Teschovirus encephalomyelitis (formerly known as porcine enteroviral encephalomyelitis) is analogous to human poliomyelitis. Severe disease is now rare; it is seen in eastern Europe and Madagascar but was last reported in western Europe from Austria in 1980. In other countries, sporadic mild disease is reported, or the disease is unrecognized.
Etiology, Epidemiology, and Pathogenesis
Until 1999, viruses causing this disease were classified within the genus Enterovirus (family Picornaviridae). However, analyses of their complete genome sequences revealed them to be very different from the enteroviruses, and they were reclassified in a new genus, Teschovirus, as the species Porcine teschovirus (the name was derived from Teschen disease). In 2015, the species was renamed to Teschovirus A to remove reference to the host species; however, the virus common name remains porcine teschovirus (PTV). Originally, 11 porcine enterovirus (PEV) serotypes were defined by virus neutralization. Of these, PEV 1–7 and 11–13 have been renamed PTV 1–10. Additional serotypes (PTV 11–13) have also recently been described, and it is likely more serotypes will be discovered in the future. PEV-8 has been reclassified as a member of a new picornavirus genus, Sapelovirus. PEV types 9 and 10, which have not been associated with neurologic disease, are distinct from the teschoviruses and remain in the Enterovirus genus. PTVs are ubiquitous in swine populations throughout the world. Many strains are nonpathogenic, but most neurotropic strains belong to one of the first three serotypes; serotype 1 includes not only the highly virulent but also many of the less virulent neurotropic strains. Although antigenic subtypes are recognized, they do not distinguish between more or less virulent strains of virus. PTV can survive in the environment for months.
Transmission is by direct or indirect contact with infected pigs. The virulent serotype 1 strain of classical Teschen disease results in high morbidity and mortality in all ages of pigs but apparently has remained confined to certain geographic areas. Mild, sporadic disease is seen elsewhere. Conventional herds are usually endemically infected, and exclusion of teschoviruses from SPF herds is difficult to maintain. Infection is mainly inapparent, and pigs usually become infected at weaning with the decline of passive maternal immunity and mixing of groups. Sporadic clinical cases of nervous disease are seen mainly around this time, although disease is more common in unweaned piglets after introduction of a serotype to which the herd has not been exposed.
Ingested virus replicates in the GI tract and associated lymphoid tissue. There is no destruction of gut epithelium, but virus is shed from multiplication sites into the feces for several weeks. In some pigs, especially those infected with virulent strains, viremia ensues and results in spread of infection to the CNS.
In acute virulent infection, clinical signs appear 1–4 wk after exposure in pigs of all ages. Ataxia is often seen first, followed by fever, lassitude, and anorexia. Seizures, nystagmus, opisthotonos, and coma may occur. Paralysis, initially evident as paraplegia but progressing to quadriplegia, is frequent in severe cases. Death is common within 3–4 days of onset of signs.
In mild disease, signs are essentially ataxia and paresis, the latter more rarely progressing to paralysis. Only young pigs (unweaned or weaned) are susceptible, and recovery is frequent.
There are no gross lesions. Microscopic changes are most prominent in the gray matter of the brain stem, cerebellum, and spinal cord. The nonsuppurative encephalitis is characterized by neuronal necrosis, neuronophagia, glial foci, and perivascular lymphocytic cuffing. Meningitis is often present over the cerebellum.
The clinical signs (especially those of locomotor disturbance), epidemiology, and absence of specific gross necropsy findings offer a presumptive diagnosis. The nature and distribution of histologic lesions provide supportive evidence. Acute and convalescent serum samples, taken ≥2 wk apart, may demonstrate a rise in neutralizing or complement-fixing antibodies. Virus isolation from the CNS is required to confirm the diagnosis. Differentiation of severe and milder forms of the disease can be based only on serologic, clinical, and epidemiologic evidence.
Differential diagnoses include the many other viral encephalitides of pigs, particularly classical swine fever, African swine fever, pseudorabies, rabies, and the encephalopathies of edema disease and water deprivation/salt intoxication. The prominent locomotor signs in teschovirus encephalomyelitis also can be confused with several toxic and nutritional neuropathies.
The different serotypes are identified either by virus neutralization, complement fixation, or ELISA using specific antisera. Genome sequence data is available for all the PTV serotypes, and molecular diagnosis by reverse transcriptase-PCR (RT-PCR) and real-time RT-PCR has been described.
Treatment and Control
There is no treatment. Live attenuated vaccine is used for control in areas experiencing severe endemic disease. In the past, eradication measures in central Europe involved ring vaccination and slaughter and also restrictions on importation of pigs and pork products. In many countries, suspected disease must be reported to regulatory authorities. In herds with endemic mild clinical disease, introduction of new breeding stock ≥1 mo before breeding should enhance passive immunity in offspring.
Last full review/revision March 2015 by Nick J. Knowles, MPhil