The VLA reports that the problem was first seen approximately three months previously. Twenty piglets reported affected on the 11 June and by the 18 June, 30 were affected. There are no further reports of affected animals prior to publication of the report.

There are 5,000 pigs on the affected farm and to date, 30 post-weaners have been reported to have died with this condition. Other age groups are not affected although an erysipelas outbreak has been reported recently with approximately 100 of the finishing pigs affected that responded to treatment.

Observations

The carcasses from a ten-week-old male and a seven-week-old female piglet were examined.

Clinical Features

There are sporadic cases of piglets going off their legs approximately three to four weeks post-weaning (piglets are weaned at four weeks). The pigs are described as going weak on the front or hind legs, or of 'going floppy' whilst being bright consistent with spinal disease.

Pigs died within a few days. Occasional animals have been dyspnoeic with nasal discharge. Pig 1 was submitted live and clinical assessment showed inability to use its hind legs or place its feet and knuckling of the fetlocks. Mentation was normal and there was no evidence of gross joint swelling. A strong withdrawal reflex was present although the absence of deep pain was suspected. Pig 2 was presented dead with a history of 'going floppy.'

Pathology

Gross pathology in both pigs showed variable degrees of pulmonary cranioventral consolidation. No other significant changes were detected. No bacteria were isolated from the brains of either of the pigs.

Bacteriology yielded mixed growth including Streptococcus suis type 2 from the lung of the first piglet, and Staphylococcus chromogenes and S. xylosus from the liver of the second piglet.

Histopathology in both pigs showed inflammation of the central nervous system (CNS) orientated on grey matter. Pig 1 had a severe multifocal sub-acute lympho-plasmacytic encephalomyelitis with unequivocal neuronophagia orientated on the spinal cord and the caudal brain stem. In some of the perivascular cuffs and areas of neuroparenchymal inflammation, a certain number of granulocytes could be detected. In addition, a focal acute to sub-acute necrotising encephalitis in the piriform lobe was present.

Pig 2 had a severe multifocal lympho-plasmacytic encephalitis orientated on the grey matter of the caudal brain stem. Apart from prominent perivascular cuffs, there were large numbers of moderately well defined glial nodules suggestive of neuronal removal as well as some larger more extensive foci associated with eosinophils and macrophages predominantly in the grey matter. The spinal cord from pig 2 was not available for examination.

The histopathology is consistent with a diagnosis of an infectious encephalomyelitis.

Based on the clinical presentation and the histopathological findings, an infection with a porcine enterovirus or a porcine teschovirus was considered the most likely aetiological agent.

Alternative diagnoses included other neurotropic viral infections such as HEV, louping-ill virus and SuHV-1, as well as bacterial encephalitides such as S. suis and E. coli. PCV-2 and PRRSV were considered since they are common porcine viruses and have been associated with encephalitides, though not in the UK. Some paramyxoviruses have been associated with encephalitis in other countries, though usually in younger animals. Protozoal infections were considered, but no protozoal-like bodies could be detected at this stage of the investigation.

IHC failed to demonstrate any louping-ill antigen. Preliminary investigations using IHC with pan-Teschovirus anti-serum (040/4B1) failed to demonstrate any antigen in pig 1. However, the test has not been fully evaluated and the results have to be interpreted with care. Other viral disease that can involve the brain such as pseudorabies, CSF, ASF, MCF, porcine paramyxoviruses, encephalomyocarditis virus, rabies and swine vesicular disease have been considered. However, epidemiology, clinical presentation and histopathology are not those typically associated with these diseases.

Because of the inconsistent bacteriology and the lesion distribution, bacterial encephalitis appears very unlikely.

Reason for Concern

There was no reason for concern on the gross pathology as it was thought to be a likely diagnosis of a spinal abscess or S. suis meningitis. Only histopathology revealed the presence of an infectious encephalomyelitis not commonly detected in the UK.

Because of the unequivocal neuronophagia in pig 1, causes of viral encephalitis such as PEV (Picornaviridae), PTV (Picornaviridae), HEV (Coronaviridae), louping-ill virus (Flaviviridae) and SuHV-1 (Herpesviridae) have been considered.

To the best of our knowledge, the epidemiology and the character of the lesions most closely resembles that of an outbreak of polioencephalomyelitis due to the infection with a porcine enterovirus as described previously in the UK and other countries (Done, et al., 2005; Pogranichniy et al., 2003).

Concurrent infections including possible PCV-2 and PRRSV infection, though they have not been confirmed in the two pigs. Mycoplasma hyopneumoniae and Streptococcus suis Type 2 inconsistently found. Initial histopathology on the two pigs, failed to detect PCV-2 or PRRSV in the two pigs examined.

No human in contact with the pigs appear to have suffered from ill health.

The VLA concludes that it has been unable to reach a definitive aetiological diagnosis and that every effort is being made to attempt the isolation of a potential viral pathogen. However, no further cases have been reported at the moment. Porcine enterovirus is the main focus of the investigation at this stage. A protocol has been set up which would allow the detection of picornaviruses as well as other potential viruses. Initial immunohistochemical investigations did fail to demonstrate any louping-ill virus associated with the lesions in pig 1.

Bibliography

1. Done S.H., C.M. Gaudie, D.A.R. Hannam, P.O.D. Higgins, T. Drew, M. Banks, M.A. Jones and R. Graham. 2005 Polioencephalomyelitis: a case report. The Pig Journal 55: 167-175.
2. Pogranichniy R.M., B.H. Janke, T.G. Gillespie, K.J. Yoon. 2003. A prolonged outbreak of polioencephalomyelitis due to infection with a group I porcine enterovirus. Journal of Veterinary Diagnostic Investigation 15(2): 191-194.
3. Zell R., M. Dauber, A. Krumbholz, A. Henke, E. Birch-Hirschfeld, A. Stelzner, D. Prager, R. Wurm. 2001. Porcine teschoviruses comprise at least eleven distinct serotypes: molecular and evolutionary aspects. Journal of Virology. Feb; 75(4): 1620-1631.

Further Reading

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