This document discusses aflatoxicosis in poultry. It begins by introducing aflatoxicosis and its etiology, caused by fungi such as Aspergillus flavus that produce aflatoxins. These mycotoxins are heat stable and immunosuppressive, affecting young birds more than adults. Clinical signs include reduced growth and increased susceptibility to other diseases. Post mortem findings can include liver damage and hemorrhaging. Diagnosis involves identifying aflatoxins in feed. Prevention focuses on proper storage and removal of contaminated feed, while treatment requires replacing toxic feed and supplementing vitamins and minerals.

1. ADVANCES IN AVIAN
PATHOLOGY
Aflatoxicosis
Sumedha Bobade
Ph.D Scholar

2. Aflatoxicosis
• Introduction
• Etiology
• Pathogenesis
• Clinical signs
• Post Mortem Findings
• Diagnostic tool
• Treatment
• Prevention and Control

3. Introduction
 An outbreak of an unknown disease in 1960 was reported and killed poultry birds The
similar incidents in was found in ducklings .This was named as Turkey- X disease.
 After investigation it was traced back as mycotoxins in groundnut meal feed imported
from Brazil..
 However subclinical mycotoxicosis result into immunosuppressant leading to
decreased vaccine efficacy, to fatty liver, buccal, comb and wattle
necrosis. Aflatoxin is a class I carcinogen
 Young birds are more sensitive than Adults .
 Ducks are 10 times more sensitive than chickens.
 Toxic substance produced by fungal toxins (mycotoxins ) are not protein in
nature like bacterial toxins, therefore are not detected by the immune system .
 Toxin can remain in the body after fungus has been removed
Synonyms:
 Bloody thigh syndrome.,Lazy leukocyte syndrome
 moldy corn toxicosis
 poultry hemorrhagic syndrome,” and Aspergillus toxicosis.

4. Sources of Aflatoxins
•

5. Etiology
• The fungus Aspergillus flavus produces most of the aflatoxins .It also
produced by A.parasiticus and Penicillium puberculum.
• Aflatoxins are highly heat stable and can withstand extreme environmental
condition.
• It remain stable once formed in grains and not destroy by grinding ,crushing
in mill and storage.
• Naturally occuring aflatoxins contain aflatoxins B1,B2, G1 and G2.(Due to
Blue or Green colour reaction to fluroscence light.AF are difuranocoumarin
compounds and include aflatoxin B1, B2, G1, G2, M1 and M2
• B1 is more toxic and found in highest concentration
• Types of mycotoxins

6. Mycotoxin
Mycotoxin Source Associated Food
Aflatoxins Aspergillus flavus and
A.parasiticus
Corn, Peanuts,cotton seed
tree nuts ,milk
Fumonisins Fusarium moniliformis
F.verticillioides,
F.proliferatum
Corn
Ochratoxin A Penicillium verrucosum,
A.ochraceus, A.nigri
Wheat,barley,corn,oats
Patulin P.expansum Apples ,pears
Trichothecenes Mainly Fusarium Cereals and other foods
Zearalenone Fusarium graminearun Cereals oil, wheat ,barley,
Starch

7. Pathogenesis
• Following absorption of AF in the upper part of the small intestine .
• AF undergoes an extensive transformation into metabolites in the liver.
• In fact, AF are not toxic but require metabolic conversion by hepatic
enzymes (the cytochrome P450 family) to the metabolically active
metabolite exo-AFB1-8, 9-epoxyde (AFBO) to exert its toxicity. This
metabolically active form of AF can bind with particular cellular
compounds (proteins, DNA and RNA) to influence normal cellular
activities, and is considered the active form responsible

8. Ma et al., 2017
Pathogenesis
AFG1 bound with the A–T residues . The binding between a ligand and a receptor, depend on
free energy , the smaller the binding free energy, the closer the binding, the folding of the
binding conformation of AFB1/AFG1 with the DNA ,the two carbonyl O atoms in the AFG1
structure all approached the interior of the DNA groove during binding, The carbonyl O also
belongs to the hydrogen bond acceptor, and moves toward the inside of the DNA groove. Three
hydrogen bonds formed between AFB1 and two DNA bases.
(Ma et al., 2017)

9. Pathogenesis
• Reduced protein synthesis results in reduced production of essential
metabolic enzymes and structural proteins for growth.
• Reduce protein synthesis decrease Ab mediated and cell mediated
immunity. Causes reduction of Bursa of Fabricus and thymus. It is toxic to
B-lymphocytes.
• Aflatoxins are metabolized in the liver to an epoxide that binds to
macromolecules, especially nucleic acids and nucleoproteins.
• Their toxic effects include mutagenesis due to alkylation of nuclear DNA,
carcinogenesis, teratogenesis, reduced protein synthesis, and
immunosuppression.
• The liver is the principal organ affected. High dosages of aflatoxins result
in hepatocellular necrosis; prolonged low dosages result in reduced growth
rate, immunosuppression, and liver enlargement.
• Aflatoxin B1 & B2 concentrate in gizzard,liver and kidney but cleared off
in 4 days .
• Aflatoxin B1 excreted in bile,urine and feces.
• T1/2 of AF B1 in laying hen is about 67 hours.

10. Clinical signs
• Decreased growth and poor feed conversion efficiency.
• Decrease in resistance to infections such as salmonellosis, coccidiosis, IBD
and candidiasis.
• Paralysis in broilers ,abnormal vocalisation,ataxia &convulsion
• Poor weight gain, feed intake , pigmentation,egg production,reproduction
performance etc.
• Adult hens-decreased egg production and reduced hatchability
• Adult breeder males -testicular weights and sperm counts will reduced.
• Insemination of hens with semen of affected males has shown decreased
fertility.
• MULTI FOCAL HAEMORRHAGE NECROPSY FINDING
• Severe intoxication ;enlarged kidney filled with urates.
• Liver is enlarged ,yellow and fragile (easily broken ).
• Small hemmorages occurs , decrease clotting factor synthesis and increse
fragility of minute blood vessel.This leads to a condition K/as Bloody
thigh syndrome.

11. Clinical signs
• Aflatoxin is toxic to B-lymphocytes .
• The clearence of blood phagocytes (a
protecteive blood cell k/as monocytes) and
those in tissue ( macrophages) are dammaged
aflatoxin affect activity and numbers of these
cells The number and movement get reduced
this condition known as Lazy leukocyte
disease.
• Cell mediated and Ab-mediated response get
reduced.

14. Diagnosis
 Clinical History and signs of the flock and mortality pattern •
 Identification and quantification of spesific toxins in feed ingredients.
 Analytical techniques like Chromatography, mass spectrometery, ELISA
etc.
 Microscopic leisons fatty change in liver

15. TREATMENT
• Level of AF B1 upto 0.38 ppm may be considered as safe
.Field levels of aflatoxin are between 20-100 ppb and may
upto 500ppb.
• Toxic feed should be replaced with unadultrated feed
• Correction of managemental practices supplimentation of
Vitamins and trace minerals along with crude protein and
dietary energy.
• Aflatoxin act as antagonist for Vitamin B2 and ointerefere
with absorption and transportation of nutrient.

16. PREVANTION AND CONTROL
• Aflatoxin can be prevented by developing mould resistant crops,
efficient harvesting, transportation and storage to minimize
contamination.(Feed manufacturing and management)
• Addition of antifungal agents in feed
• Controlled storage atmosphere ,irradiation & fumigation.
• Cleaning to remove lightweight or broken grains will often
substantially reduce mycotoxin concentration in remaining grain.
• Ammoniation reduces aflatoxin contamination in grain but is not
currently approved by the FDA for use in food animals in the USA
because of uncertainty about by-products produced.
• Detoxification with
Binding agents(Zeolite,polyvinylpolypyrrolidone).
• Ozone treatment of grains
• Ammoniation of feed/grain .

17. Control
•Use of Chemical agents like alkali (Calcium hydroide,Sodium
hydroxide,Ammonia) and acids (Benzoic acid, Copper sulphate at 0.04-0.05%).
•Use of Adsorbent or binders-
1.Inorganic toxin binders (Silica based)
Aluminosilicate,Bentonites, Zeolites
Hydrated Sodium calcium Aluminosilicate at 1%.
Activated charcoal ,clay and yeast.
2.Organic toxin binders (Carbone base)
Oat hulls,wheat bran,Alfafa fibre, yeast cell wall extract, cellulose,Hemi-cellulose
and pectin.

18. Control
•Dietary the dietary manipulation
1.Mycotoxns affects nutrient value of feed increasing the dietary the dietary
level can minimize this effect
2. Higher protein and methionine lower the effect of aflatoxin in birds.
Use of Detoxification and physical treatment
1) Exposure to sunlight for about 12-14 hrs
2) Drying at 120Cfor 2-3 hrs
3) Autoclaving ,pelleting to inhibit mould growth.
4) Density segregation (floatation).
Bio-control Measure (Use of AFLASAFE)
• This method is used at agronomic level during planting.AflasafeTM is tossed
on field soil by hand 2-3 weeks prior to flowering of crop at 10-20Kg per
hectare.