Porcine Epidemic Diarrhea

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A coronavirus causes this exotic viral diarrhea of swine that closely resembles transmissible gastroenteritis (TGE).


Porcine epidemic diarrhea (PED) occurs only in swine. In previously unexposed herds, all age groups are susceptible. The disease occurs in England, many European countries, China, Taiwan and Korea. Thus far the disease has not occurred in the western hemisphere.

Historical information

In 1971, outbreaks of watery diarrhea in feeder and fattening swine were observed in England. Suckling pigs did not sicken; otherwise, outbreaks closely resembled TGE. In 1976, a similar disease, but also affecting suckling pigs, was observed. Eventually the two diseases were referred to as PED type 1 and PED type 2.

During the 1980s a similar disease with two virulence types was prevalent in many European countries. Also, PED spread to China, Taiwan and Japan. In Europe, outbreaks now are rare, usually affect feeder and fattening pigs, and are not economically important. The disease in Asian countries, however, is highly virulent. Efforts there are under way to develop an oral vaccine for immunization of sows.

Its presence in the US was first confirmed in 2013.


A coronavirus causes porcine epidemic diarrhea. The virus is unrelated to porcine coronaviruses that cause TGE, porcine respiratory coronavirus (PRCV) and hemagglutinating encephalomyelitis virus (HEV). It does have some antigenic determinants in common with feline infectious peritonitis virus. The virus can be grown in epithelial cells from the mucosa of the small intestine of hysterectomy-derived piglets and in Vero cells. Porcine epidemic diarrhea virus induces antibodies in swine that can be identified by various laboratory techniques.


Coronavirus is disseminated in the feces of infected pigs for at least seven days post-inoculation. Fomites and vehicles can also spread virus indirectly. There is little information on the possible existence of carrier swine that could spread virus. On sites where PED is endemic and there is frequent or continuous farrowing, virus is maintained in successive generations of susceptible piglets.


The coronavirus of PED, like that of TGE, is in feces and usually is transmitted orally. It replicates primarily in enterocytes on villi of the small intestine, and to a lesser degree in cryptal cells of both small intestine and colon. In the small intestine, it causes degeneration and necrosis of enterocytes. Many enterocytes are destroyed and replaced by cuboidal or flat epithelial cells. Intestinal lesions of PED are similar to those of TGE but develop less rapidly and are less severe. Erosion and ulceration of enterocytes leads to loss of tissue fluid into the lumen and failure of the intestine to absorb adequate fluids. Diarrhea follows and leads to dehydration and depletion of electrolytes.

Clinical signs

The main sign in all age groups is watery diarrhea. The disease closely resembles TGE but spreads more slowly than TGE on a site and among adjacent farms. Infected piglets up to one week old die from dehydration after three to four days. Mortality averages about 50% but usually is lower than that of TGE. Older piglets recover in about one week. In other outbreaks, weaned pigs and older animals are severely affected but younger animals may not sicken and have little or no diarrhea. The severity of disease is quite variable.

Feeders, finishers and adult swine have diarrhea, depression, anorexia, and signs of abdominal pain. Outbreaks often start in these age groups. Morbidity may be high and affected animals are quite sick. Although recovery usually follows, there may be some mortality and occasional sudden deaths.


In piglets with PED, there usually are few gross lesions other than dehydration and a distended intestine filled with yellow fluid. In fattening hogs that die suddenly, there may be extensive necrosis of back muscles, a unique lesion. Microscopically, villi in the small intestine of piglets are atrophic. Some villi are fused with adjacent villi or poorly covered with cuboidal to flattened epithelium.


When all age groups are affected, a firm diagnosis cannot be made on the basis of clinical signs. Signs closely resemble those of TGE although PED spreads more slowly. A diagnosis of PED may be suggested by failure of baby pigs to become ill when adult animals are sick. Necrosis of back muscles in older swine is suggestive.

Diagnosis sometimes can be made after direct immunofluorescence tests on cryostat sections of the small intestine of acutely infected young pigs. The test is both rapid and reliable. It identifies virus or viral antigen in affected epithelial cells. In older, acutely infected animals, an enzyme-linked immunosorbent assay (ELISA) test on feces or intestinal content may be used to detect viral antigen. Direct electron microscope (EM) examination of feces may be helpful in identifying a coronavirus but does not differentiate PED from TGE because the viruses have similar morphology.

Several serologic tests can be used to demonstrate rising antibody titer to PED. Paired serum samples should be taken, the first at the onset of diarrhea and the second no sooner than four weeks later. Antibodies persist for at least one year.


There are no vaccines available. Pregnant sows more than two weeks away from parturition can be intentionally exposed in the face of an outbreak. This can be done by feedback of watery feces or intestinal content from acutely affected pigs. This procedure has the obvious risk of spreading other diseases.

Sanitary and quarantine measures may slow the spread of PED. There is no effective treatment other than good care and the provision of adequate water to combat dehydration.