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Are anti-ganglioside antibodies associated with proventricular dilatation disease in birds?

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The identification of Parrot bornaviruses in psittacine birds with proventricular dilatation disease (PDD) has not been sufficient to explain the pathogenesis of this fatal disease since not all infected birds develop clinical signs. One hypothesis suggests that PaBV could trigger the production of autoantibodies targeting neuronal gangliosides. These are major neuronal antigens, and PDD might therefore resemble Guillain-Barré Syndrome (GBS) in its pathogenesis. Experimental inoculation of pure gangliosides and brain-derived ganglioside extracts were used in two different immunization studies. A preliminary study on seven healthy chickens ( Gallus gallus domesticus ) was performed using a group of four chickens inoculated with a brain ganglioside extract in Freund’s complete adjuvant (FCA) and a control group comprised by three chickens inoculated only with phosphate-buffered saline (PBS). A second study with five healthy quaker parrots ( Myiopsitta monachus ) was comprised of three groups. Two quaker parrots received purified gangliosides in FCA, two received a crude brain extract in FCA, and one control quaker parrot received FCA alone. In the preliminary study, one chicken developed ataxia and weakness. None of the quaker parrots had any clinical signs that could resemble PDD or GBS. None of the chickens or quaker parrots presented any gross lesions. The chicken with clinical signs had a perivascular and perineural lymphocytic infiltrate in the proventriculus. Two of the quaker parrots (one from each treatment group) developed mild lymphoplasmacytic encephalitis and myelitis. Our results suggest that autoantibodies against gangliosides in birds are not associated with a condition resembling PDD.
Title: Are anti-ganglioside antibodies associated with proventricular dilatation disease in birds?
Description:
The identification of Parrot bornaviruses in psittacine birds with proventricular dilatation disease (PDD) has not been sufficient to explain the pathogenesis of this fatal disease since not all infected birds develop clinical signs.
One hypothesis suggests that PaBV could trigger the production of autoantibodies targeting neuronal gangliosides.
These are major neuronal antigens, and PDD might therefore resemble Guillain-Barré Syndrome (GBS) in its pathogenesis.
Experimental inoculation of pure gangliosides and brain-derived ganglioside extracts were used in two different immunization studies.
A preliminary study on seven healthy chickens ( Gallus gallus domesticus ) was performed using a group of four chickens inoculated with a brain ganglioside extract in Freund’s complete adjuvant (FCA) and a control group comprised by three chickens inoculated only with phosphate-buffered saline (PBS).
A second study with five healthy quaker parrots ( Myiopsitta monachus ) was comprised of three groups.
Two quaker parrots received purified gangliosides in FCA, two received a crude brain extract in FCA, and one control quaker parrot received FCA alone.
In the preliminary study, one chicken developed ataxia and weakness.
None of the quaker parrots had any clinical signs that could resemble PDD or GBS.
None of the chickens or quaker parrots presented any gross lesions.
The chicken with clinical signs had a perivascular and perineural lymphocytic infiltrate in the proventriculus.
Two of the quaker parrots (one from each treatment group) developed mild lymphoplasmacytic encephalitis and myelitis.
Our results suggest that autoantibodies against gangliosides in birds are not associated with a condition resembling PDD.

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