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Proventricular Dilatation Disease (PDD) affects parrots with clinico-pathological aspects similar to those of the Guillain-Barre syndrome (GBS), a human neurophathy. We observed that in sera of PPD-affected parrots antibodies to gangliosides were detectable, similarly to that observed for GBS, and that quantification of such antibodies could be diagnostic for PDD. Then, we proved that administration of purified gangliosides to parrots, elicited autoimmune response and a pathological outcome similar to that of natural PDD. We propose this model not only for better studying PDD, but also as the basis for developing a reliable animal model of GBS. Patients with Guillain-Barre syndrome (GBS) suffer from an acute onset of autoimmune neuropathy, that can lead to death or significant disability. Relatively little is known about aetiology of GBS. Early diagnosis, which is important as prompt intervention can arrest or reverse the disease, can be difficult. The presence of anti-ganglioside antibodies can confirm the diagnosis. GBS is commonly classified into four major subtypes: acute inflammatory demyelinating polyneuropathy (AIDP), acute motor axonal neuropathy (AMAN), acute motor and sensory axonal neuropathy (AMSAN), and Miller Fisher syndrome (MFS). MFS is closely associated with antibodies to GQ1b and AMAN with antibodies to GM1, but antibodies to other gangliosides have also been reported. In recent decades wasting syndrome was described in macaws and other parrot species, spreading at an alarming rate. Now known as Proventricular Dilatation Disease (PDD), it is a segmental neuropathy characterised by a non-suppurative lymphocytic, plasmacytic ganglioneuritis of central and peripheral nerve tissue. Besides the classical syndrome of weight loss associated with regurgitation and the passage of undigested food in the faeces, clinical signs also include ataxia, abnormal head movements, progressive paresis, proprioceptive deficits, anorexia, lethargy and, occasionally, sudden death. Many clinico-pathological aspects of parrot PDD resemble those of human GBS. The scientific literature is controversial about the nature and aetiology of both pathologies. For more than 30 years, PDD, similarly to GBS, has been a mysterious disease and, being a killer of captive parrots, has sent chills of terror down the spines of bird lovers. Several viral aetiological agents have been proposed 4. and immune-mediated reactions to an unknown viral agent has been hypothesized to be at the origin of the disease; however, experimental evidence is lacking. Some studies reported the presence of viral-like particles in fresh faeces from affected birds, and also in the brain. The disease was experimentally transmitted by exposing susceptible birds to a tissue homogenate presumably containing these particles; however to date, this viral-like agent has not been identified, recently, a type of bornavirus, a family of viruses that cause encephalitis in horses and livestock, has been implicated in PDD. Presently, although a presumptive diagnosis of PDD may be based on clinical signs and gross pathology, definitive diagnosis requires histology. Antemortem evaluation of crop biopsies is diagnostic in approximately 75% of birds with PDD. Detection of serum antibodies to certain viruses has been unsuccessful as a diagnostic method and in establishing a viral aetiology. We hypothesized for PPD an autoimmune mechanism involving gangliosides. Thus, we purified gangliosides from the peripheral nervous system of parrots. Anti-ganglioside antibodies were detected by ELISA and Dot blot in 121 out of 505 parrot sera, 86 (17%) corresponding to symptomatic and histology-positive birds, and 35 (7%) belonging to asymptomatic parrots. These latter were subjected to histopathological analysis, revealing periganglia infiltrates in crop biopsies, thus indicating an early stage of disease, no binding to GT1b was observed in any of the sera. All

Parrot proventricular dilatation disease: a possible model of Guillain-Barré syndrome?