Occurrence of Newcastle disease (ND) and characterization of the Avian Paramyxovirus-1 (APMV-1) amongst backyard fowls (Gallus gallus domesticus) and pigeon (Columba livia domestica) was studied. ND was suspected in two fowl flocks (100% morbidity, 86% mortality) and six pigeon flocks (21.68% morbidity, 14.16% mortality) with respiratory and/or enteric clinical signs in fowls and predominantly neurological signs in pigeons was observed. Cloacal swabs, tissue lysates or infected allantoic fluid could haemagglutinate (HA) chicken erythrocytes and pigeon convalescent serum inhibited haemagglutination (antibody titres >1/16). A 534 bp product was amplified from clinical samples and infected allantoic fluids by Reverse Transcriptase PCR (RT-PCR) targeting a partial Fusion protein gene including its cleavage site. The fowl and pigeon isolate was found to be velogenic and lentogenic respectively by virulence characterization. Fowl isolate grown in chicken embryonated eggs (CEE) showed 10-8.68 Embryo Infectious Dose (EID50) with a Mean Death Time (MDT) of 51.43 h and the Intra-Cerebral Pathogenicity Index (ICPI) in day-old chicks was 1.51. Pigeon isolate had corresponding values of 10-7.20 EID50, MDT of 92.00 h and ICPI of 0.43. Deduced amino acid sequence at Fusion protein cleavage site showed 112R-R-R-K-R*F117 velogenic motif for the fowl isolate and 112G-R-Q-G-R*L117 lentogenic motif for the pigeon isolate. Both isolates were found to be 84.1% related phylogenetically, while fowl isolate clustered with genotype XIII, the pigeon isolate clustered with genotype II and vaccine strains of APMV-1. This is the first instance of APMV-1 characterization in the region with the possibility of a vaccine spill over in pigeons.

Chickens affected with Newcastle disease virus (NDV) genotype XIII and pigeons affected with genotype II were characterized for virulence and found to be velogenic and lentogenic respectively, based on protein translation of Fusion protein (F) gene and by Mean death time (MDT) and Intracerebral Pathogenicity Index (ICPI). Clinically, respiratory and/or enteric manifestations were exhibited by the chickens, whereas pigeons showed predominantly neurological signs. It was therefore pertinent to describe the salient pathological features or differences during spontaneous infections in the respective hosts. Disease was suspected in two flocks of backyard fowl (Gallus gallus domesticus) showing 100% morbidity and 86% mortality; and in six flocks of domesticated pigeons (Columba livia domestica) exhibiting 21.68% morbidity and 14.16% mortality in a study from August 2017 to July 2018. Gross lesions and microscopic lesions were typical for those described for ND, but viscerotropic lesions were prominent in fowls, while neurotropic lesions were more vivid in pigeons. Gross lesions were suggestive of vascular injury with haemorrhagic tracheitis, enteritis and sometimes petechiae observed in other organs. No prominent gross lesions were observed in the nervous tissue except in some birds showing congestion of meninges. Histologically, haemorrhages, mononuclear infiltration and lymphoid depletion were common. Lesions in nervous tissue were more pronounced in pigeons and represented focal gliosis, loss of Nissl substances and neuronal degeneration, satellitosis and neuronophagia. There was focal gliosis of the nerve tracts in the cerebellum indicating demyelination of nerve tracts. Consistent presence perivascular oedema, endothelial hypertrophy, necrosis and medial hyalinization were noteworthy. In some cases, vacuolation was observed in Purkinjee cells together with presence of intracytoplasmic inclusions. It is speculated that the relatively less pathogenic pigeon strain has sufficient time to generate an overt neurological lesion than the virulent fowl strain. The present findings highlight the salient differences in host pathology in chicken and pigeons and are believed to assist in diagnosis of the disease, particularly while attributing a particular pathotype to a prevalent strain.

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