Foodborne pathogens It can be classified into three

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: 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 Toxin. Mediated 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-- 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 100 o. C 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 cause illness 180 F 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 (p. H > 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. , 176 F 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 o. C 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, p. H, 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 p. H 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: H 7 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 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

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 Coagulase Kinases Coagulate blood - wall off from host make boil Digest fibrin clot - allow spreading streptokinase and staphylolinase Hyaluronidase Collagenase Ig. A proteases Hemolysins Hydrolyses hyaluronic acid connective tissue Hydrolyzes collagen Destroy Ig. A 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 - 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 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 o. C 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, 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 • Pathogenesis Large number required for – Some strains of Salmonella typhi infection are not easily eliminated Bacteria adhere to • Organisms cross membrane and resist receptors on epithelial killing by macrophages 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 – 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 infected 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 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 p. H, 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 nontyphoidal 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; O 157: H 7) 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 O 157: H 7 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 O 157: H 7 “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 (O 26: H 11; O 111: H 8; O 104: H 21) does not grow well or at all at 44 -45ºC

Escherichia coli O 157: H 7 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 O 157: H 7 Epidemiological features Reservoir: cattle especially young dairy cattle wild ruminants - deer (? ) humans

Escherichia coli O 157: H 7 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 O 157: H 7 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 O 157: H 7 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 O 157: H 7 Clinical features diarrhea ranging from mild, non-bloody to virtually straight bloody stool, abdominal cramping fever is infrequent

Escherichia coli O 157: H 7 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 O 157: H 7 Clinical features Thrombotic thrombocytopenic purpura (TTP) in elderly Case fatality rate: 3 -5% (up to 50% in elderly with TTP)

Escherichia coli O 157: H 7 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 O 157: H 7 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 O 157: H 7 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 O 157: H 7 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 p. H, 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 p. H 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 (Mc. Bride’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 H 2 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 intrauterine or cervical infections spontaneous abortion (2 nd or 3 rd 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 (p. H <4. 0) storage of milk at low temperatures (<5ºC) until shipping

Listeria monocytogenes Control Processing control of factors such as p. H, 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 4 b) 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-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 Cross. Contamination (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. 2. 3. 4. 5. 6. One person responsible for the investigation Listen to complaint Get the facts Evaluate guest complaint Notify health officials if complaint appears valid 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 foodpoisoning 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