Emergence of Porcine epidemic diarrhea virus in the United States: clinical signs, lesions, and viral genomic sequences

Abstract

During the 10 days commencing April 29, 2013, the Iowa State University Veterinary Diagnostic Laboratory received the first 4 of many submissions from swine farms experiencing explosive epidemics of diarrhea and vomiting affecting all ages, with 90-95% mortality in suckling pigs. Histology revealed severe atrophy of villi in all segments of the small intestines with occasional villus-epithelial syncytial cells, but testing for rotaviruses and Transmissible gastroenteritis virus (Alphacoronavirus 1) were negative. Negative-staining electron microscopy of feces revealed coronavirus-like particles and a pan-coronavirus polymerase chain reaction (PCR) designed to amplify a conserved region of the polymerase gene for all members in the family Coronaviridae produced expected 251-bp amplicons. Subsequent sequencing and analysis revealed 99.6-100% identity among the PCR amplicons from the 4 farms and 97-99% identity to the corresponding portion of the polymerase gene of Porcine epidemic diarrhea virus (PEDV) strains, with the highest identity (99%) to strains from China in 2012. Findings were corroborated at National Veterinary Services Laboratories using 2 nested S-gene and 1 nested N-gene PCR tests where the sequenced amplicons also had the highest identity with 2012 China strains. Whole genome sequence for the virus from 2 farms in 2 different states using next-generation sequencing technique was compared to PEDV sequences available in GenBank. The 2013 U.S. PEDV had 96.6-99.5% identity with all known PEDV strains and the highest identity (>99.0%) to some of the 2011-2012 Chinese strains. The nearly simultaneous outbreaks of disease, and high degree of homology (99.6-100%) between the PEDV strains from the 4 unrelated farms, suggests a common source of virus.

Characterization of Porcine Epidemic Diarrhea Virus Isolate US/Iowa/18984/2013 Infection in 1-Day-Old Cesarean-Derived Colostrum-Deprived Piglets

“…generated experimental data are in agreement with field reports from North America suggesting that lesions of PEDV and TGEV infection are indistiguishable. 19 PEDV replication in mature enterocytes is rapid, with previous investigations demonstrating antigen or detecting nucleic acid 24 hpi. 2,7,11 In the current study, PEDV antigen and RNA were detected at 12 hpi.…”

“…18 Viral sequencing information from these initial North American breaks indicate >99% homology with 2012 Chinese isolates entered into GenBank. 6,19 More recently, North American PEDV sequences have revealed a second and distinct variant virus. 20 PEDV is transmitted by the fecal-oral route, and it causes watery diarrhea, anorexia, lethargy, and vomiting in swine of all ages, with either acute or endemic disease presentations.…”

“…Porcine epidemic diarrhea virus (PEDV) was first detected in North America 19 in April 2013 and has since infected numerous production facilities throughout the United States, Canada, and Mexico. PEDV is an enveloped single-stranded RNA virus of the Coronaviridae family 1 that was first reported in the United Kingdom, 21 but this alphacoronavirus can now be found in multiple countries worldwide.…”

Detection of African swine fever, classical swine fever, and foot-and-mouth disease viruses in swine oral fluids by multiplex reverse transcription real-time polymerase chain reaction

“…Low-virulence CSF represents yet another prominent threat to swine industries with the heightened potential for delayed detection in swine herds. 12 Finally, the spread of ASF in Russia and its emergence in wild boar in Europe, 7 and the emergence of porcine enteric coronaviruses in the United States 23 and other countries have further raised interest in new approaches to swine herd health surveillance.…”

Novel Transgenic Rice-Based Vaccines

“…PEDV causes acute diarrhea, vomiting, and dehydration with 90-95 % mortality in pigs (Stevenson et al 2013). The neutralizing epitope of PEDV, encoded by the core neutralizing epitope (COE) gene, was fused with the M cell-targeting peptide ligand Co1, which was expected to enhance the uptake of the fused antigen by M cells in Peyer's patch (Kim et al 2010a).…”