In 1996, the federal government published a review on Food Safety, which estimated 6.5-8.1 million Americans become ill from MO or their toxins in food.
More than 9,000 of these individuals will die as a consequence of their illness.
The cost in health care, lost productivity, etc. was estimated to be $5.6-22 billion.
Microbial groups able to cause foodborne illness in humans includes bacteria, fungi, virus, algae and a variety of eukaryotic parasites. Many of these organisms produce relatively minor (though uncomfortable) ailments such as diarrhea, but others may impart life-threatening conditions such as cholera or typhoid fever.
The types of foodborne illness that are caused by MO are separated into two classes:
A. Foodborne infections - live organism is consumed and no symptoms usually appear until the organism can localize (target organ or system) and grow. This is the incubation period. Examples are:
B. Foodborne intoxications - this type occurs when we consume food that contains pre-formed toxins produced by microorganisms (MO) during growth in the food. Symptoms usually occur relatively quickly after eating the toxin. Examples includes:
1. staphylococcal food poisoning
2. paralytic shellfish poisoning
Foodborne illnesses are caused by bacteria because:
1. widespread distribution
2. ability to grow rapidly whenever conditions are favorable
3. relative ease with which they can be detected in food or feces
Bacteria are by far the most commonly identified cause of foodborne disease.
In 1996, the Center for Disease Control released a 5 year (1988-1992) surveillance summary for foodborne disease that showed bacteria caused 79% of U.S. foodborne disease outbreaks, and over 90% of the cases where the causative agent was identified (CDC was able to confirm the etiological agent in only 41% of foodborne disease outbreaks - viruses are thought to be responsible for most outbreaks).
Bacterial toxins are involved in foodborne infections and intoxications. These molecules are divided into 2 groups based on chemical properties:
1. Exotoxins. Soluble, usually heat-labile proteins found in the cytoplasm or in the growth medium (as a result of autolysis). These are further subdivided by their mode of action:
a. enterotoxins stimulate gastrointestinal cells in an abnormal way.
(e.g. cholera toxin)
b. cytotoxins kill host cells by enzymatic attack. (e.g. diphtheria toxin)
c. neurotoxins interfere with normal transmission of nerve impulses..
(e.g. botulinum toxin)
2. Endotoxins. Heat stable lipopolysaccharide components of the outer membrane on Gram negative bacteria.
These toxins have similar structures and produce fever, shock, diarrhea and sometimes internal hemorrhage or abortion in hosts. Interestingly, when these toxins are administered in sublethal levels, they can confer enhanced resistance to bacterial infections.
Other Food Problems:
1. Foodborne illness is not always due to MO; sometimes allergic reactions are involved (food idiosyncrasy) which can be as mild as a skin rash or severe enough to cause death.
2. Other times the illness may be due to chemical food poisoning caused by toxic substances (natural or added) in the food e.g. poisonous mushrooms or pesticide residues.
3. Difficulty in digesting some foods may also cause gastrointestinal distress (e.g. lactose intolerance).
Specific Food-borne Diseases
A. Salmonella. Gram neg. fac. anaerobic bacteria that cause several human diseases including typhoid fever, septicemia and gastroenteritis. Different strains of salmonella are classified by somatic (O) and flagellar (H) antigens (O antigen is O polysaccharide chain, H is flagellum). The known Salmonella serovars can be separated into 3 epidemiological groups:
1. Those that only infect humans. S. typhi, S. paratyphi A & C. These strains cause typhoid and paratyphoid fevers, which are the most severe diseases caused by salmonella.
2. Host-adapted serovars. These are strains associated with a particular type of host but many can cause foodborne disease in humans. S. gallinarum (poultry), S. Dublin (cattle), S. abortus-equi (horses), S. abortus-ovis (sheep), and S. choleraesuis (swine).
3. Unadapted serovars. Pathogenic to humans and animals, include most foodborne serovars.
All salmonella share a common route of infection:
a. live cells which have been consumed penetrate the intestinal epithelium
b. multiply within membrane bound vacuoles and then lyse these vacuoles and disseminate to other parts of the body
Internalization into the host cells is very rapid (20 min.)
Salmonella food poisoning is one of the most common bacterial foodborne illnesses in
the U.S withCDC estimates between 800,000 and 4 million cases each year.
According to the last CDC 5-year survey, Salmonella was responsible for 69% of all
cases of foodborne illness caused by bacteria.
The habitat of Salmonella spp. is the intestinal tract of birds, mammals, and reptiles.
The bacteria are excreted in feces and may be transmitted through polluted water or by insects and other creatures (including humans) to a variety of salmonellosis in humans.
Eggs, poultry, meat and meat products are the most common vehicles of salmonellosis in humans.
Because they are intestinal bacteria, the contamination of meat by Salmonella is generally attributed to carcass contamination with fecal matter during slaughter and evisceration.
Eggs are a big problem and the serovar associated with eggs, S. enteritidis, is now responsible for 70% of all Salmonella cases, and this organism is believed to cause more deaths than any other foodborne pathogen. Eggs are generally sterile and are contaminated by fecal material after they are laid, but chickens with infected oviducts may lay eggs that already have Salmonella enteritidis inside them.
In 1991, the U.S. Congress required that eggs for interstate shipment be refrigerated, and U.S. grocers typically store eggs in refrigerated bins. Interestingly, the latter practice is not followed in many other developed nations.
Animal feeds can be an important source of Salmonella. In 1989, the industry-wide incidence of Salmonella in animal feeds was almost 50%.
Symptoms of Salmonella food poisoning:
1. nausea, vomiting, moderate abdominal pain, headache, chills and diarrhea
2. usually 12-14 h (but has been much longer or shorter) after ingesting sufficient numbers of bacteria
3. generally 105-109 CFU/g, but can be as few as 15-20 cells; depending on the age and health of host, and strain differences among the members of the genus
Symptoms usually last 2-3 days and are accompanied by weakness, moderate fever,
Typhoid fever is, of course, far more severe; headache and fever (which can be over 104oF or 40oC) can persist for several weeks.
Mortality for serovars other than those causing typhoid and paratyphoid fevers varies with the serovar involved is greatest in people over 50 (15%) and in children under 1 (5.8%) with a 2% rate for ages in between.
S. choleraesuis is most lethal strain with a mortality rate of 21% in people over 50. Mortality from typhoid and paratyphoid fever is about 10%. People can recover on their own with bed rest and fluid replacement, but more severe cases may require antibiotic therapy and monitoring of body fluid balance.
Biology and control:
1. optimal growth at 37oC, growth of some serovars has been noted <6o up to 45oC
2. pH optimum near neutral (6.6-8.2 ideal), growth can occur from 4.05 to 9.0.
Viability at pH values as low as 3.3 has been demonstrated in acid adapted cells
3. growth is inhibited by nitrite and if aw <0.94
4. Salmonella cannot tolerate 9% NaCl
5. readily killed at milk pasteurization temperatures (HTST: 161oF [72oC] for 15 s) or by heating foods to an internal temperature of 165oF (74oC)
6. Salmonella are quite sensitive to radiation-thus this is a useful tool for removing the bacteria from animal feeds and the use of radiation to rid Salmonella (and other pathogenic microorganisms) from raw poultry is gaining greater acceptance in the U.S.
Ultimate control of salmonella can only be achieved by eliminating the bacteria from animals and humans.
This objective is difficult because up to 5% of infected persons recover to become carriers of the disease, where the bacterium becomes established in the gall bladder and is shed every time the person goes to the bathroom and carriers do not show any symptoms of infection.
B. Staphylococcus. Genus of G+ fac. anaerobic bacteria that includes several species able to synthesize heat-resistant enterotoxins that produce the food poisoning.
Incidence: The true incidence is unknown but the Center for Disease Control estimates that 1 to 2 million cases of staphylococcal gastroenteritis occur each year in the U.S.
Ham is the most common vehicle food, and this association is thought to be due to the high salt content (3.5%), which favors growth of S. aureus (which enter from food handlers or cutting surfaces) over other MO.
Most outbreaks of staphylococcal gastroenteritis come from foods which were prepared by hand and then not refrigerated properly for several hours prior to consumption.
S. aureus and other species of staph are found on the skin and in intestinal tract of humans and animals. In general, staph can be expected in low numbers in all foods of animal origin or in those that are directly handled by humans, unless heat processing steps are used for their destruction.
Some of these coagulase (-) strains are adapted to nonhuman hosts, but they can get into human food and if permitted to grow, will produce enterotoxins in the food. Not all Staph aureus produce enterotoxin; the percentage of enterotoxigenic strains varies widely (10>60%).
The most important sources to foods, however, are nasal carriers and persons with boils or carbuncles that are allowed to handle foods.
About 50% of adults and a slightly higher percentage of children harbor S. aureus in their noses, and it is also carried by most domesticated animals.
Even when food is contaminated, the food must be handled in a manner that gives the bacterium an opportunity to grow and produce toxin.
Five factors which are most commonly associated with staphylococcal (and many other) food poisoning outbreaks:
1. Poor personal hygiene.
2. Inadequate cooking or heating of food.
3. Preparing foods too far in advance.
4. Holding food in warmers set at bacterial growth temperatures.
5. Inadequate refrigeration.
1. Pathogenesis results from the ingestion of one or more pre-formed enterotoxins.
2. Staphylococcal enterotoxins bind to helper T-lymphocytes in a manner that stimulates production of several cytokines, especially interleukin-2.
3. Overproduction of cytokines is believed to produce most of the intoxication symptoms, which include nausea, vomiting, severe abdominal cramps, diarrhea, sweating, headache and sometimes a fall in body temperature.
4. Incubation – Symptoms usually appear within 4 h (range: 1-6 h) after ingesting food that contains at least 200 ng of enterotoxin (105 CFU/g in food can produce more than enough toxin).
5. Symptoms last 24-48 h and mortality is very low.
Treatment involves bed rest and administration of fluids. Humans do not demonstrate any immunity to repeated exposure.
Biology and control:
1. Staphylococci are hardly bacteria; All enterotoxin-producing species can grow in 10% NaCl and some up to 20% NaCl.
2. S. aureus can grow between 7-47.8oC with enterotoxin production between 10-46oC (optimal toxin production between 40-45oC).
3. pH optimum is 607 but can grow over 4.0-9.8 with toxin production at pH >4.7
4. Growth has been demonstrated at aw = 0.83, although 0.86 is generally considered to be the lowest aw for growth (still the lowest of any nonhalophilic bacteria). Enterotoxin production has been demonstrated at aw values as low as 0.84.
5. Staph also do not compete well with the normal flora of many foods, especially lactic acid bacteria.
Enterotoxins are quite heat resistant. Heat inactivation of 99% pure SEB in buffer required 16.5 min at 250oF. Vegetative cells are destroyed long before toxin.
To keep toxin out of food, store foods at 4oC (40oF) or above 60oC (140oF). This practice will help to keep many disease-causing MO out of your food.
C. Shigella: Gram negative, facultative aerobic rods closely related to Salmonella and Escherichia. Worldwide it causes about 500,000 children’s deaths each year:
S. dysentariae causes dysentery
S. flexneris, S. boydii, and S. sonnei cause foodborne shigellosis
Shigella are intracellular parasites of humans and higher primates. Poor personal hygiene (the fecal-oral route of transmission) is the most common factor in foodborne shigellosis.
Like a few other pathogenic bacteria (Bordetella pertusis, Yersinia) virulence in Shigella is related to growth temperature. Cells grown at temperatures below 34oC are avirulent and cannot invade the mucosa. Growth in foods is not always necessary for infection, however, because as few as 10-100 CFU can initiate infection in susceptible people.
Prominent vehicle foods include shellfish, fruits, vegetables, chicken and salads.
Contaminated water or food handlers with poor hygiene are the most common reasons for outbreaks.
Outbreaks of dysentery occur when poor hygiene and crowding are combined (prisons, refugee camps, etc.).
Once ingested, Shigella spp. invade the colonic mucosa, multiply and then destroy the epithelial layer of the colon as they lyse infected cells and spread.
1. Incubation time ranges from 1-7 days after ingestion of live bacteria.
2. Symptoms range from mild diarrhea to severe dysentery characterized by the passage of frequent bloody mucoid small-volume stools (fever, vomiting and dehydration).
3. Symptoms may last from 4-7 days.
4. Infections are generally self-limiting, the morality rate is low in the U.S. but may be life threatening to young or malnourished people (but mortality rate among these people can be as high as 10-15%).
Treatment depends upon the severity of the disease. Severe cases or dysentery require antibiotic therapy, rest and fluid replacement.
Biology and control: Overall biology is similar to Salmonella and Escherichia
1. Growth occurs between 10-45oC.
2. pH opt is 6-8 but growth has been noted at 5.0
The only real method for control involves good hygiene and proper preparation and handling of food in homes and food service establishments.
D. Campylobacter: Gram negative, microaerophilic to anaerobic spirally curved rods. C. jejuni subsp. jejuni is by far the most common agent (>99% of human cases).
1. C. jejuni are found in the intestinal and reproductive tracts of man and animals (not carried by healthy people in U.S. or Europe, but prevalence in feces from healthy animals is 30-100%).
2. The most prominent vehicle foods in outbreaks of campylobacteriosis are poultry and raw milk.
3. About 50% of infections are associated with either eating inadequately cooked or recontaminated chicken meat or handling chickens. Studies have found that 94% of eviscerated turkeys and 72-80% of chicken carcasses were positive for C. jejuni.
4. They are also found in most other fresh meat products but at much lower rates. Rates in frozen meats are very low.
1. Actual numbers are unclear but trends in recent years suggest that, in developed nations, Campylobacter may cause as much enteric disease as Salmonella and Shigella combined (i.e. >2-4 million cases/yr in U.S.).
2. Isolation of C. jejuni from suspect food is rare because the bacteria are usually present in very low numbers, but the organism is isolated more frequently from fecal osamples of humans with diarrhea (3-14%) than Salmonella and Shigella.
3. Incidence is seasonal, with higher numbers of outbreaks in the summer and fall than in winter and spring. Most outbreaks are seen in people 10-29 years of age.
Incubation time is usually 2-4 days (up to 10 d) after ingestion of 400-500 live bacteria.
Symptoms include profuse diarrhea (sometimes with blood), abdominal pain, malaise, headache and fever and will last from 1-4 days, but relapses are not uncommon (about 25% of cases). Victims may continue to shed the organism for more that 2 months after symptoms subside.
Most infections are self-limiting and are not treated with antibiotics.
The estimated case/fatality ratio for all C. jejuni infections is 0.1 meaning one death per 1,000 cases. Fatalities are rare in healthy individuals and usually occur in cancer patients or in the otherwise debilitated (very young & old, AIDS, etc.).
Pathogenesis appears to be caused in part by the invasive abilities of the bacterium. Some, but not all, pathogenic strains have been shown to produce a heat-labile enterotoxin and a cytotoxin.
Biology and control:
1. C. jejuni cannot grow below 25oC or in the presence of 3.5% NaCl. It can remain viable, however, in vac. pkgd turkey for up to 28 d at 4oC.
2. very heat sensitive, internal (core) heating to 70oC for 10 min will destroy 107 cells in hamburger
3. requires 3-6% O2 but inhibited at 21% (atm. conc.). 10% CO2 promotes growth
4. Also sensitive to freezing, numbers die at about 1 log/day at -20oC (thus low counts in frozen meat prod.).
Control of the disease requires good hygiene practices, proper preparation and handling of food (cook it well!!), and avoiding unprocessed foods associated with Campylobacter (e.g. raw milk).
E. Clostridium: Gram+, anaerobic sporeforming rods. At least four species cause food poisoning in humans: C. botulinum, C. baratti, C. butyricum, and C. perfringens.
1. Botulism. Caused by the ingestion of a heat-labile neurotoxin produced (most frequently) by C. botulinum.
Seven types of toxin, A-G, are recognized on the basis of the serological specificity.
A, B, E, F, and G cause disease in humans
type C in fowls, cattle, mink and other animals
type D is associated with forage poisoning of cattle
1. C. botulinum cells and spores are found in soils, dust and water.
2. Spores expected in vegetable-based products as a result of soil contamination.
3. The greatest hazard continues to be home-prepared to home-canned foods that are handled improperly or given inadequate heat treatment. Many of these foods are consumed without preheating.
Adult botulism. Total cases of adult botulism in the U.S. rarely exceed 50/yr, but the high mortality rate makes the disease an ongoing concern.
1. Symptoms appear between 12-72 h after the ingestion of toxin-containing foods.
2. Nausea, vomiting, fatigue, dizziness, headache, dry skin, mouth and throat, lack of fever, constipation, paralysis of muscles, double vision. Finally, respiratory failure and death.
3. The illness may linger over 1-10 days.
4. Mortality rate varies between 30-65%.
Pathogenesis is due to the ingestion of C. botulinum neurotoxin.
1. These toxins are formed inside the bacterium and are released by autolysis.
2. Botulism toxins are the most lethal substances known; a single milligram of type A toxin will kill 15 million mice (1 mg L.D.50=30 million mice).
3. Can be absorbed into the bloodstream through the respiratory mucus membranes or thru the lining of the stomach.
1. This form of botulism is slightly more common.
2. Unlike adults, infants under 1 year of age can develop botulism from the ingestion of viable spores which germinate in their intestinal tract and produce toxin inside the child.
3. The disease can range from mild to severe, depending on how rapidly diagnosis is made.
4. Symptoms start with constipation followed by poor feeding, lethargy, and weak or altered cry. Loss of head control is dramatic.
5. The most common vehicle foods are those which do not undergo heat processing to destroy endospores (honey and corn syrup are most freq. sources). Diagnosis requires identification of botox in infant stools.
-~ 50 cases year in U.S.
1. Adults requires administration of specific antisera as quickly as possible (since binding to ganglioside is irreversible).
2. In infants, treatment primarily involves supportive care and antimicrobial therapy is not recommended.
Interestingly, the same qualities that make botulism toxin so poisonous also make it a useful therapeutic agent for dystonias. Dystonias are disorders caused by involuntary sustained muscle contractions that result in twitching, repetitive and sometimes painful movements or abnormal postures. Botox is used to partially paralyze those muscles and relieve the dystonia. In some types of dystonias, botox can provide more effective treatment than drugs or surgery.
Biology and control:
1. Complex nutritional requirements, generally competes very poorly with other MO.
2. Under optimal conditions, proteolytic strains cannot grow at refrigeration temps (range 10-50oC) but nonprt can (3.3-45oC).
3. can grow in vac. pkgd prod. like bacon without producing off odor (esp. nonprt types)
4. Toxin generally not produced at pH <4.5 (feature which determines heat processing req. in canned foods).
5. Minimum aw for growth and toxin prod. is 0.94
6. 10% NaCl or 50% sucrose are inhibitory
7. Prt strains are much more heat resistant than nonprts; type A is most heat resistant.
The best preventative steps are to use current USDA guidelines for home canning and to boil potentially suspect foods for several min, or heat to 80oC (176oF) for 10 min, either of which will destroy the neurotoxin.
2. C. perfringens food poisoning:
a. 5 variants based on the type of exotoxin produces; A-E.
b. Food poisoning cases are due to heat resistant type A, other types are associated with gas gangrene infection in wounds.
1. Type A C. perfringens are found in soils (103-104/g in virtually all samples examined), water, dust, and the intestinal tract of man and animals.
2. The bacterium or its spores get into meats directly from slaughtered animals or from contamination by containers, food handlers, or dust.
3. Foods involved in outbreaks are often meat dishes (or non-meat dishes contaminated by gravy) that were prepared one day and eaten the next because the heat prep is usually inadequate to destroy spores. During the time between prep and consumption, spores germinate and cells grow.
Actual numbers are unknown, but it appears that C. perfringens food poisoning is widespread in the U.S. and many other countries. Because of the relative mildness of the disease, it is likely that only outbreaks that affect large groups of people are ever reported and recorded. The average number of cases in outbreaks reported to CDC is about 100.
1. Incubation time is 6-24 h (esp. 8-12 h) after ingestion of 106 or more live cells.
2. Symptoms include acute abdominal pain and diarrhea. Nausea, fever and vomiting are rare and, unless the victim is immunocompromised.
3. Symptoms last less than 24 h.
4. Mortality is low and has only been fatal to older or otherwise debilitated patients. No immunity seems to develop.
Pathogenesis from type A strains is due to a heat-sensitive enterotoxin that is produced and released during sporulation. Cells may sporulate in the intestinal tract or during growth in foods and preformed toxin in foods may lead to an earlier onset of symptoms (i.e. a combination of infection and intoxication). The toxin binds irreversibly to the brush border of intestinal epithelial cells, where it moves into and damages the membrane. Water and salt uptake by infected cells is reversed and cell death results.
Biology and control:
1. opt growth temp 37-45oC, range = 20-50oC, at 45oC, generation times can be as short as 7 min
2. pH range = 5.5-8.0
3. aw req = 0.93-0.97, depending on solute but sporulation requires higher aw values
4. inhibited by 5% NaCl
5. relatively resistant to freezing (4% survival of vegetative cells after 180 d at -17.7oC and survival of spores is even higher; 11%)
6. heat resistance of endospores is variable (D100oC ranges from 0.31 to 17.6 min, depending on the strain.
7. performed toxin can be destroyed by heating at 60oC for 10 min
Control would employ all of the suggestions that apply to preventing other live pathogens in food.
F. Listeria: Gram+, aerobic or facultatively aerobic, nonsporeforming rods. Six species are recognized but L. monocytogenes is the pathogen of major concern to humans (98% of recorded human outbreaks have involved this species, only 3 known cases involved L. ivanovii, and 1 case involved L. seeligeri).
Sources and Incidence:
1. Listeria spp. are widely distributed on decaying vegetation, soils, feces, silage and water. As a consequence, the organism is present on any fresh food product of animal or plant origin, and its growth properties allow it to survive for long periods of time.
2. Microbiological surveys indicate that L. monocytogenes can be recovered from 20% of soft cheeses and processed meats, 50% of raw meat including poultry, and up to 30% vegetables.
3. Although large-scale outbreaks have attracted the greatest notoriety, sporadic disease continues to account for most cases and deaths from listeriosis in the U.S. A substantial percentage of sporadic cases have been linked to the consumption of soft cheese, food purchased from store delicatessen counters, undercooked chicken, and hot dogs which were not reheated.
Based upon the frequency with which L. monocytogenes is recovered from patients around the U.S., it is estimated that the overall rate of bacteremia or meningitis due to L. monocytogenes in this country is about 0.7 per 100,000 (approx. 1,850 cases/year) and results in approximately 425 deaths (mortality approx = 23%). Unfortunately, the rate in pregnant women is much higher (12 per 100,000) which is cause for real concern.
Because cases of foodborne listeriosis are infrequent and sporadic, important sources of Listeria in foods are not clear. Suggestions include contamination from healthy animal or human carriers (e.g. healthy cows may shed it into milk or it may come from food handlers that are carriers). Other suggestions are that the increase in foodborne outbreaks are due to coinfection with other pathogens like Salmonella or E. coli, since these bacteria are often also recovered in stools of victims.
Because Listeria are commonly found in the environment, tracing the source of L. monocytogenes in modern foodborne outbreaks can be difficult.
1. Incubation time from 1-5 weeks (ave.3 weeks) after ingestion of live bacteria.
2. The organism colonizes the intestinal tract then moves to the bloodstream where it invades other susceptible tissues including the spleen, liver and the placenta.
Listeriosis in humans is not characterized by a unique set of symptoms since the course of the disease depends on host fitness. Healthy, nonpregnant people are highly resistant, and evidence suggests that consumption of 104-105 CFU/g may not cause disease.
Far fewer numbers, however, may be enough for people predisposed to listeriosis. Factors which may predispose you to listeriosis and which are significant in the mortality rate include:
-diabetes (exp. type 1)
-people with tumors
-renal transplant patients
-people on steroid therapy
When susceptible people contract the disease, meningitis and sepsis (blood infection) are the most common symptoms and the disease may resemble infectious mononucleosis.
Pregnant women that contract it often show no symptoms or they may be like a mild case of flu. Unfortunately, abortion, premature birth or stillbirth often occur. Newborns infected at birth show symptoms of meningitis 1-4 weeks after birth.
When abortions are included in the mortality rate, the death rate from listeriosis during the 1980s ranged from nearly 50% in the United Kingdom to about 28% in the U.S.
Pathogenic strains of L. monocytogenes all produce listeriolysin O, a substance that produces β-hemolysis on erythrocytes and kills phagocytes that engulf the bacterium. Listeriolysin O is produced during exponential growth (max levels after 8-10 h of growth)
Treatment requires antibiotic therapy but this treatment is often not as effective as desired because victims are frequently immunocompromised to begin with.
Biology and control:
1. pH opt 6-8, but range is 4.1-9.6
2. grow in 10% NaCl
3. opt temp = 20-30oC, range 1-45oC
4. glucose enhances growth of all species
Fairly sensitive to heat (best way to control it):
-105-106 cells can be killed by milk past.
-cooking meat to an internal temp of 70oC (158oF) for 2 min kills L. monocytogenes
G. Escherichia coli: Gram-, fac. anaerobic rods found in the intestines of warm-blooded animals including humans. Since it is part of the intestinal microflora, E. coli is used as an indicator organism for food safety; their presence in food indicates fecal contamination. Although this bacterium was associated with outbreaks of diarrhea in nurseries during the 1940s that had mortality rates as high as 50%, e. coli was not really recognized as a human pathogen until a 1971 outbreak of gastroenteritis from imported cheese. The bacterium is now recognized as a leading cause of travelers diarrhea and the more serious disease, hemorrhagic colitis.
CDC now estimates E. coli 0157:H7 causes about 20,000 cases of illness and 250 deaths in the U.S. each year.
E. coli 0157:H7 is NOT the only strain that is able to produce Stx-1 and Stx-2, however, and other shiga-toxin-producing strains can also cause hemorrhagic colitis. As few as 10 CFU may produce the disease and the incubation period is 3-9 d (mean=4). Symptoms include bloody diarrhea, severe abdominal cramps, nausea and vomiting. Fever is rare, and symptoms may last from 2-9 d.
Although an estimated 50% of victims do not visit a physician and recover fully, EHEC infection can lead to hemolytic uremic syndrome (HUS). HUS is the leading cause of kidney failure in children, and nearly all cases are due to EHEC strains. The disease is thought to occur because cell damage by E. coli toxins leads to hemolysis, blood clotting, and ultimately loss of blood flow in the small capillaries of the kidney.
Persons with HUS may require dialysis and blood transfusions and can suffer heart failure, seizures and coma. Of the 583 people that became ill in a 1993 outbreak, 41 developed HUS and all four deaths were children that acquired HUS.
EHEC strains are associated with cattle and have been found in beef and raw milk, and will also be present in water contaminated by cattle feces. They are transmitted through food and water and by person-to-person contact. Undercooked beef and raw milk have been the primary vehicle foods, but all raw meat, poultry and seafood should be considered a possible vehicle food.
Biology and control:
-E. coli 0157:H7 can survive during refrigeration or freezing and displays good survival in acid food (e.g. apple cider @pH <4.0). Acid survival rates are increased by sublethal acid shock.
-EHEC strains are more sensitive to heat than Salmonella and this is the key to their destruction. Milk pasteurization or cooking hamburger to an internal temp of at least 155oF (68.4oC) will kill the organism. The center of hamburger patties should be gray or brown and juices should run clear without any trace of pink. Steaks aren’t a problem because only the surface is contaminated and the cooking surface is hot enough to kill the bacterium.
In response to the 1992-93 outbreak of E. coli 0157:H7 in the Pacific Northwest, the FSIS hired 160 new meat inspectors and adopted a policy that prohibits any visible contamination by feces, milk, or undigested food on beef carcasses or boneless beef. Previously small amounts of these were allowed.
FSIS is also trying to develop new approaches to meat and poultry inspection that will minimize microbiological contamination in these products, improve microbiological testing procedures and educate consumers about food handling and preparation.
The only really effective way to prevent disease, however, is to make sure the bacterium has been destroyed during food preparation. Other control steps for E. coli would include those used for other organisms transmitted by the fecal-oral route.
H. Other Bacteria
1. Vibrio: Gram negative, facultatively anaerobic rods. Four species are a concern in foodborne illness:
a. V. parahaemolyticus. Unlike most other food infection syndromes, which can be acquired from a variety of foods, V. parahaemolyticus gastroenteritis is almost always linked to seafood, especially shellfish and mollusks. Incidence in the U.S. is relatively low (generally <10 cases/yr) but it is a leading cause of food infection in Japan.
The incubation time = 3-76 h (mean = 16.7 h) after ingestion of about 105 cells of virulent V. parahaemolyticus.
Victims experience diarrhea, cramps, weakness, nausea and sometimes chills, headache and vomiting. Symptoms last 1-8 days (mean=4.6 d).
1-grow temp range is 5-44oC (opt. 30-35oC).
2-pH range for growth is 4.8 -11.0 with optimal growth between 7.6-8.6
3-grow in 1-8% NaCl, opt = 2.4%
4-under optimal growth conditions the generation time can be as short as 9-13 min.
The bacterium is considered to be heat sensitive but if high cell numbers (≥105) are present, some may linger even after 15 min at 80oC.
b. V. cholerae. Until recently, V. cholerae strains were separated into two important serological groups; strains that caused epidemic cholera all belonged to serovar 0 Group 1, while more common non-01 strains (and there are literally hundreds of these) were responsible for gastroenteritis, soft tissue infections, and septicemia in human. Both types are fairly common in warm ocean waters around California, Texas, Louisiana, and Florida.
Now, however, investigators recognize at least one non-01 strain, V. cholerae 0139, is responsible for an epidemic of cholera that started in India in 1992. It has since afflicted over 100,000 people in 11 countries in SE Asia. This is a cause for real concern because 01 vaccines do not protect against the new strain and conventional laboratory methods for identification of 01-type cannot detect this new serotype.
Because V. cholerae thrives in warm water, it is not surprising that most foodborne outbreaks involving 01 and non-01 strains in the U.S. occur during the summer. Nearly all outbreaks are linked to the consumption of raw shellfish especially oysters.
Cholera is caused by V. cholerae colonization of the intestines followed by the production of cholera enterotoxin (CT). After a 2-5 day incubation period, diarrhea, which is characterized by rice-water appearance (clear with small clumps of dead cells) can be profuse; up to 15L/day. Abdominal pain and sometimes vomiting are also symptoms. Loss of electrolytes and fluid can be fatal if treatment (oral or intravenous fluid replacement and antibiotic therapy) isn’t prompt.
c. V. vulnificus. Usually associated with wound infections, a serious form of septicemia (mortality >50%) and gastroenteritis. This is a highly invasive organism, and as few as 100 CFU may be enough to cause disease. Immunocompromised people, especially those with liver disease, are at greatest risk (people with liver disease are 200 times more likely to die after infection with this bacterium). Other risk factors include persons with iron overload (thalassemia and hemochromatosis). Men over 40 are the most frequent victims of V. vulnificus infection. Over 70% of infected persons will develop bulbous skin lesions.
Survey in Gulf states suggest an annual incidence of 0.6/100,000 and an overall mortality rate of 22%. Over 80% of individuals that developed septicemia had eaten raw oysters the week before. This bacterium is believed to be responsible for about 95% of all seafood-associated deaths in the U.S. It is frequently isolated from clams and oysters and studies in mice have found that over 80% of isolated strains were lethal upon injection. As a result, Florida now requires a label on all shellstock and shucked products warning individuals at risk not to consume these foods raw.
d. V. hollisae. Another species that causes foodborne gastroenteritis.
2. Bacillus cereus: aerobic sporeforming rod found in dust, soil and water. Grows at temp range of 4-50oC, pHs between 4.9-9.3.
Strains associated with foodborne illness produce emetic (vomiting) or diarrheal toxins in contaminated foods.
The diarrheagenic toxin is designated hemolysin BL, and it is produced during exponential growth. Production is favored in pH range of 6.0=8.5. The symdrome is relatively mild and similar to C. perfringens food poisoning. Symptoms include nausea, cramps, and diarrhea within 8-16 h (usually 12 h) after eating food contaminated with 107-108 CFU/g of B. cereus and they last another 6-12 h.
B. mycoides and a few other species of Bacillus also produce diarrheagenic enterotoxins.
Symptoms from this form of Bacillus food poisoning are more severe (similar to S. aureus food poisoning). Symptoms include nausea and vomiting, sometimes accompanied by cramps and diarrhea, 1-6 h after eating food (usually fried or boiled rice dishes) contaminated with the heat-and pH stable enterotoxin. Cell numbers as high as 109/g may be necessary to produce sufficient toxin in the food.
3. Yersinia enterocolitica: Gram-, fac. anaerobic rod found in soils and water and are also found in the intestinal tracts of animals. Although the bacterium has been isolated from a variety of foods, it is widely believed that pigs are the single greatest source in humans. Virulence results from tissue invasion after ingestion of live cells. Y. enterocolitica has been associated with several human disorders but we will only discuss the gastroenteritis syndromes.
Symptoms appear several, 1-2 d, after eating contaminated food and include fever, abdominal pain, diarrhea and sometimes vomiting. Because these symptoms mimic appendicitis, a major “complication” of yersiniosis is unnecessary appendectomy surgery. Outbreaks are more frequent in the fall than in the spring and often strike the very young and old.
-can grow between -2 to 45oC (no other pathogen displays psychrotrophic growth)
-destroyed by heating 1-3 min at 60oC, cannot survive milk past
Animal parasites that can be contracted from food include protozoa, flatworms and roundworms. Unlike bacteria, parasites cannot grow in food or on culture media and many require more than one animal host to carry out their life cycle. The definitive host is the animal in which the adult parasite carries out its sexual cycle, while the intermediate host is the one in which larval or juvenile forms develop.
Since parasites cannot be grown in culture media, their presence in food must be detected by direct examination after concentration and staining.
Giardiasis. Giardia lamblia is a flagellate protozoan that exists in water. Beaver and muskrats are major sources of this organism in water. G. lamblia produces cysts which are its primary form in water and food. Cysts excyst in the G.I. tract with the help of stomach acids and proteases and cause clinical giardiasis in some people. Estimates suggest that as many as 15% of the entire U.S. population is infected with this organism.
The infectious dose is thought to be as few as 10 cysts, and inc. time is 7-13 d, with cysts appearing in stools after 3-4 wks. Symptoms include diarrhea, abdominal pain, and weight loss (5 lbs common). Without treatment, symptoms can last months to a year or more. Giardiasis is highly contagious, with infected persons shedding as many as 9 x 108 cysts/day, and cysts can persist for 3 months in sewage.
Contaminated water is the most common source but fecal contamination of food by humans or animal pests has also been implicated in disease.
Cryptosporidiosis. Cryptosporidium parvum is a known pathogen to mammals, birds, and reptiles. Like G. lamblia, this protozoan is found in environmental waters so transmission through food involves contaminated water and fecal-oral transmission.
C. parvum produces thick-walled, environmentally-resistant oocysts that, when ingested, excyst in the small intestine and invade host cells. Symptoms include diarrhea and are self-limiting in healthy persons but can be life-threatening in immunocompromised persons like AIDS patients.
Trichinosis. This disease is caused by the roundworm Trichinella spiralis. Althought trichinosis is contracted most frequently by undercooked pork or pork products, about 75 different species can be infected with this organism including bears, cougars, and marine mammals. Birds appear to be resistant to infection.
When infected meat is ingested, stomach enzymes fee the encysted larvae, which then mature in the lumen of the intestines. They remain in the intestine for about 1 mo without producing any symptoms (unless high numbers were ingested, in which case symptoms may appear after 1-2 d), before eggs hatch and larvae penetrate the gut wall, causing nausea, abdominal pain, diarrhea and sometimes vomiting. These symptoms may persist for several days.
The larvae pass throughout the body and 7-9 d after initial symptoms, begin to penetrate skeletal muscles, especially those in the eye, tongue, and diaphragm. As the larvae burrow in, patients experience severe pain, fever, and sometimes death from heart failure. The larvae grow in the muscle then encyst in a calcified wall 6-18 mo later. They will not undergo any further development unless consumed by another animal, but can remain viable for up to 10 years in a living host.
To prevent trichinosis, USDA recommends cooking suspect meat to 170oF (76.7oC) or higher. Freezing is also effective in destroying T. spiralis; 30 days at -15oC should inactivate the larvae. Microwave cooking is a particular concern with trichinosis because rapid heating and uneven cooking can allow some larvae to persist.
Mycotoxins are toxic substances produced by a variety of molds. Analysis of the toxicity of these compounds in animal systems has shown that many are carcinogenic or mutagenic. They are produced as secondary metabolites (non-essential for growth, produced during late exponential phase). Food poisoning caused by the ingestion of mycotoxins is called mycotoxicosis.
Aflatoxins: Most widely studied and most carcinogenic of all mycotoxins. Discovered in 1960 when peanut meal for turkeys, which had been contaminated with A. flavus killed about 100,000 poults. Aflatoxins are also produced by A. parasiticus and A. nominus. 18 aflatoxins have been identified and the most potent one AFB1, is produced by all AF-positive strains. Six aflatoxins, including AFB1 fluoresce under UV light.
Aflatoxins are lethal if eaten in large dosages, sub-lethal doses can cause chronic liver disease or liver cancer. In general, young animals are more susceptible to their effects. Mutagenic effects include point mutations and frameshifts.
Aspergillus growth and aflatoxin production are favored by warm temperatures (13-35oC) and humidity (aw>0.93). Aflatoxins have been found on a wide variety of foods including meat, vegetable, dairy and grain products. Under optimal conditions, toxin may appear within 24 h, and these compounds are very difficult to destroy in most foods.
Aspergillus spp., Penicillium spp. and other genera of molds produce other important mycotoxins such as citrinin, penicillic acid, and patulin.
Ergot - Another mycotoxin has been implicated (albeit not conclusively) in one of the most bizarre epics in American history. Claviceps purpurea is a mold that usually grows on rye. Under moist, cool conditions, this mold produces a group of related alkaloids collectively referred to as ergot. The primary cleavage product of ergot upon alkaline hydrolysis is lysergic acid diethylamide (LSD), and some mycologists believe this reaction can occur in the natural state. Individuals who ingest sufficient amounts of ergot experience a type of poisoning whose symptoms are similar (but usually more severe) to those of persons that ingest LSD, and some historians believe that these behaviors may have been interpreted as bewitchment. Since young children and teenagers eat more per body mass, these individuals frequently suffer the most severe symptom of ergot poisoning so it is consistent that the witches of Salem were teenage girls.
Control of mycotoxins in food is difficult. The U.S. Food, Drug and Cosmetic Act states that any food which contains a “poisonous or deleterious substance which may render it injurious to health” is adulterated and allows the FDA to remove that food from the marketplace. Since mycotoxins are not part of the natural food composition, FDA treats them as added substances and adulterants.
FDA has established practical levels for toxins like aflatoxin (20 ppb in most susceptible commodities, 15 ppb in peanut products, 100 ppb in animal feed-except 20 ppb for dairy cattle food), but safe tolerance levels for most mycotoxins have not been established.
What can you do to prevent mycotoxicosis?
-With moldy cheese; if mold developed in fridge, O.K. – aflatoxins aren’t prod at that temp. so just trim ½ inch (1.3 cm) below growth to avoid fungal metabolites.
-don’t try to trim soft cheeses like cream or cottage cheeses
-use good sanitation, handling and storage practices to delay mold growth
-discard moldy foods outside of your kitchen to prevent high spore numbers near your food handling area
Viruses have the potential to be a leading cause of foodborne disease, but much less is known about these agents than bacteria or fungi. Like protozoa and other parasites, viruses are unable to multiply outside a living host cell. Since viruses cannot grown in food, detection requires methods to extract and concentrate these agents, usually by propagation in tissue culture. Unfortunately, tissue culture systems are not available for many of the foodborne viruses, so these agents can be very difficult to detect.
Because of these limitations, it is generally accepted that a significant percentage of the foodborne illnesses where etiologic agents cannot be identified are probably due to viruses. In fact, viral gastroenteritis is believed by some to be second only to the common cold in frequency.
Virtually any food can serve as a vehicle for virus transmission but raw or partially cooked mollusks are the most common food source because these filter feeders concentrate viruses from surrounding waters.
Hepatitis A: RNA virus identified in more foodborne outbreaks than any other virus. UT has highest rate in U.S. with >1000 cases in 1996 and about 600 in 1997. Fever, anorexia, nausea and abdominal discomfort followed by jaundice 15-45 days after ingestion of virus. Symptoms last 1-2 weeks. Chronic liver disease is rare, and lifetime immunity follows an attack. A Hep A vaccine has recently been approved by FDA.
-Outbreaks of a more serious hepatitis virus, Hep E, are linked to food in developing countries.
Rotaviruses: RNA virus first propagated in the lab in 1981. Six groups identified and 3 are known to be infectious to humans. Estimated to cause 1/3 of hospitalizations for diarrhea in kids under 5. Children 6 mo-2 yrs are most susceptible, and every U.S. child is infected by age 4. Infection produces immunity but high doses or lowered immunity can lead to mild illness in older children and adults.
Transmission usually occurs through daycare centers and water, with only sporadic foodborne transmission. Incubation time is 2 days, vomiting for 3 d, watery diarrhea for 3-8 d with abdominal pain and fever are symptoms.
Norwalk and Norwalk-like viruses; group of small, round RNA viruses that are a leading cause of gastroenteritis. Placed into 3 groups based on morphology:
1. SRSVS (small round structural viruses). Infective in older children and adults, and about 70% of U.S. adults have antibodies. Associated with travelers diarrhea and polluted water is an obvious source. Most outbreaks have been traced to raw oysters. Inc. time is 18-48 h, and symptoms include nausea, vomiting, nonbloody diarrhea and abdominal cramps. Illness lasts 1-2 days.
2. Caliciviruses. Have surface hollows, cause vomiting and diarrhea in children, 1-3 d inc. time.
3. Astroviruses. Contain a 5 or 6-pointed surface star. Cause gastroenteritis in children and adults but children <7 are most susceptible. Symptoms appear after 1-2 d and include vomiting, diarrhea and fever.
-Most Norwalk and Norwalk-like viruses are very difficult to detect due to lack of a laboratory cell culture method, so identification relies on ELISA, EM and RT-PCR.
Poliovirus can also occur in shellfish collected from polluted waters. There is a low incidence of poliomyelitis in the U.S. but relaxed immunization req. in schoolchildren could lead to new outbreaks. Disease still occurs in many nations.
Transmission of AIDS, HBV or herpesvirus has never been linked to food.
Inactivating viruses in foods:
-Some viruses can persist in foods for more than one week at 23oC and several months at 4oC.
-Heat is the most useful method. Even modest heat (e.g. milk past) will inactivate foreseeable numbers of virus.
Other Foodborne Intoxications
A. Scombroid poisoning; caused by bacterial decarboxylation of histidine to form histamine in fish or fish products. Often due to Morganella spp. But other bacteria can be involved. Histamine formation is favored by low pH and temps above 30oC. Symptoms appear within min or up to 3 h (mean = 1 h), include flushed face, sensation of heat, burning in mouth or throat, general discomfort and diarrhea followed by intense headache which diminishes to a dull ache. Dizziness, itching and faintness may also be experienced. Cooking may not destroy histamine once it has formed in food.
B. Paralytic shellfish poisoning; a syndrome associated with the consumption of toxic clams, mussels, oysters, scallops and cockles. The shellfish become toxic after eating certain species of dinoflagellates from the genus Gonyaulax. In the U.S. G. catenella occurs on the Pacific coast, while the more toxic species, G. tamarensis is found on the Atlantic coast over to northern Europe. A 3rd species, G. acatenella is found off British Columbia. Large blooms of these microbes give rise to the red tide condition on oceans.
The dinoflagellates contain a heat-stable neurotoxin called saxitoxin that causes cardiovascular and respiratory failure in humans. The maximum safe level of saxitoxin is 80 mg/100g. Symptoms appear within 2 h after eating contaminated mollusks and are characterized by tingling, numbness or burning around the mouth which spreads to the face, scalp, neck, fingertips and toes. Vomiting may also occur. There is no known antidote and the mortality rate varies between 1-22%.
Outbreaks occur between May and October on the West Coast and Aug-Oct in the East. Mollusks can be toxic even in the absence of a red tide.