Submitted to: Porcine Reproductive and Respiratory Syndrome International Symposium
Publication Type: Abstract Only
Publication Acceptance Date: September 3, 2008
Publication Date: N/A
Acute-type PRRS outbreaks were first observed in 1996. They are characterized by severe reproductive and respiratory clinical disease losses (including sow mortalities) in PRRSV “immune” herds (regularly vaccinated or systematically exposed). This study was designed to document and validate the ineffective cross-protection against clinical and pathologic disease following challenge for a putative heterologous PRRSV pair and to establish sampling protocols to investigate early post challenge local pulmonary immune responses. Medicated early-weaned pigs were immunized with VR2332 PRRSV at 4 weeks of age and challenged 8 weeks later with VR2332 or with heterologous Acute-type NCPowell. Pig treatment groups: 1) naïve control, 2) homologous challenge, 3) heterologous challenge, and 4) infection control groups. Pigs received live virulent PRRSV inoculum IN and IM. Pigs were either followed for 19+ days to assess clinical signs and pulmonary lesions or euthanized at 3 or 4 days post challenge and tissues collected. Time to recovery of normal breathing following restraint was up to 6 times longer for heterologous challenged and NCPowell infected pigs. The extent of lung inflation (interstitial pneumonia) at necropsy in these pigs was also nearly equivalent. Left cranial and caudal lung lobes were individually lavaged with HBSS, sections of right cranial and caudal lung lobes and tonsil collected for gene expression analysis. Sections of lung were formalinized for histopathologic evaluation. Viral load for each tissue will be determined by quantitative PRRSV rtPCR and PRRSV antibody by IDEXX ELISA. Cytokine production in vitro by BAL and Tracheobronchial lymph nodes (TBLN) cells, in serum, or in BAL fluid will be determined by quantitative ELISA. These data support the use of VR2332 immunization x NCPowell heterologous PRRSV challenge of pigs as a clinically and pathologically valid model for studies of immune response changes associated with ineffective cross-protection. These studies were supported by USDA PRRS CAP1 funds.