Background:

Porcine Epidemic Diarrhea virus (PEDV) is a swine enteric virus in the family Coronaviridae. It induces a malabsorptive diarrhea like that caused by the genetically related coronavirus of transmissible gastroenteritis (TGE).^6,10 The virus was discovered in England in 1971, subsequently spread throughout Europe, and was identified in China, Korea and Japan before arriving in the US in May 2013.⁶ By August, PEDV had been identified in swine herds in 16 states, including Indiana.^3,4,12 Because PEDV is widespread in Europe and Asia, it is not considered a trade-restricting disease by the USDA, but is a production-related disease.⁶ The strain of PEDV in the US is most similar, genetically, to the PEDV currently affecting China's swine herds. Since the first diagnosis in China in 2010, PEDV has caused the death of more than one million piglets.⁵ No direct connection between the current U.S. outbreak and the outbreaks in Europe and Asia has been identified.

Clinical Signs:

PEDV is usually spread by ingestion of contaminated feces or through fomites.⁴ Clinical signs may be identical to those of TGE, with vomiting and thin watery feces, with secondary dehydration and metabolic acidosis. The disease occurs mainly in young piglets; however, in previously unexposed herds, all age groups (including nursery pigs, grow/finish pigs, sows, and boars) may be susceptible. An acute outbreak in a naïve herd usually results in severe diarrhea and vomiting, with morbidity as high as 100%. Mortality can reach 95% in suckling pigs, and decreases with age.^10,11 Clinical signs develop within 12 to 36 hours of inoculation. Surviving pigs develop natural immunity over 2-3 weeks.^9,11 Neonatal piglets are protected by maternal immunity in colostrum.⁶

Associated Pathology:

The lesions at postmortem examination resemble those of TGE. The stomach is usually empty due to vomiting. The small intestine is typically thin-walled and fluid-filled with little or no absorbed chyle in lacteals.^8,10 Histologically, the small intestine has villous atrophy (short and fused villi) with cytoplasmic vacuolation and exfoliation of enterocytes.^1,8,10 A few flattened villous enterocytes have features of necrosis (hypereosinophilic cytoplasm and hyperchromatic to pyknotic nuclei). No microscopic lesions in the colon have been reported.¹

Diagnosis:

Diagnosis is based on the combination of history, clinical signs, postmortem examination, and laboratory testing. The most common ancillary test is detection of viral nucleic acid from intestinal contents by reverse transcriptase polymerase chain reaction (RT-PCR).^10,11 Other proven diagnostic methods include enzyme-linked immunosorbent assay (ELISA) and electron microscopy of feces. Currently, the U.S. Department of Agriculture, Animal and Plant Health Inspection Service, Veterinary Services (USDA-APHIS-VS) is working with the American Association of Veterinary Laboratory Diagnosticians (AAVLD) and the National Animal Health Laboratory Network (NAHLN) laboratories to enhance diagnostics.³ Porcine epidemic diarrhea virus induces antibodies in swine that can be identified by various laboratory techniques and has some antigenic determinants similar to those of feline infectious peritonitis virus.⁶

Treatment and Control:

The only treatment is symptomatic, consisting of electrolyte and fluid supplementation to prevent further dehydration. Producers should contact the herd veterinarian if any TGE-like signs appear. In addition, producers must maintain strict biosecurity protocols such as adequate quarantine, isolation of sick pigs, and disinfection to help prevent entry or spread of the disease. The virus is susceptible to many common disinfectants like bleach and Virkon S ®. In contrast to TGE, PEDV may be more tolerant to the heat of spring and summer.⁸ Thus the potential for outbreak increases as well as the need to assure equipment and trailers are properly cleaned and staff practice proper prophylactic measures. The USDA, State Animal Health Officials, the American Association of Swine Veterinarians and veterinarians at the National Pork Board are actively monitoring this disease and will make recommendations to producers as necessary.

Although PEDV infection is clinically similar to TGE and infection with Porcine Respiratory Coronavirus (PRCV), the virus is antigenically unique.² Therefore, vaccination or exposure to TGE, or exposure to PRCV will not protect against PEDV. Currently, no vaccine is available in the U.S. for PEDV. Producers who see any signs of illness in their pigs should notify their herd veterinarian immediately.

Impact:

PEDV only causes disease in swine, and does not pose any risk to humans or other animals. In addition, it poses no risk to food safety according to the USDA and the American Association of Swine Veterinarians.⁷ However, the PEDV outbreak could increase U.S. hog and wholesale pork prices as production costs increase, compounding the economic effect of last summer's historic drought.