Transcript Escherichia coli - Share My Knowledge & Experience

Foodborne pathogens
It can be classified into three forms:
foodborne intoxication
foodborne infection
foodborne toxicoinfection
Food Pathogens
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 Microrganisms that cause food borne infection
or intoxication:
E.coli
Salmonella
Listeria
Campylobacter
Botulinum
Staphylococci
Foodborne Intoxication
 illness from microbial exotoxin
 microorganism does not cause the illness, the toxin
released by the microorganism does
 common exotoxin producing microorganisms
 Staphylococcus aureus
 Clostridium botulinum
INTOXICATION
 Ingestion of FOOD CONTAINING TOXIN
causes illness
 Microbes produce toxin while growing in
food
 Ingestion of the microbes themselves
may be harmless
Food borne intoxication
some bacteria grow in food and produce a toxin
within the food which is then consumed e.g.
Bacillus cereus and Staphylococcus aureus. When
the food is consumed viable cells of the bacteria
do not need to be present.
Following ingestion, Toxins are absorbed through the
gastrointestinal epithelial lining and cause local tissue
damage and may induce inflammation resulting in
diarrhea or vomiting.
In some cases, toxins are translocated to distant
organs or tissues such as liver, kidney, peripheral, or
central nervous system where they can cause
damage.
Food Poisoning/intoxication
STAPHYLOCOCCUS AUREUS
Staphylococcal ToxinMediated Diseases:
Food Poisoning
Exotoxins
 most exotoxins are grouped according to the
tissues they adversely impact
 neurotoxins damage the nervous system
 entereotoxins upset the intestinal system
 cytotoxins afflict their damage on many different
types of cells by disrupting cellular function of by
lysing the cell
Staphylococcus aureus
 Intoxication by consumption of heat stable,
preformed toxin in food
 Symptoms
 vomiting (“projectile”)
 nausea
 abdominal cramps
 and diarrhea 1-6 hours after eating food
contaminated with toxin
 Bacteria killed by mild heat. Toxins are very
heat stable.
 Will grow with or without air; toxin not
usually produced in acid food; bacteria are
resistant to high salt (up to 15%)
Bacteria Causing Intoxications
 Staphylococcus aureus (“Staph”)
 Reservoir: Common on human skin and in nasal cavity--
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therefore commonly a problem in foods that are handled
a lot
Transmission: Must multiply in food to produce enough
toxin to cause illness
Disease: Primarily causes vomiting
Incubation period: Short; usually 2 - 4 hours
The bacteria is killed by cooking, however the toxin is not
destroyed by normal cooking!
St. aureus and food
 Staph grows and divides in food and
produces an enterotoxin
 The Staph doesn’t cause food poisoning, the
enterotoxin does
 Enterotoxin is stable to heating at 100oC for
30 minutes.
 Enterotoxin is resistant to degradation by
stomach gastric acids
St. aureus and food
poisoning
 St. aureus causes gastro-enteritis
 Food poisoning is not caused by the organism
but by the toxin that the organism secretes
 St. aureus food poisoning is the most
common form of food poisoning in the US
How did the chef get a staph
infection?
 Staph is often found on skin surfaces because they can
tolerate the low moisture and high salt content of skin
 Staph can easily spread from person to person via hand
to hand contact
 Staph can penetrate the deep tissues of skin damaged by
burns
cuts
insect bites
skin diseases—acne, eczema
Normal Flora
 the presence of normal flora
 cover potential adherence sites for invading
microorganism
bacteria found on skin
 Normal microflora : produce compounds toxic to
other microorganisms
What happens when Staph enters
a wound and how does this
relate to food poisoning ?
 Localized staph infection leading to an abscess
boils=abscesses in the skin
carbuncle=interconnected abscesses
 Rupture of the abscess leads to the release of live
bacteria and associated toxin
How do abscesses and boils
form?
 Chef cuts arm and Staph enters deeper skin layer
 St. aureus is surrounded by a capsule
thick slime layer that prevents an
immediate immune response
 Bacteria multiply at the site surrounded by the
capsule
 St. aureus establishes intimate contact with skin
cells via bacterial techoic acids and fibronectin
skin cell receptors
Staph enterotoxin causes
gastro-enteritis in two ways
 VOMITINGtoxin works on the vomiting control
center of the brain this leads to reversal of
peristalsis and vomiting
 DIARRHEAenterotoxin is a superantigen and
elicits a strong immune response in the region
where the toxin is most concentrated. Immune
response causes a loss of brush borders in
intestinal epithelial cells; these cells cannot
absorb water from the gut.
Folliculitis manifests as superficial pustules or inflammatory nodules surrounding
hair follicles.
Furuncles (boils) are tender nodules or pustules caused by staphylococcal infection.
Carbuncles are clusters of furuncles that are subcutaneously connected.
Carbuncles
Cutaneous Abscess
 A cutaneous abscess is a localized collection of
pus in the skin and may occur on any skin
surface.
Erysipelas is characterized by shiny, raised, indurated, and tender plaque-like lesions
with distinct margins. It is most often caused by β-hemolytic streptococci and occurs
most frequently on the legs and face.
Impetigo (Non-Bullous)
Non-bullous impetigo is a
superficial skin infection that
manifests as clusters of vesicles
or pustules that rupture and
develop a honey-colored crust.
Impetigo (Bullous)
Bullous impetigo is a superficial skin
infection that manifests as clusters of
vesicles or pustules that enlarge rapidly
to form bullae. The bullae burst and
expose larger bases, which become
covered with honey-colored varnish or
crust.
Ecthyma is a skin infection similar
to impetigo, but more deeply
invasive. Usually caused by a
streptococcus infection, ecthyma
goes through the outer layer
(epidermis) to the deeper layer
(dermis) of skin, possibly causing
scars.
Ecthyma gangrenosum is a bacterial skin
infection (caused by Pseudomonas aeruginosa)
that usually occurs in people with a
compromised immune system.
Necrotising fasciitis
• The action of cholera enterotoxin is shown
in Figure 21.22.
Clostridium botulinum
(anaerobic, intoxication)
 Potent, Heat labile Neurotoxin
 A few nanograms of toxin can cause illness
 180F for 10 minutes
 Spores are heat resistant
 High mortality rate
 Associated with inadequately processed home
canned food
 Widely distributed in nature
Clostridium botulinum
 Associated foods
 Low acid canned foods
 Sausages
 Meat products
 Canned vegetables
 Seafood
 Almost any type of food that is not very
acidic (pH > 4.6) can support growth and
toxin production
Exotoxins
 exotoxins are highly specific
 exotoxins are among the most lethal substances
known to man
 1 gram of the exotoxin produced from Clostridium
botulinum is capable of killing the entire population of
the United States, close to 300 million people
 the danger with exotoxins is not the ingestion of
the bacterium, but the ingestion of the toxin
Clostricium botulinum
 Clostridium botulinum (“botulism”)
 Reservoir: Spores found in soil and water (ocean/lakes)
 Transmission: Associated with improperly canned
foods and ground-harvested foods such as onions and
garlic
 Disease: Toxin causes paralysis
 Incubation period: ½ day to 3 days
 Spore is difficult to destroy, but botulinum toxin CAN
be destroyed by cooking (e.g., 176F for 10 min)
• Botulinum toxin consists of seven related
toxins that are the most potent biological
toxins known (Figure 21.20).
Botulism (C. botulinum):
 The most potent toxin known; few
cases but high mortality (25%);
destroyed by 10 min in 80 oC
 paralysis of muscles
 Common in soil and water
 How? Improper canning spore
germination toxin production
canned food used without cooking
disease
 All four types of botulism result in symmetric
descending flaccid paralysis of motor and
autonomic nerves always beginning with the
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cranial nerves. These symptoms are preceded by
constipation in cases of infant botulism.
Symptoms include:
Double or blurred vision
Drooping eyelids
Dry mouth
Difficulty Swallowing
Muscle weakness
Prevention
 Proper food preparation is one of the most
effective ways to limit the risk of exposure to
botulism toxin.
 Boiling food or water for ten minutes can
eliminate some strains of Clostridium botulinum
as well as neutralize the toxin as well. However,
this will not assure 100% elimination.
 Limiting growth of Clostridium botulinum and the
production of botulism toxin is an alternative to
their outright destruction.
 Temperature, pH, food preservatives, and
competing microorganisms are among the
factors that influence the rate and degree of
Clostridium botulinum growth.
 Growth of most strains of Clostridium
botulinum will not occur below 10 or above 50
degrees Celsius.
 Clostridium botulinum will not grow in media
with pH values lower than about 5.
 Food preservatives such as nitrite, sorbic acid,
parabens, phenolic antioxidants,
polyphosphates, and ascorbates inhibit the
growth of the microorganism.
 Clostridium botulinum will not grow in media
with pH values lower than about 5.
 Food preservatives such as nitrite, sorbic acid,
parabens, phenolic antioxidants,
polyphosphates, and ascorbates inhibit the
growth of the microorganism.
 Lactic acid bacteria including Lactobacillus,
Pediococcus, and Pactococcus can inhibit the
growth of Clostridium botulinum by increasing
the acidity of the medium.
 While the cause of roughly 85% of infant
botulism cases is unknown, in up to 15% of
infant botulism cases the causes was
ingestion of honey. Infants younger than one
year old should not be fed honey.
Avoiding Exposure
 Avoid home-processed foods if at all possible,
especially those with a low salt and acid content.
 Botulism toxin is destroyed at a temperature of
176 F, thus if you must eat home-processed
foods, boil them for 10 minutes before eating if
at all possible.
 If canning vegetables, use a pressure cooker, as it
will kill any spores because it can reach
temperatures above boiling.
Foodborne Infection
 requires consumption of microorganism
 symptomatic about 1 day following ingestion of
contaminated food
 common foodborne infecting microorganisms
 Salmonella
 poultry product infections
 Escherichia coli 0157:H7
 undercooked hamburger
Campylobacter
Salmonella
food borne infection
Infections occur when pathogens are ingested via
contaminated food and the bacteria is established
in the body
usually growing inside the intestinal tract and
irritating intestines.
The infection may involve subsequent growth in
other tissues
TRANSPORT OF THE BACTERIAL
PATHOGEN TO THE HOST
Direct contact
e.g., coughing, sneezing, body contact
Indirect contact
vehicles (e.g., soil, water, food)
ATTACHMENT AND COLONIZATION BY
THE BACTERIAL PATHOGEN
Adherence structures:
Structures such as such as pili and fimbriae and
specialized adhesion molecules on bacterium’s cell
surface bind to complementary receptor sites on host
cell surface
Colonization:
Colonization is the establishment of a site of microbial
reproduction on or within host
does not necessarily result in tissue invasion or damage
Principles of Infectious
Disease
 virulence factors are substances or features of a
microorganism that help it infect and cause
disease
 they may include
 ability to adhere
 ability to overcome host defense
 ability to evade host defense
FACTORS IMPACTING OUTCOME
OF HOST-PARASITE
RELATIONSHIPS
Factors:
number of organisms present
the degree of virulence of pathogen
virulence factors
e.g., capsules, pili, toxins
host’s defenses or degree of resistance
Attachment
Penetration into the Host
Cell
Figure 15.2
• Pathogen growth on the surface of a host,
often on the mucous membranes, may result
in infection and disease
E. coli in Small
Intestine
COLONIZATION AND GROWTH
• A pathogen must gain access to nutrients and appropriate growth
conditions before colonization and growth in substantial numbers in
host tissue can occur. Organisms may grow locally at the site of invasion
or may spread through the body.
Shigellosis
 Pathogenesis
 S. dysenteriae
 Rarely encountered in
United States
 Produces potent A-B
toxin
 Shiga Toxin
 Acts much like cholera
toxin
 Toxin associated with
fatal hemolytic uremic
syndrome
Helicobacter pylori
Gastritis
Pathogenesis
– Mucus production decreases
 Bacteria survive
extreme acidity of
the stomach
 Able to neutralize
environment
 Organism uses
flagella to corkscrew
through mucosal
lining
 Inflammatory
response begins
• Without mucus stomach lining not
protected from acidic environment
– Infection persists for years
• Possibly for a life time
Mechanisms of Pathogenesis
 colonization of host surface, then toxin production
 invading pathogen is able to grow to high numbers on
host surfaces such as the respiratory and intestinal
tract
 they then produce a toxin that is damaging to the cells
 organisms that use this mechanism include Vibrio
cholerae, which causes cholera or Corynebacterium
diphtheriae, which causes diphtheria
Mechanisms of Pathogenesis
 invasion of host tissue
 breaching body’s barriers then multiplies in the body’s
tissues
 these organisms have mechanisms that allow them to
avoid macrophage destruction
 some are also capable of avoiding detection by
antibodies
 organisms that use this mechanism include
Mycobacterium tuberculosis, causative agent for
tuberculosis, and Yersinia pestis, causative agent for
plaque
Mechanisms of Pathogenesis
 invasion of tissue, then toxin production
 breach the body’s barriers, then make toxins
 in addition to invasion, these organisms also make
toxins
 organisms that use this mechanism include Shigella
dysenteriae and Streptococcus pyogenes
Mechanisms of Pathogenesis
 in order to cause disease microorganisms
need to be able to
 adhere and colonize host tissue
 avoid the innate defenses
 avoid the adapted defenses
 cause damage related to the disease
Adherence
 to establish disease the causative agent needs to
 Adhere
 many bacteria have adhesions, generally found on the
pili
Colonization
 causative agent needs to
 multiply in order to colonize
 to multiply, they must compete successfully with the
normal flora for space and nutrients
 toxins that may be produced by the normal flora must
be overcome
Following ingestion, Toxins are absorbed through the
gastrointestinal epithelial lining and cause local tissue
damage and may induce inflammation resulting in
diarrhea or vomiting.
In some cases, toxins are translocated to distant
organs or tissues such as liver, kidney, peripheral, or
central nervous system where they can cause
damage.
Adherence

Adhesions/ligands bind to receptors on host cells so won’t
get flushed off.

Mechanisms to adhere and avoid host defenses:
 Glycocalyx Streptococcus mutans
Dextran (plaque)

Waxes
Mycobacteria
 Fimbriae
Escherichia coli
 M protein
Streptococcus pyogenes
 Tapered end w/ hooks Treponema pallidum
Capsules
Prevent phagocytosis
and help with attachment
(adherence)
 Streptococcus pneumoniae
 Klebsiella pneumoniae
 Haemophilus influenzae
 Bacillus anthracis
 Streptococcus mutans
 Yersinia pestis
Enzymes to help penetration
Many pathogens secrete enzymes that contribute to their pathogenicity:

Increase virulence by use of enzymes
 And avoid phagocytosis
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Coagulase

Kinases
Coagulate blood - wall off from host
make boil
Digest fibrin clot - allow
spreading
streptokinase and staphylolinase
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Hyaluronidase
Collagenase
 IgA proteases
 Hemolysins
Hydrolyses hyaluronic
acid connective tissue
Hydrolyzes collagen
Destroy IgA antibodies
lyse RBC’s
Hemolysins
Alpha Hemolytic Streptococci
- secrete hemolysins that cause the incomplete lysis
or RBC’s
Beta Hemolytic Streptococci
- secrete hemolysins that cause the complete lysis of RBC’s
Leukocidins
 1. Kills WBC’s which prevents phagocytosis
 2. Releases & ruptures lysosomes
 lysosomes - contain powerful hydrolytic enzymes which
then cause more tissue damage
Mechanisms of Pathogenicity
Figure 15.9
Bacteria Causing Infections
 Salmonella spp. (non-typhoid)
 Most common cause of bacterial foodborne disease
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using passive surveillance
Reservoir: many food-producing animals
Transmission: Associated with undercooked meats
(especially poultry) eggs, raw milk, and contaminated
produce
Disease: Diarrhea and systemic infections
Incubation period: ½ day - 1½ days
Salmonellosis
 Causative Agent
– Salmonella species
 Motile
 Gram negative
 Enterobacteria
– Salmonella subdivided into over 2,400 serotypes
• Salmonella typhimurium and Salmonella enteritidis most
common serotypes in United States
SALMONELLOSIS
Epidemiology - mode of transmission
 ingestion of raw, undercooked, or
contaminated food
 meat, milk, eggs, produce
 fecal-oral transmission
 contact with pets (especially infants)
 foods contaminated by infected food handler
 outbreaks usually traced to food items
SALMONELLOSIS
Epidemiology - disease frequency
 incidence highest in infants and young
children
 estimated 5 million cases annually (US)
 up to 80% are sporadic cases
 large outbreaks in hospitals, restaurants,
institutions are common
 largest outbreak in US (25,000 cases) resulted
from a nonchlorinated municipal water supply
SALMONELLOSIS
Epidemiology - disease frequency
 proportion of reported cases due to S.
enteriditis has increased from 5% in 1976 to
26% in 1994
 report in J of Infectious Diseases (1994) - 82%
of outbreaks due to S. enteriditis between
1985-1991 were traced to contaminated shell
eggs
SALMONELLOSIS
Epidemiology - disease frequency
 case fatality rate
 <1% for most forms of salmonellosis
 15% with S. dublin reported in elderly
 up to 4% with S. enteriditis (nursing homes, hospital
associated outbreaks with most being elderly)
Salmonella Epidemiology
 Etiologic Agent:
 Gram-negative bacteria in the family
Enterobacteriaciae.
 Currently, there are more than 2,460 serotypes.
 Reservoir:
 Domesticated and wild animals, including poultry,
swine, cattle, rodents, dogs, cats, birds (including pet
ducks and chicks), reptiles (including iguanas, snakes,
and turtles).
Salmonellosis:
 Gram negative enteric bacterium; all strains are
pathogenic; transmission is from sources (eggs, meats)
and by food handlers
 Colonization of of intestinal epithelium
• Two diseases:
– Enterocolitis (most commonly by S. typhimurium): 105 - 108 viable
cells; disease onset within 8 - 48 hrs; headaches, chills, vomiting,
diarrhea and fever (2-3 days); continuous shading of organism for
months/years (Typhoid Mary);
– Typhoid fever (S. typhi): Septicemia leading to high fever that can last
for several weeks; mortality is 15% if untreated; antibiotics
• Prevention: Cooked food (70 oC for 10 min); monitor for carrier state
among food handlers
Host-Parasite Relationships
 Fecal-oral transmission via contaminated
food or water
 Sources - milk & other dairy products, raw eggs,
dried or frozen eggs, meats, meat products,
poultry, roast beef, corned beef, shellfish and
undercooked whitefish, animal dyes, dried
cocoanut
 Origin - many animals are naturally infected with
various Salmonellae (especially poultry)
Cont.
 These can be found in tissues, eggs, and
excreta
 Household pets - turtles, dogs, & cats can
also transmit these bacteria
 Human carriers, especially food handlers
 Typhoid Mary
Salmonellosis
 Pathogenesis
 Bacteria sensitive to
stomach acid
 Large number required
for infection
 Bacteria adhere to
receptors on epithelial
cells of lower small
intestine
 Cells take up bacteria
through phagocytosis
 Bacteria multiply within
phagosome discharged
through exocytosis
 Inflammatory response
increases fluid secretion
resulting in diarrhea
• Pathogenesis
– Some strains of Salmonella typhi
are not easily eliminated
•
Organisms cross membrane and resist
killing by macrophages
–
Bacteria multiply within macrophages then
carried to bloodstream
•
Organisms are released when
macrophages die and invade tissues
–
Can result in abscess, septicemia, and
shock
Salmonellosis
 Epidemiology
 Bacteria can survive long
• Prevention and
periods in the environment
Treatment
 Children are commonly
– Control depends on
reporting cases and tracing
 Generally by household
source of outbreak
pets such as turtles,
iguanas, and baby chicks – Adequate cooking kills
bacterium
 Most cases have an animal
source
– Vaccine available for
 Enteric fevers, such as
prevention of typhoid fever
infected
those caused by
• Vaccine 50% to 75% effective
Salmonella typhi are
generally the exception – Surgical removal of
gallbladder eliminates carrier
 “Typhoid Mary” notorious
carrier
state
 Caused at least 53
cases over 15 years
Mary Mallon
Typhoid Mary
 Human carrier (and
reservoir) of
Salmonella typhi
Salmonella enterica serovars
 Infect domestic animals
 Eggs and contaminated meat
 One of the most prevalent
causes of food-borne illnesses
 Transmission dose as few as 10
organisms
 Attachment is key virulence
factor
Salmonella enterica serovars.
 Gram negative bacillus
 Classification based on serology and phage
susceptibility assays
Host Factors
 Very important in intestinal infections
 Gastric pH, luminar wall sheath, intestinal mobility
 Local immune factors, normal flora
 Intrinsic characteristics of pathogens
 Salmonellae = 105 organisms to cause infect.
 Shigellae = 180 – 200 orgs. to cause infect.
 ETEC = 106 - 107 orgs. to cause infect.
 Vibrios = 108 orgs.
Salmonellosis
 Sources
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Raw poultry and eggs
Raw milk
Raw beef
Unwashed fruit, alfalfa sprouts
Reptile pets: Snakes, turtles, lizards
 Signs
 Onset: 12-72 hours
 Diarrhea, fever, cramps
 Duration: 4-7 days
Clinical description of nontyphoidal Salmonella
 Other Symptoms May Include:
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Fever
Abdominal cramping
Nausea
Vomiting
Chills
Systemic symptoms – headache, myalgias, etc.
 Diarrhea usually lasts 3 to 7 days
 Mean carriage of Salmonella strains in the stool
can last 4 - 5 weeks after resolution of acute
symptoms.
Salmonella Epidemiology
 Incubation Period:
 6 - 72 hours, usually 12 - 36 hours
 Infectious Period:
 As long as bacilli appear in the stool during illness and
usually several days to several weeks thereafter.
 Prolonged shedding is more prominent in children <5
years of age.
 Approximately 1% of patients become chronic carriers
and continue to excrete organisms for more than 1
year.
Salmonella Epidemiology
 Mode of Transmission
 Transmitted through the ingestion of food and
water contaminated with human or animal waste.
 Contaminated raw vegetables or fruits have also
been implicated.
 Fecal-oral route is important, especially from
persons who have diarrhea or who are
incontinent.
Escherichia coli
 gram-negative rod-shaped bacteria
 hundreds of strains
 most strains are harmless, normal intestinal flora
of healthy humans and animals
 occurrence: ubiquitous, worldwide distribution
Categories of Escherichia coli causing diarrhea
 enterohemorrhagic (EHEC - hemorrhagic colitis;
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
O157:H7)
enterotoxigenic (ETEC- traveler’s diarrhea)
enteroinvasive (EIEC - dysentery-like)
enteropathogenic (EPEC - infant diarrhea)
enteroaggregative (infant d. in underdeveloped
countries)
diffuse-adherence (pediatric diarrhea)
Escherichia coli O157:H7
 first recognized in 1982 outbreak of hemorrhagic
diarrhea traced to hamburgers (fast food chain)
 estimated 10,000 to 20,000 cases/yr in the US
 outbreaks have been associated with other foods
such as leaf lettuce, cider, contaminated water
Escherichia coli O157:H7
 “O” and “H” designation refer to cell surface
antigen markers that are used to distinguish
serotypes
 Other serotypes of enterohemorrhagic strains
may also be implicated (O26:H11; O111:H8;
O104:H21)
does not grow well or at all at
44-45ºC
Escherichia coli O157:H7
 syndrome caused by potent cytotoxins:
verotoxins 1 and 2 (Shiga-like toxins I and II
because resemble toxins of Shigella dysenteriae)
 may also produce hemolytic-uremic syndrome
 although recognized and intensively studied for
15 years, still do not know best method of
treatment nor how animals become infected
Escherichia coli O157:H7
Epidemiological features
 Reservoir:

 cattle especially young dairy cattle
 wild ruminants - deer (?)
 humans
Escherichia coli O157:H7
Epidemiological features
 Transmission:
 ingestion of contaminated foods
 usually inadequately cooked beef (especially ground beef)
 raw milk
 other foods by cross-contamination--lettuce, apple cider, apple
juice
 person-person (families, child care facilities, institutions)
 waterborne (swimming in crowded areas, drinking water)
Escherichia coli O157:H7
Epidemiological features
 Incubation period:
 relatively long, ranging from 3-8 days
 Period of communicability:
 <1 week in adults
 may be up to three weeks in children
 prolonged carriers uncommon
Escherichia coli O157:H7
Epidemiological features
 Susceptibility and resistance
 very low infectious dose
 old-age appears to be a risk factor
 children < 5 years of age are at greatest risk of
developing hemolytic-uremic syndrome
Escherichia coli O157:H7
Clinical features
 diarrhea ranging from mild, non-bloody to
virtually
 straight bloody stool, abdominal cramping
 fever is infrequent
Escherichia coli O157:H7
Clinical features
 Hemolytic-uremia syndrome
 more common in children
 may occur in up to 10% of cases
 characterized by:
 hemolytic anemia
 thrombocytopenia
 renal failure (common cause of renal failure in children)
Escherichia coli O157:H7
Clinical features
 Thrombotic thrombocytopenic purpura
(TTP) in elderly
 Case fatality rate: 3-5% (up to 50% in elderly
with TTP)
Escherichia coli O157:H7
Control methods
 Preventive measures to reduce incidence
 slaughterhouse management to minimize
contamination of meat by intestinal contents
 pasteurization of milk and dairy products
 irradiate beef, especially ground beef
Escherichia coli O157:H7
Control methods
 preventive measures to reduce incidence
 adequately cook meat to a temp of 155°F (68°C)
 ‘pink all gone’ does not mean necessarily safe - cooking
with meat thermometer is recommended
 protect, purify, chlorinate public water supplies for
drinking
 chlorination of swimming pools
 adequate hygiene in day-care facilities
Escherichia coli O157:H7
Control methods
 control of patient and immediate environment
 report to health department (mandatory in many states)
 isolation: because of extremely small infective dose,
patients should not be allowed to handle food or
provide child/patient care until 2 negative samples are
obtained
 disinfection
 contacts with diarrhea should be handled as if infected
(no food handling, no patient care or child contact)
until two negative fecal samples are obtained
Escherichia coli O157:H7
Control methods
 treatment
 fluid/electrolyte replacement
 antibiotic treatment uncertain; TMP-SMX may lead to
hemolytic-uremia syndrome
SALMONELLOSIS
 Causative organisms: primarily S.
enteriditis, typhimurium in U.S.
 numerous serotypes, many are pathogenic
to both animals and man
 of the ~2,000 serotypes known, only ~200
recognized in the U.S.
 discovered in 1880, genus named for
American scientist Salmon in honor of his
extensive work
SALMONELLOSIS
 Microbiological features and identification
 gram-negative rod-shaped bacteria
 motile (non-motile forms are S. gallinarium,




pullorum)
heat labile
growth prevented at <7º C for most serotypes
non-spore forming, but can survive for long
periods in foods and other substrates
can survive for long periods in foods with low aw
(water activity) such as chocolate, peanut butter,
black pepper)
SALMONELLOSIS
Epidemiology - reservoir
 ubiquitous
 found in a wide range of animals, particularly poultry,
swine, cattle, pets (iguanas, turtles, terrapins,
tortoises, chicks, dogs, cats), humans
 chronic carriers common in animals and birds, less so
in humans
 S. enteriditis infects ovaries of healthy appearing
hens, thereby contaminating eggs in oviduct before
shell is formed
SALMONELLOSIS
Epidemiology - reservoir
 S. typhi, paratyphi - man only
 S. typhimurium - animals, particularly food animals
 S. enteriditis - animals, particularly food animals
 S. dublin - cattle
 S. choleraesuis - swine
 S. gallinarum, pullorum - poultry
 S. arizonae - animals, reptiles
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
Selected outbreaks in US
 1985 - 16,000 cases in 6 states
 low fat and whole milk from a Chicago dairy
 pasteurization process changed, resulting in
contamination of pasteurized milk with raw milk
 persons on antibiotic therapy more likely to be affected
 1984 - ~2700 passengers affected on 29 flights
 caused by S. enteriditis
 strongly associated with food in First Class section
only
SALMONELLOSIS
 Clinical features
 generally, salmonellosis is a milder disease than
typhoid/paratyphoid
 acute disease
 nausea, vomiting, cramping, diarrhea, fever,
headache
 more severe, even life-threatening disease can
occur in infants, elderly, immunocompromised
SALMONELLOSIS
 Clinical features
 chronic disease
 small percentage of cases develop Reiter’s syndrome
 arthritic pain, irritation of eyes, painful urination
 can last for months to years, leading to chronic arthritis
refractive to treatment
 antibiotic therapy does not seem to prevent
development of this serious sequela to acute salmonella
infection
SALMONELLOSIS
 Clinical features
 incubation period: variable - 12 to 72 hours
 illness generally lasts 4-7 days
 disease is caused by penetration and passage of
organisms from gut lumen into epithelium;
enterotoxin production (?)
 infective dose:
 as few as 15-20 cells depending on strain (4 serotypes
ingested in vehicles that buffer gastric acids)
 normally >102-3
SALMONELLOSIS
 Diagnosis
 serological identification of culture isolated from
stool
 Food analysis
 developed for many foods
 conventional methods - 5 days for presumptive
results
 rapid methods require only 2 days
SALMONELLOSIS
 Prevention and control
 FDA: ‘farm-to-table’ actions to reduce food
safety risks associated with shell eggs
farm
slaughter
processing
retail
consumer
 1 in 20,000 eggs produced annually contain
S. enteriditis
SALMONELLOSIS
 Prevention and control
 FDA/FSIS pending proposals
 38 states require refrigeration at retail level
 voluntary quality assurance programs for egg
producers
 cleaning/disinfecting hen houses
 rodent control
 proper egg washing
 refrigeration between transport and storage
 biosecurity measures
 monitoring chick mortality
 use of SE free chicks and pullets
SALMONELLOSIS
 Control
 processing - control of factors such as pH,
moisture, presence of preservatives should me
assessed at all stages using systematic approach
(HACCP)through transit, storage, foodservice, and
retail levels
 storage at low temperatures - most serotypes fail to
grow below 7ºC
 retail




handwashing
avoid food preparation by workers with diarrhea
thoroughly cook all poulty, pork, meat, egg dishes
strict sanitation practices in kitchen, including rodent
and insect control
SALMONELLOSIS
 Control
 consumer control
 FDA Recommendations
 avoid consumption of raw eggs
 avoid cross-contamination - clean utensils, disinfect
surfaces, proper hygiene, separate cutting surfaces for
raw and cooked meats and vegetables
 thoroughly cooking meat, poultry, eggs (71ºC)
 do not freeze eggs in shell
 store cooked eggs in refrigerator, discard after 1 week
 recognize risk in pets (chicks, ducklings, and
reptiles)--not recommended for small children
LISTERIOSIS
 Causative organism: Listeria monocytogenes
 common inhabitant of intestine, soil, silage, other
environmental sources
 most are pathogenic to some degree
 not recognized as a food-borne pathogen until
the 1980’s
Listeria monocytogenes
 Microbiological features and identification
 gram-positive rod-shaped
 motile, flagellated
 non spore-forming
 will grow at pH 4.4 - 9.6
 will grow in high salt concentrations (>10%)
Listeria monocytogenes
 Microbiological features and identification
 resistant to heat, freezing, drying
 able to grow at temperatures as high as 50ºC
and as low as 3ºC (psychotrophic - able to
grow at refrigerator temperatures)
 freezing has little detrimental effect on the
organism
Listeria monocytogenes
 Microbiological features and identification
 aerobic, microaerophillic
 growth on simple media (blood, trypticase soy
agar) or selective media (McBride’s agar)
 cold-enrichment techniques - too time
consuming once recognized as a food
pathogen
 now have faster methods - FDA (dairy
products); USDA (meat products)
Listeria monocytogenes
 Epidemiological features
 Reservoir
 ubiquitous
 primary reservoir is soil, silage, environment
 also present in intestinal tract of animals and
humans; asymptomatic carriers common (up
to 10%)
 seasonal use of silage followed by increase
in number of listeriosis cases in livestock
Listeria monocytogenes
 Epidemiological features
 Susceptibility and resistance
 fetuses, newborns are highly susceptible
 older aged, immunocompromised individuals
 acquired immunity unlikely
Listeria monocytogenes
 Epidemiological features
 Mode of transmission
 foodborne - outbreaks associated with
ingestion of raw or contaminated food
 milk (raw and supposedly pasteurized),
cheeses (particularly soft-ripened), ice
cream, raw vegetables, fermented raw-meat
sausage, raw and cooked poultry, raw
meat, raw and smoked fish
Listeria monocytogenes
 Epidemiological features
 Mode of transmission
 direct contact
 neonatal
 transmitted in utero
 during passage through infected birth
canal
 contaminated equipment in nurseries
Listeria monocytogenes
 Epidemiological features
 Frequency of disease
 in US - ~1,850 cases annually
 case fatality rate: 425 deaths annually
 30% in newborn infants
 up to 50% when onset within first 4 days
 nonpregnant - recent epidemic 35% (63% in
>60 yrs of age)
Listeria monocytogenes
 Epidemiological features
 Risk factors
 pregnancy (20 times more likely to get
listeriosis); 33% of cases occur during
pregnancy
 newborns - more likely to suffer serious
effects
 immunocompromised (AIDS, CA, diabetes,
renal disease, elderly)
Listeria monocytogenes
 Epidemiological features
 source of infection in selected outbreaks
 Maritime Provinces (Canada) - coleslaw made from
cabbage fertilized with sheep manure; 28% CFR
 California (1985) - Mexican-style cheese, numerous
stillbirths; 142 cases, 33% CFR; FDA now monitors all
domestic and imported cheeses
 many cases are sporadic, now thought to be
foodborne, associated with soft cheese (Brie,
Camembert, etc.)
 jellied pork tongue - cause of 279 cases, 63 deaths, 22
abortions in France in 1992
Listeria monocytogenes
 Clinical features
 Target population
 pregnant women/fetus
 Cancer patients
 immunocompromised (AIDS, steroid therapy, graft
suppression therapy)
 elderly
 healthy individuals - low risk
 antacids and H2 blockers may predispose to
infection
 outbreak among healthy individuals in
Switzerland involving heavily contaminated
cheese
Listeria monocytogenes
 Clinical features
 incubation period: variable - 3 to 70 days
 signs and symptoms:
 flu-like symptoms
 septicemia
 meningitis or meningoencephalitis
 encephalitis
 intrauterine or cervical infections
 spontaneous abortion (2nd or 3rd trimester)
 gastrointestinal symptoms (nausea, vomiting, diarrhea)
 onset time varies: few days to 3 weeks in serious
disease, > 12 hours in more mild forms
Listeria monocytogenes
 Clinical features
 infective dose varies with strain; foodborne disease
occurs with less than 1,000 organisms in susceptible
individuals (immunocompromised, elderly)
 invades monocytes, macrophages, PMN leukocytes,
hence name and pathogenesis (transplacental and
access to brain tissue)
 “circling disease” and abortions in cattle, sheep, and
goats
Listeria monocytogenes
 Diagnosis
 isolation from CSF, blood, amniotic fluid, placenta,
gastric washings
 growth on routine media
 serology unreliable
 Food analysis
 FDA method (1990) requires 5-7 days for identification
 use of specific DNA probes should afford faster and less
complicated confirmation of isolates
Listeria monocytogenes
 Control
 Prevention of listeriosis begins on the farm and
continues through processing and handling by the
consumer
 On the farm:
 silage production controlled to achieve rapid
acidification (pH <4.0)
 storage of milk at low temperatures (<5ºC) until
shipping
Listeria monocytogenes
 Control
 Processing
 control of factors such as pH, moisture,
presence of preservatives should me assessed
at all stages using systematic approach
(HACCP)
 measures to prevent contamination through
transit, storage, foodservice, and retail levels
Listeria monocytogenes
 Control
 Three major objectives of processing control
 minimize growth and multiplication of
organism in raw foods, particularly before and
during processing
 use of appropriate products to assure
destruction of organism
 minimize risk of recontamination of ready-toeat products
Listeria monocytogenes
 Control
 Storage
 temperature is a major factor affecting the risk
of multiplication; <5ºC will retard, but not
prevent, multiplication
 storage times of food should be kept to a
minimum
Listeria monocytogenes
 Control
 Consumer control
 potentially unsafe foods should not be kept
between 4ºC - 60ºC more than 4 hours between
buying and eating
 thoroughly cooking meat (71ºC), poultry (85ºC),
seafood
 thorough scrubbing of vegetables, do not cook
too far in advance since this increase
likelihood of bacterial growth
Listeria monocytogenes
 Control
 Consumer control
 avoid cross-contamination - clean utensils,
disinfect surfaces, proper hygiene, separate
cutting surfaces for raw and cooked meats and
vegetables
 thaw food in the refrigerator, then keep
refrigerated but only for short period, then
discard
 serve foods hot (>60ºC) or cold (<4ºC)
Listeria monocytogenes
 Recent multistate outbreak, 1998-1999
 at least 50 cases caused by a rare strain of Listeria




monocytogenes (serotype 4b)
reported to CDC by 11 states
onset August 2 - December 13, 1998
vehicle for transmission: hot dogs and possibly deli
meats under several brands but all by same
manufacturer: Bil Mar Foods
massive product recall in OH, NY, TN, MI, MA, VT, GA,
MN, WI, MO, AK, AL, CT, OR
Preventing food-borne disease
 Fight BAC!
 Partnership for Food Safety Education
program aimed at educating food
handlers and food preparers




Clean
Separate
Cook
Chill
Preventing food-borne disease
 HACCP
 Hazard Analysis and Critical Control
Point
 USDA/FSIS program implemented in all plants
processing meat and poulty
 Pathogen reduction standards for Salmonella
and E coli
 Implementation began in 1997, to be completed
as of Jan 2000
Preventing food-borne disease
 Food Compliance Programs
 FDA/CFSAN (Center for Food Safety Applied
Nutrition)
 Issued for 3 years; re-issued every three years or
more frequently as needed
 Guidance for inspection, investigation,
administration
 Apply to imported and domestic products







Acidified/low-acid canned foods
Milk and cheese products
Drug residue in milk
Milk safety
Mycotoxins
Medical foods
Infant formulas
Preventing CrossContamination
 Separate raw animal foods during storing,
preparing, holding, and display from raw ready-toeat food and cooked ready-to-eat food.
 Separate types of raw animal foods from each
other.
 Clean and sanitizing equipment and utensils.
 Store food in packages, covered containers, or
wrappers.
(continued)
153
Preventing CrossContamination
(continued)
 Clean hermetically sealed containers of food of
visible soil before opening.
 Protect food containers that are received packaged
together in a case or overwrap from cuts when the
case or overwrap is opened.
 Store damaged, spoiled, or recalled food separately.
 Separate fruits and vegetables before they are
washed.
154
Handwashing
Before:
Handling food
Handling clean utensils
Handling clean equipment
After:
Eating
Drinking
Smoking
Touching the face or hair
Using the toilet
Handling raw meat, poultry, or seafood
Handling soiled utensils or equipment
155
Handling a Foodborne Illness
Complaint
1. One person responsible for the investigation
2. Listen to complaint
3. Get the facts
4. Evaluate guest complaint
5. Notify health officials if complaint appears valid
6. Isolate suspected food
(continued)
156
Handling a Foodborne Illness
Complaint
(continued)
7. Cooperate with heath officials
8. Take corrective action
9. Close the complaint with the
guest
10. Index complaint
11. Follow up
157
Common Causes of Food Spoilage
 Improper storage temperatures
 Incorrect storage times
 Improper ventilation
 Failure to separate foods
 Excessive delays between receiving and storing
 Inadequate food safety standards
158
Low-Temperature Food Preservation
 Chilled storage: 50˚F (10˚C) to 59˚F (15˚C)
 Refrigerated storage: 32˚F (0˚C) to 45˚F (7˚C)
 Freezer storage: 0˚F (–18˚C) or below
159
Pasteurization
High-temperature food preservation
Food product heated to 145˚F (63˚C) for
30 minutes or to 161˚F (72˚C) for 15
seconds then immediately cooled to
50˚F (10˚C) or less.
160
Sterilization
High-temperature food preservation
Virtually kills all microorganisms and their spores.
Heating usually takes place in a large container
which is pressurized according to the food
product, its ability to withstand heat, and
packaging.
161
High risk foods
Some foods are high-risk, as they provide the ideal conditions
needed for micro-organisms to grow.
These include:
• meat and meat products;
• milk and dairy products;
• fruit.
If these foods become contaminated with food-poisoning microorganisms and conditions allow them to multiply, the risk of
food-poisoning increases.
People at high risk
Elderly people, babies and anyone who is ill or pregnant needs
to be extra careful about the food they eat.
For example, pregnant women or anyone with low resistance to
infection should avoid high risk foods such as unpasteurised soft
cheese.
Factors affecting food poisoning
Some common factors leading to food poisoning
include:
• preparation of food too far in advance;
• storage at ambient temperature;
• inadequate cooling;
• inadequate reheating;
• under cooking;
• inadequate thawing.
Factors affecting food poisoning
More common factors leading to food poisoning include:
• consuming raw food;
• improper warm holding (i.e. holding ‘hot’ food below 63ºC);
• infected food handlers;
• contaminated processed food;
• poor hygiene.
Symptoms of food poisoning
Food poisoning can be mild or severe.
The symptoms will be different depending on what type of
bacteria is responsible.
Common symptoms include:
• severe vomiting;
• diarrhoea;
• exhaustion;
• headache;
• fever;
• abdominal pain;
• tiredness.
Preventing food spoilage,
contamination and poisoning
Tips for buying food include:
• it is illegal to sell food that has passed its ‘use by’
date;
• dented, blown or rusted cans of food should not be
purchased;
• frozen food which has frozen together in the pack
should not be purchased;
• do not buy food where the packaging has been
damaged;
• only shop in clean and hygienic stores.
Preventing food spoilage,
contamination and poisoning
Tips for transporting food back home:
• buy chilled and frozen foods at the end of the
shopping trip;
• keep frozen and chilled foods cold, by using cool
boxes/bags and packing these types of foods together;
• cooked and uncooked foods
should be kept separate;
• dry and moist foods
should be packed separately;
• household chemicals
should be packed separately.
Preventing food spoilage,
contamination and poisoning
Tips for storing food in the home:
• food should be unpacked as soon as possible;
• old stocks of food should be used before buying
new ones (first in, first out theory);
• store food in the correct place, i.e. dry food, in cool,
dry clean places and chilled food in the refrigerator.
Bacteria - Clostridium botulinum
 High risk foods
Inadequately processed canned meat, vegetables and
fish (faulty canning)
 Signs and symptoms
Onset 24 – 72 hours. Voice change, double vision,
drooping eyelids, severe constipation.
Death within a week or a slow recovery over months.
Bacteria - Campylobacter
 High risk foods
Meat and poultry.
 Signs and symptoms
Onset 2 – 11 days. Fever, headache and dizziness for a
few hours, followed by abdominal pain. This usually lasts
2 – 7 days and can recur over a number of weeks.
Bacteria - Clostridium perfringens
 High risk foods
Raw meat, cooked meat dishes and poultry.
 Signs and symptoms
Onset 8 – 22 hours. Abdominal pain, diarrhoea and
nausea. This usually lasts 12 – 48 hours.
Bacteria - E Coli 0157
 High risk foods
Raw meat and dairy products.
 Signs and symptoms
Diarrhoea, which may contain blood, can lead to kidney
failure or death.
Bacteria - Salmonella
 High risk foods
Raw meat, poultry and eggs, and raw unwashed
vegetables.
 Signs and symptoms
Onset 12 – 36 hours. Headache, general aching of limbs,
abdominal pain and diarrhoea, vomiting and fever. This
usually lasts 1 – 7 days, and rarely is fatal.
Bacteria - Staphylococcus aureus
 High risk foods
Meat, dairy products and poultry.
 Signs and symptoms
Onset 1 – 6 hours. Severe vomiting, abdominal pain,
weakness and lower than normal temperature. This
usually lasts 6 – 24 hours.
Bacteria - Listeria Monocytogenes
 High risk foods
Unpasteurised milk and dairy products, cook-chill foods,
pate, meat, poultry and salad vegetables.
 Signs and symptoms
Ranges from mild, flu-like illness to meningitis,
septicaemia, pneumonia. During pregnancy may lead to
miscarriage or birth of an infected baby.
Bacteria - Bacillus cereus
 High risk foods
Rice, meat, seafood, salads, potatoes, and noodles.
 Signs and symptoms
Ranges nausea and vomiting and abdominal cramps and
has an incubation period of 1 to 6 hours .
This usually lasts less than 24 hours after onset.
Review of the learning objectives
 To recognise the seriousness of food poisoning.
 To identify high risk foods
 To identify people at risk of food poisoning.
 To identify factors affecting food poisoning.
 To identify methods of shopping safely to prevent food
poisoning.
 To recognise common bacteria involved in food
poisoning.
Food-Borne Diseases
People get sick with a food-borne
disease when they consume foods or
beverages contaminated with diseasecausing microbes, chemicals, insects or
other harmful substances