Mycotoxin and Mycotoxicoses
History
Ergot poisoning -cereal grains -Claviceps purpura & the toxin
compounds were identified in 1875.
black, elongated, fruiting bodies grow
in the ears of the cereals
“St. Anthony’s fire,” whereby narrowing of
blood vessels would occur, and would often
lead to changes in mental behaviour, as well
as weakness, nausea, vomiting, gangrene
and worse.
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In Russia (1913), the disease alimentary toxic aleukia (ATA)
outbreak - due to the consumption of mold cereal grains.( T-2 toxins) -
nausea, vomiting, diarrhea, and sometimes death.
First, well-documented outbreak of animal mycotoxicosis - East
Anglia, England in 1960 -1,00,000 turkey poults died of an unknown
disease (Turkey X disease).- groundnut meal - presence of Aspergillus
flavus mycelia and the toxic metabolites by thin layer chromatography
- called aflatoxins.
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General features of mycotoxin formation
Greek word – ‘mykes’ meaning ‘fungus’ and the Latin word –
‘toxicum’ meaning ‘poison’.
Many of the toxigenic fungi, over 300 known species, are capable of
elaborating mycotoxins.
The same mycotoxin can be produced by different fungi and the same
fungus can produce different mycotoxins.
Toxin production occurs only under specific conditions of moisture,
temperature, suitability of substrate and appropriate oxygen tension.
The optimum conditions for toxin production are relatively specific for each
fungus.
e.g. Fusarium elaborates its toxin at freezing temperature,
A. flavus requires a temperature of 250C.
Damage to the seed coat by insects, mechanical harvesting, severe frost
or
other factors may predispose crops to fungal attack. Insects may also serve
as carriers of fungal spores.
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The fungal associated with cereal grains have been divided
mainly into two types.
1.Field fungi invade the grains before harvest and required
greater water activity for growth
e.g. Fusarium, Helminthosporium and cladosporium
2. Storage fungi invade the grains after harvest during drying
and in storage e.g. Aspergillus, Penicillium
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Mycotoxins
Species Toxins
A.flavus and Aflatoxins
A.parasiticus
A. ocheraceus Ochratoxin
Fusraium roseum Trichothecane (t-2) toxin
Pencillium citrinum Citrinin
A.nidulans and Sterigmatocyosin
A.versicolor
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Characteristics of mycotoxins
.
low molecular weight, non-antigenic, heat stable secondary
fungal metabolites. (approx. 400 – so far identified)
activate at low concentrations.
wide spectrum of toxic effects, like carcinogenic, mutagenic,
teratogenic and immunosuppressive.
Acquired immunity does not occur following exposure.
Each toxin affects specific target organs or tissues
Target organs/ tissues Toxins
Vascular system Aflatoxins
Digestive system Aflatoxins
Mucous membrane Trichothecane (t-2) toxin
Urinary system Ochratoxin
Reproductive system Zearalenone (Fusarium toxin)
Cutaneous system Sporidesmin
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Mycotoxicosis
Mycotoxicosis in animals is determined by several factors
Species of toxigenic fungus
Concentration of mycotoxin in the food
Age, sex and health status of the exposed animal
Target organs or tissue affected
Duration of exposure to contaminated feed.
Mycotoxins can enter the system of birds and animals by ingestion, inhalation
or direct skin contact.
Mycotoxicosis occurs in three forms.
1. Acute primary mycotoxicosis
Due to high to moderate amounts of mycotoxins are consumed.
Causes marked signs of disease or death.
2. Chronic primary mycotoxicosis
Due to moderate to low levels of mycotoxin intake.
reduced productivity , reproductivity and inferior market quality.
3. Secondary mycotic diseases
Due to intake of very low concentration of specific mycotoxins,
impairment of immune system results in predispose to infectious diseases such as
Salmonellosis, candidiasis and coccidiosis.
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Clinical features of mycotoxicosis
Disesase produced are not transmissible to contact animals.
Outbreaks are often seasonal and sporadic, and may be
associated with certain batches of stored food or particular types of
pasture.
Initially, the signs of illness are decreased growth rate or
immunosuppression
Recovery depends on the type and amount of mycotoxin ingested
and the duration of the exposure to contaminated feed.
Evidence for the presence of mycotocoses in animals -laboratory
demonstration of mycotoxins in suspected food, or in the tissues,
secretions or excretions of affected animals.
Characteristic lesions in target organs of affected animals are
important supporting diagnostic evidence.
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Mycotoxicosis of domestic animals and poultry
Disease Fungus Crop or Mycotoxin Animals
substrate affected
Aflatoxicosis Aspergillus Ground nut, Afaltoxins B1, Cattle, pig,
flavus maize, oats, B2, G1,G2 poultry and
Aspergillus barley, rice dogs
parasiticus and nut crops
Ergotism Claviceps Seed heads of Ergotamine and Cattle, Sheep,
purpura many grasses ergometrine Pig, Horse and
and grains Poultry
Facial Eczema Pithomyces Pasture, litter Sporidesmin Sheep and
charatarum Cattle
Oestrogenism Fusarium Maize, Barley Zearalenone Pigs
graminareum and cereals
Leukoencephalo Fusarium Maize Fumonisins B1 Horses and
malacia- moniliforme (A1, A2, B2) Donkey
Trichothecane Many fusarium Cereals T-2 toxin, Many species
toxicosis species diacetoxy -
seripenol
Ocharatoxicosis A. ochraceus Barley, wheat Ochratoxin -A Pigs and
P. viridicatum and Maize Poultry.
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Depigmentation -ochratoxin
Oral-Lesion_T2 toxin
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Aflatoxico
The name aflatoxin derives from Aspergillus flavus toxin.
sis
Group of approx. 20 related toxic compounds produced by some
strains of A. flavus and A.parasiticus - maize, cotton seed and groudnuts. .
Aflatoxins are a group of related bisfuranocumasin compounds with
toxic, carcinogenic, teratogenic and mutagenic activity.
The four major aflatoxins are B1, B2, G1 and G2. - named according
to their position and fluorescent color on thin layer chromatography (TLC).
Aflatoxins M1, M2 are hydroxylated metabolites of B1 and B2 that
are excreted in the milk of lactating animals such as dairy cows.
Concentration of aflatoxin B1 in excess of 100μg /kg of feed are
considered toxic for cattle
B1 – most encountered in animals and humans
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Biological effects of aflatoxin
Aflatoxin B1 is the most hepatogenic, carcinogenic,
teratogenic and embryotoxic effects
Acute toxicity
Hepatic injury and nervous signs such as
ataxia and convulsions.
Death may occur suddenly.
Chronic toxicity
There is reduction in efficiency of food conversion,
depressed daily weight gain, decreased milk production in
dairy cattle and enhanced susceptibility to intercurrent
infections due to immunosuppression.
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Sympto
ms
Prominent signs in calves include blindness, circling, grinding of
teeth, diarrhoea, tenesmus and convulsions.
Aflatoxicosis has ben described in goats. But sheep are highly
resistant.
In dairy cattle afalatoxin M1 and M2 are excreted in the milk.
In pigs, signs include drowsiness, inappetance, jaundice, weight
loss and yellow urine.
Ducklings are considered to be the most susceptible avain
species to aflatoxins.
Signs include anorexia, poor growth rate, ataxia and opisthotonus
followed by sudden death.
In birds over three weeks of age, subcutaneous haemorrhages of
legs and feet.
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Lesi
ons
Principle target organ is liver.
Depending on the severity of intoxication, hepatomegaly
with necrosis, marked bile duct hyperplasia will occur.
Acute hepatic failure and massive haemorrhage due to
impaired blood clotting, increased capillary fragility leading to
death may occur with higher doses.
In chronic toxicity, in additon to liver damage, degenerative
changes in the kidney, thymus cortical aplasia leading to
decreased cell mediated immune response will occur.
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Diagnosis
Chemical identification of mycotoxins in food samples and
biological assays for toxicity are important confirmatory steps.
Demonstration of toxigenic strains of Aspergillus flavus and
Aspergillus fumigatus and of potentially toxic levels of mycotoxins
in the food, tissues, secretions are helpful for diagnosis.
Thin layer chromatography and HPLC are more sensitive
analytical methods for determing aflatoxins levels in the food.
Radio immuno assay and ELISA methods are also available.
Biological assays
Ducklings are mostly susceptible. Bile duct proliferation in one-
day-old ducklings and chick embryo bioassay are highly useful.
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Control and prevention
Prevention of contamination at all stages of food production,
storage and use is the preferred method of preventing
aflatoxicosis.
Deconatmaination procedures like physical removal and
chemical treatment of aflatoxin contaminated feeds such as acids,
alkalies, aldehydes, oxidizing agents of selected gases (ammonia)
have been used for degrading aflatoxins.
High affinity inorganic compounds such as benzoic and
propionic acid have been widely used as preservatives for stored
agricultural products.
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Mycotoxin binders
Inorganic binders : Hydrated sodium
calcium aluminosilicate (HSCAS): egs:
clay, bentonite, montmorillonite, zeolite,
phyllosilicates
A common toxin binder used in animal
feed.
Organic binders or biopolymers are
complex indigestible carbohydrates
(cellulose, polysaccharides in the cell
walls of yeast and bacteria such as
glucomannans, peptidoglycans, and
others) and synthetic polymers such as
cholestyramine can adsorb mycotoxins
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Aspergillus clavatus intoxication is a highly fatal neuromycotoxicosis of
ruminants, especially cattle.
caused by the ingestion of infected sprouting grain and sorghum beer
residue.
Locomotor disturbances, tremors and paralysis are observed.
mycotoxins such as patulin, cytochalasin E
isolated mainly from soil and dung, but also occurs on stored products
(mainly cereals) with high moisture content, e.g. inadequately stored rice,
corn and millet
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Kunkers or leeches – necrotic yellowish
coral like droppings
Equine cutaneous pythiosis – Pythium insidiosum
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