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Semester 2 Infection > L17: E Coli > Flashcards

L17: E Coli Flashcards

1
Q

What is E Coli?

A

Escherichia Coli
Gram Negative Rods (red/pink) staining
Typically lactose fermenting
Facultatively anaerobic
Often Motile
Numerous serotypes–> Different antigens (O, K F, H)
Consitutuent part of large bowel, microbiota of many animals including human

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2
Q

What is meant by ‘one health’ ecology of E Coli?

A

E Coli spread between animals, humans and the environment –> interconnectedness
Includes pathogenic and resistant strains
Challenge of controlling spread–> antibacterial resistance

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3
Q

What is the structure of an E Coli under the microscope?

A

Rod shaped

Plasma membrane, cell wall, nucleoid, ribosome

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4
Q

How can E Coli be identifies in the laboratory?

A

E Coli uses sugar lactose as an energy source
Produces lactic acid as waste product
MacConkey agar contains lactose and a pH indicator
Goes red with lactic acid
Others such as Pseudomonas aeruginosa–> non lactose fermenting–> yellow colonies

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5
Q

How are the many different species of E Coli known about?

A

Different typing technologies discovered different species

1) Serology–> using antibodies to detect the different antigens- O, K, F and H
2) Metabolic profiling–> variation in biochemical pathwaus
3) Genomic diversity –>
- DNA hybridisation,
- multi-locus enzyme electrophoresis (MLEE),
- multi-locus sequence typing (MLST),
- whole genome sequencing

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6
Q

What is an added advantage of genome sequencing?

A

Determine strain

Also can determine who passed it on to who

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7
Q

What are the different antigens present on E Coli?

A

O–> lipopolysaccharide antigen
–> Body detect O antigen (PAMP) –> Inflammatory response
–> Different O antigens on different strains allows for invasion–> evades immune system
H–> antigen on flagellum
K–> Capsule antigens
F–> Fimbriae antigens

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8
Q

What did whole genome sequencing show?

A 
1509 EColi cultures were sequences 
70,000 different genes identified
885 genes present in all 1509 isolates
--> 885 genes say it is E Coli
--> Rest unknown function--> may make them pathogenic
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9
Q

What is meant by E Coli in health and disease?

A

EColi found in the large bowel–> normal part of gut flora
Possibly protects against invasion by pathogenic species such as Salmonella
Can also cause:
- Intestinal infections
- Toxin-mediated disease
- Extra-intestinal infections

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10
Q

What are some of the extra-intestinal infections?

A 
Urinary tract
Intra-abdominal 
Biliary tract 
Bloodstream infection 
Neonatal meningitis
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11
Q

What causes E Coli to causes disease?

A

Different strains have different virulent factors

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12
Q

What are the causes of diarrhoea linked to E Coli?

A

6 different pathotypes of diarrhoeagenic E Coli

  • -> Enterotoxigenic E Coli (ETEC)
  • -> Enteropathogenic E Coli (EPEC)
  • -> Enteroaggregative E Coli (EAEC)
  • -> Enteroinvasive E Coli (EIEC)
  • -> Diffusely adherent E Coli (DAEC)
  • -> Shiga toxin-producing E Coli (STEC) aka Verocytotoxin-producing E Coli (VTEC) or Enterohaemorrhagic E Coli (EHEC)
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13
Q

Which ones are the most common in children? Immunocompromised patients?

A

EPEC and EIEC–> common in children in developing country

EAEC most common in immunocompromised

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14
Q

What is Enterotoxigenic E Coli?

A

Diarrhoeal illness–> Travellers’ diarrhoea
Low income countries
Faeco-oral transmission
ETEC produces two toxins–> Heat stable toxin (ST) and Heat-labile toxin (LT)

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15
Q

How does enterotoxigenic E Coli cause diarrhoea? What other symptoms? For how long?

A

Produced two toxins–> heat-stable toxin (ST) and heat-liable toxin (LT)
Stimulates lining of intestines causing them to secrete excessive fluid–> profuse watery diarrhoea and abdominal cramping
Symptoms–> Nausea with/without vomiting, fever, chills, loss of appetite, headache, muscle aches and bloating
Last 3-4 days (onset 1-3 days after exposure)

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16
Q

How does enteropathogenic E Coli cause diarrhoea?

A
  1. Localised effacement of microvilli from enterocytes
  2. Attaches to host surface, forms channels via Type III mediated secretion machinery forming translocation tube
  3. Bacterial proteins sent into cell including Tir receptor (bacterial receptor)
  4. Tir receptor embeds into plasma membrane of infected cell
  5. Intimin secreted by bacteria EColi attached to pathogen derived protein–> Tir receptor
  6. EColi attached to membrane
  7. Signalling pathway –> reorganisation of host actin cytoskeleton–> formation of pedestal base
17
Q

What does Shiga toxin-producing E Coli (STEC) cause?

A

Haemorrhagic colitis (bloody diarrhoea) and haemolytic uraemic syndrome (acute renal failue, haemolytic anaemia and thrombocytopenia)

18
Q

How does the STEC work?

A
  1. 5 beta subunits associated with alpha subunit form toxin
  2. Bind to Globotriaosylceramide (Gb3) on host cell surface
  3. Toxin is endocytosed and transported to the golgi apparatus and ER
  4. Intracellular transport–> A chain cleaved into A1 (enzymatically active) and A2
  5. Kept together by a disuphide bond until they reach the ER
  6. A1 fragment is released and translocated to the cytosol
  7. A1 inactivates ribosomes–> inhibiting protein synthesis–> results in cell death
19
Q

What are a few of the STEC outbreaks? Why?

A

Oregon and Michigan 1982–> meat from a fast food restaurant
Scotland 2016–> Dunsyre Blue Cheese–> Unpasteurised cows milk–> cows faeces in milk
Germany 2011–> Contaminated bean sprouts

20
Q

What are Extra-intestinal pathogenic E Coli? What causes the diease?

A

Strains of E Coli capable of causing disease outside the intestinal tract
Wide range of virulence factors: Adhesion, iron acquisition systems, protectin and invasins, toxins and others etc…

21
Q

How do urinary tract infections occur?

A

Uropathogenic E Coli transfer from the rectum to the urethra and then migrate to the bladder causing cystitis
Occurs more frequently in women as its closer
Often self-limiting e.g. not treated will probably go away
However can cause further complications

22
Q

How do the virulence factors lead to UTIs (cystitis)?

A

Adhesion
–> Type 1 fimbriae–> adhesive tips attach to alpha-D-mannosylated proteins on uroepithelium–> mediates adhesion, invasion and formation of intracellular bacterial communities
Toxin
–> LPS
–> Alpha-haemolysin–> pore forming toxin, cytotoxic towards epithelial cells
Iron acquisition
–> Avaliability of iron is restricted
–> Bacteria produce their own iron-complexing proteins (siderophores) to acquire iron

23
Q

What can happen if UTI are not treated?

A

Can lead to cause kidney infection

Bloodstream infections

24
Q

Whats is significant about E Coli and bloodstream infections?

A

Commonest cause of bloodstream infection

High mortality rates–> 2016/17–> 14.8% 30 day all-cause mortality

25
Q

What are other causes of EColi caused bloodstream infections?

A

50% UTIs –> ineffective antibiotic treatments
21% urinary catheters
16% hepatobiliary infections
7% gastrointestinal infections

26
Q

How are diarrhoeal EColi infections managed/prevented?

A

Prevention

  • -> Avoid potentially contaminated food and drinks
  • -> Avoid raw fruits and vegetables, raw seafood or undercooked meat or poultry, unpasteurised diary products, food from street vendors and untreated waters in areas lacking adequate chlorination
27
Q

How are diarrhoeal EColi infections treated?

A

Most recover within a few days without treatment
Clear liquids–> prevent dehydration and loss of electrolytes
Oral rehydration solutions
Avoid antibiotics–> may make illness worse

28
Q

How are UTIs caused by Ecoli treated?

A

Antibiotic–> Trimethoprim and nitofurantoin

60% Ecoli isolates tested are trimethoprim resistant

29
Q

If 60% isolates of Ecoli are trimethoprim resistant why is it still prescribed?

A

Drs only send UTI samples of ones difficult to treat
Probably very specific strains
Not representative of all Ecoli species

30
Q

Why is resistance to EColi increasing?

A

Resistance genes frequently on plasmid
Horizontal gene transfer common
40-50% isolates resistant to co-amoxiclav
Variable but increasing prevalence of carbapenemase genes
Resistance linked to sequence type–> ST131, ST69 etc…

Semester 2 Infection (20 decks)

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