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Mycotoxicosis in Broilers

Mycotoxicosis in Broilers. Professor Doctor/ Wafaa Abd El-Ghany Poultry Diseases Department Faculty of Veterinary Medicine, Cairo University. Mycotoxins. Mycotoxicosis.

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Mycotoxicosis in Broilers

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  1. Mycotoxicosisin Broilers Professor Doctor/ Wafaa Abd El-Ghany Poultry Diseases Department Faculty of Veterinary Medicine, Cairo University

  2. Mycotoxins

  3. Mycotoxicosis • Generic term describing diseases conditions caused by different chemical secondary metabolites(A compound that is not necessary for growth or maintenance of cellular functions but is synthesized, generally, for the protection of a cell or micro-organism, during the stationary phase of the growth cycle), of toxogenic fungi.

  4. Types of Fungi 1. Field fungi fungi that attack plants grow in the field (prior to harvest) & grow under special conditions (Fusarium). 2. Storage fungi Invade grain during storage (Aspergillus and Penicillium). The development of fungi is influenced by: • Moisture content of the stored grain (14% or more), • Temperature (24-28C), • Length of storage time. • Bad storage conditions as aeration (ventilation). • Presence of insects that damage the grains.

  5. Economic losses

  6. Economic losses

  7. Aflatoxicosis • Disease condition resulted from feeding on contaminated ration with aflatoxin and characterized by hepatotoxicity. • Mostly often presents as a uncertain, sub-acute or chronic condition Low doses for long period).

  8. Etiology Chemical metabolites of certain toxogenic fungi (Aspergillus flavus and Aspergillus parasiticus) Hepatotoxic & carcinogenic Stable compounds Include B1, B2, G1 and G2. the most toxogenic and carcinogenic one is B1. They give Blue or Green fluorecens under UV lamp

  9. Susceptibility

  10. Mechanism of toxicologic damage

  11. Mechanism of toxicologic damage

  12. Mechanism of toxicologic damage

  13. Mechanism of toxicologic damage Inhibit protein synthesis (immunoglobulins) Cause atrophy of lymphoid organs

  14. Factors affecting signs severity

  15. Clinical signs Acute: • Increasing mortalities. • Soft droppings containing un-digested food particles. • Nervous signs in ducklings & turkey poults. • Egg production losses. Chronic: • Decreased mortalities. • Retardation of growth. • Severe anaemia. • Distention of abdomen with fluid (ascitis).

  16. Lesions Acute: • All types of haemorrhages on muscles. • S/C gelatinous exudates (oedema). • Atrophy of lymphoid organs (thymus, bursa and spleen). • Atrophy and pale bone marrow. • The liver is: • Enlarged, • Sub-capsular haemorrhages, • Carries necrotic foci with mild fatty degeneration.

  17. Lesions Chronic: • Haemorrhages on the breast and thigh muscles. • Hydropericardium. • Ascitis. • The liver is: • Shrinked (fibrosed), Cirrhosed (rubbery). • Complete fatty degeneration (fatty or yellow liver syndrome especially in layers).

  18. Differential diagnosis • Haemorrhagic syndrome. • Big liver disease (ALC). • Nacl poisoning. • Vit. E & Selenium def. (Exudative diathesis). • Paratyphoid (Keel septicaemia). • Duck viral hepatitis. Differential diagnosis based on detection and determination of toxin in ration.

  19. Ochratoxicosis • It is the type of food intoxication characterized by Kidney damage and nephrotoxicity as well as hepatotoxicity.

  20. Etiology

  21. Mechanism of toxicologic damage

  22. Clinical signs Acute: • Perfuse whitish diarrhea. • Severe dehydration. • Sudden death. Sub-acute: • Retardation of growth. • Pale shank and peak (severe anaemia & depigmentation). • Rickets like signs. • Egg production losses (soft shell).

  23. Lesions • The kidneys show enlargement (swollen), pale, whitish foci distributed and embedded in the tissues (ureates). 2. The ureters are distended with ureates. 3. Deposition of ureates in the visceral organs and serous membranes (visceral gout), also in the joints (articular gout). 4. Soft bone and rubbery peak.

  24. Differential diagnosis • Infectious nephritis nephrosis syndrome. • Gumboro disease. • Gout (nutritional imbalance). • Oosporin and citrinin mycotoxins • Rickets or osteomalacia Differential diagnosis based on detection and determination of toxin in ration.

  25. TrichothecenceT2- intoxication • Diseased condition caused by ingestion of contaminated feed with trichothecence and characterized by necrosis and ulceration in oral cavity which may extend to oesophagus, proventriculus and intestine.

  26. Etiology

  27. Mechanism of toxicologic damage

  28. Clinical signs • Necrosis and ulcers at peak commeasure, tongue, hard palate and the lesion is extend to esophagus, proventriculus and intestinal tract producing bloody diarrhea. 2. Anorexia and growth retardation. 3. Anaemia. 4. Nervous signs. 5. Decrease in egg production, egg shell quality and hatchability.

  29. Lesions 1. Oral necrosis and ulcers. 2. Proventricular ulcers. 3. Haemorrhagic enteritis. 4. Bone marrow paleness. 5. Atrophy of lymphoid organs. 6. Mottled (yellow tan) friable liver.

  30. Differential diagnosis • Wet form of fowl pox. • Vit. A deficiency. • Candidiasis. Differential diagnosis based on detection and determination of toxin the ration.

  31. Other mycotoxins types

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