The immunological and pathological changes in poultry induced by ochratoxin A

The mvcotoxin ochratoxin A (OA) can contaminate a wide variety of feedstuffs and be nephrotoxic to domestic animals and poultry. The objective of this work was to study the clinical, pathological and immunological effects induced by feeding OA to broilers and turkeys from hatch as well as its effects on production characteristics and teratogenicity in quail. Some basic immune mechanisms were studied.

OA caused growth depression in broilers and turkeys but not in quail. There was a loss of carotenoid pigments in the shank of broilers.

The principal pathological effects were in the kidney especially in the proximal convoluted tubules (PCT) where the mitochondria were the organelles most sensitive to OA-damage although other intracellular elements were involved together with a marked increase in lysosomal activity. OA localised within PCT and glomeruli. Ring-form mitochondria in the PCT and the accumulation of glycogen in the liver were considered to be of diagnostic significance.

In the lymphoid organs, widespread degeneration was a consistent feature of OA-toxicity, suggesting a direct effect on immunity, OA induced a marked depression of both humoral and cell-mediated immune (CMI) responses in broilers and turkeys. Total serum levels(IgG-IgM,IgA) were reduced in broilers but only IgM levels were depressed in turkeys. Tissue immunoglobulins were also depressed. Delayed hypersensitivity responses were reduced in broilers and turkeys. Graft-versus-host reactions, evaluated by a chick embryo splenomegaly test, were depressed in OA-fed broilers.

It was not possible to elicit a distinct Arthus reaction in turkeys in contrast to broilers.

In general, granulocytes, particularly heterophils and eosinophils, and vascular endothelial cells appeared to clay a significant role in CMI responses in poultry.

OA-contaminated feed resulted in reduced egg production, fertility and hatchability in a dose-related fashion in Japanese quail and an increase in embryonic mortality and a number of developmental defects.