Lecture 14 Ecoli_shigella(1)

8/13/2019 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


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


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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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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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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Lecture 14 Ecoli_shigella(1)

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