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4.2 Medical Microbiology > STEC > Flashcards

STEC Flashcards

1
Q

List some of the different variants of E. Coli

A

Enteropathogenic E. Coli (EPEC)
Enterotoxigenic E. Coli (ETEC)
Diffusely adherent E. Coli (DAEC)

Enterohaemorrhagic E. Coli (EHEC)
Enteroinvasive E. Coli (EIEC)

Enteroaggregrative E. Coli (EAEC)

Uropathogenic E. Coli (UPEC)

Neontal meningitis E. Coli (NMEC)

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2
Q

EPEC, ETEC and DAEC cause infections where in the body?

A

Colonise the small bowel and cause diarrhoea

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3
Q

EHEC and EIEC cause infections where?

A

They cause disease in the large bowel

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4
Q

EAEC infects what part of the body?

A

Can colonise both the small and large bowels

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5
Q

Where does UPEC cause infection

A

Uropathogenic E. Coli enters the urinary tract and travels to the bladder to cause cystitis and if left untreated can ascend durther into the kidneys to cause pyelonephritis

It can also spread to blood and cause urosepsis

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6
Q

Where does NMEC cause infection

A

It can cause septicaemia

Neonatal meningitis E. Coli can cross the blood brain barrier into the central nervous system and cause meningitis

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7
Q

What E. Coli strains colonise the small bowel and cause diarrhoea

A

EPEC
ETEC
DAEC

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8
Q

What E. Coli strains cause disease in the large bowel

A

EHEC
EIEC

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9
Q

What E. Coli strains colonoise both the small and large bowel

A

EAEC

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10
Q

What E. Coli strains cause septicaemia

A

UPEC
NMEC

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11
Q

Who are most at risk of urosepsis

A

Elderly women -> UTIs progress into septicaemia

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12
Q

How do the E.coli strains differ from one another

A

They differ in terms of pathogenicity

some inherit toxins such as shiga toxin in EAHEC

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13
Q

What is VTEC

A

Verotoxigenic E. Coli

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14
Q

What are the genes for VTEC, what do they encode

A

Stx1 and Stx2

Verotoxins encoded on bacteriophages

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15
Q

What are the genes for EHEC and what is their function

A

vtx1, vtx2, eae genes

Haemorrhagic colitis hence enterohaemorrhagic E. Coli

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16
Q

How was E. Coli traditionally serotyped?

A

Traditionally classified on basis of the reaction of antibodies with three types of antigens: O, K and H antigens

According to this method there is over 170 O, 103 K and 56 H antigens -> this is always increasin

A combination of O and H antigens have been identified to type strains

NB: these arent useful predictors of virulence

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17
Q

Give some examples of E. Coli strains named according to O, H and K antigens

A

O157:H7
O104:H4
O26
O103
O111

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18
Q

Where did verotoxigenic E. Coli get its name

A

VTEC comes from the old assay that was used to identify verotoxin producing e. coli

Vero monkey cells

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19
Q

What two organisms produce shiga toxin

A

Shigella dynsentriae type 1
Shiga toxin-producing E. Coli

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20
Q

Traditionally how was functionally active shiga toxins detected?

A

Using vero cell toxicity test

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21
Q

What strains will be vero cell toxicity test positive?

A

Verotoxin or verocytotoxin-producing E. Coli (VTEC)

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22
Q

What does shiga toxin cause?

A

Diarrhoea
Haemorrhagic colitis
Haemolytic uremic syndrome (HUS)
Enterohaemorrhagic E. Coli (EHES)

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23
Q

Technically speaking Shiga toxin could be produced by any E. Coli why is this?

A

Since the gene for it is transferred via bacteriophage so technically any strain can take it up

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24
Q

Talk about STEC/Shiga toxin E. Colli, what is it, how many different types are there

A

These produce 1 or more types of shiga toxin (stx):
- stx 1 or stx2

There are over 400 E. Coli serotypes which harbour stx genes

270 serotypes have been associated with clinical infection
- virulence may differ between strains

Genes are located on distinct phage elements - mobile genetic elements

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25
Q

Is stx1 or stx2 more toxigenic

A

Stx2 is 1000 times more toxic

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26
Q

What is the best studied strain of STEC

A

E. Coli O157:H7

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27
Q

When was O157:H7 first discovered

A

First recognised as a pathogen in 1982

It was identified as the cause of two outbreaks of bloody diarrhoea:
- fast food chains across several states on the west coast - undercooked burgers - caused 700 cases and 4 deaths

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28
Q

How did O157:H7 develop

A

There is lots of plasticity in the E.Coli genome -> theres a great ability to lose and acquire genetic material

Done through genomic islands and integrated prophages from bacteriophages

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29
Q

What did O157:H7 develop from, how did it evolve?

A

Prior to the initial outbreak it had never been isolated

It started of as an EPEC gene -> H7 was already present in enteropathogenic E. Coli first

EPEC then acquired a prophage which encoded the STX2 gene

PO157 plasmid was then collected

Plasmid encodes a haemolysin but lost the ability to fermen sorbitol and Bgluc

O polysaccharide was then changes

NB: we dont know what was the reservoir for all of these genetic changes

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30
Q

Give a quick breakdown on the development of O157:H7

A

Initially was an EPEC O55:H7
Stx phage was inherited -> EPEC O55:H7
Plasmid O157 inherited -> conversion to an EHEC O157:H7
Loss of abiliity to ferment sorbitol and Bglu to form the EHEC O157:H7 we know today

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31
Q

How is O157:H7 transmitted

A

There are multiple routes of transmission
Really low infectious dose needed
Direct contact and person to person spread

Cows are the reservoir -> spread to meat, unpasteurised foods or ready to eat foods, bodies of water etc -> ingestion by person - person to person spread

Outbreak associated with unpasteurised apple juice

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32
Q

What were the three main O157:H7 outbreaks studied in America

A

Spinach (SP)
Taco Bell (TB)
Taco John (TJ)

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33
Q

How do we detect polymorphisms in E. Coli

A

Lineage-specific polymorphism assay-6

Puts polymorphisms into lineages e.g. LI, LII etc
- there are three different lineages

Can be further broken down into Clades
- there are 8 different clades

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34
Q

How do lineages of O157:H7 vary from country to country?

A

Different lineages predominate in different countries e.g. L1 predominates in Canadda and US while LI/II predominates in australia and Argentina etc

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35
Q

How do Clades of O157 differ from contry to country

A

There are 8 different clades, 8 is hypervirulent

Clade 7 predominantes in Australia (92%) while clade 8 predominates in Argentina (81-91.4%)

In the netherlands the only clade identified is 8 (38.8%)

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36
Q

How many known differnet SNP genotypes are there for O157:H7?

A

39 SNP Genotypes
20% SNP difference at 96 loci
9 distinct clades

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37
Q

What is clade 8 of O157:H7 associated with?

A

Hypervirulence

but also clinical illness and more frequently reported blood diarrhoea

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38
Q

What are clades 2, 7, and 8 of O157:H7 associated with?

A

These are the clades associated with clinical illness

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39
Q

What are clades 2 and 8 of O157 associated with?

A

Clades 2 and 8 are associated with increased reports of bloody diarrhoea

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40
Q

What are the reservoirs for O157?

A

Generally considered to be cattle
Studies have recovered both O157 and non O157 from ruminants of both food producing and wild animals such as birds
Some animals can be super shedders

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41
Q

What are super shedders in terms of O157 reservoirs

A

Animals that shed greater than 10^4 CFU/g faeces

These animals are colonised at the recto-anal junction

These animals are more likely to spread the disease

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42
Q

Talk about O157 colonisation in animals

A

Some animals will be transiently culture positive
- short durations - few days
- not colonised at the RAJ mucosa
- passive shedders
- seen in cattle
- shed bacteria for an average of 1 month but less than 2 months

In rare cases animals can be colonised for a long time and can shed bacteria for 3-12 months or longer

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43
Q

Talk about non-O157 EHEC, what are they and how common are they?

A

Non-O157 EHEC infections are linked to the ‘Big 6’
- 70 to 75% are 1 of 6 specific strains
- 20 to 30% are other non-O157 STECs

These are becomig a lot more common
Rates ever increasing since bringing in molecular methods of typing EHECs
The disease association with these is unknown as research has focused on O157 but theyre all considered moderate risk compared to the high risk O157

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44
Q

What are the Big 6 Non-O157 EHECs

A

O26 - this is the most common in Ireland -> actually more common than O157
O45
O103
O111
O121
O145

45
Q

Which of the non-O157 strains are most common

A

O26
O111
O103
O145

In this order -> O26 and O111 similar numbers

46
Q

What factors contribute to the virulence of O157:H7

A

adhesion
LEE
Haemolysin (encoded by plasmid)
ToxB -> prophage

Mobile genetic elements:
- phages
- genomic islands
- plasmids

47
Q

What is LEE in O157

A

Locus of enterocyte effacement
Its a pathogenicity island that inserts itself into the E. Coli genome
It allows for really unusual binding
It already existed in EPEC the E. Coli strain that O157 evolved from

48
Q

What is special abobut the O157 adhesion to host epithelial cells?

A

Formation of attaching and effacing (A/E) lesions
Histopathological alteration of the intestine
Locus of enterocyte effacement (LEE) pathogenicity island -> unusual binding of EPEC
Unusual tight binding to epithelium cells
Alteration of the binding site

49
Q

Need detailed descripion of tight binding of O157:H7 to epithelium

A
50
Q

Talk about EHEC adherance to intestinal mucosa

A

EHEC can adhere to intestinal mucosa
EHEC has the eae gene which encodes intimin
eae = Attaching and effacing lesion
Intimin is used for the effacement of microvilli -> inimin binds closely and causes colonisation of the intestine

EHE colonises the intestinal mucosa and induces a characteristic histopathological lesion referred to as attaching and effacing A/E lesions

The geness responsible for A/E lesions map to 13 regions which have been designated the locus of enterocyte effacement (LEE)

51
Q

What is eae

A

attaching and effacing lesion
Its a gene that encodes intimin
Its responsible for the effacement of microvilli in EHEC

52
Q

What is an A/E lesion

A

A histopathological lesion characteristic to EHEC
Known as attaching and effacing lesion
Theyre encoded by genes found in LEE
Presence of AELs are associated with infection but bacteria cn still cause major disease without them

53
Q

Talk about LEE expression

A

The presence of the LEE is stongly associate with disease

The LEE of E. Coli O157:H7 is conserved in EPEC

54
Q

Talk about the LEE of O157

A

The LEE of O157 has an additional 7.5kb prophage sequence compared to its EPEC ancestor

The LEE is made of 41 different genes organised into three major regions:
- TTSS
- Intimin and TIR
- Esp

55
Q

What is the TTSS of the LEE of O157?

A

A type III secretion system that exports effector molecules

Its a type 3 injector type mechanism
Bacteria needs contact with host for this mechanism to work

56
Q

What is the intimin and TIR of O157?

A

Intimin is an adhesion
TIR is its translocated receptor which is translocated into the host cell membrane via the TTSS

57
Q

What is the intimin and TIR of O157?

A

Intimin is an adhesion
TIR is its translocated receptor which is translocated into the host cell membrane via the TTSS

58
Q

What is the Esp of the LEE of O157?

A

Several secreted proteins (Esp) as a part of the TTSS

Resopnsible for modification of host cel signal transsduction during the formation of A/E lesions

59
Q

Explain in your own words how O157 attached to epithelium

A

Bacteria will bind to host cell initially with bundle forming pilus

Bacteia alter the cytoskeleton of host cell
A pedesal is formed
Host cell forms a receptor that the bacteria further bind to
Effacement will contibute

60
Q

Give an indep description of how the LEE of O157 allows for binding of the bacteria to epithelium (video on brightsapce)

A
61
Q

Talk about the plasmid of O157

A

Non-conjugative F-like plasmid a range size from 92 to 104 kb

pO157 shows a dynamic structure

mobile genetic elements such as transposons, prophages, insertion sequences (IS) and parts of other plasmids all together

19 genes found on the plasmid

62
Q

What 19 genes are found on the plasmid of O157

A

a haemolysin (ehxA)
a catalase-peroxidase (katP)
a type II secretion system apparatus (etp)
a serine protease (espP)
a putative cytotoxin (toxB)
A zinc metalloprotease (stcE)
And an eae conserved fragment (ecf)

63
Q

What is the haemolysin of O157 responsible for?

A

Haemorrhagic colitis

64
Q

Talk about the carrying of shiga-toxin genes by phages

A

Stx-coding genes are carried by lambdoid prophages
Role of prophages is essential to microbial evolution
Increase evolutionary fitness
Rearrangement of genomic regions
Acquisition of foreign DNA
Spreading of phages has contributed to the emergence of different Shiga toxin producing E. Coli types

65
Q

What are the effects of shiga toxins on cells in general

A

A-B toxins
They have a really potent cythopathic effect on many cell lines
Theyre particularly active on endothelial cells
Theyre lethal for laboratory animals
They inhibit protein synthesis

a = catalytic, biologicaly active part of toxin

66
Q

How does shiga toxin affect the human host

A

Causes vascular damage mostly in the colon and kidneys

two major complications:
- haemorrhagic colitis (inflammation of the gut)
- haemolytic uremic syndrome

67
Q

How does stx1 and xtx2 comapre t o each other

A

They both share the same enzymatic activity and structural features
However they are immunogically distinct
Stx2 is much more potent than stx1 in humans
Both are associated with the same haemorrhagic colitis and HUS
STEC strains encoding Stx2 are more likely to cause severe disease

68
Q

What are the different parts of the shiga toxin

A

A divided into A1 and A2:
- Active site: glutamic acid
- Ribsome interaction region
- ER translocation region

B part is divided into 5 pentamiers

69
Q

What is the mode of action of the shiga toxin - how is it activated?

A

A2 cleaved from A
The resultant A1 subunit is a highly specific N-glycosidase
This cleaves adenine 4324 from 28S rRBA comonent of eukaryotic 60S ribosomal subunit
Inhibiting elongation factor 1 (EF 1) dependent
Aminoacyl tRNA binding and peptide elongation

70
Q

How does the toxin bind to and get into cells

A

Toxin (5b pentamers) binds to GB3 receptors expressed on endothelial cells in kidney and brain

Toxin GB3 complex is internalised by endocytosisi

Toxin-Gb3 complex undergoes retrograde transport through Golgi apparatus

Proteolysis leaves A1 and A2 subunits linked by a disulphide bond on the stem of a cleaved loop

In ER, the enzymatically active A1 fragment is liberated from the A2 fragment through disulphide-bond reduction

The A1 fragment cleaves an adenine in the 28S rRNA of 60S ribosomal subunits

This results in inhibition of protein synthesis and the induction of ribotoxic stress

71
Q

How many subtypes and variants of stx are there?

A

There are 107 different subtypes and variants of these toxins
The stx2 toxins are associated with sever disease

72
Q

How many subtypes and variants of stx2 are there?

A

7 subtypes (a-g)
35 variants

73
Q

Talk about disease and certain subtypes of Stx2

A

Stx2 is more frequently associated with HUS and haemorrhagic colitis

Theres an association between HUS and the subtypes Stx2a, Stx2c and Stx2d

These trigger thombotic miroaniopathy (TMA)

74
Q

What is Thrombotic microangiopathy

A

Thrombocytopenia < 150
Non immune haemolytic anaemia with a Hct <30%
Azotemia/high creatinine levels

75
Q

How does shiga toxin affect endothelial cells

A

Enhanced expression of functional tissue factor that could contribute to microvascular thrombosis

Damage to or activation of endothelium, red cells and platelets

Damage to or activation of cellular responses such as cytokine expression and apoptosis caused by ribotoxic stress -> this then leads to inflammation along with infection

76
Q

What are the main contributers to pathogenesis of O157

A

Phagosome island LEE
Shiga toxins
Plasmid O157

RpoS -> acid, heat and salt resistance
Iha -> adherence-conferring molecule
EAST1: enterotoxin
Various other LEE reulators and effectors

77
Q

How are the effects of shiga toxin different in the brain

A

We see thrombotic effects to a lesser extent in the brain

78
Q

How do the symptoms of O157 differ in terms of intestinal vs systemic infection

A

Intestinal:
- asymptomatic
- watery diarrhoea develops into HC
- haemorrhagic colitits

systemic:
- haemolytic uremic syndrome (HUS)
- microangiopathic haemolytic thromboytopenia
- anaemia

79
Q

How does VTEC disease progress, how many recover vs die etcc

A

95% will recover but 5% will develop HUS

Out of this 5%:
- 3-5% will die
- 5% will siffer chronic renal failure, stroke and other major sequelae
- 30% will suffer proteinuria and other minor sequelae
-60% will resolve

80
Q

Talk about the rate of HUS development from VTEC in different age groups

A

15.3% in those <5years old
7.9% in those 5-9 years
3.4% in those 10-17 years
1.2% in those 18-59
3.8% in those >60years old

NB: those 60+ had the highest rate of death due to VTEC whether or not they developed HUS

The frail and immunocompromised and pregnant are especially vulnerable

81
Q

What are the HUS Risk Factors

A

Pathogen and host factors
Children most at isk
Leading cause of renal failure in children in the UK and USA
Some studies suggest female gender association
Association with Stx2a and severe disease

82
Q

How is HUS treated

A

The use of antibiotics in the prevention of HUS area of intense speculation and debate

Plasma exchange to remove the toxin

Immunoadsorption

Future therapies such as shiga toxin binding or neutralisation therapies

83
Q

Why is the use of antimicrobials for HUS debated?

A

As antimicrobials can stimulat the phages to produce more toxin

There have been outbreaks where they use antibiotics and the outcomes havent been any worse but its definitey not the recommended route

This is probably why we tend to see less resistance in STEC strains

84
Q

Talk about research on EHEC non-O157 strains

A

There is relatively little known compared to O157
Limited knowledge as focus has been on O157 since 1982
Undestanding of ecology, reservoirs, transmission, virulence etc is all dependent on O157 research

85
Q

How do the genes of O157 differ than non-O157

A

O157 possess classic EHEC genes such as:
- stx1/stx2
- LEE PAI
- pO157
- these maximise disease-causing potentia

Non-O157 are more viable:
- stx1 or stx2
-pO157 may be missing
- LEE PAI

86
Q

Talk abou disease progression in non-O157 strains, who recovers who doesnt

A

Incubation of 3-4 days
Results in non-blood diarrhoea and abdominal cramps (60% recover at this point)
40% progress to bloody diarrhea after 1/2 days
98% resolve
Rare that HUS develops (less than 2%)

87
Q

What is the ‘pathogenic paradigm shift’ in terms of E. coli

A

Germany outbreak marked the outing of E. Coli O104:H4 also known as enteroadherent haemorrhagic E. Coli (EAHEC)
This strain didnt have the classical virulence markers we would associate with normal EHEC but it was still extrardinarily virulent

88
Q

What does EAHEC stand for?

A

Enteroadherent haemorrhagic E. Coli

89
Q

Talk about the virulence factors of EAHEC

A

Lacked classical EHEC markers:
- LEE PAI
- pO157

Possessed:
- Stx2 (Stx2a)
- enteroaggregative E. Coli (EAEC) virulence factors
- aggregative adherence factor (AAF)

90
Q

What was the EAEC outbreak?

A

Outbreak of a new strain in sprouts in germany in 2011

Toxin gene (stx2) was transferred via phage to an EAEC bacterium

New combination with additional resistance genes resulted in EAHEC O104:H4

91
Q

Why is O104:H4 concidered a hybrid pathogen

A

It has the virulence of a VTEC STx2 strain as well as the adherence o an EHEC strain

92
Q

Talk about adherence in O104:H4

A

AAF pilli encoded by aagR results in aggregation and adherence fimbriae

Stacked brick adherence

Thought to be down to unusual really tight binding on gut epithelium which allows for the quicker and increased delivery of toxins resulting in severe disease and a prolonged incubation period

93
Q

Talk about the spread of EAHEC

A

Its an emerging pathogen but its spreading globally
It caused sporadic infections first in Asia and across Europe
Its endemic to central africa

94
Q

What are the reservoirs for EAHEC

A

Not animals
Humans
Irrigation water contamination may be a source of EAHEC

95
Q

What common EAEC virulence factors does O104:H4 also encode

A

AAF specifically AAF/I on pAA virulence plasmid
SPATE proteases
Dispersin aap gene
AggR global regulator

96
Q

What additional virulence factors does O104:H4 encode that EHEC doesnt

A

Encodes a Stx2 within a lysogenize lambdoid bacteriophage

Plasmid that encodes an extended spectrum B-lactamase CTX-M-15
- Recent addition and not in the 2001 strain

97
Q

Compare the disease progression of normal EHEC O157 vs STEC O1O4:H4

A

Only 5-10% of O157 develop HUS while 22% of O104 H4 will develop HUS

98
Q

Why is there an increased risk of HUS with O104 than O157?

A

Aggregative adherence
Biofilm formation
Stx production
Prolonged release of toxin in this strain

99
Q

How large was the initial O104:H4 outbreak?

A

Caused 4000 cases
Caused 53 deaths
Caused 855 cases of HUS

This was a really large outbreak, unusual, mortality and severe disease was high unlike other E. Coli strains

100
Q

What did a retrospective study on the O104 outbreak reveal

A

Strain originated in sprouts
Tones of vegetables had to be dumped until the source was discoered -> was originally thought to be in cucumbers
Originated first in Egypt -> sprouts were only germinated in germany
Sprouts consumed in april, may and june

Outbreak began in may but was seen across all german hospitals -> sent to reference lab for toxn gvene detection and sequencing -> this was really the first time whole genome sequencing was done in real time, results ready in 4 days -> detected in leftover sprouts but never detected in original sporuts -> dont know how they got to sprouts etc

101
Q

Talk about the epidemiology of the O104 outbreak

A

Young children who would normally be afected by E. Coli strains werent affected
Women were more commonly infected then males
- probably down to dietary choices and no other reason

102
Q

Talk about epidemiology of STEC asociated HUS in Ireland (in general)

A

Trends in ireland generally mimic those described globally
90 cases between 2012 and 2014
83 culture positives
58% female
90% HUS<15
57% <5 years
3 HUHS cases in over 65s -> high mortality

103
Q

What STEC serogroups in HUS and non-HUS are most common in Ireland

A

5 of the big 6 are seen (O26, O91, O145 O55, O103)

Rarer O91 serorgoup starting to see more of it in Ireland but it hadnt been one of the big six in the past
O157 = 50% of HUS cases
O25 = 33% of HUS cases

104
Q

What toxin genotypes are seen in Ireland

A

4 stx 1s
33 stx 2s
15 stx 1 and 2

stx 2 has a higher risk of developing HUS (x4 times higher)

Any O157s had an stx2

105
Q

Talk about the genetics of the HUS in Ireland

A

Predominance of Stx2 genotypes
13.5% were eae negative
67% were hylA negative

Small but important evolving STEC causing HUS

Any viable STEC has potential to cause HUS

Dont limit investigations in either clinical or food samples to merely the big 6 serogrous with eae positivity to define a virulent STEC strain

106
Q

Why dont we use antibiotics for STEC

A

Ciprofloxacin signals SOS response
The phage will continuously be transcribed then resulting in continuous shiga toxin production
Hence why we dont treat with antibiotics just toxin neutralisers instead

Hence why we have little to no resistance
STEC strains are much slower to acquire resistance

107
Q

Talk about resistance in O157:H7

A

Resistance to sulfonamide and tetracycline is common in O157:H7

There has been the detection of a shiga-toxin producing ESBL O157:H7 human clinical isolate in Denmark in 2013:
-blaTEM and blaCTX-M-1 blaTEM104 blaCTX-M-28

108
Q

What resistance is seen in STEC O104

A

ESBL
Resistance to ampicillin, cefotaxime, ceftazidine, sulfamethoxazole, streptomycin, trimethoprim, tetracycline and naladixic acid

109
Q

ESBLS have been seen in what other STEC strains other than O104

A

Three human isolates og O26 carrying either a blaCTX-M-3, blaCTX-M-18 or blaTEM-52

An O157 chicken isolate carrying a blaCTX-M-2 gene

4.2 Medical Microbiology (20 decks)

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