FOODBORNE
DISEASE
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:
1. salmonellosis
2. dysentery
3. cholera
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
3. botulism
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.)
Incidence:
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.
Sources:
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,
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.
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.
Sources:
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.
Symptoms:
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 childrenÕs deaths each year:
S.
dysentariae causes dysentery
S.
flexneris, S. boydii, and S. sonnei
cause foodborne shigellosis
Sources:
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.
Symptoms:
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).
Sources:
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.
Incidence:
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.
Symptoms:
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
Sources:
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.
Incidence:
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.
Symptoms:
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.
Infant botulism
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.
Treatment:
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.
Sources:
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.
Incidence:
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.
Symptoms:
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.
Symptoms:
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
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.
Sources:
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 arenÕt 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).
Biology
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 (³105) 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) isnÕt 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.
Diarrheal symdrome:
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.
Emitic syndrome:
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 ÒcomplicationÓ 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
PARASITES
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
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 Òpoisonous or deleterious substance which may render it injurious to healthÓ
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 arenÕt prod
at that temp. so just trim ½ inch (1.3 cm) below growth to avoid fungal
metabolites.
-donÕt
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
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.