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

Jianhua Guo,Jeann Leal De Araujo,Raquel R Rech,Aline Rodrigues Hoffmann,J Jill Heatley,Ian Tizard

doi:10.7717/peerj.3144

Abstract

The identification of Parrot bornaviruses (PaBV) 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. Although the most accepted theory indicates that PaBV directly triggers an inflammatory response in this disease, another hypothesis suggests the disease is triggered by autoantibodies targeting neuronal gangliosides, 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. The first study was performed on 17 healthy chickens (Gallus gallus domesticus): 11 chickens were inoculated with a brain ganglioside extract in Freund’s complete adjuvant (FCA) and six chickens inoculated with phosphate-buffered saline. A second study was performed five healthy quaker parrots (Myiopsitta monachus) that were divided into 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. One chicken developed difficult in walking. Histologically, only a mild perivascular and perineural lymphocytic infiltrate in the proventriculus. Two quaker parrots (one from each treatment group) had mild lymphoplasmacytic encephalitis and myelitis. However, none of the quaker parrots developed myenteric ganglioneuritis, suggesting that autoantibodies against gangliosides in birds are not associated with a condition resembling PDD.

Highlights

Parrot bornaviruses (PaBV) are consistently isolated from psittacine birds with proventricular dilatation disease (PDD) (Honkavuori et al, 2008; Kistler et al, 2008), the pathogenesis of this condition still remains unclear since not all infected birds develop clinical signs
The pathogenesis of PDD has been linked to two main hypotheses: the first and most accepted theory states that parrot bornaviruses (PaBV) spreads throughout the nervous system and directly triggers the inflammatory and immunological changes that lead to damage in the central nervous system (CNS), the enteric nervous system and peripheral nerves (Piepenbring et al, 2016)
This study aimed to evaluate the relationship between the experimental inoculation of gangliosides or crude nervous tissues and the development of neurologic disease in chickens (Gallus gallus domesticus) and PaBV-free quaker parrots (Myiopsitta monachus) that could resemble PDD

Summary

Introduction

Parrot bornaviruses (PaBV) are consistently isolated from psittacine birds with proventricular dilatation disease (PDD) (Honkavuori et al, 2008; Kistler et al, 2008), the pathogenesis of this condition still remains unclear since not all infected birds develop clinical signs. Several mechanisms have been proposed to explain how PaBV causes ganglioneuritis as well as the encephalomyelitis in birds (Piepenbring et al, 2012). The second hypothesis proposes the pathogenesis of PDD in psittacine birds is caused by the production of autoantibodies targeting components of the nervous system (Rossi, Crosta & Pesaro, 2008), a similar mechanism to an autoimmune condition of humans called Guillain–Barré syndrome (GBS)

Objectives

Methods

Results

Conclusion