By Dr Peter Evans
Porcine Epidemic diarrhoea (PED) is a disease caused by a Group 1 Coronavirus of family Coronaviridae. Transmissible Gastroenteritis (TGE) and Porcine Corona Respiratory disease (PRCD) also fall into this group.PED type 1 was diagnosed in the UK for the first time in 1971. The disease was primarily a disease of fattening pigs. The initial name given to the disease was Epidemic Viral Disease (EVD).
A second outbreak of acute diarrhoeas which now included suckling pigs (and all other ages of pigs) was investigated in Europe in 1976.This disease was called EVD type 2.
In 1978 researchers were able to identify that these outbreaks were caused by a coronavirus which was different to TGEv. In 1982 the name Porcine Epidemic diarrhoea was adopted.
The disease was identified in many countries in Europe in the 1980’s, India in 2003, China (1992), Korea (1993) and Japan (1983). 55% of Spanish farms were serologically identified to have PEDv in 1992/3.
At that time there were no reports of PEDv in the Americas.
(One must keep in mind that the years indicated are years that surveys/research was done and does not indicate a timeline of spread of the virus).
Britain reported a clinical outbreak during 1998 and Hungary in 1995. In Czech Republic about 12% of samples tested in 2003/4 were in combination with other enteric viruses. In 2005/6 Italy experienced acute outbreaks, while Spain experiences an average of five cases per year (European strain) causing 10-25 % deaths in suckling pigs
Japan had severe outbreaks during 1993 and ’94 with mortalities ranging from 30—100%; followed by a severe outbreak on 108 farms in 1996 (70% mortality). Korea also had similar problems in the 1990’s.
More recent situation (post 2010)
Until 2013 Americas were free of PEDv. After outbreaks in USA, slaughter pigs in the UK were tested serologically – 10% were positive to PEDv (European strain).
During the period 2010-12 there was a rapid spread of an especially virulent PEDv in China which also affected Philippines and South Korea. During 2013 Japan experienced a severe outbreak after a seven-year lull.
The PEDv virus that affected the USA was soon found in other countries in the Americas: 2013 in Mexico; spread into Colombia, Dominican Republic and Peru by March 2014.
By March 2014, 30 US states were affected. The PEDv has been shown to be 99% similar to Chinese strains. Despite the best efforts to keep the disease out of Canada, the disease was diagnosed in Ontario in January 2014.
In March 2014 a new virus was diagnosed, causing diarrhoea, but not as virulent as PEDv. The virus was identified as a DeltaCorona virus (PEDv is an alphacoronavirus). Porcine Delta Coronavirus (PDCoV) has been identified in 17 US states by August 2014.
How was the virus introduced and spread into the USA?
Many of the farms that became infected with PEDv were biosecure conscious and had good systems in place. The first case was on a farm in Ohio closely followed by three other farms. It soon became apparent that these farms shared feed sources. All fours sites became positive within one week of changing feed.
Unfortunately feed tested negative for PEDv, but clinical signs suggest otherwise.
The possibility of feed being the source was supported by the introduction into Canada. Canada had been proactive in attempting to keep the disease out: heightened biosecurity; inspections of trucks from the US, in-depth risk assessment and environmental surveillance. The Canadian suspected transportation of feed after case seven was identified on the remote Prince Edward Island (18 of 20 farms used the same feed supplier).
The US now suspects that imported porcine plasma was probably the cause of the outbreak. Further research into plasma protein has revealed that PEDv is killed during processing which leads one to believe that if imported plasma protein was the source, it would have been contaminated post processing.
The spread within the US is attributed to the high levels of movement of pigs in multi-site operations; from site to site and to abattoirs. Coupled to the highly infectious nature of PEDv.
In addition, extremely high levels of PEDv are shed in faeces. It is calculated that 28g of PEDv infected manure has the equivalent viral load to 1t of TGEV infected manure. Thus indirect spread by mechanical vectors (cats and flies), contaminated equip and personnel, becomes significant.
The risk odds of being infected by a neighbour are 8,4 @ 1 mile; 6,3 @ 2 miles; and from >3 miles no increase in odds between farms.
Interestingly the size of farm has no role in risk level, but breeding farms have 8.8 odds of spread to other farms compared to farrow to finish where the odds are 6,4.
PEDv is viable in slurry lagoons for 16 weeks (compared to nine weeks of shedding in sows). Highlighting the importance of environmental control and biosecurity is important.
Current research in the US and other countries is developing a basic understanding of both conronaviruses. There is now development diagnostic tests both to identify the virus and to determine exposure (serology of immune responses).
Researchers also want to understand the transmission of the virus and in the environment. This would allow one to improve prevention protocols.
What we know at this point is:
- Only pigs
- Pigs need to ingest the virus = Faeco oral
- Replicates in enterocytes
- Short incubation period pigs are sick with 48 hours
- Virus is shed for seven to 28 days in mucous from the intestines
- Immune response takes seven to 14 days to develop
- pH range 5-9 @ 4°C
- Survives in: -Fresh faeces – 7days; Manure 14- >28 days; water 7 days
- Survive in: – Wet feed 28 days; dry feeds < 14 days
- Survives in: – Plasma protein 7 days @22°C; 14 days 12°C; 21 days @ 4°C
- Sureties on truck surfaces for 24 hours at 20°C – 25% pigs become infected.
Clinically the main symptoms are a watery diarrhoea affecting suckling pigs; 50 to 90% die with the highly virulent strain of PEDv. If less virulent, 20-40% will die.
Weaned/fattening have scouring without significant increase in mortality but some decrease in ADG noted.
Within a period of 8-12 weeks the disease become endemic, mortalities decline and growth rates return to normal. The reduction coincides with increase in maternal immunity once all breeding females have been exposed. Vaccines are being developed, but in the interim a number of feed-back programmes were practiced.
A big unknown at present is whether a herd with an endemic European strain induced immunity will be protected against the US strains (and Asian strains).
What we do know is that there is no cross immunity with TGEV.
How is South Africa reacting
South Africa has taken note of the situation in America and Asia. We continue to monitor progress in diagnostic tests to ensure that we do not get the disease into the country.
Although South Africa has never tested for European strains of PEDv we have not had any reported clinical cases.
Our import protocols for genetic material are being amended to address PEDv.
The risk in meat is considered low as we have a VPN for imported meat in place.
Romagosa Anna. 2014. Presentation SAPPO congress.
Barbara Straw et al. 2006. Diseases of Swine 9th Edition,
KJ Yoon. 2014. The Emergence of porcine epidemic diarrhoea in US Swine: Surprises in the road to prevention and control. Proceedings of the 23rd IPVS congress, pp 64-66
Website: University of Minnesota Swine Disease Eradication Center
Website: National Pork Board
Website: USDA. Swine Health Monitoring Project
Website: AASV. American Association of Seine Veterinarians