Lecture 14 Ecoli_shigella(1)
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Transcript of Lecture 14 Ecoli_shigella(1)
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Lecture 14- Foodborne Disease:
Pathogenic E. coli
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E. coli
Gram-negative rod
Facultative anaerobe
Motile Non-sporeforming
Normal inhabitant of intestinal tract of
humans and warm-blooded animals and birds
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http://en.wikipedia.org/wiki/File:EscherichiaColi_NIAID.jpghttp://en.wikipedia.org/wiki/File:EscherichiaColi_NIAID.jpg -
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E. coli: Pathogens vs Non-Pathogens
Most E. coli are nonpathogenic Nonpathogenic E. coli may be beneficial in intestine
Use of E. coli as indicator microorganism
E. coli as a model organism
Used to study many cellular processes due to its rapid
growth rate and simple nutritional requirements
E. coli K12
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Pathogenic E. coli
Only a few strains of E. coli are pathogenic These strains belong to six groups, which cause different
types of infection
ETEC
EPEC
STEC
EIEC
DAEC
EAEC
Target populations Everyone, but young are mostseverely affected
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Natural Habitat and Presence of E. coli in Foods
Present in high numbers in intestines of certain animals:106/g of contents of large intestine
ETEC, EPEC, EIEC, DAEC, EAEC: Only humans are natural hosts Foods contaminated directly or indirectly through human fecal
contamination
Produce Hand-prepared foods or foods with high human handling
EHEC: Intestines of food producing animals
Foods contaminated directly or indirectly through fecalcontamination
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Pathogenic E. coligrowth requirements and sensitivities
Mesophiles Temperature range: 10-45C
Optimum temp: 37C
Grows at pH 4.5-9
Grows at NaCl
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ETEC
Worldwide problem: Major cause of travelers diarrhea
Waterborne and foodborne pathogen
Problem in infants in developing countries
Disease symptoms: Severe watery diarrhea
Some vomiting
Fever
Infective dose: 108-109 cells
Onset:
Duration: 3-4 days
Severity:
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Mechanism of ETEC Pathogenesis
Intoxication
Both toxins inhibit Na+ and Cl-
absorption
Stimulate Cl- and H2
0 secretion
ETEC
LT
ST
Cl-
H2O
Fig 25.3, Ray and Bhunia
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EPEC
Worldwide problem: Waterborne and foodborne pathogen
Problem in infants in developing countries
Disease symptoms: Severe watery diarrhea with mucus
Some vomiting
Severe abdominal pain, with intestinal inflammation
Fever
Infective dose: 106-109 cells
Onset: 17h 72h
Duration: 6h 3d
Severity: 5-6% mortality rate
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Mechanism of EPEC Pathogenesis
Attach to epithelial cells Using bundle forming pili
Forms an attaching andeffacing lesion (A/Elesion) on epithelial cells
Result: Malabsorption,diarrhea, pain, intestinalinflammation
A/E lesion
EPEC
bfp
Actin
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Images of EPEC Adhesion
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STEC (formerly EHEC)
Emerging pathogens
Common serovars: O157:H7
O26, O111, O103, O121, O45 and O145 (i.e., non-O157:H7)
Produce Shiga-like toxins (Stx)
Disease symptoms: (Enterohemorrhagic colitis)
Bloody diarrhea
Some vomiting
Severe abdominal cramping
Occasional fever
HUS
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EHEC
Infective dose: 10-100 cells
Onset: 3-9 d
Duration: 4-10 d
Severity: 1-2% mortality rate
Food industry response: Zero tolerance for O157:H7;public comment period for non-O157:H7 in ground beef
and beef trim
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Mechanism of EHEC Pathogenesis- Intestinal phase
Adhesion via intimin
Forms an A/E lesion
Produces Stx-
EHEC
A/E lesion
Stx
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Stx A-B Type Toxin
B subunit binds to hostreceptor Gb3
Kidney cells have highlevels of Gb3
A subunit enters kidneycell and inhibits proteinsynthesis cell dies
Kidney pain Bloody urine
Renal failure
death
Mechanism of EHEC Pathogenesis- HUS phase
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EIEC
Worldwide problem: Food and water-borne outbreaks
Disease symptoms: Dysentery (like Shigella) Abdominal cramps
Profuse diarrhea
Fever, headache and chills
Infective dose: 106 cells
Onset: 8-24h
Duration: 7-12 days
Severity: ~1%
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EIEC Mechanism of Pathogenesis
Adhesion
Invasion Several invasion proteins
Produces diarrheal toxinonce inside cell
Survival inside host cell-
Cell-to-cell spreadEIEC
Diarrhealtoxin
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Treatment of Foodborne E. coli Infection
Most are self-limiting
Antidiarrheal medications not recommended
Antibiotics:
May help to kill pathogen in severe cases
Controversial for EHEC infections
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Prevention of Foodborne E. coli Infection
On-farm Prevention of E.colicontamination of water/soil
Prevention/limitation of EHEC in animals
Hygiene
Subtherapeutic antibiotics, probiotics
Food industry Processing steps
Sanitation
Routine testing of products and plant environment
Food retail/at home Avoid contamination by human handlers hygiene
Proper cooking
Refrigeration
Avoid cross contamination
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E. coli O1O4:H4
May 21 July 26 2011, Germany, largest documented outbreak
Initially the outbreak was associated with consumption ofcucumbers
Subsequent investigations: consumption of fresh sproutedseeds from a single sprouted seed producer in Germany.
Contaminated seeds used for the sprout production were themost likely source.
STEC isolates responsible for the outbreaks in France andGermany were found to be indistinguishable. It was thereforeconcluded that there was a common source for both outbreaks.
One consignment (lot) of fenugreek seeds imported from Egypt
was the most likely link between the outbreaks STEC O104 is a very rare serogroup in humans
A total of 3911 cases were reported to the ECDC and WHO
773 cases of HUS
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Natural Habitat and Presence of Shigella in Food
Intestines of humans and some primates is only naturalhabitat
Contaminates food via fecal contamination
Common Food Association:
Produce
Foods with high human handling vegetable salads, deli salads(potato, tuna, chicken), shellfish
Can grow in foods, but does not cause spoilage
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Incidence of Shigellosis
U.S. - 450,000 cases/yr
All other industrialized nations: 1.5 million cases/yr
Developing countries- 164.7 million cases/yr
Mortality rate: 5-15%
For weeks-months after infection, humans can be
asymptomatic carriers
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Shigella Mechanism of Pathogenesis
1- Invasion of intestinal epithelium
Invades epithelial cells and spreads from cell to cell
Taken up by M-cells and passed to macrophages
Causes apoptosis of infected cells and weakens intestinal
epithelial barrier
Fig 25.4, Ray and
Bhunia
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Shigella Mechanism of Pathogenesis
2- Production of toxin and induction of diarrhea
Once inside of epithelial cells, Shigella produces Shiga toxin
Shiga toxin damages intestinal epithelial cells, preventingnutrient uptake and inducing fluid loss
Fig 25.4, Ray and
Bhunia
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Shigella Mechanism of Pathogenesis
3- Triggers Inflammation and further damages intestinal epithelium
The infected epithelial cells and macrophages produce chemokines
that attract white blood cells
Further weakens the intestinal epithelial barrier, allows morebacteria to invade
Fig 25.4, Ray and
Bhunia
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Complications Resulting from Shigellosis
Hemolytic Uremic Syndrome (HUS)
High fever and seizures
Reiters Syndrome
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Diagnosis of Shigellosis
Fecal samples tested for Shigella
Classic microbiological methods
DNA-based methods
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Treatment for Shigellosis
Mild infections self limiting
All others antibiotic therapy
Potential problems with antibiotic therapy
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Prevention of Shigellosis
Shigella-carriers should not handle foods
Sanitation for food handlers
Sanitation practices for field workers
Access to toilets and hand-washing stations
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Shigellosis Outbreak
2000 S. sonnei and Senor Felix 5-Layer Bean Dip
410 people in CA, OR, WA
Traced to infected employee with no paid sick leave
GMP violations at food processing plant
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