This coronaviral diarrhea (not yet recognized in the western hemisphere) affects pigs of all ages and clinically resembles transmissible gastroenteritis (TGE, see Intestinal Diseases in Pigs: Transmissible Gastroenteritis in Pigs) in several respects.
Etiology and Epidemiology
The porcine epidemic diarrhea (PED) virus is not related to any other member of the Coronaviridae. Pigs are the only known host. Antibodies to the virus have not been found in wild pigs or in other animal species. Infections have been seen in most European countries and in China. Large epidemics occurred in -Europe in 1969; no antibodies have been found in sera collected before 1969. Since then, the virus has become widespread and endemic in several European countries, and acute outbreaks have become rare. On large breeding farms, the virus persists in consecutive litters of pigs after weaning and after they lose their immunity from antibody in the milk. On these farms, the virus may be associated with weaning diarrhea. In Belgium, the virus is most frequently associated with diarrhea in feeder pigs, which develops shortly after they are gathered from different breeding farms and assembled in large fattening units. The virus was demonstrated in fecal material in 80% of these groups. Epidemiologic data from other countries are scarce. Spread of the virus mainly occurs directly through infected pigs and indirectly through virus-contaminated fomites and via transport trucks.
The pathogenesis and immune mechanisms are similar to those reported for TGE. Oral infection results in viral replication in the epithelial cells of the small intestinal villi. Cells on colonic villi also become infected. No other tissue tropisms have been shown. Virus is excreted in the feces.
Diarrhea is the only direct virus-induced clinical sign observed. An acute outbreak on a susceptible breeding farm resembles a TGE outbreak and is characterized by watery diarrhea in pigs of all ages. However, as compared with TGE, the incubation period is longer (3–4 days), not all the litters of suckling pigs may become sick, and mortality in neonatal pigs is lower (average 50%). Also, the disease within the farm spreads more slowly. In all outbreaks, signs are most consistently seen in feeders, finishers, and adults, which appear to be most susceptible because outbreaks often start in these age groups. Older pigs are more lethargic and depressed with PED than with TGE. Sick pigs appear to have colic.
Acute outbreaks in susceptible finishing pigs are characterized by watery diarrhea, but a markedly increased number of acute deaths may be seen, particularly in pigs infected toward the end of the finishing period and in stress-sensitive breeds. Death may even occur during the incubation period.
Macroscopic lesions are confined to the small intestine with villous shortening as the main characteristic. These lesions closely resemble those seen with TGE. No lesions have been described in the colon. A consistent finding is acute necrosis of back muscle.
Clinical differentiation from TGE is difficult. TGE in its typical epidemic form causes a rapidly spreading diarrhea in animals of all ages with high mortality in neonates. With PED, the diarrhea spreads at a slower rate, and although diarrhea is seen in most of the litters, some litters may remain healthy even in the absence of immunity. Morbidity is 100% in older pigs, and they are severely sick. Acute deaths in adults and finishing pigs due to muscle necrosis and occurring during an outbreak of diarrhea are typical of PED and are not seen with any other infectious diarrhea.
Laboratory diagnosis in neonates is made by direct immunofluorescence on cryostat sections of small intestine or colon. ELISA to detect viral antigens in feces or intestinal contents is more useful for older pigs. Antibodies can be detected in paired serum samples through ELISA-blocking.
No specific treatment is available. Measures taken during an outbreak are of a general nature. Pigs with diarrhea should have free access to water, and finishing pigs should have feed withheld for 1–2 days.
On breeding farms, in the face of an outbreak, spread of virus to the farrowing house can be prevented temporarily by sanitary measures and, if performed together with a deliberate infection of pregnant sows, losses in neonates may be lowered. No vaccine is available.
Last full review/revision March 2012 by D. L. Hank Harris, DVM, PhD