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Latest Changes - All Parts
See the differences
file for a complete, chronologically ordered sequence of changes.
IV. Spoilage & Toxins, Especially Botulism (Part 8)
A. Home Canned Food Spoilage--What went wrong???A.1.1 I've got some bad jars. What did I do wrong?
Prepared by Susan Brewer/Foods and Nutrition Specialist/Revised, 1992
EHE-669
A.1.2 I have some unsealed jars and spoiled food--What do I 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.
B.1 Detoxification Method 1
B.2 Detoxification Method 2
Cover jar and food with chlorine bleach. Let stand 24 hours. Dispose of as above.
B.3 Detoxification Method 3
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
The word from the FDA, courtesy of Henry Hilbreath, aka souris. Besides what's discussed here, there is another discussion of many of these topics that is a little more up to date availble from the Colorado State University at http://www.ext.colostate.edu/pubs/foodnut/09305.html
Food and Drug Administration Foodborne Pathogenic Microorganisms and Natural Toxins 1992
_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. [Botulism is derived from the German word for sausage. :)]
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.
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.
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.
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.
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.
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.
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).
All people are believed to be susceptible to the foodborne intoxication.
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.
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.
Documented examples include:
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 G. --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.
D. 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.
E. 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.
Common sense is a first step in the prevention of botulism.
For instance:
[JTE on 7/10/2003 has added this paragraph based on recent USDA research which can be found at http://www.uga.edu/nchfp/questions/FAQ_canning.html#31]
Herbs, garlic and the like as well as oils are low-acid and together could support the growth of the
disease-causing Clostridium botulinum bacteria. Oils may be flavored with these items if they are made up
for fresh use, stored in the refrigerator and used within 2 to 3 days. There are no canning recommendations.
Fresh herbs must be washed well and dried completely before storing in the oil. The very best sanitation
and personal hygiene practices must be used. Pesto is an uncooked seasoning mixture of herbs, usually
including fresh basil and garlic, and some oil. It may be frozen for long term storage; there are no home
canning recommendations.
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.
F. 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://www.cfsan.fda.gov/~mow/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 94 mowNOSPAM@vm.cfsan.fda.govG. 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 develop 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/Aflatoxicosis
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 related 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 encountered in tree nuts, peanuts, and other oilseeds, including corn and cottonseed.
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 proportions; 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, exposure 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 metabolic 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 carcinogenic potential. The relative 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 outbreak, 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 peculiar and very notable feature of the outbreak: the appearance of signs of disease in one village population was preceded by a similar disease in domestic 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 outbreak 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.
6. Associated Foods:
In the United States, aflatoxins have been identified in corn and corn products, 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 aflatoxicosis, the chances
of human exposure to acute levels of aflatoxin is remote in well-developed countries. In
un-developed countries, human susceptibility 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 aflatoxins 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 analysis 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
mowNOSPAM@vm.cfsan.fda.gov