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Pathological, Immunohistochemical and Molecular Findings Associated with Senecavirus A-Induced Lesions in Neonatal Piglets

This study investigated the cause of the mortality of piglets with cutaneous, enteric and neurological disorders from seven pig farms located in different geographical regions of Brazil. Twelve 1- to 5-day-old piglets were submitted for pathological evaluation. The principal gross findings included faint rib impressions on the pleural surface of the lungs (n = 9), diphtheritic glossitis (n = 6) and ulcerative lesions at the coronary band (n = 5). Histopathology revealed interstitial pneumonia (n = 12), myocarditis (n = 6), diphtheritic glossitis (n = 3), encephalitis (n = 3) and atrophy of intestinal villi with vacuolation of the superficial epithelial cells (n = 6). Immunohistochemistry with monoclonal antibodies specific for Senecavirus A (SenV-A) demonstrated immunoreactivity of the choroid plexus of the cerebrum, degenerate epithelium of ulcerative lesions of the tongue, the urothelium of the kidney and urinary bladder, and the superficial cells of the intestine. Reverse transcriptase polymerase chain reaction (PCR), PCR and/or quantitative PCR assays were used to investigate viral agents associated with vesicular and/or enteric diseases. Antigens and RNA of SenV-A were identified in multiple tissues of all piglets; molecular assays for all other viruses evaluated yielded negative results. These findings confirm the participation of SenV-A in the multiple lesions observed in these piglets. Several theories are proposed: SenV-A may be eliminated via the urinary system, neurological disease may occur due to initial invasion of choroid plexus, enteric disease may be related to atrophy and fusion of villi of the small intestine, and vertical transmission could be a form of dissemination.

Leme RA, Oliveira TE, Alfieri AF, Headley SA, Alfieri AA; Pathological, Immunohistochemical and Molecular Findings Associated with Senecavirus A-Induced Lesions in Neonatal Piglets; J Comp Pathol. 2016 Aug-Oct;155(2-3):145-55. doi: 10.1016/j.jcpa.2016.06.011. Epub 2016 Jul 26. PMID: 27473601 DOI: 10.1016/j.jcpa.2016.06.011