Teschen, Talfan and reproductive diseases caused by porcine enteroviruses

Teschen, Talfan and reproductive diseases caused by porcine enteroviruses

T J L ALEXANDER

Introduction

With the exception of swine vesicular disease (SVD), most infections with porcine enteroviruses, which belong to the family Picornaviridae, cause no apparent disease, but some strains are capable of causing polioencephalomyelitis (Teschen and Talfan), reproductive disorders (stillbirths, foetal mummification, embryonic death and infertility — known collectively by the acronym SMEDI) and, less commonly, pneumonitis or peri- and myocarditis.

Most mammals and birds have their own host-specific array of enteroviruses which are sub-classified into serotypes by serum neutralization and other serological tests.1, 4, 5, 8 Pigs are no exception. They have 11 known serotypes: Teschen/ Talfan disease is caused by serotype 1, and SVD (see Swine vesicular disease) is caused by a distinct porcine enterovirus which is related to the human enterovirus, coxsackie virus 5. With the exception of SVD virus, the porcine enteroviruses are ubiquitous. Although the majority of infections are subclinical, type 1, the Teschen/Talfan virus, may cause polioencephalomyelitis.1, 5, 6 Teschen is the more severe form of polioencephalomyelitis and was first recognized in 1930 in Teschen, which is on the border of the Czeck Republic and Germany. It is endemic in Central Europe, southern Zaire and Madagascar.11 Talfan disease, named after a hill in Wales and known in Denmark as benign enzootic paresis, is a milder disease which has occurred in North America, France, Belgium, Britain, Ireland, Denmark, Greece, Australia and north-east Europe.8, 11 Serotypes 1, 3, 6 and 8 have been reported to be causes of theSMEDIsyndrome,1, 2, 3, 5, 7 which is also caused by porcine parvovirus (Porcine parvovirus infection), encephalomyocarditis virus (Encephalomyocarditis virus infection) and, to some extent, the virus responsible for the porcine reproductive and respiratory syndrome (Porcine reproductive and respiratory syndrome) infections.

Others, for example porcine enterovirus serotype 2, when given experimentally to colostrum-deprived piglets, may produce microscopic lesions of pneumonitis9, 10 but no clinical signs although they may trigger off other pathogenic infectious agents, such as Mycoplasma hyopneumoniae. Serotype 2 has also produced mild polioencephalomyelitis, fibrinous pericarditis and myocarditis in colostrum-deprived piglets.9

Aetiology

The genus Enterovirus is one of five in the family Picornaviridae, the others being Cardiovirus (see Encephalomyocarditis virus infection), Rhinovirus, Hepatovirus, and Aphthovirus.

Enteroviruses (see the introduction, Picornaviridae, and Foot-and-mouth disease) are spherical, 25 to 31 nm in diameter and non-enveloped, with a buoyant density in cesium chloride of 1,34. They contain a core of single-stranded RNA, which is surrounded by a protein capsid but no lipids. They can be grown in porcine epithelial cell cultures, (usually kidney cells) but some can be cultured in cell lines derived from other species.1, 5, 13

Porcine enteroviruses are relatively resistant to heat, pH 2 to 9, commonly used disinfectants and environmental factors.

Epidemiology

Infected pigs shed virus in their faeces, sometimes in large quantities, which contaminates the environment and infects other pigs. The oral–faecal route of infection is probably the most important. Being relatively resistant, the virus can persist for long periods in piggeries and in slurry. Enteroviruses are highly infectious and can be readily carried to other pig farms on boots, clothes, vehicles or other vectors.1, 10

Pathogenesis

Since porcine enteroviruses are so widespread in pig populations, sows tend to have a strong humoral and mucosal-associated immunity. Thus the enteroviruses endemic in a herd are prevented from multiplying in the alimentary tracts of the piglets by secretory IgA derived from their dam’s colostrum. After weaning, however, this rapidly disappears, leaving their alimentary tracts more susceptible to infection. 1, 10 They still have a high level of circulating colostrumderived antibodies, some of which enter the intestinal lumen, reducing the level of multiplication of enteroviruses. The humoral antibodies also prevent spread of these viruses from the alimentary tract into the bloodstream. Low-level multiplication in the intestines in such circumstances stimulates the lymphoid system to produce both mucosal-associated IgA and humoral antibodies which prevent clinical disease and eventually inhibit viral multiplication in the body.5 Individual young pigs thus go through a sequence of subclinical infections with different serotypes during the growing period.1, 10

Natural infection of pigs by enteroviruses is by the oral route.5, 13 The virus multiplies in the intestines and lymph nodes of susceptible pigs and, in the absence of circulating antibody, causes a transient viraemia lasting several days. Virus can be found in most tissues and organs.5, 13 Depending on the strain involved, infection may be silent or may induce the formation of lesions in target organs and clinical signs of disease.

Teschen/Talfan virus invades the central nervous system causing polioencephalomyelitis and paresis, in some animals leading to paralysis of the limbs, particularly the hind limbs.6 Serotypes 1, 3, 6 and 8 may invade the foetuses and cause...

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