Occurrence: Europe, Eastern Asia, the USA and Central America.
Age affected: All ages.
Causes: Porcine Epidemic Diarrhoea (PED) virus – related to TGE and PRCv viruses.
Effects: Diarrhoea, retarded growth, vomiting, death in piglets.
Porcine Epidemic Diarrhoea (PED)
Occurrence: Europe, Eastern Asia, the USA and Central America.
Porcine Epidemic Diarrhoea (PED) is caused by a coronavirus distinct from that of Transmissible Gastroenteritis (TGE). The virus requires trypsin (a digestive enzyme) for successful cell culture. A classical serotype has been present for many years in Europe and Eastern Asia, but variant genotypes have developed in China and have spread particularly to the USA and Central America. The virus can survive at low temperature for long periods but is less tolerant of acid and alkali at high temperatures. Infection is oral and the virus infects mature absorptive cells of the small intestinal lining and destroys them.
Levels of digestive enzymes such as lactase in sucking piglets are reduced markedly. The villi (finger like extensions of the lining) contract and absorption of nutrients decreases, allowing undigested food and fluid to pass to the large intestine for fermentation and giving rise to diarrhoea. In partially-immune piglets, only a small part of the small intestine may develop villous atrophy. Colostral and milk antibody protects piglets but disappears within 5-13 weeks and active immunity then develops within 2-4 weeks of infection. The presence of serum antibody in a nursing sow does not rule out the development of epidemic diarrhoea in her litter. Antibody levels on infected farms peak at 4 months and decline from then onwards.
Infection is oral, from virus present in the faeces of infected pigs. As the diarrhoea in affected pigs is so profuse and watery, the faeces can be distributed widely within a herd by contact and also by aerosol and spread within a building is extremely rapid. Recovered pigs carry and shed the virus for weeks. The virus can survive for long periods when frozen and remains stable in neutral conditions.
Transmission between farms is usually by the movement of infected pigs, but transport, contaminated clothing and aerosol spread have all been documented and mechanical spread by bird movement can occur. The virus has been identified in feed and may have been associated with spray-dried plasma.
PED occurs as an explosive outbreak of diarrhoea in non-immune weaned pigs or in pigs of all ages. After an incubation period of 1-3 days, piglets develop watery diarrhoea and may vomit. Illness occurs in almost all non-immune piglets on the farm and mortality rates amongst the youngest piglets can approach 100%. Fewer young piglets die if piglet drinkers are available. The disease spreads rapidly in the unit. Twenty to thirty percent of the older pigs may be affected with vomiting and diarrhoea. Inappetence may occur in all pigs, especially in breeding stock. In herds with partial immunity, sucking and young weaned pigs under 32 kg live weight are rarely affected. Affected weaned pigs are dull and unwilling to rise. Fever is rare.
The diarrhoea in weaned pigs is greenish-brown in colour and very fluid, often coating the pig completely. Signs of dehydration are common. Vomiting is prominent in some outbreaks. The acute stage of vomiting and diarrhoea lasts approximately 3 days but complete recovery takes a further 7-8 days. Few pigs die where water is freely available unless other diseases are present. Affected feeding pigs take about 14 days longer to reach 90 kg due to loss of condition. Agalactia in sows may cause mortality in their litters.
The occurrence of an acute, rapidly spreading scour with vomiting and inappetence in weaned pigs or throughout the herd suggests the presence of PED or TGE. Mortality in young piglets may be lower in PED than in TGE but can still be considerable. In a partially immune herd, only a few piglets may develop the disease and it is difficult to differentiate from other causes of piglet diarrhoea. The presence of PED is confirmed by laboratory tests. Commercially-available penside tests utilise specific antibody to detect virus particles and antigen in faeces, and the Polymerase Chain Reaction (RTPCR) can detect the viral RNA. ELISA tests can detect antibody in the sera or milk of recovered pigs. Dual infections with TGE and PED can occur in the same pigs, so TGE tests are often included.
These are generally seen in piglets as mortality is highest in this age group. Carcases are dehydrated. The stomach may be empty and the intestines fluid-filled. The stomach lining may be inflamed, the intestinal contents are fluid with flakes of milk and villous atrophy may be present allowing the milk flakes to be seen through the thinned small intestinal wall. Weaned pigs rarely die of PED alone, but carcases of those that do so are covered with fluid faeces and are dehydrated.
The stomach of weaned pigs examined post-mortem is usually empty or filled with bile-stained fluid and both large and small intestines are pale and thin-walled, often with fluid contents. Villous atrophy is present. The presence of the virus can be demonstrated in the intestinal epithelium by fluorescent antibody or immunoperoxidase, and its presence confirmed by RTPCR.
There is no specific cure, just supportive therapy for affected pigs. Sucking pigs and recently-weaned pigs should be given glucose:glycine electrolyte solutions to reduce mortality and aid recovery. Adequate water and milk substitute should be provided for the piglets of affected sows lose their milk, and water should be freely available to all affected stock. The effects of an outbreak of the disease may be reduced by isolating all sows within 14 days of farrowing, and by infecting all those due to farrow in more than 14 days. Weaners may also be infected in order to reduce the duration of the outbreak.
Where swine dysentery or other disease is present in weaned pigs, recovery from Porcine Epidemic Diarrhoea is hastened by the treatment for these diseases. Sow vaccines have been described, but are not universally available. PED usually enters a herd in carrier pigs, so isolation of the herd and the purchase of breeding stock from herds known to be free from the disease can keep it out. To prevent virus spread, footwear and vehicles need to be thoroughly cleaned and disinfected, protective clothing worn on the farm and vehicles excluded where possible.