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...