Senecavirus A: First clinical case in an Ontario commercial swine herd

Josepha DeLay, Ryan Tenbergen, Margaret Stalker, Tim Blackwell, Davor Ojkic, Jim Fairles

Animal Health Laboratory, University of Guelph, ON (DeLay, Stalker, Ojkic); Demeter Veterinary Services, St. Nicolas, ON (Tenbergen); Ontario Ministry of Agriculture, Food, and Rural Affairs, Elora, ON (Blackwell)

AHL Newsletter 2019;23(4):9-10.

In June 2019, Senecavirus A (SVA) was detected in a farrow-to-finish, multi-site Ontario herd. Initially, 40% of lactating sows were acutely anorexic and pyrexic, and 10% of affected sows developed vesicles and ulcers on snouts and at coronary bands (Fig. 1A and 1B). Concurrently, diarrhea was identified in 50% of neonatal litters <7days of age, with high mortality (70%) among affected piglets.  The Canadian Food Inspection Agency (CFIA) was immediately notified when vesicles were observed, and a full investigation excluded foreign animal diseases, including: foot and mouth disease, swine vesicular disease, and vesicular stomatitis.  SVA was confirmed by PCR as the cause of vesicular lesions. 

Biofeedback was initiated to control the outbreak.  Clinical disease continued in the sow herd and among nursing piglets but gradually resolved, with increases in preweaning mortality, sow mortality and stillborn and mummified fetuses over the next 3-4 weeks.  Progression and monitoring of herd infection were accomplished by SVA PCR on oral fluids, carried out at the Animal Health Laboratory. Among piglets infected during the initial outbreak, PCR-based evidence of infection persisted for variable time periods and through all stages of production, although vesicular lesions were identified only in nursing and gestating sows and in gilts in the developer unit, and diarrhea was seen only in neonates.  Surviving nursing and nursery pigs were unthrifty, with uneven growth.  In a sample of piglets euthanized at weaning, postmortem examination identified lymphoplasmacytic inflammation in multiple organs including kidney, heart, liver, and brain.

Figures 1A and 1B. Snout (A) and coronary band (B) ulceration in Senecavirus A-infected sows.

Figures 1A and 1B. Snout (A) and coronary band (B) ulceration in Senecavirus A-infected sows.

Pathology investigation is ongoing into the association of widespread inflammatory lesions in nursery pigs with SVA. Animal and environmental monitoring continues for SVA elimination in the herd. Further investigation is in progress to determine the source of SVA infection in this outbreak. Although SVA has been detected at assembly yards in Ontario since 2016 and lesions have been observed in cull sows at these sites, this is the first case of SVA-associated disease in a commercial swine herd in Ontario.


1. Canning P et al. Neonatal mortality, vesicular lesions, and lameness associated with Senecavirus A in a U.S. sow farm. Transboundary and Emerg Dis 2016;63: 373-378.

2. Leme RA et al. Pathological, immunohistochemical, and molecular findings associated with Senecavirus  A-induced lesions in neonatal pigs.  J Comp Path 2016;155: 145-155.

3. Segalés J et al. Senecavirus A: An emerging pathogen causing vesicular disease and mortality in pigs? Vet Pathol 2017;54(1): 11-21.

Edema disease as the cause of neurologic signs in nursery pigs

Josepha DeLay, Đurđa Slavić, Clint Lichty

Animal Health Laboratory, University of Guelph, ON (DeLay, Slavić); South West Ontario Veterinary Services, Stratford, ON (Lichty)

AHL Newsletter 2019;23(4):10.

An acute episode of diarrhea and neurologic deficits involved 25% of nursery pigs in a 1200 head herd.  Post-weaning colibacillosis and bacterial meningitis due to Streptococcus suis were the main clinical differential diagnoses. Field postmortems were conducted on 2 euthanized pigs and samples were forwarded to the Animal Health Laboratory for evaluation. 

Colibacillosis was confirmed in both pigs based on histologic evidence of adherent bacilli at the luminal surface of enterocytes lining small intestinal villi, and isolation of Escherichia coli from feces of both pigs.  Both pigs also had variably severe atrophic enteritis suggestive of concurrent viral enteritis due to porcine rotaviruses or coronaviruses (no further testing pursued for confirmation).  Typical lesions of bacterial meningitis were not present, however focal edema was identified histologically in brainstem white matter of 1 pig.  Genotyping of fecal E.coli isolates confirmed the presence of F18 and stx2e toxin genes, compatible with the profile for the subset of E.coli responsible for edema disease in swine. F4/K88, F5/K99, and F41 fimbrial genes of other enterotoxigenic E.coli strains were not identified in the isolates, and F4/K88 and F5/K99 antigens were not detected by agglutination serotyping.

In this case, both diarrhea and cerebral edema leading to neurologic disease were attributed to F18 Stx2e-positive E.coli.  Stx2e toxin is produced by E.coli in intestine and is absorbed into the systemic circulation. The toxin acts at sites distant from intestine, targeting and injuring blood vessels in various organs causing edema.  Although clinical disease is dramatic, with a rapid and fatal course, gross and histologic lesions may be subtle.

Edema disease is rare, but is an important differential diagnosis for neurologic disease in nursery and early grower pigs. To date, 4 cases of edema disease have been diagnosed at the AHL in 2019. The diagnosis relies on identifying compatible gross and histologic lesions, in conjunction with culture of F18, Stx2e-positive E.coli from intestine. Palpebral and gastric mural edema may be seen grossly.  Diarrhea is often absent, and histologic evidence of intestinal colonization by the bacteria is uncommon. As a result, intestine is often not included for culture in pigs with neurologic signs, and the correct diagnosis can be missed.


Fairbrother JM and Nadeau, E. Colibacillosis in Diseases of Swine, 2019. JJ Zimmerman, LA Karriker, A   Ramirez, KJ Schwartz, GW Stevenson, J Zhang, ed.  p807-834.