While Avian Borna Virus (ABV) appears to be the causative agent of PDD, the relationship of ABV in the pathogenesis of this disease remains unclear. In an epidemiological survey, ABV was present in many but not all parrots with symptoms of PDD1- 3. The signifi cance of this disjunct suggests that there may be at least an additional factor at play. This discrepancy may result from the fact that PDD-like symptoms may be induced by ABV as well as by other, unrelated viruses or bacteria that induce an auto-immune ganglioneuritis or undiscovered ABV strains with divergent genomes may exist. There have been no studies directed to address this discrepancy in testing for parrots with symptoms of PDD that are negative for ABV. Studies in humans have demonstrated that an infection with the intestinal pathogen Campylobacter jejuni may lead to Guillain-Barrè Syndrome (GBS), a ganglioneuritis very similar to PDD. Abs against the ganglioside GM1 have been demonstrated in GBS patients. In order to assess if a similar role may exist in parrots, we tested a serum collection of parrot for C.jejuni lipooligosaccharide (LOS). There was a 93% cross reactivity with sera from clinically positive parrots with PDD symptoms that were also positive for anti gangliosides using the ELISA-test. There was no reactivity in unaffected control parrots. This suggests a possible role of C.jejuni infection, besides that of ABV, in the pathogenesis of the clinical symptoms of parrots with PDD.