13ch37 Lecture

Brock Biology of Microorganisms
Twelfth Edition
Madigan / Martinko Dunlap / Clark
Chapter 37
Food Preservation and Foodborne Microbial Diseases
Lectures by Buchan & LeCleir
Copyright 2009 Pearson Education Inc., publishing as Pearson Benjamin Cummings
II. Microbial Sampling and Food Poisoning
37.4 Foodborne Diseases and Microbial Sampling 37.5 Staphylococcal Food Poisoning 37.6 Clostridial Food Poisoning
37.4 Foodborne Diseases and Microbial Sampling

Food Poisoning (also called food intoxication)
Disease that results from ingestion of foods containing preformed microbial toxins The microorganisms that produced the toxins do not have to grow in the host
Food Infection
Microbial infection resulting from the ingestion of pathogen-contaminated food followed by growth of pathogen in the host
Annual Foodborne Disease Estimates for the United States
Food Poisoning/Intoxication
Results from the ingestion of preformed toxin in food product Rapid onset of vomiting/diarrhea in 4-12 hrs Common causes Clostridium botulinum Clostridium perfringens Staphylococcus aureus Bacillus cereus
37.5 Staphylococcal Food Poisoning

Food poisoning is often caused by toxins produced by S.
aureus
S. aureus can grow on common foods and some strains produce heat-stable enterotoxins
Gastroenteritis occurs within a few hours of consumption
It is estimated that 185,000 cases of staphylococcal food poisoning occur each year Enterotoxins of S. aureus classified as superantigens produce large T cell response and an inflammatory response
Staphylococcus aureus
Figure 37.4
37.6 Clostridial Food Poisoning

Clostridium perfringens and Clostridium botulinum cause serious food poisoning
Produce endospores that may not be killed during cooking/ canning process
C. perfringens is the most commonly reported form of

food poisoning, with 248,000 annual cases
Large numbers of cells (>108) must be ingested Enterotoxin is produced in the intestinal tract 7-15 hours after consumption
Clostridium perfringens
Figure 37.5
37.6 Clostridial Food Poisoning

Botulism is a severe and often fatal food poisoning
Caused by an exotoxin produced by Clostridium botulinum Botulinum toxin is a neurotoxin, but is destroyed by heat Average of 24 cases annually Over 60% of all botulism cases in the U.S. are in infants 25% of cases are fatal
Home-prepared foods are most common source of illness

Infant cases can be caused by consumption of raw honey
Botulism in the United States
Figure 37.6
Botulism
Symptoms Begins 12 to 36 hours post ingestions of contaminated foods Begins with dizziness, dry mouth and blurred vision Abdominal symptoms include pain, nausea, vomiting and diarrhea or constipation Progressive paralysis ensues Paralysis of respiratory muscles most common cause of death Paralysis distinguishes botulism from other forms of food poisoning
Botulism
Causative agent
Clostridium botulinum
Gram (+), spore forming rod shaped
Endospores generally resist boiling for hours

Killed by autoclaving
Produces toxin
7 different toxins
A, B, C1, D, E, F, G All produced by different strains A, B, E, F responsible for most human cases
Botulism
Pathogenesis
Spores germinate in favorable environment
Bacterial growth results in toxin release
Toxin resist digestion and is absorbed by small intestine
Toxin can circulate in blood stream for 3 weeks or more
Toxin is neurotoxin
Acts against nervous system One of most powerful poisons known Toxin attaches to motor nerves blocking function of neurotransmitter
Botulism
Epidemiology Bacteria are widely distributed in soils and aquatic sediments In early 20th century foodborne outbreaks common Infant botulism more common than foodborne Intestinal occurs in small children to 6 months of age Results in disease ranging from mild lethargy to respiratory insufficiency Wound botulism
Botulism
Prevention and Treatment

Prevention depends on proper sterilization and sealing of canned food Heating food to 100C for 15 minutes just prior to eating generally makes food safe to eat
Cant rely on smell, taste or appearance to detect contamination
Treated by intravenous administration of antitoxin ASAP

Antitoxin only neutralizes circulating toxin Affected nerves recover slowly Artificial respiration may be required for prolonged periods
III. Food Infection
37.7 Salmonellosis 37.8 Pathogenic Escherichia coli 37.9 Campylobacter
37.10 Listeriosis
37.11 Other Foodborne Infectious Diseases
37.7 Salmonellosis
Salmonellosis is a gastrointestinal illness caused by foodborne Salmonella infection
40,00045,000 documented cases per year Food production animals such as chickens and pigs may harbor Salmonella Onset of the disease occurs 848 hours after ingestion Disease normally resolves in 25 days
Salmonella ingested in food or water invades

phagocytes and grows as an intracellular pathogen
Salmonellosis
Symptoms Generally characterized by Diarrhea Abdominal pain Nausea Vomiting Fever Symptoms vary depending on virulence of strain and number of infecting organisms Symptoms are generally short-lived and mild
Salmonellosis
Causative Agent
Salmonella enterica
Gram negative Motile, H2S +
Enterobacteria
Salmonella subdivided into over 2,400 serotypes

Salmonella Typhimurium and Salmonella Enteritidis most common serotypes in United States, Salmonella Typhi produces typhoid fever
Salmonellosis
Salmonella typhi cause of Typhoid Fever 10% fatality rate Therapy is supportive + antibiotics Resulting from poor sanitation
Water or food sources
Salmonellosis
Epidemiology
Bacteria can survive long periods in the environment Children are commonly infected
Generally by household pets such as turtles, iguanas, and baby chicks

Control depends on reporting cases and tracing source of outbreak Adequate cooking kills bacterium Vaccine available for prevention of typhoid fever
Vaccine 50% to 75% effective
Most cases have an animal source

Enteric fevers, such as those caused by Salmonella Typhi are generally the exception Typhoid Mary notorious carrier
Surgical removal of gallbladder eliminates carrier state
Caused at least 53 cases over
Salmonellosis in the United States, 19752005
Figure 37.7
37.8 Pathogenic Escherichia coli

Most strains of E. coli are non-pathogenic
All pathogenic strains are intestinal parasites and a few

produce potent enterotoxins Enterohemorrhagic E. coli (EHEC, i.e. O157:H7) produce verotoxin, similar to Shiga toxin
Verotoxin causes bloody diarrhea and kidney failure
50 deaths in the U.S. per year
Other types of E. coli are classified as ETEC and EPEC
Escherichia coli Gastroenteritis
Symptoms
Depends largely on virulence of infecting strain Symptoms can range from vomiting and a few loose stools to profuse water diarrhea to severe cramps and bloody diarrhea Fever not usually prominent Recovery usually occurs within 10 days
Pathogenesis
Possesses two important virulence factors
Production of enterotoxin Adherence to cells of small intestine
Virulence factors foster spread
Causative Agent
Most diarrhea causing E. coli fall into four groups
Enterotoxigenic E. coli (ETEC)
Most common cause of travelers diarrhea
Enteroinvasive E. coli (EIEC)

Disease closely resembles that of Shigella species
Enteropathogenic E. coli (EPEC)

Causes outbreaks in hospital nurseries and bottle fed infants in developing
countries
Enterohemorrhagic E. coli (EHEC)

Epidemiology
Epidemics occur from
Person-to-person spread Contaminated food and water Unpasteurized milk and juices

Prevention directed at
Hand washing Pasteurization of drinks Proper food preparation
Humans, domestic and wild animals all sources of pathogenic strains
Treatment includes
Replacement of fluids and electrolytes Infants may require antibiotics
Antibiotics tend to prolong disease in adults
37.9 Campylobacter
Campylobacter spp.
The most common cause of bacterial foodborne infections in the United States More than 2,000,000 cases of bacterial diarrhea per year
Transmitted to humans via contaminated food

Poultry, pork, raw shellfish, or in surface waters After ingestion, Campylobacter replicates in the small intestine Infections cause a high fever, headache, malaise, nausea, abdominal cramps, and bloody stools
Campylobacter jejuni
Figure 37.8
Campylobacteriosis
Symptoms
Fever Vomiting Diarrhea Abdominal cramps Dysentery
Occurs in only about 50% of cases
Bacteria recognized in 1972

Estimated 2.4 million cases annually
Less than 1,000 fatalities
Fatalities mostly in elderly and immunocompromised
Causative Agent
Campylobacter jejuni
Motile Gram negative Curved rod Cultivated from feces
Campylobacteriosis
Pathogenesis
Small infecting dose
Only 500 organisms required to initiate disease
Organisms penetrate intestinal epithelium Bacteria multiply in and under cells and initiate inflammation
Campylobacteriosis
Epidemiology
Numerous foodborne and waterborne outbreaks have been
reported
Most cases sporadic
Causative agent lives in intestine of variety of domestic animals

Particularly poultry One drop of juice from raw chicken can contain infective dose
Epidemics have occurred due to unpasteurized milk

Person-to-person spread rare
Campylobacteriosis
Prevention and Treatment Prevention directed at proper treatment of water and food Pasteurization of drinks and proper cooking and handling of raw food
Most cases of campylobacteriosis subside without antimicrobial

treatment in about 10 days Erythromycin recommended for severe cases
37.10 Listeriosis
Listeria monocytogenes is the cause for listeriosis
May lead to bacteremia and meningitis Virtually no food product is safe from contamination Psychrotolerant
L. monocytogenes is an intracellular pathogen

Uptake of the pathogen by phagocytes results in the growth and proliferation of the bacterium
Mortality rate of listeriosis is 20%

Listeria monocytogenes
Figure 37.9
Shigellosis
Symptoms
Classic symptom is dysentery Other symptoms include
Headache Vomiting Fever stiff neck Convulsions (rare) Joint pain
Causative Agent
Four species of Shigella
S. flexneri S. boydii S. sonnei S. dysenteriae
Commonly fatal for infants in developing countries
All species can cause shigellosis
Shigellosis
Pathogenesis
First step is phagocytosis of bacteria by cells in the large intestine Cells transport bacteria beneath epithelium Bacteria adhere to specific receptors near base of epithelial cells Bacteria multiply at high rate Shigella are non-motile
Move from cell to cell via actin tails
Tails push bacteria from one cell into another
Dead cells slough off

Initiates intense inflammatory response Areas covered with pus and blood
Responsible for pus and blood in feces
Shigellosis
Epidemiology
Humans are only reservoir
Transmitted fecal-oral route
Organism not easily killed by stomach acid

Low infecting dose
As few as 10 organisms
Transmission occurs most often as a result of overcrowding

Also common in day cares and among homosexual men
Contaminated food and water also responsible for outbreaks

Shigellosis

Controlled by sanitary measures and surveillance of food handlers
and water supplies No vaccine available Most important treatment is fluid and electrolyte replacement Antimicrobials often used to shorten duration of symptoms
Also shorten time bacteria discharged in feces
However 20% of Shigella species are resistant to antibiotics of choice

Other Bacteria
Yersinia enterocolitica causes foodborne infections due to contaminated meats and dairy products
Can lead to life-threatening enteric fever
Bacillus cereus grows in food that is cooked and left to

cool slowly
Causes diarrhea and vomiting
Shigella spp. cause nearly 100,000 cases of severe foodborne invasive gastroenteritis each year

Viruses
The largest number of annual foodborne infections are
thought to be caused by viruses
Noroviruses are responsible for most infections 9,000,000 annual cases of foodborne disease
Human Norovirus
Figure 37.10
Norovirus
Responsible for 23 million cases of viral gastroenteritis in
United States annually

Originally called Norwalk Virus Symptoms Causative Agent
Nausea Vomiting Norovirus
Small Nonenveloped Single stranded RNA genome Belongs to calcivirus family
Watery diarrhea
Symptoms generally subside
in 12 to 60 hours
Norovirus
Epidemiology
Transmission via fecal-oral route
Sometimes contracted from eating shellfish
Incubation period 12 to 48 hours Typically infects children and adults Infected individuals eliminate virus in feces
Only for a few days

Protists
Can be spread in foods contaminated by fecal matter in
untreated water used to wash, irrigate, or spray crops Fresh foods such as fruits are often the source of these infections
Cyclosporiasis
Symptoms
Incubation period approximately 1 week Symptoms include
Fatigue Loss of appetite Slight fever Vomiting
Causative Agent
Clyclospora cayetanensis
Cysts passed in feces
Do not yet contain sporocysts
Under favorable conditions 2 sporocysts develop from each oocyst

Each sporocyst will give rise to two sporozoites
Watery diarrhea
Relapses can occur for up to 4 weeks
Development occurs outside the body
Cyclosporiasis
Pathogenesis
Little is known of pathogenesis There is conformation that both sexual and asexual forms are
Epidemiology
Person-to-person spread unlikely
Due to noninfectious state of eliminated oocysts
present in infected intestine
Most infections occur in spring and summer Travelers to tropical areas at greater risk of infection Fresh produce implicated in numerous epidemics
Especially imported raspberries
Protists Transmitted in Food
Figure 37.11

Prions
Proteins that adopt novel conformations that inhibit normal protein function and cause degeneration of neural tissue
New variant Creuzfeldt-Jakob Disease

Linked to bovine spongiform encephalopathy (BSE), a prion disease
180,000 European cattle have been diagnosed with BSE
Transmissible Spongiform Encephalopathies

Symptoms
Early symptoms
Vague behavioral changes Anxiety Insomnia Fatigue
These symptoms progress weeks to months to hallmark symptoms

Muscle jerks Lack of coordination Dementia Deteriorating intellectual function Impaired judgment Memory loss
Disease often progresses to death within a year

Transmissible Spongiform Encephalopathies

Causative agent
Proteinaceous infectious particles
a.k.a prions Appear to be new class of infectious agent
Differ from bacteria, viruses and viroids
Main characteristics
Increase in quantity during incubation period Resist inactivation via UV and ionizing radiation Resist inactivation by formaldehyde and heat Not readily destroyed by proteases Not destroyed by nucleases Much smaller than smallest virus Composed of protein coded by normal cellular gene
Modified after transcription
Transmissible Spongiform Encephalopathies Prevention and Treatment

Prions inactivated by autoclaving in 1N NaOH No treatment All forms are fatal
A Brain Section From a Cow with BSE
Figure 37.12

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Brock Biology of Microorganisms

Madigan / Martinko Dunlap / Clark

II. Microbial Sampling and Food Poisoning

Copyright 2009 Pearson Education Inc., publishing as Pearson Benjamin Cummings

37.4 Foodborne Diseases and Microbial Sampling

Annual Foodborne Disease Estimates for the United States

Copyright 2009 Pearson Education Inc., publishing as Pearson Benjamin Cummings

37.5 Staphylococcal Food Poisoning

Gastroenteritis occurs within a few hours of consumption

Copyright 2009 Pearson Education Inc., publishing as Pearson Benjamin Cummings

Copyright 2009 Pearson Education Inc., publishing as Pearson Benjamin Cummings

37.6 Clostridial Food Poisoning

C. perfringens is the most commonly reported form of

Copyright 2009 Pearson Education Inc., publishing as Pearson Benjamin Cummings

37.6 Clostridial Food Poisoning

Home-prepared foods are most common source of illness

Botulism in the United States

Copyright 2009 Pearson Education Inc., publishing as Pearson Benjamin Cummings

Copyright 2009 Pearson Education Inc., publishing as Pearson Benjamin Cummings

Endospores generally resist boiling for hours

Copyright 2009 Pearson Education Inc., publishing as Pearson Benjamin Cummings

Toxin can circulate in blood stream for 3 weeks or more

Copyright 2009 Pearson Education Inc., publishing as Pearson Benjamin Cummings

Prevention and Treatment

Treated by intravenous administration of antitoxin ASAP

Copyright 2009 Pearson Education Inc., publishing as Pearson Benjamin Cummings

III. Food Infection

37.7 Salmonellosis 37.8 Pathogenic Escherichia coli 37.9 Campylobacter

Copyright 2009 Pearson Education Inc., publishing as Pearson Benjamin Cummings

Salmonella ingested in food or water invades

Copyright 2009 Pearson Education Inc., publishing as Pearson Benjamin Cummings

Salmonella subdivided into over 2,400 serotypes

Copyright 2009 Pearson Education Inc., publishing as Pearson Benjamin Cummings

Water or food sources

Copyright 2009 Pearson Education Inc., publishing as Pearson Benjamin Cummings

Prevention and Treatment

Most cases have an animal source

Surgical removal of gallbladder eliminates carrier state

Caused at least 53 cases over

Salmonellosis in the United States, 19752005

Copyright 2009 Pearson Education Inc., publishing as Pearson Benjamin Cummings

37.8 Pathogenic Escherichia coli

All pathogenic strains are intestinal parasites and a few

50 deaths in the U.S. per year

Other types of E. coli are classified as ETEC and EPEC

Copyright 2009 Pearson Education Inc., publishing as Pearson Benjamin Cummings

Escherichia coli Gastroenteritis

Copyright 2009 Pearson Education Inc., publishing as Pearson Benjamin Cummings

Escherichia coli Gastroenteritis

Enteroinvasive E. coli (EIEC)

Enteropathogenic E. coli (EPEC)

Enterohemorrhagic E. coli (EHEC)

Escherichia coli Gastroenteritis

Prevention and Treatment

Humans, domestic and wild animals all sources of pathogenic strains

Copyright 2009 Pearson Education Inc., publishing as Pearson Benjamin Cummings

Transmitted to humans via contaminated food

Copyright 2009 Pearson Education Inc., publishing as Pearson Benjamin Cummings

Bacteria recognized in 1972

Copyright 2009 Pearson Education Inc., publishing as Pearson Benjamin Cummings

Copyright 2009 Pearson Education Inc., publishing as Pearson Benjamin Cummings

Causative agent lives in intestine of variety of domestic animals

Epidemics have occurred due to unpasteurized milk

Person-to-person spread rare