We have already studied about the food borne diseases and their classification.
Food borne intoxications are basically food borne illness caused due to
ingestion of toxin produced my microorganisms (mycotoxins, bacterial toxins).
Natural toxins present in food may also result in food poisoning in humans.
Food poisoning is also caused by consuming old, used, residual, fermented,
spoiled, contaminated, toxic and bacteria infested food.
and legumes contain a number of toxic substances such as protease inhibitors,
lathyrogens, and flavism causing agents, cyanogens, haemaglutinins and
paponins which are discussed below:
acid. It thus interferes with the normal growth of animals fed with such
glycoside by the enzyme α-glucosidase, hydrogen cyanide is liberated. A
cyanides content of 10-20 mg per 10 gm of pulses is considered safe. Many
legumes excepting limabean (Phaseolus lunatus) contains cyanide within
soyabean, swordbean and jackbean. Toxic saponins cause nausea and
vomiting and can be removed by soaking the beans prior to cooking.
state of iodine deficiency in the thyroid and eventually goitre.
associated with consumption of kesari dal regularly as high as 300g daily.
In lathyrism, the toxic substances interfere with formation of normal
collagen fibers in the connective tissue.
broadbeans or by inhaling pollen of its flowers. Flavism is hemolytic
anemia. In several cases, death may occur within 24-48 hours of the onset of
poisoning in certain individuals.
vegetables e.g. protease inhibitor in cereals and potatoes, saponins in
spinach and asparagus and goitrogens in rapeseed mustard, cabbage and
related species. Goitrogens cause hypothyroidism and thyroid enlargement
adverse responses when eaten. Some algae like Gymnodinium and
Gonyaulax are toxic. Heating does not destroy these substances.
ingestion of fish or shellfish that have fed upon algae toxic to human beings.
Paralytic shellfish poisoning is caused by ingestion of shellfish such as
scallops, clams and mussels which have consumed toxic dinoflagellates.
distress, parasthesia of the lips and fingertips followed by ataxia, muscular
uncoordination and ascending paralysis. Death may occur within 2 to 12
hours from cardiovascular collapse or respiratory failure. The human lethal
dose of toxin is considered to be 3 to 4 mg.
most of the toxic factors in them. Heat causes denaturation of the proteins
responsible for trypsin inhibition and haemagglutination and of the enzyme
causing hydrolysis of cyanogenic glycosides. Fermentation also destroys toxic
factors and yield more digestible products of high nutritive value.
the production, spoilage and safety of food. Molds have not only served to
synthesize antibiotics but also to produce some foods. Fermented foods such as
some cheese, soy sauce, miso, tempeh and other oriental delicacies are prepared
with the help of molds.
elaborate the toxin in large macroscopic fruiting bodies; for example, the toxin
produced by certain species of Amanita, a poisonous mushroom. Other fungi
always grow and sporulate as parasites on living host plants, and sometimes
will do so only on a specific host.
fungi and it produces mycotoxins. In contrast to fungi that are parasitic on
living plants another group of fungi is saprophytic and causes destruction of
dead plants and animal material.
molds in atmosphere and are found to inhabit stored grain and dried products
and hence have been referred to as “storage fungi”. These molds include
Cladosporium, Fusarium, Penicillium, Aspergillus and Alternaria.
causes illness or death when ingested by man or animals. The primary
metabolites are those that are essential for growth whereas secondary
metabolites are formed during the end of the exponential growth phase and
have no apparent significance to the producing organism relative to growth.
mycotoxins commonly encountered in food are around one million times less
toxic than most lethal of the botulism toxin. But long term chronic toxicity is of
special concern because several of the mold metabolites are carcinogenic and
influence the immune response of a number of animal species. The syndrome
resulting from ingestion of toxin in a mold contaminated food is referred to as
considerable suffering and mortality. They were alimentary toxic aleukia
(ATA) in Russia, caused by consumption of corn contaminated with T-2 toxin
produced by Fusarium sporotrichoides and yellow rice disease in Japan,
associated with Penicillium islandicum.
aflatoxicosis caused by consumption of corn contaminated with Aspergillus
flavus were reported from India involving approximately 1000 people of whom
nearly 100 died.
tremorgens are associated with animal feeds and forages which affect the
quality of meat and other animal products. It is also seen that mycotoxins
present in animal feed get into human foods because they pass through the food
chain in either their original or metabolized form.
mold growth. Many mycotoxigenic species are able to produce several
mycotoxins. It is likely, therefore, that contaminated foods will contain a
cocktail of toxins that can interact synergistically.
Some major mycotoxins found in foods
existence dates from 1960, when more than 100,000 turkey died in England
after eating peanut meal imported from Africa and South America. From the
poisonous feed were isolated Aspergillus flavus and a toxin produced by this
organism that was designated aflatoxin (Aspergillus flavus toxin- A-fla-toxin).
related toxins are known. Aflatoxin B1 is the most important of this large family
of compounds and is produced by Aspergillus flavus, A. parasiticus and
A.nominus. The toxicity of the six most potent aflatoxins decreases in the
following order: B1>M1>G1>B2>M2≠G2.
aflatoxicosis maybe produced in a wide range of tropical and subtropical food
commodities such as figs, tree nuts and cereals. The most important crops are
corn and groundnut, but it can also occur in temperate crops such as wheat.
post harvest crops stored at inappropriate temperatures and water activities, it is
now known that these compounds can be present in the field before harvest.
A.flavus and A. parasiticus may infect healthy plants at a very early stage.
carcinogenic in some animal species as rat. Aflatoxin B1 is acutely toxic to our
species and is responsible for liver necrosis. The toxicological effect of the
aflatoxins are influenced by their metabolism after intake into their body
milk. Although M1 and M2 are less toxic than the parent compound B1, M1
retains its toxic and carcinogenic ability in many animals. The LD50 of AFB1
for rats by the oral route is 1.2mg/kg and 1.5 to 2.0 mg/kg for AFG1.
an insidious combination of acute and chronic toxicity, it is prudent to control
their presence in food. Many countries have legislation establishing maximum
like nuts maybe possible or to use technologically sophisticated equipment to
sort and discard the contaminated units. It may also be possible to control the
production of aflatoxin in the field by an integrated programme of agricultural
management that may include plant breeding, improved irrigation and
replacement of aflatoxigenic strains by non- aflatoxigenic strains of A. flavus.
isocoumarin produced by Penicillium verrucosum in temperate climate and by
several species of Aspergillus in warmer and tropical parts of the world.
has also been isolated from meat and fish, however the occurrence of
ochratoxin A in meat products is usually due to transmission into muscle,
kidney and blood in animal fed on contaminated animal feed such as barley.
Ochratoxin may also be transferred from dietary intake into milk.
ochraceus is common on coffee beans, spices, soybeans, groundnut, rice and
corn. Ochratoxin is heat resistant and is not destroyed by roasting or
autoclaving though the ochratoxin producing fungi are capable of growth and
mycotoxin production at temperature below 10ºC.
in humans known as Balkan endemic nephropathy. There is increased evidence
that it can also be considered as a carcinogen with genotoxic property as well as
a potent nephrotoxin.
demonstrated that ochratoxin is quite widespread in foods and its presence in
human body fluids confirms that there is a significant exposure with the human
population. Ochratoxin is immunosuppressive and inhibits protein biosynthesis.
Cancer (IARC) as a possible human carcinogen. Low doses as 70μg/kg body
weight can induce kidney tumors in male rats. Its oral LD50 in rats is 20 to 22
mg/kg, and it is both hepatotoxic and neprotoxic.
by most forms of food processing. Cooking with or without previous soaking
removes a significant amount of ochratoxin from beans but does not lead to
total destruction. Beans still contain 16% to 60% of the initial ochratoxin
contamination and it seems probable that the material may have leached out
rather than destroyed.
Aspergillus and Paeciliomyces but the most important in the context of human
food production is P. expansum, a soft rot pathogen of apple and pears. Patulin
is an unsaturated lactose and is sensitive to sulphur dioxide and is unstable in
alkali but stable in acid.
in fruit juice is a indication that the juice was extracted from poor quality fruit
which is undesirable and should be avoided with good manufacturing practices.
This mycotoxin has also been found in moldy bread, sausage, fruits (including
bananas, pears, pineapples, grapes and peaches) and other products.
mg/kg and has been shown to be teratogenic, immunotoxic and neurotoxic and
to cause gastrointestinal disturbances in rats. Patulin is quite rapidly excreted
from animals. It causes chromosomal aberrations in animal and plant cells and
is a carcinogen.
confined to the region of damaged tissue and simply removing the lesions
reduces the toxin by 90%, but if 1cm around the lesion is also removed, no
patulin is detectable in rest of the apple.
reduce levels of patulin. Although pasteurization (using high temperature, short
time treatment of ten seconds at 90ºC) causes some reduction in patulin in fruit
juices, it is only of the order of 20%, which is not sufficient to make a badly
contaminated food product acceptable.
produce toxic substances that have been found in apples, tomatoes, blueberries
and others. The toxins produced include alternariol, alternariol monomethyl
ether, altenuene, tenuazonic acid and altertoxin-I.
fungi. It has been recovered from polished rice, moldy bread, country cured
hams, wheat, oats, rye and other similar products. It is a known carcinogen.
large number of fungi, including many Penicillia as well as members of the
A.ochraceus. One of the best producers is P.cyclopium, it has been found in
corn, beans and other field crops. Its LD50 in mice by subcutaneous route is 100
to 300 mg/kg and it is a proved carcinogen.
like the latter, they cause hepatocarcinogenic activity in animals. Among the
organisms that produce them are Aspergillus versicolor, A. nidulans,
A.rugulosus. The LD50 for rats by intra-peritoneal injection is 60 to 65 mg/kg.
which produce members of the trichothecene family of mold metabolites like
deoxynivalenol, neosolaniol and T-2 toxin etc.
trichothecene and is produced by species such as F. graminearum and F.
culmorum. LD50 of DON is 70mg/kg. The trichothecenes are remarkably stable
compounds, and DON will survive both dry milling and wet milling processes
of corn. The baking of bread has relatively little effect on trichothecenes such as
little acute toxicity, but there should be some concern about chronic exposure to
a compound known to be estrogenic. It may be produced, together with DON
and other trichothecenes, in a wide range of cereals including corn, barley and
southern leaf blight- damaged corn seed as a water soluble toxin. The LD50 for
mice has been reported to be 20.9 mg/kg for females and 29.1 mg/kg for males.
At toxic doses moniliformin causes rapid death without obvious overt cellular
damage, although acute degenerative lesions in the myocardium are reported.
human health are the fumonisins produced by species of Fusarium, such as F.
moniliforme. Like a number of mycotoxins, the fumonisins are relatively heat
stable and would not be significantly destroyed by drying processes for corn or
heat treatments used for the production of maize derivatives.
water-soluble is known to be responsible for equine encephalomalacia, porcine
pulmonary edema syndrome and hepatic cancer in rats and maybe involved in the epidemiology of esophageal carcinoma in humans in southern Africa and
parts of China.