Porcine transmissible gastroenteritis

GENERAL INTRODUCTION: CORONAVIRIDAE

Introduction

Transmissible gastroenteritis (TGE) is a highly contagious disease of swine. It is characterized by vomiting, diarrhoea and high mortality (up to 100 per cent) in seronegative piglets less than two weeks of age. The causative agent (TGEV) is an enteric coronavirus that was first detected in the United States (US) in 1946 from outbreaks of acute diarrhoea with high mortality in piglets.¹ The disease has since been reported in most parts of the world where intensive pig farming is practised, including Europe, Asia (Japan, Korea, Malaysia, Taiwan), the Americas (North, Central and South) and Africa (Zaïre, Ghana). It was a major cause of disease and death in piglets in the US, Europe and elsewhere from the 1960s-1980s, notwithstanding the widespread application of vaccines. Since the emergence and rapid spread throughout Europe of porcine respiratory coronavirus (PRCV),² a deletion mutant of TGEV with respiratory tropism, a large proportion of the  pig population has become immune to that virus and, consequently, also to TGEV. The endemic status of PRCV has thus markedly decreased the clinical and economic importance of TGEV (see Porcine respiratory coronavirus infection).

Aetiology

Being a member of the family Coronaviridae and genus Alphacoronavirus,TGEV is a single-stranded RNA virus. Virions are pleomorphic (diameter of 60 to 160 nm) with a fringe of widely spaced, club-shaped projections 12 to 25 nm in length.³ They are composed of three structural proteins: the nucleocapsid protein (N), a small membrane glycoprotein (M, formerly labelled E1), and a large glycoprotein constituting the viral projections (S, formerly named E2). The S glycoprotein bears an epitope that induces neutralizing antibodies as well as several epitopes that induce non-neutralizing antibodies.⁴

There is only one serotype of TGEV, although some antigenic variation exists between field strains with different geographical origins, and between virulent and attenuated strains. Transmissible gastroenteritis virus is antigenically closely related to PRCV, canine coronavirus, feline enteric coronavirus and feline infectious peritonitis coronavirus,^{5, 6} and is distantly related to porcine epidemic diarrhoea virus (PEDV)⁷ and human coronavirus 229E.^{8, 9}

The virus is sensitive to lipid solvents and to various disinfectants, such as formaldehyde, sodium hypochloride, iodine and quaternary ammonium compounds. It is inactivated within a few days at 37°C and within a few hours when exposed to sunlight. Most strains of TGEV are only moderately sensitive to trypsin and are stable at pH3. The physicochemical properties of TGEV are provide elsewhere.^{10, 11}

Epidemiology

Pigs are the only animals for which TGEV is pathogenic. Other non-porcine hosts, such as dogs, cats and foxes, can be infected experimentally but do not develop signs of illness. Whether these or other species are natural hosts of this virus is uncertain.

Transmission of TGEV is direct, i.e. pigs excreting the virus come into contact with susceptible individuals or indirect through contact of susceptible animals with virus contained in faeces or contaminated fomites. In experimentally infected pigs, TGEV was shed for approximately 14 days in faeces.¹² TGEV can also be detected in lungs of some pigs.¹³

Herd immunity can be accomplished by intentionally exposing the sows to virulent TGEV to boost lactogenic (milk) immunity.^{14, 15} On isolated small farms, herd immunity is accomplished and TGEV infection is self-limiting. Conversely, on large farms (more than 200 sows) with a continuous farrowing system and continual influx of susceptible animals, TGEV can become endemic after the primary outbreak. Subsequent groups of pigs become infected after weaning when their maternal immunity wanes and they in turn infect other groups. The only clinical evidence of infection in these groups is mild diarrhoea at weaning. Typical TGE in young piglets that is associated with high mortality occurs when gilts or sows are TGEV seronegative or they fail to provide passive protection in the colostrum and milk to their offspring.

Generaly, outbreaks of TGE occur in winter suggesting that TGEV preservation in the frozen state in faeces or at cold temperatures can facilitate its transfer. Additionally, starlings (numerous in feedlots in winter) ¹⁶ and house flies ¹⁷ were indicated as potential mechanical vectors for TGEV transmission. It is not known how the virus survives the summer, but viral persistence on endemically- infected farms (in pigs, non-porcine reservoirs such as cats ¹⁸ and dogs ¹⁹ and mechanical vectors) is likely to be the main mechanism.¹⁰

Since the emergence of PRCV, typical and severe outbreaks of TGE with high mortality in new-born...