Food-borne Diseases Flashcards

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1
Q

Microbial groups able to cause foodborne diseases:

A

bacteria, fungi, virus, algae and a variety of eukaryotic parasites

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2
Q

Types of foodborne illness

A

Foodborne infections

foodborne intoxications

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3
Q

Food-borne infection

A

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:

        1. salmonellosis
        2. dysentery
        3. cholera
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4
Q

Food-borne intoxication

A
  • 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
    3. botulism
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5
Q

Foodborne illnesses are caused by bacteria because

A
  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
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6
Q

most commonly identified cause of foodborne disease

A

Bacteria.
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).

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7
Q

Types of bacterial toxins:

A

Exotoxins and endotoxins

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8
Q

Types of exotoxins:

A

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)

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9
Q

endotoxin

A

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.

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10
Q

Other Food Problems:

A
  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).
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11
Q

Salmonella

A

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).

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12
Q

3 epidemiological groups of Salmonella:

A
  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.
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13
Q

All salmonella share a common route of infection:

A

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.)

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14
Q

Incidence of Salmonella:

A

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 bacteri

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15
Q

Sources of Salmonella:

A

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.

animal feeds

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16
Q

what is responsible for 70% of all salmonella cases?

A

eggs.

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17
Q

How eggs get infected with salmonella

A

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.

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18
Q

symptoms of Salmonella

A
  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,
and drowsiness.
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

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19
Q

most lethal strain of Salmonella

A

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.

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20
Q

Biology and control of Salmonella

A
  1. optimal growth at 37oC, growth of some serovars has been noted <0.94
  2. Salmonella cannot tolerate 9% NaCl
  3. readily killed at milk pasteurization temperatures (HTST: 161oF [72oC] for 15 s) or by heating foods to an internal temperature of 165oF (74oC)
  4. 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.

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21
Q

Staphylococcus food poisoning

A

Genus of G+ fac. anaerobic bacteria that includes several species able to synthesize heat-resistant enterotoxins that produce the food poisoning.

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22
Q

incidence of staph food poisoning:

A

1-2 million cases in US/year

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23
Q

Most common food vehicle for staph

A

ham

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24
Q

Sources of S. aureus

A

S. aureus and other species of staph are found on the skin and in intestinal tract of humans and animals

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25
Q

The most important sources to foods,

A

nasal carriers and persons with boils or carbuncles that are allowed to handle foods

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26
Q

Five factors which are most commonly associated with staphylococcal (and many other) food poisoning outbreaks

A
  1. Poor personal hygiene.
    1. Inadequate cooking or heating of food.
    2. Preparing foods too far in advance.
    3. Holding food in warmers set at bacterial growth temperatures.
    4. Inadequate refrigeration.
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27
Q

Symptoms of staph food intoxication

A
  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.
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28
Q

Treatment to staph food intoxication

A

involves bed rest and administration of fluids. Humans do not demonstrate any immunity to repeated exposure

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29
Q

Biology and control of S. aureus

A
  1. Staphylococci are hardy 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.

30
Q

Shigella

A

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
31
Q

Sources of Salmonella

A

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.).

32
Q

_________ (the fecal-oral route of transmission) is the most common factor in foodborne shigellosis

A

Poor personal hygiene

33
Q

Shigella pathogenesis

A

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.

34
Q

symptoms of shigella food poisoning

A
  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%).
35
Q

Treatment of shigellosis

A

depends upon the severity of the disease. Severe cases or dysentery require antibiotic therapy, rest and fluid replacement.

36
Q

Biology and control of shigella

A

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.

37
Q

Campylobacter

A

Gram negative, microaerophilic to anaerobic spirally curved rods. C. jejuni subsp. jejuni is by far the most common agent (>99% of human cases).

38
Q

Sources of campylobacter

A
  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.
39
Q

Incidence of campylobacter

A
  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
40
Q

Symptoms of Campylobacter:

A

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

41
Q

pathogenesis of campylobacter

A

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.

42
Q

Biology and control of C. jujuni

A
  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).

43
Q

Clostridium

A

Gram+, anaerobic sporeforming rods. At least four species cause food poisoning in humans: C. botulinum, C. baratti, C. butyricum, and C. perfringens.

44
Q

Botulism

A

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

45
Q

Sources of C. botulinum

A
  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.
46
Q

Incidence of botulism

A

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.

47
Q

Symptoms of botulism

A
  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%
48
Q

Pathogenesis of C. botulinum

A

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.
49
Q

Infant Botulism

A
  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.

50
Q

Treatment of botulism

A
  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

51
Q

Biology and control of C. botulinum:

A
  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.
52
Q

best preventative steps for C. botulinum

A

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

53
Q

C. perfringens food poisoning

A

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.

54
Q

Sources of C. perfringens

A
  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.
55
Q

Incidence of C. perfringens

A

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

56
Q

Symptoms of C. perfringens

A
  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
57
Q

Pathogenesis of C. perfringens

A

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.

58
Q

Biology and Control of C. perfringens

A
  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.

59
Q

Listeria:

A

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).

60
Q

Sources and Incidence of Listeria:

A
  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.
61
Q

Incidence of Listeria

A

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.

62
Q

Listeria symptoms

A
  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:
      -AIDS
-alcoholism
      -diabetes (exp. type 1)
      -cardiovascular disease
      -people with tumors
      -renal transplant patients
      -people on steroid therapy
      -pregnancy
63
Q

When susceptible people contract listeriosis, _____ and _________ are the most common symptoms and the disease may resemble infectious mononucleosis

A

meningitis and sepsis

64
Q

Pathogenic strains of L. monocytogenes all produce

A

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)

65
Q

Treatment to listeriosis

A

Treatment requires antibiotic therapy but this treatment is often not as effective as desired because victims are frequently immunocompromised to begin with.

66
Q

Biology and control of listeria

A
  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
67
Q

Escherichia coli

A

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.

68
Q

CDC now estimates E. coli 0157:H7 causes about

A

20,000 cases of illness and 250 deaths in the U.S. each year.

69
Q

Other E. coli strains

A

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.

70
Q

sources of E. coli

A

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.

71
Q

Biology and control of E. coli

A
  • 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.