm to host cell cytoplasm, damaging mucosa
- Symptoms include malabsoptive diarrhoea
8
Q
EHEC
A
- Adheres intestinal epithelial cells + produces toxic proteins/Shiga-like toxin
- Toxic proteins introduced directly into host cytoplasm
- Or Shiga-like toxin enters bloodstream + travels to kidney
- Toxic proteins can cause (often) bloody malabsorptive diarrhoea symptoms
- Shiga-like toxins can cause kidney failure
9
Q
AB toxin
A
- Examples include Heat labile toxins
- A = Active domain, the main killing component of the toxin
- B = Binding domain, that stimulates uptake + entry into the cell
- These components are common in many toxins
10
Q
ETEC virulence factors
A
- CFs
- Labile Toxin AB
- Stable toxins
- Adhesins
- Serine protease
- Metabolism
- Motility
- Biofilm formation
- Iron scavenging + uptake
- Oxygen sensing
11
Q
Verbatoxin/Shiga toxin
A
- B domain binds to neutral glycolipids
- A domain is transferred to cytosol, N-glycosidase hydrolyses 28S rRNA, between ribose + adenine, killing the cells
- This can lead to Haemolytic Uremic Syndrome (HUS), vessel damage, clotting + kidney damage, then death
- Proposed ciprofloxacin treatment against O157:H7 + O1o4:H4 in fact exacerbated symptoms
- Lambdaphage under lysogeny in E. coli can trigger shiga toxin production when antibiotics are introduced
12
Q
The means of acquisition of mobile genetic elements
A
- Bacteriophage ie Shiga toxin
- Transposon insertion ie Stable toxin, heat stable toxin of ETEC
- Plasmid trasnfer ie Labile toxin of ETEC
- Pathogenicity islands (PAIs) ie PATs-1, -2 of UPEC, LEE of EHEC + EPEC, kps PAI of MNEC
- Evolution
13
Q
Types of Adhesins
A
- Pili/Fimbriae
- Type IV pili
- Gram positive
- Outer membrane proteins
- Autotransporters
- Tirs
14
Q
Requirements of adhesion + roles + methods of mediation
A
- The first step in colonisation
- Non-specific or reversible
- Can be specific recepotr-ligand interaction
- Anchors to tissue, inanimate objects + biofilms
- Downstream signalling to then cause inflammation + beginning invasion once adhered
- Overcome cell-cell electrostatic repulsion is a must
- Extend beyond antiphagocytic capsule or the S layer
15
Q
Why have multiple adhesins?
A
- Multiple adhesins encoded in a single genome
- Differential expression in response to nutrition status/environmental status reults in physiological changes
- Different tissues + different host specificity
- Redundancy in targets to bind to can ensure binding , which may be a snapshot into evolution
