Lecture 17 -B. Cereus, C. Perfringens(1)

8/13/2019 Lecture 17 -B. Cereus, C. Perfringens(1)

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Foodborne Toxicoinfections:

Bacillus cereus

Clostridium perfringens

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Bacillus cereus

Gram-positive rods

Spore former

Motile

Grows optimally in aerobic conditions

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Growth temperature range: 450C,

pH of 4.99.3

NaCl < 10%.

Vegetative cells

Spores resistant to thermal processes

Including cooking and pasteurization

B. cereus growth requirements and sensitivities

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Vegetative cells and spores primarily in soil

Dust

Intestines of 10% of humans

Present mostly in foods of plant origin

Rice

Produce

Commonly associated with temperature-abused foods

Natural Habitat of B. cereus and presence in food

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Two forms: Emetic and Diarrheal disease

Infective dose: 105-108 cells

May occur separately or simultaneously Both diseases are caused by toxins

Most toxins produced at optimum growth temp

Mortality rate


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Emetic disease caused by a heat stable emetic toxin Onset: 0.5-5h

Duration: 24h

Symptoms: Nausea, vomiting, abdominal pain, occasional

diarrhea, no fever

Diarrheal disease caused by a heat labile enterotoxin

Onset: 6-12h Duration: 24h

Symptoms: Profuse watery diarrhea, abdominal pain, novomiting, no fever

Disease caused by B. cereus

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Emetic v. Diarrheal

FS 362, 12-7-09 7


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Sequence of events leading to

toxicoinfection/intoxication

Spores or cells are initially present in the food product

Conditions allow spore germination and/or vegetative cellgrowth

Temperature abuse

Cells may or may not produce toxin while in food

These cells may produce one of the toxins or both of the toxins

Vegetative cells (maybe toxins) are consumed in food

Emetic toxin released in the stomach

Diarrheal toxin released in the intestine

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Mechanism of B. cereus Pathogenesis

Emetic toxin: Binds to a receptor on the vagus nerve

in stomach, and induces vomiting

Cereulide

of logarithmic phase, highest level ofproduction at early stationary phase of growth,

not associated with sporulation

12 to 37 C, although maximal production ofemetic toxin appears to occur between 12 and

22 C

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Mechanism of B. cereus Pathogenesis

Diarrheal toxin: Stimulates Na+, Cl- secretion

from intestinal epithelial cells, causes water

loss

Hbl, Nhe and CytK cytotoxins are the main

virulence factors in B. cereus foodborne

diarrheal disease

Pore formation in intestinal epithelial cells

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Treatment/Prevention ofB. cereus Illness

Treatment: Self limiting, rehydration

Prevention:

We cannot eliminate B. cereus in foods

We can prevent it from reaching dangerous levels in

foods

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B. cereus Outbreak

Day-care center in Virginia

22 children, 6 adults ill with vomiting and diarrhea

Lunch catered by a local Chinese restaurant

Rice prepared the day prior to the lunch

Cooled at room temperature prior to refrigeration

overnight

Morning of the lunch: Rice was pan-fried with chicken andheld at room temperature prior to serving

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Clostridium perfringens

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C. perfringens

Gram positive rods

Motile

Sporeformers

Facultative anaerobe

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Growth temperature range: 10-52C

Optimum temperature: 45C

pH >5.0

NaCl < 5%

Generation time in optimal conditions:

Vegetative cells:

Spores:

C. perfringens growth requirements and

sensitivities

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Vegetative cells and spores found in: Intestinal tract ofanimals, birds and humans, and soil

Meat/meat products

Milk

Produce

Soups/stews or dishes with many meat or soil-associated

ingredients C. perfringens tends to be associated with large outbreaks

(hundreds+ of infected individuals)

Natural habitat of C. perfrigens and presence in food

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Disease caused by C. perfringens

Gastroenteritis Toxicoinfection caused by enterotoxin

5 types of C. perfringens

A-E

Toxins produced >10C

Infective dose 106 vegetative cells

Onset 8-24h; Duration 24h

Symptoms Explosive diarrhea, abdominal pain

Mortality


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Sequence of events leading to

toxicoinfection/intoxication

Spores or cells are initially present in the food product

Conditions allow spore germination and/or vegetativecell growth

Temperature abuse

Food consumed with high levels of vegetative cells

Enterotoxin usually produced/released in the intestinal

tract

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Mechanism of C. perfringens Pathogenesis

Enterotoxin produced in host intestine

Binds to receptor on epithelial cell membrane

Leads to loss of Na+, Cl-,

C. perfringens ferment carbohydrates in intestine and

produces gas

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Treatment/Prevention ofC. perfringens

Illness

Treatment: Self limiting, rehydration

Prevention:

We cannot eliminate C. perfringens in foods

We can prevent it from reaching dangerous levels in

foods

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C. perfringens Outbreak

2002: Connecticut steel factory

Employee Thanksgiving holiday banquet (over 1000

served in 12 h period)

642 people ill with diarrhea, sometimes explosive

Traced to contaminated meat gravy

Spores in original product survived cooking

Improper cooling - spore germination

Gravy kept warm during banquet vegetative cell

growth

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Lecture 17 -B. Cereus, C. Perfringens(1)

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