EXPERIMENTAL DISEASE Comparison of the Pathogenicity of Two US Porcine Reproductive and Respiratory Syndrome Virus Isolates with that of the Lelystad Virus

The Lelystad virus or one of two US isolates (VR2385, VR2431) of porcine reproductive and respiratory syndrome virus were given intranasally to 25 4-week-old cesarian-derived colostrum-deprived pigs. Pigs from these groups were necropsied at 1, 2, 3, 5, 7, 10, 15, 21, or 28 days postinoculation. The Lelystad virus and VR243 1 induced mild transient pyrexia, dyspnea, and tachypnea. VR2385 induced labored and rapid abdominal respiration, pyrexia, lethargy, anorexia, and patchy dermal cyanosis. All three isolates induced multifocal tan-mottled consolidation involving 6.8% (n = 9, SEM = 3.4) of the lung for Lelystad, 9.7% (n = 9, SEM = 2.7) of the lung for VR2431, and 54.2% (n = 9, SEM = 4.4) of the lung for VR2385 at 10 days postinoculation. Characteristic microscopic lung lesions consisted of type 2 pneumocyte hypertrophy and hy- perplasia, necrotic debris and increased mixed inflammatory cells in alveolar spaces, and alveolar septal infil- tration with mononuclear cells. Lymphadenopathy with follicular hypertrophy, hyperplasia, and necrosis was consistently seen. Similar follicular lesions were also seen in Peyer's patches and tonsils. Lymphohistiocytic myocarditis and encephalitis were reproduced with all three isolates. Clinical respiratory disease and gross and microscopic lung lesion scores were considerably and significantly more severe in the VR238 5-inoculated pigs. All three viruses were readily isolated from sera, lungs, and tonsils throughout the 28 days of the study. The lymphoid and respiratory systems have the most remarkable lesions and appear to be the major site of replication of these viruses. This work demonstrated a marked difference in pathogenicity of porcine reproductive and respiratory syndrome isolates. The Lelystad virus (LV) was isolated in The Neth- erlands in 1991,*l and porcine reproductive and re- spiratory syndrome (PRRS) virus (PRRSV) was iso- lated in the United States in 1 992.'.2 Both viruses were isolated from swine herds with outbreaks of repro- ductive failure in adults and respiratory disease in 1- 16-week-old pigs. LV and PRRSV have since been characterized and tentatively classified along with lac- tate dehydrogenase elevating virus, simian hemor- rhagic fever virus, and equine arteritis virus in the newly proposed virus family Arteriviridae.'IZL Methods to isolate and propagate LV and PRRSV and serum antibody detection techniques for these viruses have been described.'~~~,~ ~ Antigen detection in tissues by use of a streptavidin-biotin immunoperoxidase technique demonstrated that PRRSV replicates primarily in macrophages in the respiratory and lymphoid sys- tem~.~,~