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History of a killer - the rise of Porcine Epidemic Diarrhea

It’s been described as one of the biggest threats to the North American pork industry since Foot and Mouth disease. It’s hard to control, difficult to contain, and a common axiom suggests a single thimblefull of infected feces could kill every piglet in Canada. The road to identifying what we now call Porcine Epidemic Diarrhea (PED) started on a laboratory slide in Great Britain over 40 years ago. Back in 1971, cases of chronic diarrhea were identified among young hogs in the United Kingdom were, at first, thought to be common Transmissible Gastroenteritis Virus (TGEv,) but researchers were puzzled when tests for the pathogen kept coming up negative.


As the 70s wore on, more and more cases of this TGEv—like virus showed up in swine populations across western and central Europe, specifically in England, Germany, Spain, France and Holland. Dubbed Epidemic Viral Diarrhea by veterinarians, the disease affected swine of all ages, but proved especially deadly for suckling pigs. By the late 1970s, veterinary researchers managed to isolate it as a coronavirus, confirming early theories suggesting this new disease was similar to other coronavirus infections, including TGEv. While virologically in the same family as speciesspecific enteritis and bronchitis-causing coronaviruses (including the infamous SARS virus,) PED bears no serological similarities to anything identified thus far, nor does it respond to existing coronavirus inoculations or treatments. Additionally, while PED was proving just as contagious as TEGv, the PED virus seemed to be able to survive longer outside of its host than similar coronaviruses. Hog farms in Holland were hard hit, with PED becoming endemic in both finishing and breeding herds, common in both young gilts and sows for about two years after the initial infection. Cases were also popping up on farms in eastern Europe, including Hungary, the Czech Republic and Romania.


By the early 1990s, Taiwan became the first country outside of Europe to report infections, soon followed by northern India, China, Korea, Japan and Southeast Asia. Unlike its somewhat mild experience in Europe, PEDv hit Asia with a vengeance. Korea saw almost 60 per cent of its swine herd in the early 1990s infected, with Japan taking an even heavier hit. Nearly 15,000 deaths were recorded in Japan’s swine herd during an eight month stretch in 1993, with a 1996 outbreak across 108 Japanese farrow-to-finish farms only sparing 20,000 out of the country’s nearly 60,000 piglets. More recent Asian outbreaks include one in 2007 in Thailand, several between 20092011 across China and isolated cases in Vietnam, Laos and the Philippines. It certainly appears that North America’s exposure to PEDv is closely paralleling the Asian experience – and with good reason. According to a report published last October by the American Society for Microbiology, three distinct strains of PED are currently making the rounds in the United States. In an interview with Western Hog Journal , Dr. Paul Sundberg, vice president of science and technology the National Pork Board, said researchers at Virginia Tech managed to genetically isolate the genome of the American viruses and trace their lineage to a strain responsible for a severe outbreak in China. Researchers were even able to determine that the American strains originated from an outbreak in Anhui province, near Shanghai. “The virus has been sequenced, and it has 99.6 per cent the same sequences as the virus in China,” Dr. Sundberg said. “That, however, doesn’t mean it came to the U.S. from China. We don’t know how it got into the U.S., we’re still looking into that.” The American Society for Microbiology report also found that these Asian strains bore striking genetic similarities to a coronavirus commonly found in bats, suggesting that the virus is capable limited transmission between species.


While Porcine Epidemic Diarrhea affects hogs of all ages, its effects are especially felt in younger animals. The mortality rate for suckling pigs is very close to 100 per cent, which drops off dramatically once animals are weaned, with death only occurring in one to five per cent of finisher animals. Similar to TGEv, PED presents in infected animals with copious amounts of watery diarrhea. As this is the only outward sign of the disease, sure diagnosis of PEDv can only be made in the laboratory. While older animals normally recover in a few weeks, the prognosis for piglets under a week old is almost always fatal — usually coming after only three days from acute dehydration. Animals usually present symptoms less than 24 hours after infection. Viral replication takes place almost immediately after entering its host, normally in the epithelial cells of the animal’s lower digestive tract. Laboratory analysis shows intestinal cells start showing irreversible effects from the virus within 10 to 14 hours of infection.


Like many entertis-causing coronaviruses, the virus infects enterocytes — epithelial cells that make up the villi in an animal’s intestines. Villi are microscopic fingerlike projections that line the intestinal walls of most animals. Ranging from half a millimetre to two millimetres in length, a villus serves to increase the surface area of the intestine, allowing a greater amount of nutrients to be absorbed from passing food, as well as providing a fertile breeding ground for the PED virus. Mortality seems to be correlated in the length of the host animal’s intestinal villi, as neonatal hogs have exceptionally long villi that shrink as the pig matures past its first week of life. As a piglet is born and it starts to suckle from its mother, its long villi serve to absorb nutrients from her milk while the animal rapidly grows in its first few weeks of life. The infection ravages the piglet’s villi, either by blunting the vellum or causing them to slough off the intestinal walls, quickly rendering large portions of the animal’s intestinal tract incapable of absorbing nutrients or water. With its mother’s milk passing through the piglet’s system undigested, the animal will eventually die of dehydration. Post mortem analysis often reveals intestines full of undigested milk curds. As the virus is capable of extremely rapid growth within an infected animal, the animal’s near-constant diarrhea contains a massive amount of infected enterocytes stripped from the animal’s small intestine. This fertile bed of viral material is easily spread to another animal through feed or water, or transported off the farm in the treads of a boot or a feces-splashed transport truck – ready to spread to another herd.

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