Porcine epidemic diarrhea is a condition caused by the porcine epidemic diarrhea virus that leads to severe gastrointestinal disease in pigs. It is closely related to the agent responsible for transmissible gastroenteritis in pigs. Piglets are most susceptible to the disease, as are young adults during periods of stress. Transmission is via the fecal-oral route. The porcine epidemic diarrhea virus belongs to the family Coronaviridae, and it only affects pigs. PED is harmless to other farm animals and poses no food safety risk. The virus is enveloped, single-stranded, and has a positive sense RNA. The epithelial cells of the small intestine are the target of the virus, causing severe diarrhea and dehydration. However, when endemic, PED exhibit lower morbidity in suckling and recently weaned piglets.
History PED is closely related to the agent responsible for transmissible gastroenteritis in pigs. Transmission is via the fecal-oral route and by aerosols. The first case of PED was seen in the United Kingdom in 1971. By the early 1980s, it began circulating to other European countries. Porcine epidemic diarrhea has been endemic in Europe and Asia but not reported in the United States until spring 2013. However, recently, PED has been identified in various herds across multiple states in the U.S. The U.S. PED strains underwent evolutionary divergence, which resulted in two sublineages. The three emergent U.S. strains are most closely related to a strain isolated in 2012 from China, which might result from multiple recombination events between different genetic lineages or sublineages of PED.
Infection route PED targets intestinal epithelial cells and replicates in the small intestine villi. Infected pigs show reduced intestinal villus height and decreased transepithelial resistance.Trypsin facilitates PED entry and release by cleaving the S protein into two subunits, enabling efficient viral replication and spreading in vitro. However, some cell-adapted attenuated PED strains can support PED reproduction without trypsin. As a result of viral infection, distinct cytopathic effects, including cell fusion, vacuolation, syncytium, and detachment, are produced in infected cells. Once in the body, PED promotes fusion between cells, resulting in continuous cell necrosis, severe diarrhea, and even death in piglets. At the same time, PED is sensitive to the porcine liver, resulting in abnormal cholesterol metabolism genes and thus disrupting the metabolic homeostasis of cholesterol. PED uses endocytosis as the entry mechanism for infecting host cells. The virus relies on serine proteolysis and low pH to invade cells. Following entry, PED utilizes viral components to evade innate immune responses. Extensive research has shown that interferon plays a vital role as a signaling molecule to block viral infection upon invasion.
Signs and symptoms In adult swine, the disease is very mild and mortality is rare. The primary signs are a watery diarrhea and mild systemic signs such as pyrexia, anorexia and lethargy. The virus presents itself differently in the ages of swine. However, weaners and growers exhibit profuse, watery diarrhea that lacks blood or mucus, is typically yellow-green, and is accompanied by vomiting and anorexia. It may lead to a 100% mortality rate of piglets under a week of age. In piglets, excessive scouring, diarrhea, vomiting, dehydration, and increased pre-wean mortality are primary indicators. The incubation period is typically two to four days; clinical signs occur within four days when PED first enters the herd.
Clinical signs The clinical signs vary widely and depend on previous exposure and the immunological and endemic status of the infected area, including the farm and region. The initial clinical finding is watery feces that may be coagulated, malodorous, and can accompanied by vomiting. Dehydration and metabolic acidosis may be secondary signs. If swine recovers, it is usually within 7 to 10 days. Some conducted studies in the United States and the United Kingdom suggest that the incubation period of PED is well before clinical signs are detected and can range from 1 to 7 days (US PED) or 5–8 days (UK PED).
Clinical symptoms A common symptom of PED is gross lesions, which are limited to the digestive tract. Gross lesions are characterized by thin, transparent intestinal walls that accumulate considerable amounts of yellow fluid within the lumen. The stomach is filled with curdled milk, most likely a side effect of the reduced intestinal peristalsis. The virus infects many areas of the digestive tract; congestion of the mesenteric vessels is frequently detected with infection, along with fluid-filled mesenteric lymph nodes. Infected pigs commonly exhibit a lack of intestinal lacteals, which serves as an indicator of malabsorption. Despite persistent severe diarrhea, infected pigs had low to moderate appetite 3–5 days after the onset of diarrhea, after which they began to decline. Histological lesions are another symptom seen in piglets infected with PED. These lesions consist of acute diffuse, severe atrophic enteritis, mild vacuolation of superficial epithelial cells, and sub-epithelial edema in the cecum and colon. In various studies during incubation, infected pigs exhibited standard villous lengths; however, the vacuolated enterocytes underwent necrosis. After the onset of diarrhea, infected pigs showed severe villous shortening for 1–3 days. Piglets euthanized at a later stage of infection had moderate to severe villous atrophy, which is indicative of continued cellular necrosis. Following PED infection, markers for proliferating cells are seen. One study concluded that the time of onset and severity of diarrhea induced by PED may vary depending on the extent of villous atrophy and the rapidity of replacement by the stem cells.
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