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Archive-name: food/preserving/part5
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Rec.Food.Preserving FAQ
FREQUENTLY ASKED QUESTIONS (FAQ) in the newsgroup preserving
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Copyright 1998-2002 by Eric Decker, as a work of literature. Distribution
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Disclaimer: No author represented in this FAQ is qualified to establish
scheduled processes nor is any author a competent processing authority in
the sense of 21 CFR 113.83 et alia.
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Part 5 of 6
13. Spoilage, Especially Botulism
13.1 [Okay, I've got some bad jars. What's growing in them? How can I
dispose of them?]
----
HOME CANNED FOOD SPOILAGE--WHAT WENT WRONG??
0.1 Jars and lids that are not sterile. Food placed in unsterilized jars
or even air contact with non-sterile lids provide a bacteria source that
can ramp up in numbers VERY rapidly. Processing times are deemed for
uncontaminated food and vessels.
-----------------
1. Fresh food was decayed, unwashed, unpeeled or untrimmed. This results
in a high microbial load. A larger than normal number of microorganisms can
take a longer processing time for complete sterilization than is usually
recommended.
2. Food packed too tightly in jars. Temperature in the geometric center
of the jar was not high enough long enough to result in complete
sterilization of the food. Pack food loosely, prepare according to USDA
Guidelines (1/2 inch slices, halves, etc.) then use the recommended time,
pressure, temperature.
3. Jars became un-sterile soon after being filled. If lids are not placed
on jars and processing is not started immediately after jars are filled,
microorganisms may start to grow and reach very high levels prior to
processing.
4. Inaccurate heat-processing time was used; this may occur if old
recommendations are used (food is underprocessed) or if the timing
was interrupted (power failure, pressure fluctuation, etc.)
5. Food was not processed at the correct temperature:
A. Pressure Canner (240F, 115C).
1. Failed to test dial gauge yearly.
2. Failed to exhaust canner 10 min with full steam flow.
3. Failed to make an adjustment for elevation (11 PSIG versus 10 PSIG
in Illinois due to average 1000 above sea level altitude)
4. Failed to keep pressure accurate (high enough).
B. Boiling Water Bath Canner
1. Water was not covering jar tops by 2" or more.
2. Water was not maintained at a rolling boil.
3. Processing time was too short.
4. Failed to make an adjustment for altitude (addition of 2 minutes
for every 1000 ft above sea level).
6. Use of Open Kettle Canning, Microwave Canning, or Oven Canning Methods.
These methods do not get the canned food hot enough long enough to destroy
microorganisms so the food may spoil, may contain dangerous microorganisms
and their toxins, or both.
7. Improper cooling of jars after processing:
A. Failure to remove jars from canner at the end of processing time or
when gauge reads "0". As jars cool, they may suck water (containing microbes
or spores) back into the food.
B. Failure to properly cool jars. Very slow or very rapid cooling may
interfere with formation of a seal.
8. Use of paraffin to seal jelly jars. Paraffin is no longer recommended
for sealing jams, jellies or preserves. Mold, which is the most common
spoiler of sweet spreads, can send "roots" down along the edge of the
paraffin and produce toxic substances into the spread.
9. Improper storage of home-canned foods:
A. Home canned foods which are exposed to temperatures in excess of 95F
may spoil. Sterilization recommendations used for home canning do not
necessarily kill some of the "thermophiles" or heat-loving microorganisms.
These organisms tolerate high temperatures and will grow at high temperatures.
If they are still present, they may grow and spoil the food, or alter the food
so that other microorganisms can grow.
B. Home canned foods which are stored in the sunlight may get very hot
inside--the light goes in, changes to heat as it is absorbed by the food,
allows the air in the headspace to expand breaking open the seal allowing
microorganisms to come in.
C. Keeping very acid foods (pickled or fermented products, some juices)
for a long period of time may give the food acid time to eat away at and
deteriorate the lid resulting in pinholes which allow microorganisms to get
into the jar. Discard any home canned food with damaged or flaking metal on
the lid.
D. Lids on home canned foods stored in a damp place may rust through
allowing microbes to get into the food.
Prepared by Susan Brewer/Foods and Nutrition Specialist/Revised, 1992
EHE-669
----
UNSEALED JARS AND SPOILED FOOD--WHAT TO DO
Occasionally even the most careful home canner has jars which become
unsealed during storage resulting in food spoilage. Exposure to high
temperatures or water during storage may cause the seals to break open or
the lids to rust through allowing microorganisms access to the food inside.
Any time a jar of home-canned food looks suspicious, treat it as though it
were spoiled. Low-acid home-canned foods such as vegetables, meat, poultry
and seafood are a special problem because of their association with botulism,
so spoiled in these food categories should be detoxified before they are
disposed of.
1. Do not taste food from an unsealed jar or any food which appears to be
spoiled. Presence of black discoloration, gas, swelling of the lid,
unnatural odors, spurting liquid and mold growth (blue, white, black or
green) indicate spoilage.
2. Spoiled, low-acid foods (including tomatoes) may have no evidence of
spoilage, so if they are suspect:
A. Swollen but still sealed jars can be put in the garbage (in
a heavy bag) or buried.
B. Unsealed jars should be detoxified.
3. Detoxification:
A. Place containers and lids on their sides in a large pot (8 qt
or more).
B. Wash hands well.
C. Cover containers with water to at least 2" over them.
D. Put lid on pot and bring to a boil.
E. Boil 30 minutes.
F. Cool and discard (in trash bag or bury).
G. Scrub all counters, containers, equipment (including the can
opener), clothing and hands that may have had contact with
the food. Throw away sponges, wash cloths, etc. used in the
clean-up.
ALTERNATE DETOXIFICATION METHODS:
Cover jar and food with chlorine bleach. Let stand 24 hours. Dispose of as
above.
Cover jar and food with a strong lye solution and let stand 24 hours.
Dispose of as above.
NOTE: Do not mix chlorine bleach and lye (sodium hydroxide) together.
[Pick a detox method and stick with it.--LEB].
Prepared by Susan Brewer/Foods and Nutrition Specialist/Revised, 1992
EHE-680
----
13.1.2 [Botulism. What is it?]
The word from the FDA, courtesy of Henry Hilbreath, aka souris..
Food and Drug Administration Foodborne Pathogenic
Microorganisms and Natural Toxins 1992
1. Name of the organism: Clostridium botulinum
Clostridium botulinum is an anaerobic, Gram-positive, spore-forming
rod that produces a potent neurotoxin. The spores are heat-resistant and can
survive in foods that are incorrectly or minimally processed. Seven types (A,
B, C, D, E, F and G) of botulism are recognized, based on the antigenic
specificity of the toxin produced by each strain. Types A, B, E and F cause
human botulism. Types C and D cause most cases of botulism in animals.
Animals most commonly affected are wild fowl and poultry, cattle, horses and
some species of fish. Although type G has been isolated from soil in
Argentina, no outbreaks involving it have been recognized.
Foodborne botulism (as distinct from wound botulism and infant
botulism) is a severe type of food poisoning caused by the ingestion of foods
containing the potent neurotoxin formed during growth of the organism. The
toxin is heat labile and can be destroyed if heated at 80C for 10 minutes or
longer. The incidence of the disease is low, but the disease is of
considerable concern because of its high mortality rate if not treated
immediately and properly. Most of the 10 to 30 outbreaks that are reported
annually in the United States are associated with inadequately processed,
home-canned foods, but occasionally commercially produced foods have been
involved in outbreaks. Sausages, meat products, canned vegetables and seafood
products have been the most frequent vehicles for human botulism.
The organism and its spores are widely distributed in nature. They
occur in both cultivated and forest soils, bottom sediments of streams,
lakes, and coastal waters, and in the intestinal tracts of fish and mammals,
and in the gills and viscera of crabs and other shellfish.
2. Name of the Disease:
Four types of botulism are recognized: foodborne, infant, wound, and a
form of botulism whose classification is as yet undetermined. Certain foods
have been reported as sources of spores in cases of infant botulism and the
undetermined category; wound botulism is not related to foods.
Foodborne botulism is the name of the disease (actually a food-borne
intoxication) caused by the consumption of foods containing the neurotoxin
produced by C. botulinum.
Infant botulism, first recognized in 1976, affects infants under 12
months of age. This type of botulism is thought to be caused by the ingestion
of C. botulinum spores which colonize and produce toxin in the intestinal
tract of infants (toxico infectious botulism). Honey is the only implicated
food source for C. botulinum spores. The number of confirmed infant botulism
cases has increased significantly as a result of greater awareness by health
officials since its recognition in 1976. It is now internationally
recognized, with cases being reported in more countries.
Wound botulism is the rarest form of botulism. The illness results
when C. botulinum by itself or with other microorganisms infects a wound and
produces toxins which reach other parts of the body via the blood stream.
Foods are not involved in this type of botulism.
Undetermined category of botulism involves adult cases in which a specific food
or wound source cannot be identified. It has been suggested
that some cases of botulism assigned to this category might result from
intestinal colonization in adults, with in vivo production of toxin. Reports
in the medical literature suggest the existence of a form of botulism similar
to infant botulism, but occurring in adults. In these cases, the
patients had surgical alterations of the gastrointestinal tract and/or
antibiotic therapy. It is proposed that these procedures may have altered the
normal gut flora and allowed C. botulinum to colonize the intestinal tract.
3. Nature of the Disease:
Infective dose - a very small amount (a few nanograms) of toxin can
cause illness. Onset of symptoms in foodborne botulism is usually 18 to 36 hours
after ingestion of the food containing the toxin, although cases have varied
from 4 hours to 8 days. Early signs of intoxication consist of marked
lassitude, weakness and vertigo, usually followed by double vision and
progressive difficulty in speaking and swallowing. Difficulty in breathing,
weakness of other muscles, abdominal distention, and constipation may also be
common symptoms.
Clinical symptoms of infant botulism consist of constipation that
occurs after a period of normal development. This is followed by poor
feeding, lethargy, weakness, pooled oral secretions, and wail or altered
cry. Loss of head control is striking. Recommended treatment is primarily
supportive care. Antimicrobial therapy is not recommended. Infant botulism
is diagnosed by demonstrating botulinal toxins and the organism in the
infants' stools.
4. Diagnosis of Human Illness:
Although botulism can be diagnosed by clinical symptoms alone,
differentiation from other diseases may be difficult. The most direct and
effective way to confirm the clinical diagnosis of botulism in the laboratory
is to demonstrate the presence of toxin in the serum or feces of the patient
or in the food which the patient consumed. Currently, the most sensitive
and widely used method for detecting toxin is the mouse neutralization test.
This test takes 48 hours. Culturing of specimens takes 5-7 days.
5. Associated Foods:
The types of foods involved in botulism vary according to food
preservation and eating habits in different regions. Any food that is
conducive to outgrowth and toxin production, that when processed allows
spore survival, and is not subsequently heated before consumption can be
associated with botulism. Almost any type of food that is not very acidic
(pH above 4.6) can support growth and toxin production by C. botulinum.
Botulinal toxin has been demonstrated in a considerable variety of foods,
such as canned corn, peppers, green beans, soups, beets, asparagus, mushrooms,
ripe olives, spinach, tuna fish, chicken and chicken livers and liver pate,
and luncheon meats, ham, sausage, stuffed eggplant, lobster, and smoked and
salted fish.
6. Frequency:
The incidence of the disease is low, but the mortality rate is high
if not treated immediately and properly. There are generally between 10 to
30 outbreaks a year in the United States. Some cases of botulism may go
undiagnosed because symptoms are transient or mild, or misdiagnosed as
Guillain-Barre syndrome.
7. The Usual Course of Disease and Complications:
Botulinum toxin causes flaccid paralysis by blocking motor nerve
terminals at the myoneural junction. The flaccid paralysis progresses
symmetrically downward, usually starting with the eyes and face, to the throat,
chest and extremities. When the diaphragm and chest muscles become fully
involved, respiration is inhibited and death from asphyxia results.
Recommended treatment for foodborne botulism includes early administration of
botulinal antitoxin (available from CDC) and intensive supportive care
(including
mechanical breathing assistance).
8. Target Populations:
All people are believed to be susceptible to the foodborne intoxication.
9. Food Analysis
Since botulism is foodborne and results from ingestion of the toxin of
C. botulinum, determination of the source of an outbreak is based on
detection and identification of toxin in the food involved. The most widely
accepted method is the injection of extracts of the food into passively
immunized mice (mouse neutralization test). The test takes 48 hours. This
analysis is followed by culturing all suspect food in an enrichment medium
for the detection and isolation of the causative organism. This test takes
7 days.
10. Recent Outbreaks:
In the last 10 years, two separate outbreaks of botulism have occurred
involving commercially canned salmon. Restaurant foods such as sauteed
onions, chopped bottled garlic, potato salad made from baked potatoes and
baked potatoes themselves have been responsible for a number of outbreaks.
[Root crops, pattern?--LEB] Also, smoked fish, both hot and cold-smoke
(e.g., Kapchunka) have caused outbreaks of type E botulism.
In October and November, 1987, 8 cases of type E botulism occurred, 2
in New York City and 6 in Israel. All 8 patients had consumed Kapchunka, an
uneviscerated, dry-salted, air-dried, whole whitefish. The product was made
in New York City and some of it was transported by individuals to Israel.
All 8 patients with botulism developed symptoms within 36 hours of consuming
the Kapchunka. One female died, 2 required breathing assistance, 3 were
treated therapeutically with antitoxin, and 3 recovered spontaneously. The
Kapchunka involved in this outbreak contained high levels of type E botulinal
toxin despite salt levels that exceeded those sufficient to inhibit C.
botulinum type E outgrowth. One possible explanation was that the fish
contained low salt levels when air-dried at room temperature, became toxic,
and then were re-brined. Regulations were published to prohibit the
processing, distribution and sale of Kapchunka and Kapchunka-type products
in the United States.
Most recently, a bottled chopped garlic-in-oil mix was responsible
for three cases of botulism in Kingston, N.Y. Two men and a woman were
hospitalized with botulism after consuming a chopped garlic-in-oil mix that
had been used in a spread for garlic bread. The bottled chopped garlic relied
solely on refrigeration to ensure safety and did not contain any additional
antibotulinal additives or barriers. The FDA has ordered companies to stop
making the product and to withdraw from the market any garlic-in-oil mix
which does not include microbial inhibitors or acidifying agents and does
not require refrigeration for safety. Since botulism is a life-threatening
disease, FDA always initiates a Class I recall.
The botulism outbreak associated with salted fish mentioned above is reported
in greater detail in Mortality and Morbidity Weekly Report (MMWR) 36(49):
1987 Dec 18. A botulism type B outbreak in Italy associated with eggplant in
oil is reported in MMWR 44(2):1995 Jan 20.
An incident of foodborne botulism in Oklahoma is reported in MMWR 44(11):
1995 Mar 24. [Traced to a 3 day-old pot of beef stew left sitting at room
temperature on the stove burner. Yikes!--LEB]
In the late 1900's a MD in northern Canada was found guilty in the death of a
young woman. Autopsy showed she died of botulism. The doctor misdiagnosed the
problem and the patient died a couple of days later. Botulism is sneaky, deadly
and not seem much anymore. Be VERY careful in your canning as the doctor
treating you or your family just might make an error based on a lack of
experience with said toxin. - ED.
mow@vm.cfsan.fda.gov
----
Botulism poisoning is due to ingesting toxin(s) produced by the anaerobic
bacterium _Clostridium botulinum_. There are seven isoforms of botulism
toxins (Types A-G). Botulism toxins are colorless, odorless, and
tasteless, but highly potent neurotoxins. To explain the physiology of
the toxin a little farther, you might remember that nerve impulses are
electrical signals (charge gradient that runs along the length of an axon),
while the connection between muscles and nerves are mediated by chemical
signals. The end of an axon releases synaptic vesicles filled with
chemical neurotransmitters. These synaptic vesicles travel a short
distance to the synaptic plate on muscle cells, then bind and release
neurotransmitters. Current research indicates that botulism toxins bind
and cleave several proteins on the outside of synaptic vesicles. Those
vesicles cannot then bind to the next synaptic plate and unload the
neurotransmitter. Thus, the connection between nerve and muscle
impulses is cut biochemically, at the place where the chemical signal is
delivered. Muscle control is lost, especially fine facial muscles.
Symptoms of botulism toxin poisoning usually occur within 12-36 hrs after
ingestion. They include muscle weakness, slurred speech, blurred vision
(all fine muscle movements); followed by an inability to hold up the head.
Death occurs by respiratory failure.
If you recognize these symptoms after trying a canned food, call 911
immediately. Whoever is able should reclose the jar, wrap well, put in
a ziploc bag, close, bring to the hospital. Wash your hands carefully
after this procedure! [Other food poisoning symptoms are listed below in
question IV.5--LEB]
Treatment for botulism is straightforward. Often the antisera to the
toxin is given, and the victim is placed on a respirator. Survival
depends on the amount of toxin ingested, and how quickly the victim got
treatment. Recovery is quite slow, taking months. The United States
case/fatality rate has dropped in recent years, but the *number of cases*
in the US increases slightly in proportion to the popularity of home
canning. Interesting cultural comparison: botulism cases in Europe tend
to come from cured meats, from Japan from salted fish, from the US from
canned vegetables.
13.1.3 [I'm confused about when the toxin is produced. Tell me more about
the bacterium.]
There are three varieties of _C. botulinum_; 2 of these varieties (A, C)
live and grow in soil under anaerobic (without oxygen) conditions, while 1
variety (E) can be found in fresh and saltwater, also under anaerobic
conditions.
Under aerobic (oxygen) conditions, all varieties of _C. botulinum_ encyst,
producing a spore. Under normal *aerobic* conditions, both oxygen and your
immune system take care of the few dormant spores that you meet in everyday
life. NOTE: This is the dormant spore, *not* the bacterium. The bacterium
is what you could find in a badly processed can. However, while the
encysted, dormant form does *not* produce the toxin (only the bacterium does),
the _C. botulinum_ spore is much more resistant to extreme conditions than
the bacterium, making it harder to kill.
Deadly problems can occur in situations where you attempt to preserve food by
creating an *anerobic* state; namely, when you create a vacuum seal using
heat and a 2-piece lid, sometimes when you preserve food in oil, or when you
smoke meat. In each of those situations, the _C. botulinum_ spores can
develop ("hatch" is a good way of thinking of it) into the bacterium, which
then produce the toxin in your canned goods, oil, or on your smoked meat.
For this reason, _C. botulinum_ spores in canned/smoked food must be killed
or must be kept dormant. You, as a food preserver, using good common sense
and a bag of tricks can accomplish this.
13.3.4 [How can I be absolutely, positively sure that those spores are killed?]
You know, I think someone could make a mint by inventing the "home botulism
test kit" that would work in the same way that a home pregnancy test kit
does. But we don't, so...
Remember, that despite the bacterium's fearsome reputation, _C. botulinum_
is still a microbe, and can be killed using a little basic microbiology.
Preserving recipes utilize at least one of these 5 microbiological facts,
good recipes often use several.
1. _C. botulinum_ bacterium dies at 212 F/ 100 C.
2. _C. botulinum_ spores die at 240 F/ 116 C.
3. Botulism toxin denatures at 185 F/ 85 C.
**(All temperatures must be maintained for least 15 minutes, and
the heat must be consistent throughout the food, fluid, and jar.)**
4. _C. botulinum_ spores cannot hatch in strong acid solutions
of pH 4.6 or below. (Some sources claim pH 4.7.)
5. _C. botulinum_ cannot grow, develop, or multiply in food
with a water content of less than 35%. (Food dehydrators have another
set of toxic pests to worry about, see IV.6 about aflatoxin.)
Common sense is a first step in the prevention of botulism.
For instance: 1.) _C. botulinum_ bacteria and spores usually live in soil.
Thus clean foods of soil, dust, grit, etc, using fresh, cold water. Change
wash water often. Don't can "drops", fruit that has dropped to the ground.
Pay special attention to cleaning root crops (including garlic!), shucking
skins or peeling that produce if need be.
2.) One variety of _C. botulinum_ (E) lives in flat water. So, you want to
make your brines, etc, with fresh cold water. Start with fresh, cold water
if you are boiling to sterilize, or perform other operations.
3.) Botulism spores remain dormant under high acid conditions. Fruit is
quite high in acid but also contains a lot of sugar, so the fruit still
tastes sweet. Vinegar is added to vegetables to pickle them. You can can
foods like this in a boiling waterbath. However, the concentration of acid
(ionic strength) is also very important, so you want to use vinegars of a
known strength (5% or 5 grain); add the recommended amount of vinegar, citric
acid, or ascorbic acid described in your recipe; can just-ripe fruits. For
safety's sake, you shouldn't cut down the amount of vinegar in a recipe, take
a cue from fruit and add a little bit of sugar to cut down the extreme acid
taste. Vegetable pickles should be immersed in the vinegar or brine. *BTW,
finding out that honey is a source of botulism spores (infant botulism),
means that I'm not thrilled about the idea of substituting honey for sugar,
as the Rodale Institute appears to be.*
4.) Botulism spores, bacterium, and the toxin are killed by high heat.
However, all the contents of the jar has to get to the target temperature,
no matter the volume, and the temperature should be sustained for about 15
minutes. Follow recipes exactly, including jar sizes and treatment of the
jars. Process at least for the times indicated, but remember that you have
to increase processing time or pressures depending on your altitude. (Water
boils at lower temperatures the higher your altitude.) Note that larger
size jars usually require longer processing time, because the heat has to
penetrate through the jar.
Acid and heat are each used in canning things that are borderline acid, such
as tomatoes, tomato vegetable mixes (like salsa and spaghetti sauce),
vegetable relishes, and other vegetable mixes. The idea here is that you
can't increase one thing to avoid other procedures. (You can't increase acid
to avoid pressure canning).
5.) Botulism cannot grow or develop without water.
In making jams or jellies, enough sugar and pectin is added to form a gel,
depressing the amount of free water available for bacteria to grow. This
is one of the reasons why special care has to be taken if the jam or jelly
is extremely runny.
Foods preserved in oil (raw garlic, chilis, dried tomatoes) create a special
case. Oil contains no water, as it is centrifuged out during processing.
If an item is dependably dry, under 35% water content, adding it to the oil
should not cause problems, as long as your items are well immersed (1 inch
of oil covering). Dry herbs, seeds and spices, dried chiles, even sundried
tomatoes should not cause problems. (N.B: Research from the Australian
Extension Service--sundried tomatoes are more acid than hydrated ones: pH
4.0 for dried, 4.6 for hydrated--LEB). However, the dehydrated food must be
properly dried, conditioned, and not case hardened (case hardened things are
hard and crunchy on the outside, soft and gooey on the inside). The jury is
out on wet herbs.
If you try to preserve a lot of "wet" items in oil (garlic cloves, chopped
onions, ginger root, fresh chiles), you might have a heap of trouble. Oil
doesn't contain much dissolved oxygen, so it is a good anaerobic medium.
Raw garlic, onions, ginger are all rootcrops, and each contain over 35%
water. Chilies often are added to oil in a non-dried state. Generally, you
want to "pickle", or at least allow your wet, raw item to take up some 5%
vinegar for about 15-20 minutes before putting into the oil. Chunky items
(i.e. garlic cloves) should be smashed, crushed, or chopped to get the
vinegar into the item.
Simple, but through, sauteing of your chosen flavoring in your oil can also
get rid of spores, since they evaporate free water, and the oil can be heated
to above 240 F. Yet another idea is to refrigerate your flavored oils, as
bacterial growth is very slow below 40 F/4 C.
In addition, the garlic-in-oil botulism problem began when garlic pastes in
olive oil were introduced in grocery stores. Many of the botulism
poisonings occurred when these pastes were used in cold pasta, salads, and
salad dressings. If you are going to be using your flavored oil for sauteing,
stir fry, or deep fat frying you will easily heat your oil to above any of
the target temperatures described above.
Since the toxin is denatured at 185 F/85 C, if you are concerned about a
canned good the usual procedure is as described in the above section (to
hard boil the contents for 15 minutes). NOTE: This will denature the
botulism toxin. Other toxins, such as those caused by _Staphococcus_, will
not denature until temps of 240 F/116 C are reached and sustained for 30
minutes. As a matter of fact, a hard boil in that case will break open the
bacteria, and more toxin would be released into the food.
13.1.5 [I don't feel so good. What do I have/had/will have?]
This is a generalized list of food poisoning symptoms pulled from the Bad
Bug Book on the FDA site: http://vm.cfsan.fda.gov/~mov/app2.html.
[If you are actually in the throes of food poisoning, do not use this as a
substitute for a doctor's diagnosis and care. I merely list this as a
subject useful to food preserver--LEB.]
Associated
Onset time Predominant organism
to symptoms symptoms or toxin
__________________________________________________________________________
Upper gastrointestinal tract symptoms (nausea, vomiting) occur first or
predominate:
Less than 1 h Nausea, vomiting, unusual Metallic salts
taste burning of mouth.
1-2 h Nausea, vomiting, cyanosis, Nitrites
headache, dizziness, dyspnea,
trembling, weakness, loss of
consciousness.
1-6 h, mean Nausea, vomiting, retching, Staphylococcus
aureus
2-4 h diarrhea, abdominal pain, and its enterotoxins
prostration.
8-16 h Vomiting, abdominal cramps, Bacillus cereus
(2-4 h emesis diarrhea, nausea.
possible)
6-24 h Nausea, vomiting, diarrhea, Amanita species
thirst, dilation of pupils, mushrooms
collapse, coma.
Sore throat and respiratory symptoms occur:
12-72 h Sore throat, fever, nausea, Streptococcus
pyogenes
vomiting, rhinorrhea, sometimes
a rash.
2-5 days Inflamed throat and nose, Corynebacterium
spreading grayish exudate, diphtheriae
fever, chills, sore throat,
malaise, difficulty in swallowing,
edema of cervical lymph node.
______________
Lower gastrointestinal tract symptoms (abdominal cramps, diarrhea) occur
first or predominate:
2-36 h, mean Abdominal cramps, diarrhea, Clostridium perfringens,
6-12 h putrefactive diarrhea Bacillus cereus,
associated with C. perfringens, Streptococcus faecalis,
sometimes nausea and vomiting. S. faecium
12-74 h, mean Abdominal cramps, diarrhea, Salmonella species
18-36 h vomiting, fever, chills, (including S. arizonae),
malaise, nausea, headache, Shigella, enteropatho-
possible. Sometimes bloody genic Escherichia coli,
or mucoid diarrhea, cutaneous other Enterobacteriacae,
lesions associated with V. Vibrio parahaemolyticus,
vulnificus. Yersinia Yersinia enterocoliticia,
enterocoliticia mimics Pseudomonas aeruginosa
flu and acute appendicitis. (?),Aeromonas hydrophila,
Plesiomonas shigelloides,
Campylobacter jejuni,
Vibriocholerae (Ol and
non-Ol) V.vulnificus, V.
fluvialis
3-5 days Diarrhea, fever, vomiting Enteric viruses
abdominal pain, respiratory
symptoms.
1-6 weeks Mucoid diarrhea (fatty stools) Giardia lamblia
abdominal pain, weight loss.
1 to several Abdominal pain, diarrhea, Entamoeba histolytica weeks,
constipation, headache, drowsiness, ulcers, variable --
often asymptomatic.
3-6 months Nervousness, insomnia, hunger Taenia saginata,
pains, anorexia, weight loss, T. solium
abdominal pain, sometimes
gastroenteritis.
....---....
Neurological symptoms (visual disturbances, vertigo, tingling,
paralysis)
occur:
Less than l h *** SEE GASTROINTESTINAL AND/OR Shellfish toxin
NEUROLOGIC SYMPTOMS (Shellfish Toxins)
(this Appendix)
Gastroenteritis, nervousness, Organic phosphate
blurred vision, chest pain,
cyanosis, twitching, convulsions.
Excessive salivation, perspir- Muscaria-type
ation, gastroenteritis, mushrooms
irregular pulse, pupils
constricted, asthmatic breathing.
Tingling and numbness, Tetradon (tetrodotoxin)
dizziness, pallor, gastro- toxins
hemmorrhage, and desquamation
of skin, fixed eyes, loss of
reflexes, twitching, paralysis.
1-6 h Tingling and numbness, gastro- Ciguatera toxin
enteritis, dizziness, dry mouth,
muscular aches, dilated pupils,
blurred vision, paralysis.
Nausea, vomiting, tingling, Chlorinated hydrocarbons
dizziness, weakness, anorexia,
weight loss, confusion.
2 h to 6 days, Vertigo, double or blurred Clostridium botulinum
usually vision, loss of reflex to and its neurotoxins
12-36 h light, difficulty in swallowing.
speaking, and breathing, dry
mouth, weakness, respiratory
paralysis.
More than 72 h Numbness, weakness of legs, Organic mercury
spastic paralysis, impairment
of vision, blindness, coma.
Gastroenteritis, leg pain, Triorthocresyl
ungainly high-stepping gait, phosphate
foot and wrist drop.
______________
Allergic symptoms (facial flushing, itching) occur:
Less than 1 h Headache, dizziness, nausea, Histamine
(scombroid)
vomiting, peppery taste, burning
of throat, facial swelling and
flushing, stomach pain, itching
of skin.
Numbness around mouth, tingling Monosodium glutamate
sensation, flushing, dizziness,
headache, nausea.
Flushing, sensation of warmth, Nicotinic acid
itching, abdominal pain, puffing
of face and knees.
_____________
Generalized infection symptoms (fever, chills, malaise, prostration, aches,
swollen lymph nodes) occur:
4-28 days, mean Gastroenteritis, fever, edema Trichinella spiralis
9 days about eyes, perspiration,
muscular pain, chills,
prostration, labored breathing.
7-28 days, mean Malaise, headache, fever, cough, Salmonella typhi
14 days nausea, vomiting, constipation,
abdominal pain, chills, rose
spots, bloody stools.
10-13 days Fever, headache, myalgia, rash. Toxoplasma gondii
0-50 days, Fever, malaise, lassitude, Etiological agent not
mean 25-30 anorexia, nausea, abdominal yet isolated -- probably
days pain, jaundice. viral
Varying periods Fever, chills, head- or joint Bacillus anthracis,
(depends on ache, prostration, malaise, Brucella melitensis, B.
specific swollen lymph nodes, and other abortus, B. suis, Coxi-
illness) specific symptoms of disease ella burnetii, Franci-
in question. sella tularensis,
Listeria monocytogenes,
Mycobacterium tubercu-
losis, Mycobacterium
species, Pasteurella
multocida, Strepto-
bacillus moniliformis,
Campylobacter jejuni,
Leptospira species.
Gastrointestinal and/or Neurologic Symptoms - (Shellfish Toxins):
0.5 to 2 h Tingling, burning, numbness, Paralytic Shellfish
drowsiness, incoherent speech, Poisoning (PSP)
respiratory paralysis. (saxitoxins)
2 - 5 min to Reversal of hot and cold Neurotoxic Shellfish
3 - 4 h sensation, tingling; numbness Poisoning (NSP)
of lips, tongue & throat; muscle (brevetoxins)
aches, dizziness, diarrhea,
vomiting.
30 min to Nausea, vomiting, diarrhea, Diarrheic Shellfish
2 - 3 h abdominal pain, chills, fever Poisoning (DSP)
(dinophysis toxin,
okadaic acid, pecteno-
toxin, yessotoxin)
24 h (gastroin- Vomiting, diarrhea, abdominal Amnesic Shellfish
testinal) to pain, confusion, memory loss, Poisoning (ASP)
48 h disorientation, seizure, coma (domoic acid)
(neurologic)
_________________________________________________________________
Text last edited: 21 Jan 92
Hypertext last edited: 26 Jul 94mow@vm.cfsan.fda.gov
13.1.6 [Aflatoxin. What is it?]
Food dehydrators have another set of toxic pests to worry about. While
bacteria need free water to reproduce, molds can grow and spread, and de-
velop their toxins under much drier conditions. The most famous mold is
that of ergot, which when ingested causes hallucinations. The molds of
most concern here are those of _Aspergillus_, which produces aflatoxin.
The Bad Bug MO of aflatoxin is listed below.
Aflatoxins
U S Food & Drug Administration Center for Food Safety & Applied
Nutrition Foodborne Pathogenic Microorganisms and Natural Toxins 1992
(Bad Bug Book)
1. Name of Toxin: Aflatoxins
2. Name of Acute Disease: Aflatoxicosis
Aflatoxicosis is poisoning that results from ingestion of aflatoxins in
contaminated food or feed. The aflatoxins are a group of structurally re-
lated toxic compounds produced by certain strains of the fungi _Aspergillus
flavus_ and _A. parasiticus_. Under favorable conditions of temperature and
humidity, these fungi grow on certain foods and feeds, resulting in the
production of aflatoxins. The most pronounced contamination has been encoun-
tered in tree nuts, peanuts, and other oilseeds, including corn and cotton-
seed.
2. Aflatoxins:
The major aflatoxins of concern are designated B1, B2, G1, and G2. These
toxins are usually found together in various foods and feeds in various pro-
portions; however, aflatoxin B1 is usually predominant and is the most toxic.
When a commodity is analyzed by thin-layer chromatography, the aflatoxins
separate into the individual components in the order given above; however,
the first two fluoresce blue when viewed under ultraviolet light and the
second two fluoresce green. [Could a black light be useful to monitor dried
items?--LEB]. Aflatoxin M a major metabolic product of aflatoxin B1 in
animals and is usually excreted in the milk and urine of dairy cattle and
other mammalian species that have consumed aflatoxin-contaminated food or
feed.
3. Nature of Disease:
Aflatoxins produce acute necrosis, cirrhosis, and carcinoma of the liver in
a number of animal species; no animal species is resistant to the acute
toxic effects of aflatoxins; hence it is logical to assume that humans may
be similarly affected. A wide variation in LD50 values has been obtained in
animal species tested with single doses of aflatoxins. For most species, the
LD50 value ranges from 0.5 to 10 mg/kg body weight. Animal species respond
differently in their susceptibility to the chronic and acute toxicity of
aflatoxins. The toxicity can be influenced by environmental factors, expo-
sure level, and duration of exposure, general health, and nutritional status
of diet.
Aflatoxin B1 is a very potent carcinogen in many species, including nonhuman
primates, birds, fish, and rodents. In each species, the liver is the primary
target organ of acute injury. Metabolism plays a major role in determining
the toxicity of aflatoxin B1; studies show that this aflatoxin requires meta-
bolic activation to exert its carcinogenic effect, and these effects can be
modified by induction or inhibition of the mixed function oxidase system.
4. Normal Course of Disease:
In well-developed countries, aflatoxin contamination rarely occurs in foods
at levels that cause acute aflatoxicosis in humans. In view of this, studies
on human toxicity from ingestion of aflatoxins have focused on their carcin-
ogenic potential. Therelative susceptibility of humans to aflatoxins is not
known, even though epidemiological studies in Africa and Southeast Asia,
where there is a high incidence of hepatoma, have revealed an association
between cancer incidence and the aflatoxin content of the diet. These studies
have not proved a cause-effect relationship, but the evidence suggests an
association.
One of the most important accounts of aflatoxicosis in humans occurred in
more than 150 villages in adjacent districts of two neighboring states in
northwest India in the fall of 1974. According to one report of this out-
break, 397 persons were affected and 108 persons died. In this outbreak,
contaminated corn was the major dietary constituent, and aflatoxin levels of
0.25 to15 mg/kg were found. The daily aflatoxin B1 intake was estimated to
have been at least 55 ug/kg body weight for an undetermined number of days.
The patients experienced high fever, rapid progressive jaundice, edema of the
limbs, pain, vomiting, and swollen livers. One investigator reported a pe-
culiar and very notable feature of the outbreak: the appearance of signs of
disease in one village population was preceded by a similar disease in domes-
tic dogs, which was usually fatal. Histopathological examination of humans
showed extensive bile duct proliferation and periportal fibrosis of the
liver together with gastrointestinal hemorrhages. A 10-year follow-up of the
Indian outbreak found the survivors fully recovered with no ill effects from
the experience.
A second outbreak of aflatoxicosis was reported from Kenya in 1982. There
were 20 hospital admissions with a 60% mortality; daily aflatoxin intake was
estimated to be at least 38 ug/kg bodyweight for an undetermined number of
days.
In a deliberate suicide attempt, a laboratory worker ingested 12 ug/kg body
weight of aflatoxin B1 per day over a 2-day period and 6 months later, 11
ug/kg body weight per day over a 14-day period. Except for transient rash,
nausea and headache, there were no ill effects; hence, these levels may
serve as possible control levels for aflatoxin B1 in humans. In a 14-year
follow-up, a physical examination and blood chemistry, including tests for
liver function, were normal.
5. Diagnosis of Human Illnesses:
Aflatoxicosis in humans has rarely been reported; however, such cases are
not always recognized. Aflatoxicosis may be suspected when a disease out-
break exhibits the following characteristics:
- the cause is not readily identifiable
- the condition is not transmissible
- syndromes may be associated with certain batches of food
- treatment with antibiotics or other drugs has little effect
- the outbreak may be seasonal, i.e., weather conditions may
affect mold growth.
The adverse effects of aflatoxins in animals (and presumably in humans) have
been categorized into two general forms.
A. (Primary) Acute aflatoxicosis is produced when moderate to high
levels of aflatoxins are consumed. Specific, acute episodes of disease ensue
may include hemorrhage, acute liver damage, edema, alteration in digestion,
absorption and/or metabolism of nutrients, and possibly death.
B. (Primary) Chronic aflatoxicosis results from ingestion of low to
moderate levels of aflatoxins. The effects are usually subclinical and dif-
ficult to recognize. Some of the common symptoms are impaired food conver-
sion and slower rates of growth with or without the production of an overt
aflatoxin syndrome.
6. Associated Foods:
In the United States, aflatoxins have been identified in corn and corn pro-
ducts, peanuts and peanut products, cottonseed, milk, and tree nuts such as
Brazil nuts, pecans, pistachio nuts, and walnuts. Other grains and nuts are
susceptible but less prone to contamination.
7. Relative Frequency of Disease:
The relative frequency of aflatoxicosis in humans in the United States is
not known. No outbreaks have been reported in humans. Sporadic cases have
been reported in animals.
8. Target Populations:
Although humans and animals are susceptible to the effects of acute afla-
toxicosis, the chances of human exposure to acute levels of aflatoxin is
remote in well-developed countries. In un-developed countries, human sus-
ceptibility can vary with age, health, and level and duration of exposure.
9. Analysis of Foods:
Many chemical procedures have been developed to identify and measure afla-
toxins in various commodities. The basic steps include extraction, lipid
removal, cleanup, separation and quantification. Depending on the nature of
the commodity, methods can sometimes be simplified by omitting unnecessary
steps. Chemical methods have been developed for peanuts, corn, cottonseed,
various tree nuts, and animal feeds. Chemical methods for aflatoxin in milk
and dairy products are far more sensitive than for the above commodities
because the aflatoxin M animal metabolite is usually found at much lower
levels (ppb and ppt). All collaboratively studied methods for aflatoxin anal-
ysis are described in Chapter 26 of the AOAC Official Methods of Analysis.
10. History of Recent Outbreaks:
Very little information is available on outbreaks of aflatoxicosis in humans
because medical services are less developed in the areas of the world where
high levels of contamination of aflatoxins occur in foods, and, therefore,
many cases go unnoticed.
Text last edited: 21 Jan 92
Hypertext last edited: 19 Apr 95 mow@vm.cfsan.fda.gov
(end of part 5)
User Contributions:Comment about this article, ask questions, or add new information about this topic: |
Throughout history, we can see how we have been strategically conditioned to come to this point where we are on the verge of a cashless society. Did you know that Jesus foretold of this event almost 2,000 years ago?
In Revelation 13:16-18, we read,
"He (the false prophet who deceives many by his miracles--Revelation 19:20) causes all, both small and great, rich and poor, free and slave, to receive a mark on their right hand or on their foreheads, and that no one may buy or sell except one who has the mark or the name of the beast, or the number of his name.
Here is wisdom. Let him who has understanding calculate the number of the beast, for it is the number of a man: His number is 666."
Speaking to the last generation, this could only be speaking of a cashless society. Why? Revelation 13:17 tells us that we cannot buy or sell unless we receive the mark of the beast. If physical money was still in use, we could buy or sell with one another without receiving the mark. This would contradict scripture that states we need the mark to buy or sell!
These verses could not be referring to something purely spiritual as scripture references two physical locations (our right hand or forehead) stating the mark will be on one "OR" the other. If this mark was purely spiritual, it would indicate both places, or one--not one OR the other!
This is where it really starts to come together. It is amazing how accurate the Bible is concerning the implantable RFID microchip. Here is information from someone named Carl Sanders who worked with a team of engineers to help develop this RFID chip:
"Carl Sanders sat in seventeen New World Order meetings with heads-of-state officials such as Henry Kissinger and Bob Gates of the C.I.A. to discuss plans on how to bring about this one-world system. The government commissioned Carl Sanders to design a microchip for identifying and controlling the peoples of the world—a microchip that could be inserted under the skin with a hypodermic needle (a quick, convenient method that would be gradually accepted by society).
Carl Sanders, with a team of engineers behind him, with U.S. grant monies supplied by tax dollars, took on this project and designed a microchip that is powered by a lithium battery, rechargeable through the temperature changes in our skin. Without the knowledge of the Bible (Brother Sanders was not a Christian at the time), these engineers spent one-and-a-half-million dollars doing research on the best and most convenient place to have the microchip inserted.
Guess what? These researchers found that the forehead and the back of the hand (the two places the Bible says the mark will go) are not just the most convenient places, but are also the only viable places for rapid, consistent temperature changes in the skin to recharge the lithium battery. The microchip is approximately seven millimeters in length, .75 millimeters in diameter, about the size of a grain of rice. It is capable of storing pages upon pages of information about you. All your general history, work history, criminal record, health history, and financial data can be stored on this chip.
Brother Sanders believes that this microchip, which he regretfully helped design, is the “mark” spoken about in Revelation 13:16–18. The original Greek word for “mark” is “charagma,” which means a “scratch or etching.” It is also interesting to note that the number 666 is actually a word in the original Greek. The word is “chi xi stigma,” with the last part, “stigma,” also meaning “to stick or prick.” Carl believes this is referring to a hypodermic needle when they poke into the skin to inject the microchip."
Mr. Sanders asked a doctor what would happen if the lithium contained within the RFID microchip leaked into the body. The doctor replied by saying a terrible sore woul (...)