In the past we have demonstrated that the pathogenesis of the often fatal syndrome known as “Proventricular Dilatation Disease” (PDD) in parrot is an autoimmune reaction. During the PDD development, intramural myoenteric ganglia are progressively damaged by anti-ganglioside specific auto-antibodies and sensitized lymphocytes and monocytes. We have shown the presence and localization of these auto-antibodies by IHC and immunoelectron microscopy in the crop or gastrointestinal ganglia of parrots, some of which showing severe clinical signs of PDD. In 85% of 40 parrots (34 parrots) belonging to different genera and species, with various clinical signs and positive crop biopsies for PDD, we have evidenced an high titre of anti-gangliosides antibodies, detected by an ELISA test. Of these 34 parrots, 60% (20 parrots) showed avian bornavirus P40 protein specific antibodies in the ELISA test. EM examination showed the presence of dense deposits (probably antibody-complement complexes) over presynaptic motor axons, accompanied by ultrastructural signs of damage. Using immuno-electron microscopy, we observed deposits of antibodies equally distributed on both neuronal and perisynaptic Schwann cells (pSC) membranes, and ultrastructural evidences of injury at both sites. These data demonstrated that both presynaptic neuronal membranes and pSCs are targets for anti-ganglioside antibodies and that probably specific complement components might mediate the injury to both sites. In our opinion this pathogenetic mechanism is independent of a specific aetiological agent (i.e. Bornavirus, Paramyxovirus or other viruses or bacteria). To validate our hypothesis, we tested the 40 sera of PDD affected birds also for lipo-oligosaccharide (LOS) from Campylobacter jejuni, which shows a remarkable structural and antigenic similarities with the gangliosides. The presence of cross-reactivity strengthens the autoimmune theory as the cause of the syndrome.
PARROT'S PDD IS A MULTIFACTORIAL DISEASE? NEW PATHOGENETIC EVIDENCES FOR AN AUTO-IMMUNE GANGLIONEURITIS
ROSSI GIACOMO;GALOSI LIVIO;PICCININI ANDREA;
2014-01-01
Abstract
In the past we have demonstrated that the pathogenesis of the often fatal syndrome known as “Proventricular Dilatation Disease” (PDD) in parrot is an autoimmune reaction. During the PDD development, intramural myoenteric ganglia are progressively damaged by anti-ganglioside specific auto-antibodies and sensitized lymphocytes and monocytes. We have shown the presence and localization of these auto-antibodies by IHC and immunoelectron microscopy in the crop or gastrointestinal ganglia of parrots, some of which showing severe clinical signs of PDD. In 85% of 40 parrots (34 parrots) belonging to different genera and species, with various clinical signs and positive crop biopsies for PDD, we have evidenced an high titre of anti-gangliosides antibodies, detected by an ELISA test. Of these 34 parrots, 60% (20 parrots) showed avian bornavirus P40 protein specific antibodies in the ELISA test. EM examination showed the presence of dense deposits (probably antibody-complement complexes) over presynaptic motor axons, accompanied by ultrastructural signs of damage. Using immuno-electron microscopy, we observed deposits of antibodies equally distributed on both neuronal and perisynaptic Schwann cells (pSC) membranes, and ultrastructural evidences of injury at both sites. These data demonstrated that both presynaptic neuronal membranes and pSCs are targets for anti-ganglioside antibodies and that probably specific complement components might mediate the injury to both sites. In our opinion this pathogenetic mechanism is independent of a specific aetiological agent (i.e. Bornavirus, Paramyxovirus or other viruses or bacteria). To validate our hypothesis, we tested the 40 sera of PDD affected birds also for lipo-oligosaccharide (LOS) from Campylobacter jejuni, which shows a remarkable structural and antigenic similarities with the gangliosides. The presence of cross-reactivity strengthens the autoimmune theory as the cause of the syndrome.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
