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The largest outbreak of highly pathogenic avian Influenza A virus(HPAIV) infection in U.S. history began in December 2014 resulting in the euthanasia of millions of birds and collateral economic consequences to the U.S. poultry industry. We describe 2 cases of H5N2 HPAIV infection in laying hens in Iowa. Following a sharp increase in mortality with minimal clinical signs, 15 dead birds, from 2 unrelated farms, were submitted to the Iowa State University Veterinary Diagnostic Laboratory. Common lesions included diffuse edema and multifocal hemorrhage of the comb, catarrhal exudate in the oropharynx, and multifocal tracheal hemorrhage. Less common lesions included epicardial petechiae, splenic hemorrhage, and pancreatic necrosis. Influenza A virusnucleoprotein was detected by immunohistochemistry in multiple cell types including ependymal cells, the choroid plexus, neurons, respiratory epithelium and macrophages in the lung, cardiac myocytes, endothelial cells, necrotic foci in the spleen, Kupffer cells in the liver, and necrotic acinar cells in the pancreas. Real-time polymerase chain reaction and sequencing confirmed H5N2 HPAIV with molecular characteristics similar to other contemporary U.S. H5N2 HPAIVs in both cases.

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 Coronaviridaeproduced 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.

The role of Bovine viral diarrhea virus(BVDV) in the development of Porcine circovirus-2(PCV-2)-associated disease (PCVAD) was investigated in 2 experimental studies. In the first, separate groups of germ-free pigs were inoculated with filtered tissue homogenate (from diseased pigs) containing PCV-2b + BVDV-1–like virus (group 1), PCV-2a + BVDV-1–like virus (group 4), BVDV-1–like virus only (group 3), or PCV-2b + BVDV-1–like virus following a BVDV vaccination protocol (group 2). This last group was used to test if BVDV vaccination would prevent clinical PCVAD in this model. Many of the inoculated pigs had mild multisystemic inflammation consistent with classic PCVAD. One vaccinated, dually inoculated pig had acute respiratory distress followed by death at 21 days postinfection. Lesions in this pig resembled the severe form of PCVAD observed in the field since the fall of 2004, suggesting a role of ruminant pestiviruses and/or vaccination in the development of this disease. In the second study, cesarean-derived, colostrum-deprived pigs were inoculated with PCV-2b and a cytopathic strain of BVDV-1 (cpBVDV-NADL) either alone or in combination. Clinical signs of PCVAD were seen in a single animal inoculated only with PCV-2b. This pig had growth retardation followed by acute respiratory distress leading to death 30 days postinfection. Pulmonary lesions in this animal were similar to those seen in the pig that died in the first study. Infection with cpBVDV-NADL did not enhance PCV-2b replication or lesion formation.

Porcine teschovirus(PTV) was isolated in cell culture and/or demonstrated by polymerase chain reaction in samples of brain and/or spinal cord in pigs in Indiana during the 2002–2007 period. Testing was initiated on pigs originating from populations exhibiting nervous clinical disease and/or pigs with microscopic lesions in central nervous tissues, indicating viral encephalitis and/or myelitis. Virus was demonstrated in pigs with and without lesions as well as with and without nervous clinical disease. Nucleotide sequence analysis of the 5′-nontranslated region of the viral genome revealed that these isolates had low-level genetic heterogeneity but were homologous to porcine PTV serotype 1 (PTV-1). These findings indicate that low-to-moderate virulence strains of PTV with some homology to PTV-1 are endemic in many swineherds of Indiana and are associated with subclinical and clinical nervous disease in weaned pigs.