Rebecca Egan, Josepha DeLay, Davor Ojkic, Jim Fairles, Marty Misener, Clint Lichty

Animal Health Laboratory, University of Guelph, ON (Egan, DeLay, Fairles, Ojkic); South West Ontario Veterinary Services, Stratford, ON (Misener, Lichty)

AHL Newsletter 2020;24(1):10-11.

In December 2019, neurologic signs (predominately ataxia) were initially observed in a low number of pigs (~0.5%) upon entry to the nursery or within 1-4 weeks of placement. Disease was unresponsive to antibiotic therapy and progressed to death in all affected pigs within 24 to 48 hours of first signs. At its peak, the overall morbidity rate reached approximately 12% in this nursery, and while the majority of deaths occurred 2-4 weeks following placement, some deaths occurred as late as 5 to 7 weeks. Similar clinical signs were also identified in pigs in a second nursery barn sourced from the same closed sow herd. Two field postmortems were performed, and tissues were submitted to the AHL for histologic examination.  The following day, 3 live pigs were brought to the AHL for euthanasia and immediate postmortem. Non-suppurative encephalomyelitis was identified histologically in both sets of pigs (Fig. 1). Inflammation and neuronal necrosis were concentrated in gray matter of midbrain, brainstem, and cervical spinal cord. Porcine hemagglutinating encephalomyelitis virus (PHEV), rabies virus, and bacteria were not detected in brain by PCR (viruses) or culture (bacteria). 

Representative brain samples from 2 pigs were forwarded to the Iowa State University Veterinary Diagnostic Laboratory for porcine sapelovirus, porcine teschovirus, and porcine astrovirus 3 testing. Porcine sapelovirus DNA was detected by PCR in both brain samples, and porcine teschovirus nucleic acid was detected concurrently in the brain of 1 pig. Although the clinical syndrome seen in this case (low mortality) was not typical of the immediately notifiable “Teschen disease” form of teschovirus infection, detection of teschovirus necessitated reporting to the Canadian Food Inspection Agency (CFIA). Further investigation was required, and these sapelovirus and teschovirus isolates were sequenced by the CFIA.

Historically, porcine enteroviruses (serotypes 1 to 11) have been members of the genus Enterovirus in the Picornaviridae family. Recent reclassification has resulted in the generation of two new genuses, the Teschovirus genus (serotypes 1-7 and 11-13, now porcine teschovirus) and the Sapelovirus genus (serotype 8, now porcine sapelovirus A). Porcine enterovirus serotypes 9 and 10 (PEV-9 and PEV-10) remain in the Enterovirus genus. Enteric infection with these viruses is often acquired post-weaning, coinciding with waning maternal antibodies and mixing of animals; however, most infections remain asymptomatic. Infection with virulent strains may produce clinical neurologic disease in 2 typical forms: a severe and highly fatal form (Teschen disease), and a milder form (Talfan disease).

In recent years, similar cases of neuroinvasive sapelovirus infection have been reported in pigs in the United States and Europe. While entero-like viruses including sapeloviruses are commonly carried in the intestinal tract of healthy animals, factors precipitating spread to the central nervous system have yet to be elucidated. To date, sapelovirus-associated neurologic disease has not been reported in other species. In an acute outbreak of neuroinvasive sapelovirus infection reported elsewhere, all affected animals were from a single nursery source and were placed in two different finisher barns at 9 weeks of age. Over the following 3-week period, the onset and progression of clinical signs was variable in affected pigs, and included decreased feed/water consumption, dullness, ataxia, incoordination, paresis, and paralysis. Deep pain perception and withdrawal reflexes were maintained in hind limbs, and cranial nerve deficits were not observed. Histologic lesions were similar to those described in our case, and PCR testing for porcine enterovirus, porcine teschovirus and porcine sapelovirus consistently detected porcine sapelovirus. Overall, the reported morbidity and case fatality rates were 20% and 30%, respectively.  These rates differ from the Ontario cases, which had a lower morbidity rate (~12%) and higher case fatality (~100%). In light of these recent findings, porcine sapelovirus and teschovirus encephalomyelitis should be included as differential diagnoses in cases of neurologic disease, particularly in nursery pigs. AHL

References

1. Schock A et al. Investigation into an outbreak of encephalomyelitis caused by a neuroinvasive porcine sapelovirus in the United Kingdom. Veterinary Microbiology 2014;172:381-389.

2. Arruda PHE et al. Detection of a novel sapelovirus in central nervous tissue of pigs with polioencephalomyelitis in the USA. Transboundary and Emerging Diseases 2017;64:311-315. https://onlinelibrary.wiley.com/doi/epdf/10.1111/tbed.12621 [1]

3. Arruda PHE et al. Identification of a divergent strain of sapelovirus associated with a severe polioencephalomyelitis outbreak in the US.. Swine Health Information Center. https://www.swinehealth.org/sapelovirus/ [2]

4. Cantile C, Youssef, S. Enterovirus/teschovirus polioencephalomyelitis of pigs. In: Jubb, Kennedy, and Palmer's Pathology of Domestic Animals, 6th ed. Maxie MG, ed. Elsevier, 2016; vol 2:372-373.