CPB 697 RESEARCH SEMINAR

 

 

 

 

DEPARTMENT OF COMPARATIVE PATHOBIOLOGY

 

 

 

Huiling Wei, BVM, MSVPM

Graduate Student in Virology

Department of Comparative Pathobiology

Purdue University

 

 

 

Porcine Respiratory Disease Complex

 

 

 

Thursday, March 27, 2008

VPTH 112

3:30 pm

 

Abstract:

Respiratory disease is a major health problem in growing swine. Cases of respiratory disease involving multiple pathogens as concurrent infection with viral and/or bacterial agents are often referred to as porcine respiratory disease complex (PRDC). Pathogens involved in PRDC can be classified as initiators (primary) or followers (secondary). Primary pathogens have the ability to cause disease in healthy pigs by damaging alveoli, defense mechanisms of the lungs and preventing oxygen diffusion. When damage in the lungs occurs the lungs become susceptible to secondary infection which starts replicating in high numbers. Pigs showing clinical signs of PRDC will be characterized by slow growth, decreased feed efficiency, lethargy, anorexia, fever, cough and dyspnoea. Porcine reproductive and respiratory syndrome (PRRS) and swine influenza virus (SIV) are common viral pathogens associated with PRDC. Co-infections with PCV2 have now been documented frequently in cases of PRDC. Prolonged and unusually severe clinical disease, unique histologic lesions of lymphoid depletion and airway fibrosis, and abundant PCV2 antigen within these lesions suggest that PCV2 is playing an important role in PRDC. Therefore, pathogens like PRRSV and SIV that cause the death of epithelial cells and lead to regeneration of damaged epithelium of airways may indirectly enhance the replication of PCV2. Based on the replicative cycle of PCV2, which requires and makes use of actively replicating cells, it is likely that factors that affect the replication of epithelial cells of airways would affect PCV2 replication and increase the number of infected cells. Furthermore, immune activation and assumedly cytokine secretion stimulated by vaccination or other pathogens have been demonstrated to up regulate PCV2 replication and result in more severe disease. Although increasing attention has been paid to PRDC recently, it is still unknown how PCV2 and other pathogens act synergistically to increase the severity of PRDC.