Porcine epidemic diarrhoea (PED) is a disease caused by the virulent porcine epidemic diarrhoea virus (PEDv), which is an alphacoronavirus similar to, but genetically distinct from the transmissible gastroenteritis (TGE) virus. PED is characterised by acute, rapidly spreading viral diarrhoea. Pigs are the only known hosts of PEDv. There are no public health or food safety concerns associated with PED.
PED is primarily a production loss disease. There is no effective treatment other than control of secondary infections. PED vaccines are available in Japan, South Korea and China, and more recently in the United States (US). Economic losses have not justified vaccine development in Europe. PED is not currently a listed disease for the World Organization for Animal Health (OIE).
PEDv is a member of the family coronaviridae. Coronaviruses are divided into three known genera: alpha, beta and gammacoronavirus. A fourth genus, deltacoronavirus, has been proposed. Coronaviruses are enveloped, single-stranded RNA viruses. Different strains of PEDv exist with virulence dependent upon the spike gene sequence. Currently, it is not possible to differentiate strains in terms of virulence by laboratory tests.
PEDv is transmitted by the faecal-oral route, with subclinical carrier pigs the biggest risk for infection of naive populations. Virus may also be introduced to a farm by contaminated equipment, fomites or people. Experimentally, the incubation period of PEDv has been demonstrated to be approximately 36 hours from inoculation until the appearance of clinical signs. The incubation period for PEDv is typically longer than for TGE. Acute outbreaks of PED on susceptible farms often occur within 4-5 days after sale or purchase of pigs.
The duration and severity of clinical disease and accompanying production losses depend primarily on the speed of development of consistent herd immunity. Therefore, the disease is more likely to become endemic in larger herds and those that have regular entry of naive, susceptible animals resulting in persistent diarrhoea in pigs post-weaning.
After an outbreak of PED has occurred on a breeding farm, the PEDv may either disappear or become enzootic. The enzootic status can be established if sufficient litters of pigs are produced and weaned so that the virus is maintained through infection of consecutive litters of pigs that have lost their lactogenic immunity at weaning.
Introduction of PEDv into a naive herd typically results in acute outbreaks of severe diarrhoea, vomiting, high morbidity (up to 100%) and variable mortality. Mortality rates can be extremely high in piglets < 1 week old (50-100%), but are generally low in growing and adult pigs (1-3%).
Clinical signs include vomiting, acute watery diarrhoea, loss of appetite, dehydration, and metabolic acidosis in piglets; diarrhoea and depression in grower pigs; depression, anorexia, diarrhoea and 'belly ache' in breeders.
A diagnosis of PED cannot be made on a clinical basis only. Acute PED outbreaks where diarrhoea is observed in pigs of all ages cannot be clinically differentiated from TGE. Laboratory testing is required for identification.
Specific polymerase chain reaction (PCR) assays, immunohistochemistry and virus isolation can be used to detect PEDv infected animals, although virus isolation may be difficult. Samples to collect for testing include faeces or intestinal contents, intestine, colon and oral fluids. Optimal samples to collect are from live acutely-affected pigs within 24 hours of diarrhoea onset. Necropsy samples must be taken as soon after death as possible.
PEDv is thought to be widespread throughout most regions of Western and Central Europe and Southeast Asian countries, including China and Japan. Severe outbreaks with high mortality are typically rare in Europe, but China has seen a large increase in outbreaks since 2010, and the emergence of new strains has been attributed to this increase. PED has also been reported in Canada and Mexico and is suspected in Central America, Colombia, Peru, and the Dominican Republic.
In 2013, a highly virulent form of PED was first reported in the US, which quickly spread throughout the country. PEDv appeared in multiple, widely distributed pig herds within days implying its spread within the country was through a common point-source utilised regularly by the pig industry. No explanation of how the virus arrived in the US was confirmed. The predominant isolate circulating in the US pig herd is 99.4% homologous with a strain known to be circulating in China in 2012. Recently, the situation in the US has been complicated by the discovery of a clinically avirulent variant of PEDv.
PED is not present in Australia.
Strict biosecurity measures are the main line of defence against PEDv entry into Australia. Live pigs are not permitted entry into Australia. The importation of stockfeed of terrestrial animal origin (blood meal, meat meal, tissues etc) is only currently permitted from New Zealand, which does not have PEDv. People and imported feed ingredients for stockfeed from countries with PEDv pose the highest risk of introduction of PEDv into Australia.