#09-127

Complete

Date Full Report Received

07/25/2011

Date Abstract Report Received

07/25/2011

Investigation

Institution: , ,
Primary Investigator:

Porcine respiratory disease complex (PRDC) is a multifactorial disease process with a variety of infectious agents contributing to disease. The complex cannot be simply explained as infection with multiple pathogens as other factors, such as immune status and management practices contribute to disease occurrence and severity. Swine influenza virus (SIV) is a known contributor to PRDC and may predispose to secondary bacterial infection. The time following SIV infection in which a pig remains susceptible to secondary bacterial disease is unknown, and is an important point from a management perspective. To determine if SIV predisposes or enhances secondary Haemophilus parasuis (Hps) infection, studies were performed to evaluate disease severity to Hps challenge in pigs previously infected with SIV. Two separate studies were performed in which pigs were challenged with Hps 5 or 10 days following SIV infection. In the first study, 4-week old pigs were challenged with SIV and 10 days later, infected with Hps. There was no significant difference in Hps colonization in SIV/Hps-infected or Hps-only infected pigs, although host immune responses were significantly increased in the SIV/Hps group compared to the Hps- or SIV- alone groups. In the second study, in an attempt to bypass maternal immunity, 8-week old pigs were used. Pigs were challenged with SIV and then 5 days later, challenged with Hps. Hps colonization 1 day following Hps challenge was not significantly effected by prior SIV infection, nor were host immune responses significantly different between SIV/Hps challenged pigs compared to Hps-only. However, the Hps challenge was virulent, as disease in both the SIV/Hps group and Hps-only group was severe enough to warrant euthanasia of the pigs prior to the scheduled necropsy. Lesions were consistent with Glassers disease, and Hps was recovered from several systemic sites. The results from these studies highlight the need for methods to evaluate Hps immune status, both for research studies as well as field susceptibility. Results regarding the susceptibility to secondary bacterial infection following SIV are mixed, but our results did generate a model that has now been used to evaluate Hps pathogenesis and associated virulence factors.