Mycotoxicosis in Poultry
Introduction
·
A mycotoxicosis is a disease caused
by a natural toxin produced by a fungus.
·
In poultry, this usually results
when toxin-producing fungi grow in grain and feed.
·
Hundreds of mycotoxins have been
identified, and many are pathogenic.
Major mycotoxins and its etiology
|
Fungus
|
Mycotoxin
|
|
Aspergillus
species
|
Aflatoxin
(B1, B2, G1, G2)
Ochratoxin
A
Patulin
|
|
Fusarium
species
|
Fumonisin
Zearalenone
Trichothecene
(T2 Toxin, Deoxynivalenol (DON or Vomitoxin), Diacetoxyscirpenol (DAS)
|
|
Penicillium
species
|
Ochratoxin
A
Patulin
|
|
Claviceps species
|
Ergot
alkaloids
|
|
Mycotoxcosis
|
Cause
|
Clinical
signs
|
Organs
affected
|
Gross
pathology
|
|
Aflatoxicosis
|
Aspergillus
flavus,
A.
parasiticus
|
§ General unthriftiness
§ High morbidity and mortality.
|
§ Liver
§ Lymphoid organs
§ Hematopoeitc functions
|
§ Reddened due to necrosis and congestion or yellow due to
lipid accumulation.
§ Hemorrhages may occur in liver and other tissues.
§ In chronic aflatoxicosis, the liver becomes yellow to gray
and atrophied.
§ Ascites
|
|
Fusariotoxicosis
|
F.
verticillioides
F. verticillioides
F. graminearum
|
§ Feed refusal,
§ Drop in egg production
§ Cynosis in comb and wattles in layers.
|
§ Oral mucosa
§ GI tract
§ Lymphoid organs
|
§ Necrosis and ulceration of the oral mucosa
§ Reddening of the GI mucosa
§ Diarrhoea
§ Mottling of the liver
§ Atrophy of the spleen and Bursa.
§ Lesions in proventriculus, and gizzard
|
|
Ochratoxicosis
|
Aspergillus
ochraceus
Penicillium
viridicatum
|
§ Depression
§ Huddling
§ Hypothermia
§ Diarrhoea
§ Rapid weight loss
|
§ Kidney
§ Liver
§ Lymphoid organs
§ Bone marrow
|
§ Damage of kidney
§ Fatty liver
§ Atrophy of the spleen and Bursa
§ Pale bone marrow
§ Ascites
|
|
Ergotism
|
Claviceps species
|
§ Discolored toe in chicks
§ Atropied comb, wattles in adults
§ Vesicles and ulcers develop on the shanks of the legs and
on the tops and sides of the toes
|
§ Nervous system
|
|
Mycotoxin decontamination methods
A)
Physical methods
Antimycotic agents:
Antimycotic agents like sorbic acid and
sorbate; propionic acid and propionate, benzoic acid, benzoates and parabens;
and acetic acid and its derivatives are the chemicals that prevent mould growth
and interfere with mycotoxin production.
Irradiation:
Gamma or electronic irradiation is highly
effective for destroying the fungal spores. Fluorescent or ultraviolet (UV)
rays decompose aflatoxins and ochratoxins.
Mechanical separation:
Toxin levels decrease as clean product is
physically separated from contaminated grains.
B)
Chemical detoxification
Ammoniation:
Treatment with aqueous and gaseous ammonia or
ammonium hydroxide, with or without heat and pressure to destroy the mycotoxin
in contaminated food and feed is currently the best and effective method.
Ammoniation not only detoxified several mycotoxins (85-100% reduction), but
also inhibited mould growth.
Sodium hydroxide:
Warming of grain to 1050C in the presence of
0.5% sodium hydroxide detoxified various mycotoxins in the feed.
C)
Biological Inactivation
1.
Mycotoxin-binding agents:
Numerous
agents like, activated carbons (charcoal), bentonites, clay, hydrated sodium
calcium alumino silicate, and zeolite, have currently been used to counteract
the mycotoxicosis in poultry and its carry over effect through meat and eggs. These sorbents are nutritionally inert and
reduce the bioavailability of various mycotoxins by absorption on their surface
in intestinal tract.
Activated
charcoal:
It has high ability of binding with several mycotoxins. The adsorption property
of AC was found effective against aflatoxin B1 and ochratoxin A up to 95% and
91%, respectively. Charcoal at 2% level had shown beneficial effects.
Bentonites: Bentonites (hydrated
aluminium silicate) are sorbents with layered (lamellar) crystalline
microstructure and variable composition. Their absorption property mainly
depends on the interchangeable cations (Na+ , K+ , Ca++ and Mg++) present in
the layers. Sodium bentonite is more effective than calcium bentonite.
Bentonite could bind aflatoxin to the extent of 66% while it was of little use
in adsorbing OTA.
Hydrated
sodium calcium alumino silicate (HSCAS): Molecular surface of HSCAS gets
saturated with water and attracts the polar structure of various mycotoxins. In
young broiler chicks, HSCAS (0.5%) was effective at reducing the toxicity of
aflatoxin as well as combined toxicity
with OTA. However, its protective properties are very low towards OTA,
zearelenone and nil towards trichothecenes.
2.
Microbiological binding agents: Mannan oligosaccharide (MOS) extracted from
the cell wall of Saccharomyces cerevisiae has shown broad-spectrum efficacy
against most of the mycotoxins. Saccharomyces cerevisiae was found to have
beneficial effect in poultry during mycotoxicosis and MOS was believed to be
the responsible factor and showed significant binding over zearelenone, T2
toxin and moderate binding over OTA (25.5%), during in vitro studies
D)
Antioxidant substances
The
protective properties of antioxidants are probably due to their ability to act
as superoxide anion scavengers, thereby protecting cell membranes from the
mycotoxin induced damage.
Ascorbic
acid (Vitamin C):
The
addition of vitamin C to the diet containing OTA, partially protected laying
hens against the toxic effect. The OTA induced reduction in feed intake was
counteracted at 250C by vitamin supplementation.
Phenolic
compounds:
The
phenolic antioxidants, gallic acid, vanillic acid, protocatechuic acid, 4-
hydroxybenzoic acid, catechin, caffeic acid, and chlorogenic acid were found to
be effective against the fungal growth of ochratoxigenic Aspergilli and the OTA
production.
Vitamin
A:
Vitamin
A possesses the antioxidant properties against the mycotoxin-induced damage.
Carotenoids, mainly carotenes and xanthophylls present in carrots, palm oil and
maize, not only possessed the antioxidant property but also had antimutagenic
and anticarcinogenic properties and reduced the toxicities of OTA.
Vitamin
E/Selenium:
Supplementary
vitamin E administration to chickens partially counteracts the formation of
lipid peroxides due to single and combined exposure to OTA and T2 toxin. Higher
vitamin E intake partially ameliorated oxidative stress caused by OTA. It is
known that reduced vitamin E (alpha tocopherol radicals) can be regenerated
following single electron reduction by ascorbic acid. Vitamin C should,
therefore, enhance the biological efficacy of vitamin E especially under stress
condition. Vitamin E and selenium are involved in the formation of glutathione
peroxidase, a compound vital in the cellular detoxification mechanism.
E)
Food components and additives
Numerous
food components, ingredients, or additives with or without antioxidant
properties have been found to have ameliorative properties against
mycotoxicosis.
Aspartame:
Aspartame
(L- aspartyl- L- phenylalanine methyl ester), a structural analogue of both OTA
and phenylalanine, has been shown to have protective effect against OTA induced
cytotoxicity in animals. Aspartame prevents typical cytotoxic effects of OTA
including inhibition of protein synthesis, lipid peroxidation and leakage of
certain enzymes, such as lactate dehydrogenase, gamma glutamyl transferase and
alkaline phosphatase.
Crude
proteins:
Raising
the protein levels of diet from 14-18% to 22-26% counteracted the OTA effects.
Dietary
lipids:
Inclusion
of cottonseed oil at 2, 6, or 16% level into semi-purified diets containing 10
ppm aflatoxin, not only improved the body weight, but the mortality was also
significantly reduced. The higher levels of dietary fat reduced mortality and
in some instances, improved the body weights. Lipids exerted their effects in
part by interfering with absorption of the aflatoxin. Supplementation with
olive oil and safflower oil, both sources of unsaturated fatty acids, also
improved body weight which suggested that diets containing higher levels of
linoleic acid supported better feed conversion and lower mortality in chicks
fed diets with aflatoxin.
L-Methionine:
It
has been reported to have a protective effect against many oxidant drugs. It
plays an important role in preserving the structure of cell membrane and in
modulating the antimicrobial activity of polymorphonuclear leucocytes in
periodontal disease as well as behaving as a chemotherapeutic agent in
hepatitis treatment.
Treatment
·
The
most effective treatment is removal of the source of toxins.
·
Addition
of antifungal feed preservatives is also helpful.
·
Increasing
protein level in the feed until mortality reduces may also be beneficial.
·
Administration
of soluble vitamins and selenium. (Vit. A, D, E, K, C)
