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The emergence of PEDV for the first time in the USA in 2013 has caused tremendous losses as a result of baby pig mortality. It has stimulated a wealth of research on the virus, the PED disease and its pathogenesis.This has led to useful viewpoints but sometimes with a speculative “tone”. Is this US virus more virulent than the strain CV777 originally isolated in Europe from diseased baby pigs in 1977? Is indeed the disease now more devastating than it was in the seventies in Europe? Too often, genome analyses have led to denominating isolates as “variants with increased virulence” and to hasty conclusions based on sequence data rather than comparative pig inoculation experiments.
The author of the present article has been directly involved with PED in Europe from its first stages in the early seventies and his group has isolated PEDV for the first time (reference strain CV777). It may thus be interesting to make some considerations and to go back to some facts of the past that one tends to forget.
In 1971, a veterinary surgeon (Oldham) reported in a British journal “Pig farming supplement” a brief report entitled “How it all began”. Here, he described on English pig farms a new diarrheal syndrome which was characterised by acute diarrhea in feeder pigs, fattening swine and sows while suckling pigs were not affected at all. The syndrome was called TOO, standing for “The Other One” and referring to its clinical similarity to transmissible gastroenteritis (TGE), but it was still different insofar that baby pigs did not become sick. A laboratory diagnosis of TGEV, a common cause of viral diarrhea at that time, remained negative. The name TOO was quickly abandoned and changed to “epidemic diarrhea”. This epidemic diarrhea soon spread to the European continent and was, in the early seventies, also observed in Belgium. On Belgian farms, the clinical picture was similar to that in the UK. Once started on a farm, the diarrhea spread quickly particularly within a fattening pig population. Spread was slower among the sow population on breeding farms and baby pigs did not become sick. It was even striking that lactating mothers showed severe diarrhea while their suckling pigs remained healthy and only suffered from a temporary agalactia of their mother. Losses on the affected swine farms were minimal and the diarrheal outbreak was self limiting. An additional feature in Belgium were the sudden deaths in adult fatteners with mortality rates as high as 3%. These deaths occurred in pigs with the “porcine stress syndrome” that was very common in Belgian Landrace and Pietrain breeds at that time.
The cause of this new epidemic diarrhea was assumed to be of viral origin as antibiotic treatments were unsuccessful but all the attempts to isolate a virus in cell cultures failed and, based on serological examination, TGEV was systematically excluded as the possible cause. The origin of the “new”virus from the early seventies has never been revealed but a virus jump from another animal species, as often seen with coronaviruses, was and still is to be considered.
This clinical picture rather suddenly changed in the mid seventies as baby pigs also became sick with diarrhea. Now, the disease became totally similar to TGE since baby pigs became sick within 1 to 2 days after birth. Pig mortality, even though varying from one farm to the other, could reach up to 90 % in pigs infected prior to the age of 6 days with an average of 50 %. The disease was now called “porcine epidemic diarrhea” and suddenly attracted much more attention not only from practical but also from a scientific point of view.
Virus isolation attempts were intensified and the disease was experimentally reproduced in baby pigs in isolation with the strain denominated CV777. The causative coronavirus was visualised by electron microscopy and immuno-electron microscopy showed it to be different from the other porcine coronaviruses known at that time, TGEV and hemagglutinating encephalitis virus.
Of course, genomic analyses of the “TOO strain” and the CV777 could not be done at that time but it was clear that the early virus had undergone some genetic change resulting in a greater ability to infect intestinal cells in baby pigs. Pathogenesis studies in pigs with CV777 using immunofluorescent staining showed a striking similarity with that caused by TGEV.
