Sequence analysis showed heterogeneity among 74 strains and distinct molecular characteristics of highly virulent strains and variants.

In 1987, porcine reproductive and respiratory syndrome (PRRS) was recognized in the USA as a new disease of swine causing late-term reproductive failure and severe pneumonia in neonatal pigs. The syndrome is caused by an RNA virus referred to as PRRS virus (PRRSV), which is classified in the family Arteriviridae. Swine macrophages are the only indigenous cell type known to support PRRSV replication. Direct contact between infected and naive pigs is the predominant route of PRRSV transmission. Exposure of a mucosal surface to PRRSV leads to virus replication in regional macrophages, a prolonged viremia and systemic distribution of virus to other macrophage populations. Reproductive failure induced by PRRSV infection in late-gestation sows is characterized by premature farrowing of stillborn, partially autolyzed, and mummified fetuses. Pneumonia caused by PRRSV infection is more severe in young pigs compared to adults and may be complicated by concurrent bacterial infections. Gross lung lesions associated with PRRSV infection vary from none to diffuse consolidation. In addition, multiple lymph nodes may be markedly enlarged. Microscopically, PRRSV-pneumonia is characterized by multifocal, interstitial thickening by macrophages and necrotic cell debris in alveoli. Other less common microscopic lesions of PRRSV infection include myocarditis, vasculitis, encephalitis, and lymphoid hypertrophy and hyperplasia. In acute or subacute PRRSV infections, serum and lung are the best specimens for diagnosis. Persistent PRRSV infections can be produced by transplacental or intranasal infection. Persistent PRRSV infections are an important factor for virus survival and transmission within a swine herd and will complicate control programs.

In late summer through early winter of 1998, there were several outbreaks of respiratory disease in the swine herds of North Carolina, Texas, Minnesota, and Iowa. Four viral isolates from outbreaks in different states were analyzed genetically. Genotyping and phylogenetic analyses demonstrated that the four swine viruses had emerged through two different pathways. The North Carolina isolate is the product of genetic reassortment between H3N2 human and classic swine H1N1 influenza viruses, while the others arose from reassortment of human H3N2, classic swine H1N1, and avian viral genes. The hemagglutinin genes of the four isolates were all derived from the human H3N2 virus circulating in 1995. It remains to be determined if either of these recently emerged viruses will become established in the pigs in North America and whether they will become an economic burden.

In February 2014, porcine deltacoronavirus (PDCoV) was identified in the United States. We developed a PDCoV real-time reverse transcription PCR that identified PDCoV in 30% of samples tested. Four additional PDCoV genomes from the United States were sequenced; these had ≈99%–100% nt similarity to the other US PDCoV strains.

Abstract. One-, 4-, and lo-week-old pigs were exposed to porcine reproductive and respiratory syndrome virus (PRRSV) to determine the effect of age on clinical signs, hematologic alterations, the onset and duration of viremia, routes of virus shedding, antibody production, and microscopic lesions produced by PRRSV isolate ATCC VR-2332. The response to PRRSV infection was similar among age groups. Fever, usually prolonged, and a marked dyspnea with cutaneous erythema when restrained for sample collection were the most consistent clinical signs. Prolonged periocular edema was unique to the l-week-old pigs. The white blood cell count was decreased on day 4 postexposure (PE) due to decreases in neutrophils and lymphocytes. The virus was isolated from buffy coats at day 1 PE and was isolated from serum, buffy coat, or plasma at each sample collection period through the end of the trial (day 28 PE). Virus was most consistently isolated from lung, lymph node, spleen, and tonsil on day 7 PE and exclusively from lymph node, spleen, and tonsil on day 28 PE. Virus was infrequently isolated from urine and fecal and nasal swabs. Consistent microscopic changes in all age groups included interstitial pneumonia and lymph node hypertrophy and hyperplasia on days 7 and 28 PE, lymph node necrosis on day 7 PE, and subacute mononuclear myocarditis on day 28 PE. Findings presented here indicate that interstitial pneumonia, lymphoid necrosis, and mononuclear myocarditis are characteristic lesions of PRRSV isolate ATCC VR-2332 infection in 1-, 4-, and lo-week-old pigs.Porcine reproductive and respiratory syndrome (PRRS), a recently emerging disease of swine, causes pneumonia and late term abortion characterized by stillborn pigs, partially autolyzed fetuses, and weak live-born pigs. [8][9][10][11][14][15][16]18,24,25 In conventional pigs, this virus causes fever, marked dyspnea ("thumping"), flulike signs, and an increase in pneumonia from opportunistic bacteria. ll,14,l6,18 Clinical signs in PRRS virus (PRRSV)-infected gnotobiotic pigs are inappetence, fever, diarrhea, hyperpnea, dyspnea, and rough hair coats.9 Clinical signs of the disease are reported to be more severe in neonatal pigs. The disease is caused by a positive-strand enveloped RNA virus closely related to lactate dehydrogenase-elevating virus (LDEV), equine arteritis virus (EAV), and simian hemorrhagic fever virus (SHF) and will probably be classified in the family Arteriviridae. 4,17,20 To determine the effect of age on disease, l-, 4-, and 10-week-old pigs were intranasally exposed to PRRSV. Hematologic alterations, onset and duration of vireFrom the Departments of Veterinary Diagnostic Medicine (Rosmia, routes of virus shedding, antibody production, and gross and microscopic lesions were evaluated. Materials and methodsAnimals. Thirty-two pigs (16 4-wk-old pigs and 16 10-wk-old pigs) and 2 sows with litters (each litter containing 9 1-wk-old piglets) were obtained from a swine herd seronegative for PRRS. The source herd was also seronegative for antibodies to pseu...

The pathogenesis of porcine reproductive and respiratory syndrome virus (PRRSV) was determined in gnotobiotic pigs by studying the sequential development of microscopic lesions and sites of virus distribution and replication. Thirty-two pigs (three pigs/infected group and one pig/control group) were inoculated by nasal instillation of either PRRSV isolate ATCC VR-2332 (total dose 10(2.6) TCID50) or uninfected cell culture supernatant. Infected and control pigs were euthanized at 12 hours, and 1, 2, 3, 5, 7, 14, and 21 days postexposure (PE). Gnotobiotic pigs experimentally infected with PRRSV were viremic by 12 hours PE and subsequently developed pneumonia, lymphadenopathy, vasculitis, myocarditis and encephalitis. Lung lesions developed by day 3 PE, persisted through day 21 PE and were characterized by alveolar septa thickened by macrophages, alveolar proteinaceous and karyorrhectic debris, alveolar syncytial cells, and multifocal type II pneumocyte hypertrophy. Lymph node lesions varied in distribution and severity and were characterized by germinal center hypertrophy and hyperplasia, lymphocyte necrosis, multiple cystic spaces, and polykaryocytes within the cystic spaces. Heart lesions were a late feature of infection and all infected pigs had heart lesions on day 21 PE characterized by subendocardial, myocardial, and perivascular foci of lymphocytes. Vasculitis also varied in distribution and severity and affected all sizes of vessels. Results of this experiment indicate that PRRSV is a multisystem disease characterized initially by viremia with subsequent virus distribution and replication in multiple organs causing interstitial pneumonia, vasculitis, lymphadenopathy, myocarditis, and encephalitis.

European-like field isolates of porcine reproductive and respiratory syndrome virus (PRRSV) have recently emerged in North America. The full-length genomic sequence of an index isolate characterized in 1999, strain EuroPRRSV, served as the reference strain for further studies of the evolution and epidemiology of Europeanlike isolates (type 1) in the United States. Strain EuroPRRSV shared 90.1 to 100% amino acid identity with the prototype European strain, Lelystad, within the structural and nonstructural open reading frames (ORFs) and 95.3% overall nucleotide identity. The 5 untranslated region and two nonstructural regions within ORF 1 were closely examined due to significant divergence from strain Lelystad. A 51-bp deletion in a region within ORF 1a, coding for nonstructural protein 2 (NSP2), was observed. Sequence analysis of the structural ORFs 2 to 7 of additional European-like isolates indicated that these isolates share 93% nucleotide identity with one another and 95 to 96% identity with the Lelystad strain but only 70% identity with the North American reference strain VR-2332. Phylogenetic analysis with published PRRSV ORF 3, 5, and 7 nucleotide sequences indicated that these newly emerging isolates form a clade with the Lelystad and United Kingdom PRRSV isolates. Detailed analysis of four of these isolates with a panel of 60 monoclonal antibodies directed against the structural proteins confirmed a recognition pattern that was more consistent with strain Lelystad than with other North American isolates.

Rotavirus C (RVC) is a major cause of gastroenteritis in swine. Between December 2009 and October 2011, 7520 porcine samples were analyzed from herds in the US and Canada. RVC RNA was detected in 46% of the tested samples. In very young pigs (≤3 days old) and young piglets (4-20 days old), 78% and 65%, respectively, RVC positive samples were negative for RVA and RVB. RVC RNA was also detected in 10% of tested lung tissues. Additionally, we investigated the porcine RVC molecular diversity by sequencing the VP7 gene segment of 65 specimens, yielding 70 VP7 gene sequences. Based on pairwise identity frequency profiles and phylogenetic analyses, an 85% nucleotide classification cut-off value was calculated using the novel sequence data generated in this study (n=70) and previously published RVC VP7 sequences (n=82), which resulted in the identification of 9 VP7 RVC genotypes, G1 to G9.