Swine vesicular disease

D K J MACKAY

GENERAL INTRODUCTION: PICORNAVIRIDAE

Introduction

Swine vesicular disease (SVD) is a vesicular condition of pigs resulting from infection with a specific enterovirus. It is classified as a List A disease by the Office International des Épizooties (OIE) not because of the severity or contagiousness of the disease itself, but because the lesions produced by SVD virus are indistinguishable from those produced by another agent on List A, foot-and-mouth disease (FMD) virus. Swine vesicular disease is a disease that has emerged relatively recently. The causative virus was first identified in Italy in 1966 as an enterovirus responsible for a vesicular condition in pigs that was not FMD.²⁶ The same agent was detected in Hong Kong in 1971, where it has remained endemic ever since. The disease was given the name swine vesicular disease following its appearance in the UK in 1972. During the 1970s and early 1980s outbreaks occurred in several European countries, particularly Italy and the UK. By 1985 the disease had been eradicated from Western Europe with the exception of Italy. Since then it has remained endemic in Italy, despite an eradication campaign financed by the European Union. In the early 1990s, outbreaks occurred in a number of European countries due to the long-distance movement of pigs between member states of the European Union. Worldwide, the disease is also still present in Taiwan Province of China, in Hong Kong, and possibly in other countries of the Far East.

Aetiology

Swine vesicular disease virus (SVDV)is an enterovirus within the family Picornaviridae. It is antigenically related to the human coxsackie virus B5 (CB5).¹⁵ As a typical enterovirus, it is a small, non-enveloped RNA virus with an icosahedral capsid approximately 30 nm in diameter. The genome consists of a single strand of positive sense RNA, 7,4 KB in length, coding for the four capsid proteins and a number of non-structural proteins. Swine vesicular disease virus is capable of surviving a wide range of temperatures and pH: for example a pH greater than 12 or less than 2 is required to inactivate it, the time taken to achieve inactivation at a given pH is dependent on the temperature.¹⁴

This is of particular relevance to the epidemiology and control of the disease. There is only one serotype of SVDV, but antigenic and genomic differences can be recognized between isolates collected at different times and from different areas.²

Genetic analysis (Figure 122.1) shows a gradual evolution of the virus over time from the first isolation in 1966.²

Epidemiology

As the name suggests, SVD is principally a disease of pigs. Cattle do not support replication of SVDV and, although it can replicate in the pharynx of sheep exposed to infected pigs, sheep are not important in the epidemiology of the disease. ⁵ Infection of pigs can occur through damaged skin, and by ingestion or inhalation. Pigs that are moved or mixed often fight with each other and in this way receive small cuts and grazes, which can serve as portals of entry for the virus. The dose of virus required to initiate infection across damaged skin is as little as 10^1,5 PFU, which is 1 000-fold less than that needed to infect pigs orally.²² Taken together, these factors explain why recent outbreaks in Europe have been characterized by clinical disease in pigs which have recently been moved and, presumably, exposed to infection either during transport or at their destination. Airborne spread of SVDV does not occur other than by short-distance aerosol transmission between pigs in contact with each other.²⁸ Infection can occur through ingestion of contaminated food. Whether virus enters directly across the mucosa or through damaged epithelial surfaces is not known. The virus in muscle is not inactivated by the fall in pH that occurs due to rigor mortis. Frozen meat from animals slaughtered during the viraemic phase can therefore remain as an almost indefinite source of infection and the virus can survive even in some processed meat for several months.²³

The severity of the disease depends on both the strain of virus¹⁰ and the conditions under which the animals are kept. Recent European isolates of SVDV are generally less virulent than European isolates from the 1970s,¹⁹ and completely avirulent strains have been isolated in Japan.¹⁶

Figure 122.1 Phylogenetic analysis of the nucleotide sequence of part of the VP1 gene of SVD viruses isolated between 1966 and 1993.¹⁵ Several distinct genetic groups are seen and there is a progressive evolution of the virus with time. After 1966, each group contains representative viruses from Asia suggesting repeated introductions into Europe from an origin in the Far East

Figure 122.2  Ruptured and unruptured vesicles along the coronary bands of the hoof of the accessory digit in a pig infected with an isolate of SVDV isolated from Italy in 1993 (ITL/9/93). The junction between the coronary band and the bulb of the heel is a common site for vesicle formation.

The most frequent means of transmission of SVDV between herds is the movement of infected animals. The frequently mild or subclinical nature of the disease means that apparently healthy pigs can readily be moved from an undetected source of infection. Disease only becomes apparent due to the appearance of clinical signs in animals subjected to the stress of movement or in susceptible...