First experimental proof of Rotavirus A (RVA) genotype G18P inducing the clinical presentation of 'young pigeon disease syndrome' (YPDS) in domestic pigeons (Columba livia)
Young pigeon disease syndrome (YPDS) is characterized as a seasonally occurring, acute and primarily enteric medical condition of mainly juvenile domestic pigeons (Columba livia) with highly variable mortality reaching more than 50%. Although the syndrome has been known in Europe for almost three decades, its aetiology remains largely obscure. Recently, a previously unknown pigeon-associated clade of Rotavirus A (RVA) genotype G18P was detected in Europe and Australia in association with fatal diseases resembling YPDS. Here we show for the first time, that peroral inoculation of healthy juvenile homing pigeons with two genetically different cell culture isolates of RVA G18P (106.3 foci-forming units per bird) induces an acute and self-limiting YPDS-like disease in all infected birds. Clinical signs included regurgitation, diarrhoea, congested crops, anorexia and weight loss, as described for naturally RVA-infected pigeons. In agreement with the original outbreaks, RVA isolate DR-7 induced more pronounced clinical signs as compared to isolate DR-5, indicating strain-dependent virulence factors to contribute to variable disease outcomes observed in the field. All inoculated birds developed rotavirus-reactive antibodies starting at seven days after inoculation. High levels of viral RNA and infectious virus were detectable in cloacal swabs and faecal samples already three days after inoculation. While shedding of infectious virus subsided within few days, moderate viral RNA levels were still detectable in cloacal swabs, faeces, and tissue samples at the end of the experiment three weeks after inoculation. Histopathological analysis at this time point revealed inflammatory lesions in spleens and livers of pigeons from both infected groups. In summary, we fulfilled Henle-Koch's postulates and confirmed RVA G18P as a primary cause of YPDS-like diseases in domestic pigeons. By establishing an infection model, we provide a crucial tool for future research, such as identification of transmission routes and establishing vaccination regimes.
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