5-week-old male Yorkshire crossbred, Sus scrofa domestica, pig.Three early weaned piglets, each weighing approximately 9 kg, were submitted alive with listlessness and mostly hind limb ataxia and paresis of 4 days duration. One had been treated with dexamethasone and penicillin, with no results. Morbidity was qualified as moderate and mortality was not recorded at time of submission. No other clinical signs were reported. All other affected piglets recovered.
No significant gross lesions were seen (the whole CNS was examined in all piglets).
Spinal cord: There is an extensive, moderate nonsuppurative poliomyelitis involving mainly the ventral horns.Â It is characterized by mild to moderate lymphocytic perivascular cuffing, gliosis mostly in the form of glial nodules, and degeneration/ necrosis in large ventral horn (motor) neurons with neuronal loss and neuronophagia.Â The necrotic neurons perikaryon is either swollen, markedly vacuolar and fibrillar or shrunken and hypereosinophilic; nuclei are either absent or pycnotic/ karyorrhectic.Â Microglial cells/macrophages can be seen around and within necrotic neurons (neuronophagia).Â Mostly in the dorsal funiculi, there is Wallerian degeneration characterized by dilated myelin sheaths with axonal loss and occasional necrotic macrophages (myelinophage).Â Similar lesions were present in all sections of cervical, thoracic and lumbar spinal cord examined.
Brain (not provided): there were similar but milder lesions with minimal neuronal changes in the brain stem; a mild multifocal nonsuppurative leptomeningitis was also present.
Moderate and extensive nonsuppurative poliomyelitis with marked neuronal necrosis and loss, and neuronophagia (ventral horns).
Enterovirus was isolated from a pool of fresh brainstem and spinal cord samples; it was not serogrouped.
No microscopic lesions were seen in other organs.Â Based on case history, microscopic lesions and isolation of enterovirus, a diagnosis of enteroviral polioencephalomyelitis, most consistent with Talfan disease, was given.Â Enteroviruses (genus Enterovirus, family Picornaviridae) are found in the enteric tract of humans and animals.Â Porcine enteroviruses (PEVs) were classified into 13 serotypes (PEV 113) that are antigenically related strains with variable virulence.Â These serotypes have further been grouped into groups I (PEV serotypes 17 and 1113), II (PEV-8), and III (PEVs 9 and 10).Â Group I is now reclassified as Teschovirus.(7)
PEVs are ubiquitous and intestinal infection is frequent but most infections are asymptomatic.Â PEVs undergo local replication in the large intestine and ileum, mucosal lymphoid tissues and lymph nodes, followed by viremia that can lead to the central nervous system infection.Â The infrequent disease can appear in the postweaning period (generally 6 to 10 week-old pigs) secondary to mixing of pigs from different sources and decreased maternal immunity, and can result in mild to severe neurological disorders.(2) PEV serotype I is highly virulent and the causative agent of Teschen disease.Â Clinical signs are acute and include fever, ataxia, seizures, convulsions, opisthotonos, coma and death; mortality is high.Â Milder infections (also known as Talfan disease, poliomyelitis suum, benign enzootic paresis and Ontario encephalomyelitis) are linked to less virulent strains and clinical signs include ataxia, limb paresis, flaccid paraparesis or paraplegia; mortality is usually low and most pigs can recover.Â
There are no gross lesions in enteroviral polioencephalomyelitis.Â Microscopically, lesion distribution depends on the involved strain, but the cerebrospinal axis from the olfactory bulb to the lumbar cord is consistently involved.(3) As described above, there is progressive lymphocytic perivascular cuffing and infiltration of mononuclear cells (nonsuppurative polioencephalomyelitis) into the neuropil secondary to motor neuron degeneration in the ventral gray column.Â Neuronophagia and glial nodules, characteristic of CNS viral infections, are key features.Â Gray matter of the spinal cord and adjacent dorsal root ganglia (ganglioneuritis) are more involved than white matter, and changes in the dorsal horn are milder than in the ventral horn.(6) Other changes may be present, such as vacuolation at the periphery of the soma of neurons.Â There is relative sparing of the cerebral and cerebellar cortices, contrary to the deep substance of the cerebellum that is consistently and severely involved.Â Lesions can also be found in the pontine nuclei, medulla, thalamus and periaqueductal gray matter.(5) Leptomeningitis may be patchy and sometimes severe in the cerebellum in the older pigs in which the course is prolonged.(3)
Transmission electron microscopic examination reveals separation of ribosomes from the endoplasmic reticulum and loss of Nissl body clusters that provoke a progressive dilation of the endoplasmic reticulum.(5)
Survival is possible sometimes with sequelae.Â Extraintestinal infections are relatively transient, whereas the virus persists in the large intestine for several weeks.(2)
In this case, differential diagnoses included Teschen disease, Talfan disease and hemagglutinating encephalomyelitis virus (HEV) infection.Â To our knowledge, Teschen disease is not known to occur in North America and is associated with high mortality rates.Â HEV was not isolated and would also have induced higher mortality rates.Â Porcine reproductive and respiratory syndrome (PRRS) should also be considered in cases with concomitant pulmonary lesions.Â
PEV are specific and are not zoonotic.Â Although PEV are different from the human enterovirus (poliovirus) that is responsible for acute flaccid paralysis called polio, histological lesions induced by poliovirus are quite similar to those described above.(4)
Other enteroviruses are encountered in swine (Swine Vesicular Disease virus) and in mice (Theilers murine encephalomyelitis virus infection).Â The virus causing avian encephalomyelitis, formerly classified as an enterovirus, has now been reclassified as a hepatovirus.(1)
Spinal cord, ventral horns: Neuronal necrosis, multifocal, marked, with gliosis, satellitosis, neuronophagia, and dorsal funiculi axonal degeneration.
The contributor provided the most common examples of viruses that are typical ruleouts for this disease.Â Other viral etiologies considered by conference participants were rabies virus, porcine herpesvirus 1 (pseudorabies), and Japanese encephalitis virus.Â With rabies virus infection, there is perivascular cuffing, focal gliosis, hemorrhage, neuronal degeneration, vacuolation of neurons and neuropil, and intracytoplasmic Negri bodies (3).Â Pseudorabies presents histologically as a nonsuppurative meningoencephalitis with trigeminal ganglioneuritis, with marked neuronal degeneration and necrosis and eosinophilic intranuclear inclusion bodies can be seen within numerous cells in the CNS (8).Â Japanese encephalitis virus is often found in stillborn and neonatal piglets, and is histologically very similar to Teschen/Talfan disease.Â Gross lesions include hydrocephalus, cerebellar hypoplasia, hypomyelinogenesis, and anasarca (3).
Another rule out that was regarded by conference participants was toxic poliomyelomalacia caused by selenium; however, this would present as a bilaterally symmetric malacia with distribution in the white and gray matter, with loss of neurons and endothelial and glial proliferation (3).Â
This case provides wonderful examples of neuronophagia, neuronal necrosis, and satellitosis, which are characteristic of this and other cases of viral encephalitis.Â It is difficult to distinguish neurogenic viral etiologies by histology alone, and special diagnostic techniques are usually required.
There was some variation between slides in this case, most notably in the number of spinal nerves, some of which had perivascular inflammatory cells.Â .Â
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