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African swine fever (ASF) is a devastating haemorrhagic disease of domestic pigs, which can cause mortality up to 100%. Sudden mortality in pigs following an acute course of systemic disease was investigated in Mizoram state of India and confirmed the outbreak as ASF. Affected pigs suffered from severe depression, high fever, bloody diarrhoea, cutaneous haemorrhages and showed haemorrhagic lesions in visceral organs. The outbreak was confirmed by detection of p72, p54 and the central variable region of B602L genes by PCR in representative tissue samples collected from dead pigs. The nucleotide and phylogenetic analyses of p72, p54 and B602L characterized the ASFV as genotype II. Interestingly, the analysis of B602L gene has revealed that the ASFV from Mizoram state of India is more closely linked to the Eurasian ASFV strains isolated prior to 2014 and discriminated the Indian strains in two separate groups indicating that the source of origin for the Mizoram outbreak could be different from that of the other states of India. [ABSTRACT FROM AUTHOR]

This study reports for the first time a natural outbreak of highly pathogenic porcine reproductive and respiratory syndrome (HP‐PRRS) caused by HP‐PRRS virus (HP‐PRRSV) in wild pigs characterized by sudden onset of depression, anorexia, respiratory distress, and high fever. The disease has caused severe haemorrhagic pneumonia, haemorrhagic lymphadenitis, enlarged spleen with areas of infarction, and petechial haemorrhages on the myocardium and on the surface of kidneys. HP‐PRRSV was detected in representative tissue samples by reverse transcription‐PCR, and the field strain was isolated in the MA104 cell line. The phylogenetic analyses based on the whole genome sequences and nucleotide sequences of open reading frame 5 (ORF5) gene showed close grouping with the subtype IV of lineage 8/8.7 of PRRSV II, which represents the HP‐PRRSV strains that predominate in the pig population of China since 2010. The amino acid sequence analysis of the ORF5 gene revealed the replacement of leucine (L) at position 39 to isoleucine (I) in the primary neutralizing epitope. Among the four potential N glycosylation sites, the N34 was mutated and found to be restricted to only three N glycosylation sites. The present findings have indicated that HP‐PRRSV can cause fatal outbreaks and may emerge as a major threat to the wild pig population. [ABSTRACT FROM AUTHOR]