10 - E.coli Flashcards
Is North America strongly affected by mortality from diarrhea in children under 5?
No
E.coli is a gram ______, motile, nonsporulating, rod-shaped, and a facultative anaerobe
negative
Does E.coli produce spores?
No
T OR F: E.coli is part of the normal microbial population of the intestinal track of humans, and other warm blooded animals?
T
T OR F: Most strains of E.coli are pathogenic
F
E. coli can be categorized into different _________ based on their ability to produce toxins, ability to adhere to epithelial cells, and ability to invade epithelial cells (the pathogenic traits have mostly been acquired through horizontal gene transfer)
pathotypes
AIEC =
Adherent invasive E.coli
ETEC =
Enterotoxigenic E.coli
EAEC =
Enteroaggregative E.coli
STEC =
Shiga toxin producing E.coli
EIEC/Shigella =
Enteroinvasive E.coli
DAEC =
Diffusely adherent E.coli
EPEC =
Enteropathogenic E.coli
UPEC =
Uropathogenic E.coli
E. coli can also be differentiated into serotypes based on three major surface antigens: _ (LPS), __ (flagella), and __(capsule)
O
H
K
The O antigen defines the ________ of a strain, and the H antigen identifies the _________
serogroup
serotype
Several serogroups fall into multiple __________
pathotypes
E. coli strains can be grouped into 5 main phylogenetic groups:
A B1 B2 D E
*EIEC/Shigella also forms additional phylogroups (black)
T OR F: Pathotypes do not always group together in the same phylogroup.
t
Name the main 4 parts of the small intestine:
- villi
- crypt
- enterocyte
- microvilli
The E.coli genome is very _____________
plastic
There are about _______ genes in the E.coli core genome, and ___________ genes in its pan-genome
1,700
16,400
Several _________, ____________, and ___________ regularly moving in and out of bacterial genomes
prophages
genomic islands
plasmids
Most virulence factors (toxins, and colonization factors) of E. coli are derived from _________________________
mobile genetic elements
The phenotype (and disease caused) by each phenotype is determined by which virulence factors they have picked up via _____________________
horizontal gene transfer
What are the genes that are considered virulence factors in humans:
LEE or Shiga toxins
Give me some characteristics of EPEC:
- has the ability to form distinctive lesions on the surfaces of intestinal epithelial cells
- carries LEE genes (the locus of enterocyte effacement)
- mainly affects children less than 1 year old in developing countries
- only transmitted via the fecal-oral route, humans are the only identified carrier
What can you do to prevent transmission of EPEC?
- proper hygiene methods
- have clean fresh water supplies
EPEC does not generally have ________________
enterotoxins
In EPEC the effacement of microvilli may lead to a decrease in absorptive surfaces thereby __________________________
contributing to diarrhea by increasing water in the small intestine
*Tight junctions may also be disrupted, this could lead to increased intestinal permeability
STEC is defined by the presence of Shiga toxin 1 & 2 which is acquired by _______________
bacteriophage infection
STEC causes what:
mild to bloody diarrhea and haemolytic uremic syndrome (HUS)
HUS is caused by what:
The destruction of red blood cells. The damaged red blood cells clog the filtering system in the kidneys, which can lead to life-threatening kidney failure
Does STEC have the LEE genes?
Yes and STEC can also form lesions on the microvilli like EPEC
____________ is the most common serotype of STEC
O157:H7
What is the transmission route for STEC:
fecal-oral route
______________________ are responsible for sporadic and outbreak related illnesses of STEC
Contaminated food and water
Stx toxins are carried on a __________ phage which may become ___________ during bacterial stress, for this reason __________ are not recommended
lysogenic
lytic
antibiotics
EIEC and Shigella are ______________________ pathogens
facultative intracellular
EIEC / Shigella are ______________ that divide in the intracellular milieu of intestinal cells
invasive
T OR F: EIEC / Shigella destabilize the epithelial tight junctions, and induce epithelial cell death
T
Generally, EIEC and Shigella have the same virulence strategies, though ___________ has increased virulence
Shigella
Explain the multistep process infection by EIEC/Shigella
cells penetrate the epithelial barrier, induce macrophage cell death, invade intestinal epithelial cells, engagement in intra- and intercellular movement, and degrade epithelial integrity
Symptoms of EIEC/Shigella include:
- mild watery diarrhea
- fatigue
- malaise
- fever
- anorexia
What happens later in the disease of EIEC/Shigella
- abdominal cramps
- blood or mucus in diarrhea and dehydration
*usually self-limiting and more serious in the developing world
Since Shigella also carries the Stx toxins, _____ can also result
HUS
What is one difference between STEC and EIEC/Shigella:
in the case of EIEC/Shigella antibiotics seem to protect against HUS unlike with STEC
______________may be the most common bacterial pathogen identified in patients with diarrhea
EAEC
________is a causative agent for traveler’s diarrhea
EAEC
T OR F: EAEC is often transmitted through food and water contaminated with fecal material, such as salads, deserts, salsa – food workers can also be carriers and must practice hygienic measures to keep infection from spreading
T
What is the 3-part infection model for EAEC infection?
1- cells adhere to intestinal mucosa
2- cells produce enterotoxins and cytotoxins
3 - the mucosa becomes inflamed due to toxins and the immune system (diarrhea)
The identifying factor of EAEC is that the combination of virulence factors required for the three steps above are all encoded on the _________ plasmid
pAA virulence
ETEC is also a major cause of _________
traveler’s diarrhea
ETEC can produce either or both _________ or _______ enterotoxin and produces several colonization factors for adherence to the intestinal epithelium
heat-liable
heat-stable
No ________________ are in the core-genome of ETEC
virulence factors
Acquisition of _____________ toxins and __________ factors may be the driving force behind ETEC pathogenesis
plasmid-borne
virulence
ETEC is the only E. coli to have a ___________, therefore, is a defining characteristic
heat-stable toxin
How does the heat-stable toxin produced by ETEC acts:
it acts by inducing chlorine and fluid secretion into the lumen, thus diarrhea
ETEC also affects the ______ industry
swine
What are the symptoms associated with ETEC?
- mild to severe (non-bloody) diarrhea which rapidly leads to dehydration
- headaches
- fever
- abdominal cramping
- nausea/vomiting
Are antibiotics recommended for ETEC?
Antibiotic treatment is not generally recommended, since it will clear up on its own, and antibiotic use must be weighed against the possibility of antimicrobial resistance
T OR F: DAEC attach to epithelial cells, but do not follow the classical patterns of adherence, such as attachment and effacement of microvilli
T
What is special about DAEC?
its diffuse pattern of adherence to epithelial cells (adherence occurs over the entire surface of the epithelial cell
T or F: Adults can become asymptomatic carriers, but it has been speculated that carrying DAEC leads to chronic inflammatory intestinal disease
T
What happens when DAEC binds to epithelial cells:
it induces actin rearrangement and destroys microvilli, tight-junctions become leaky
What is the defining virulence factor of DAEC:
the Afa/Dr family of adhesins which allow for the diffuse binding to epithelial cells
What is the only treatment for DAEC:
oral rehydration
______________ has been implicated as a causative agent of Crohn’s Disease, which is a cause of inflammatory bowel disease (IBD)
AIEC
____ are most related to UPEC
AIEC
___% of patients with Crohn’s disease carry AIEC
30
EPEC and LEE-positive STEC are ________________ pathogens that attach to the intestinal epithelium and efface microvilli, forming characteristic A/E lesions.
extracellular
ETEC uses _______________- for attachment to host intestinal cells
colonization factors (CFs)
________ forms biofilms on the intestinal mucosa, and bacteria adhere to each other as well as to the cell surface to form an aggregative adherence pattern (AA) known as “stacked brick.”
EAEC
_______ is dispersed over the surfaces of intestinal cells, resulting in a diffuse adherence (DA) pattern.
DAEC
_______ colonizes the intestinal mucosae of patients with Crohn’s disease and is capable of invading epithelial cells as well as replicating within macrophages.
AIEC
EIEC/Shigella are __________________ that penetrate the intestinal epithelium through M cells to gain access to the submucosa. EIEC/Shigella escape submucosal macrophages by induction of macrophage cell death followed by basolateral invasion of colonocytes and lateral spread.
intracellular pathogens
Acquisition of genes is generally from mobile elements such as _____________, ___________, and __________
transposons
prophages
plasmids
ETEC isolates carry enterotoxins __ and ___ solely or together on plasmids, as well as colonization factors (CFs).
LT
ST
DAEC isolates have fimbriae that enhance adherence, called the ______
Afa/Dr
EAEC virulence factors are found the __________
pAA plasmid.
EIEC/Shigella gained the ability to invade cells mainly through the _______ plasmid and acquired additional virulence traits in the form of ______
pINV
PAIs
nes involved in the pathogenesis of ______ are unclear
AIEC
Important virulence factors include genes that encode the ability to:
- Adhere to epithelial cells
- Produce toxins
- Invade epithelial cells
What are the most common E.coli pathotypes in food (4):
STEC
ETEC
EAEC
EIEC
