A diverse group of diseases are caused by closely related viruses in the family Picornaviradae; the virus family has recently been reorganized. Enterovirus was one of seven genera in the family under the former taxonomy and contained numerous virus species to which swine were known to be susceptible, with virus species further designated by a serotyping scheme. Around 2000, the taxonomy was revised based on genomic sequence data. Currently, porcine enterovirus 1 (PEV 1, the prototype “Teschen virus” and “Talfan virus”), PEV 2 through 7, and PEV 11-13 have been moved to a new genus called Teschovirus. Porcine enteroviruses 8-10 remain in the original Enterovirus genus. Diseases manifested by the different viruses vary widely and include polioencephalomyelitis, female reproductive failure, myocarditis, pericarditis, pneumonia, and diarrhea.
Porcine picornaviruses are ubiquitous. They occur only in swine and most infections are asymptomatic. Teschen disease, the most virulent picornaviral infection, causes polioencephalomyelitis (PEM). The disease occurs only in central Europe and parts of Africa. Talfan disease, a similar but less severe disease, causes PEM in Europe, North America and Australia. Outbreaks in North America have occurred infrequently and been of minor significance.
Teschen disease first was reported in Czechoslovakia over 65 years ago. Talfan disease was reported over 40 years ago. Both diseases, and other rather pathogenic picornaviral diseases, are well controlled and confined geographically and do not cause widespread problems in leading swine-raising countries. Other serogroups can occasionally cause polioencephalomyelitis outbreaks in the US.
Picornaviruses were once believed to be major causes of female reproductive failure and to cause stillbirths, mummification of fetuses, embryonic deaths and infertility (SMEDI). Although picornaviruses rarely can cause these abnormalities and occasional abortions, they are much less important than other known viral causes of reproductive failure. The picornaviruses are believed to cause other lesions or signs (including myocarditis, pericarditis, pneumonia and diarrhea), occur infrequently and seldom result in severe losses.
There are more than 50 strains of porcine picornavirus. They can be grown readily in cell cultures of porcine origin. They are classified into 14 serogroups in the family Picornaviridae. Porcine enterovirus 1 (the prototype “Teschen virus” and “Talfan virus”), PEV 2 through 7, and PEV 11-13 have been moved to a new genus called Teschovirus. Porcine enteroviruses 8, 9 and 10 remain in the original Enterovirus genus. There is little cross reactivity among all these viruses. Picornaviruses are single-stranded RNA viruses, relatively stable, and highly resistant to environmental influences and many disinfectants. They can be inactivated by sodium hypochlorite.
All picornaviruses are assumed to have similar epidemiology. Less virulent strains of virus are endemic in most herds. The viruses are shed in the feces and transmission usually is fecal-oral. Spread of virus usually is by direct or indirect contact with infected pigs. Infected fetuses born alive sometimes are a source of viral exposure of other pigs. Fomites can carry the relatively stable viruses. All ages of swine are susceptible if they have not previously encountered a picornavirus of that serogroup.
Picornavirus is ingested and replicates in the tonsil, intestinal tract and probably in lymphoid tissue in the lamina propria. The milder strains usually remain confined to the intestinal tract. Epithelial cell destruction is not a feature of picornaviral infections. With the more virulent strains, viremia occurs and virus may spread to the central nervous system (CNS) or pregnant uterus and fetuses.
Infections of the CNS vary in extent and severity and can affect that system from the olfactory bulbs to the lumbar cord. More often the lesions occur from the hypothalamus to the medulla. In prolonged cases there may be lymphocytic meningitis, particularly in the cerebellum and brain stem. Spinal cord lesions are largely confined to the gray matter of the ventral horns. There is a gradient in the severity of lesions and the outcome in an infected pig depends on location, severity and extent of lesions.
Teschen disease, the most virulent porcine picornaviral infection, affects all age groups of swine. Morbidity and mortality are high. Early signs include anorexia, listlessness and fever which are soon followed by ataxia, abnormal postures and recumbency. There may be opisthotonus, convulsions, nystagmus and coma. Death occurs within a few days. Occasional cases survive but may have residual paralysis.
Talfan disease, a similar but less severe disease, results in lower morbidity and mortality. It usually occurs in young pigs, weaned or unweaned. Signs are similar to those of Teschen disease but milder. Although pigs often show ataxia and paresis, the paresis seldom progresses to paralysis and most pigs recover. Less virulent strains produce only mild or no CNS signs.
In the United States, occasional outbreaks of ataxia and posterior paresis are associated with other serogroups of picornavirus. Clinical signs are as described. Outbreaks are usually transient until herd immunity is established.
There are no specific gross lesions caused by picornaviruses nor are there any microscopic lesions in the intestinal tract. In Teschen disease, Talfan disease and sporadic epidemics with the other newly classified viruses, there is a nonsuppurative inflammation prominent in the gray matter of the brain stem, cerebellum and spinal cord (polioencephalomyelitis). In affected areas many neurons are degenerate or necrotic. In prolonged cases there may be lymphocytic meningitis over the cerebellum and brain stem. Lesions tend to be more marked and extensive with Teschen disease than in cases caused by less virulent picornaviruses.
Typical clinical signs and absence of gross lesions are suggestive of the diagnosis, especially in areas where outbreaks occurred previously. Microscopic lesions in the CNS are suggestive of viral infection but not pathognomonic. Paired serum samples taken at least two weeks apart may show a rising titer in serum neutralization or complement fixation tests. Virus isolation in tissue culture and identification by immunofluorescence or identification of viral antigen in tissue by similar technique are useful. These techniques are not available in all diagnostic laboratories in the United States since virulent porcine picornaviral infections seldom occur. Neurotropic picornaviral diseases must be differentiated from other diseases associated with CNS disease (see the table, Diseases Associated with CNS Signs). Polymerase chain reaction (PCR) techniques have been widely reported and can helpful in both detection and identification of the virus. Picornavirus detected in nervous tissue should be considered diagnostic; when detected simply through serology or in enteric tissues further work should be completed in order to establish the significance of the virus. Many non-pathogenic strains can be routinely recovered from both normal and clinically ill pigs.
In herds where picornaviruses have caused reproductive or other problems, new breeding stock should be introduced into the herd at least a month before breeding begins. They usually will be exposed to the endemic picornaviruses and develop an active immunity to them prior to breeding. It may be preferable to expose new stock to a composite sample of feces from the herd to which they are to be added. This can be done either by exposing them to pen contact with feces or mixing some feces with their feed.
In Europe, Teschen disease and Talfan disease have been controlled by slaughter and ring vaccination around premises or areas where outbreaks have occurred. Both live-attenuated and inactivated tissue culture vaccines have been used. In addition, there usually has been restriction of importations from endemic areas of infection.
In the US, occasional outbreaks of disease occur in nursery/grower stages. Most are transient but losses can be significant. Herd immunity is the goal but with segregation of ages, sometimes difficult to achieve.
Outbreaks of disease of unusual severity suspected of being caused by any of the virulent types of picornaviral infection should be reported immediately to livestock disease control authorities. Thus far, import regulations on swine and pork products have kept the United States free of most highly virulent porcine