Dr. Fabio Vannucci, a University of Minnesota swine pathologist and his graduate student Dr. Talita Resende collaborated with a team from South Dakota State University to study the pathogenesis of Senecavirus A in finishing pigs. The results of their experiments were published online a few weeks ago in the Journal of General Virology and the printed version should be following shortly.
The importance of Senecavirus A in swine production resides in a striking resemblance in clinical signs with Food and Mouth Disease. Indeed, Senecavirus A causes vesicular lesions around the mouth and on the feet of pigs.
The collaborative work showed that Senecavirus A viremia occurred between 3 to 10 days post-inoculation (dpi), and that the neutralizing antibody response started 5 dpi. Clinical signs first observed 4dpi, lasted up to 10 days.
This study advances our understanding of Senecavirus A pathogenesis to hopefully be able to better manage it in the future.
Abstract: Senecavirus A (SVA) is an emerging picornavirus that has been recently associated with vesicular disease and neonatal mortality in swine. Many aspects of SVA infection biology and pathogenesis, however, remain unknown. Here the pathogenesis of SVA was investigated in finishing pigs. Animals were inoculated via the oronasal route with a contemporary SVA strain SD15-26 and monitored for clinical signs and lesions associated with SVA infection. Viremia was assessed in serum and virus shedding monitored in oral and nasal secretions and feces by real-time reverse transcriptase PCR (RT-qPCR) and/or virus isolation. Additionally, viral load and tissue distribution were assessed during acute infection and following convalescence from disease. Clinical signs characterized by lethargy and lameness were first observed on day 4 pi and persisted for ~2-10 days. Vesicular lesions were observed on the snout and feet, affecting the coronary bands, dewclaws, interdigital space and heel/sole of SVA-infected animals. A short-term viremia was detected between days 3-10 post-inoculation (pi), whereas virus shedding was detected between days 1-28 pi in oral and nasal secretions and feces. Notably, RT-qPCR and in situ hybridization (ISH) performed on tissues collected on day 38 pi revealed the presence of SVA RNA in the tonsil of all SVA infected animals. Serological responses to SVA were characterized by early neutralizing antibody responses (5 days pi), which coincided with a progressive decrease in the levels of viremia, virus shedding and viral load in tissues. This study provides significant insights on the pathogenesis and infectious dynamics of SVA in swine.