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Transcript of Foodborne pathogens It can be classified into three forms: foodborne intoxication foodborne...
Foodborne pathogens
It can be classified into three forms:
foodborne intoxication
foodborne infection
foodborne toxicoinfection
Food Pathogens www.textbookofbacteriology.net Todar's Online Textbook of Bacteriology
Microrganisms that cause food borne infection or intoxication:
Salmonella
BotulinumE.coli
ListeriaCampylobacter
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.
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--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
burnscutsinsect bitesskin diseases—acne, eczema
Normal Flora
the presence of normal flora cover potential adherence sites for
invading microorganism
Normal microflora : produce compounds toxic to other microorganisms
bacteria found on skin
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 skincarbuncle=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 VOMITINGtoxin works on the vomiting
control center of the brain this leads to reversal of peristalsis and vomiting
DIARRHEAenterotoxin 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.
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.
Non-bullous impetigo is a superficial skin infection that manifests as clusters of vesicles or pustules that rupture and develop a honey-colored crust.
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.
Impetigo (Bullous)Impetigo (Non-Bullous)
Ecthyma gangrenosum is a bacterial skin infection (caused by Pseudomonas aeruginosa) that usually occurs in people with a compromised immune system.
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.
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 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 infectionInfections 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
Direct contacte.g., coughing, sneezing, body contact
Indirect contactvehicles (e.g., soil, water, food)
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:number of organisms presentthe degree of virulence of pathogen
virulence factorse.g., capsules, pili, toxins
host’s defenses or degree of resistance
• Pathogen growth on the surface of a host, often on the mucous membranes, may result in infection and disease
• 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
Bacteria survive extreme acidity of the stomach Able to neutralize
environment
Organism uses flagella to corkscrew through mucosal lining
Inflammatory response begins
– Mucus production decreases
• 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.
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
Adherence
CapsulesPrevent phagocytosis and help with attachment
(adherence) Streptococcus
pneumoniae Klebsiella pneumoniae Haemophilus influenzae Bacillus anthracis Streptococcus mutans Yersinia pestis
Many pathogens secrete enzymes that contribute to their pathogenicity: Increase virulence by use of enzymes And avoid phagocytosis
Coagulase Coagulate blood - wall off from host make boil
Kinases Digest fibrin clot - allow spreading
streptokinase and staphylolinase
Hyaluronidase Hydrolyses hyaluronic acid connective tissue
Collagenase Hydrolyzes collagen IgA proteases Destroy IgA antibodies Hemolysins lyse RBC’s
Enzymes to help penetration
HemolysinsAlpha 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
Bacteria Causing Infections
Salmonella spp. (non-typhoid) Most common cause of bacterial foodborne
disease 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 periods in the environment
Children are commonly infected Generally by household
pets such as turtles, iguanas, and baby chicks
Most cases have an animal source
Enteric fevers, such as those caused by Salmonella typhi are generally the exception
“Typhoid Mary” notorious carrier Caused at least 53
cases over 15 years
• Prevention and Treatment
– 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
– Surgical removal of gallbladder eliminates carrier state
Mary Mallon
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
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 non-typhoidal Salmonella Other Symptoms May Include:
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; 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 eggsfarm
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-to-eat 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 Cross-Contamination
Separate raw animal foods during storing, preparing, holding, and display from raw ready-to-eat 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.
153(continued)
Preventing Cross-Contamination
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
(continued)
HandwashingBefore:
Handling foodHandling clean utensilsHandling clean equipment
After:EatingDrinkingSmokingTouching the face or hairUsing the toiletHandling raw meat, poultry, or seafoodHandling soiled utensils or equipment
155
Handling a Foodborne Illness Complaint
1. One person responsible for the investigation
2. Listen to complaint3. Get the facts4. Evaluate guest complaint5. Notify health officials if complaint
appears valid6. Isolate suspected food
156(continued)
Handling a Foodborne Illness Complaint
7. Cooperate with heath officials8. Take corrective action9. Close the complaint with the
guest10.Index complaint11.Follow up
157
(continued)
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 preservationFood 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 preservationVirtually 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 micro-organisms 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 foodsUnpasteurised milk and dairy products, cook-chill foods, pate, meat, poultry and salad vegetables.
Signs and symptomsRanges 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 foodsRice, meat, seafood, salads, potatoes, and noodles.
Signs and symptomsRanges 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.