E. coli O157:H7
Kang, Dong-Hyun
Associate Professor
Department of Food Science and Human Nutrition
Washington State University
Foodborne illness processes
Infection
Intoxication
Toxicoinfection
Infections
A disease state caused by the presence
of viable, usually multiplying organisms
at the site of inflammation
Intoxication
A disease state caused by exposure to
a toxic chemical
Toxicoinfection
A disease state that is caused by
exposure to a toxic chemical produced
by the presence of viable, usually
multiplying organisms at the site of
inflammation
Major Foodborne Pathogens
E. coli O157:H7
Listeria monocytogenes
Salmonella
Campylobacter
Shigella
Vibrio
Yersina
Staphylococcus
Clostridium botulinum perfringens
Bacillus cereus
E. coli
Major Foodborne
Pathogens in E. coli Group
Taxonomy
Biochemical tests
Production of indole (indole positive)
Use of citrate (citrate positive)
Serological tests
Pathogenic strains is partially based on serology
with 173 O (somatic), 56 H (flagella), and 80 K
(capsular) antigen
E. coli
Major Foodborne
Pathogens in E. coli Group
ETEC
EPEC
EHEC E. coli O157:H7
EAEC
EIEC
Serotypes of pathogenic E.coli
Table 1. Serotypes characteristic of the pathogenic E. coli categories
aO antigen untypeable by conventional methods.
Enterohemorrhagic E. coli
E. coli O157:H7
Escherichia coli O157:H7
Major Outbreaks
2007
E. coli O157:H7 in ground beef from the
Topps Meat Company in Elizabeth, New
Jersey. As of 2007, it is the second-largest
beef recall in United States history
E. coli O157:H7
Escherichia coli O157:H7
Major Outbreaks
2006
E. coli O157:H7 from Taco Bell in South
Plainfield, New Jersey and Long Island.
They suffered from hemolytic uremic
syndrome - 39 people in central New Jersey
and on Long Island were sickened
E. coli O157:H7
Escherichia coli O157:H7
Major Outbreaks
2006
E. coli O157:H7 in bagged spinach
packaged by Natural Selection Foods and
most likely supplied by Earthbound Farm in
San Juan Bautista. 3 dead, and 198 people
reported sickened by the outbreak across 25
US States
E. coli O157:H7
Escherichia coli O157:H7
Major Outbreaks
2002
E. coli O157:H7 in ground beef from ConAgra. 19
people became ill in California, Colorado,
Michigan, South Dakota, Washington and
Wyoming as a result of eating tainted hamburger.
The company recalled over 19 million pounds of
ground beef it had manufactured, in the third
largest recall in history
E. coli O157:H7
Escherichia coli O157:H7
Major Outbreaks
1997
E. coli O157:H7 in ground beef from
Hudson Foods Company of Rogers,
Arkansas.
The company recalled over 25 million
pounds of ground beef it had manufactured,
in the second largest recall in history.
E. coli O157:H7
Escherichia coli O157:H7
Major Outbreaks
1996
E. coli O157:H7 in unpasteurized apple
juice from Odwalla
E. coli O157:H7
Escherichia coli O157:H7
Major Outbreaks
1993
E. coli O157:H7 in undercooked
hamburgers from Jack in the Box. Four
people died and hundreds of others became
sick in the Seattle area and other parts of the
Pacific Northwest.
E. coli O157:H7
E. coli O157:H7
Escherichia coli O157:H7
Gram negative bacillus, generally motile
Non-sporeforming bacteria
73,480 cases/year – 500 deaths
Relatively high toxicity as 44°C
survive well during freezing
pH: optimum near neutrality, but
tolerant of a number of conditions,will
grow well down to 4.5
E. coli O157:H7
Mode of Infection
Once ingested, the organisms make
their way to the large intestine, where
they cause inflammation.
Adhere to intestinal epithelium
Adhering bacteria destroy the villi of the
intestinal epithelial cells
create a lesion – severe diarrhea
E. coli O157:H7
Mode of Infection
When the lesion becomes deep enough,
Break the lamina propria – affect the
underlying blood vessels – Hemorrhage and
bloody stools
Outpouring of a toxin into the blood
circulation – leading to damage of small blood
vessels in the kidneys, brain, other organs
E. coli O157:H7
Mode of Infection (Toxin)
The Shiga-like toxins - general class of AB toxins. -
The B component binds to molecules on the surface
of target cells.
The toxins are then taken up into the target cells by
endocytosis, at which point the A component enters
the cytoplasm and carries out some toxic enzymatic
reaction inside the cell.
Structural division between the cell-surface
recognition function (B subunit) and toxic enzymatic
action.
E. coli O157:H7
Mode of Infection (Toxin)
The A component attacks the 28 S
ribosomal RNA, deaminates a single
adenine at position 4342. by clipping a
particular nucleotide from one of the
ribosomal RNAs. This blocks protein
synthesis and leads to the death of the
cell.
Pathogenesis
Three-stage model of EPEC
pathogenesis. (A) The first
stage is characterized by initial,
relatively distant interaction of
bacteria with the enterocyte
layer. This initial attachment is
thought to be mediated by the
bundle-forming pilus. (B) In
the second stage, eae and other
genes are activated, causing
dissolution of the normal
microvillar structure. (C) In the
third stage, the bacterium binds
closely to the epithelial
membrane via the protein
intimin. Other bacterial gene
products mediate further
disruption of the cytoskeleton
and phosphorylation of cellular
proteins.
Pathogenesis
Virulence factors (BFP)
BFP
Pathogenesis
Pedestal-like structure
EHEC
A toxin
Shiga Like Toxin Glycolipid
B toxin
28 S ribosomal RNA
E. coli O157:H7
Illness
Onset: 3 - 9 days, average 4 days
Duration: 2 - 9 days
Symptoms: abdominal cramps, watery diarrhea,
grossly bloody diarrhea described as "all blood
and no stool", abdominal pain described as equal
in intensity to labor pains
Hemolytic Uremic Syndrome (HUS)
Thrombotic Thrombocytopenic Purpura (TPP)
Questions ?