Date Full Report Received04/18/2013
Date Abstract Report Received04/18/2013
InvestigationInstitution: National Animal Disease Center, USDA-ARS
Primary Investigator: Susan Brockmeier
Funded ByNational Pork Board
The appearance of highly-pathogenic porcine reproductive and respiratory syndrome virus (PRRSV) isolates in Asia necessitates investigation into the clinical repercussions of these viruses if the strains were to appear in the US. Epidemiologic data from Asian outbreaks suggest that disease severity was associated with both the PRRSV isolates from these cases and secondary bacterial infections. Previous reports have indicated that US isolates of PRRSV predispose to secondary bacterial infections as well, but outbreaks like the ones described in Asia have not been reported in the US. The objectives of this research were to compare the pathogenesis of Asian and US PRRSV isolates with regard to their ability to cause disease and predispose to secondary bacterial infections in swine. The experiment consisted of 10 groups of 9-10 pigs each. At 6 weeks of age, half the groups were inoculated with a bacterial cocktail of Streptococcus suis, Haemophilus parasuis, and Actinobacillus suis and 1 week later 4 bacterial colonized groups and 4 non-bacterial colonized groups were inoculated with 1 of 2 Asian HP-PRRSV strains (JXwn06 or SRV07) or 1 of 2 US PRRSV strains (SDSU73 or VR2332). JXwn06 was isolated during the initial outbreaks of Porcine High Fever Disease in China in 2006, whereas SRV07 was isolated after the disease had spread to Vietnam in 2007.
The HP-PRRSV strain JXwn06 caused severe disease compared to the North American prototype strain VR2332, which caused the least disease of the isolates tested. A virus like JXwn06 could be devastating to the swine industry in the US, causing severe disease and mortality, whether entering from a foreign country or emerging from similar evolution of endemic viruses in the US. Disease caused by the Vietnamese strain SRV07 and the US strain SDSU73 fell somewhere between that of VR2332 and JXwn06. Although SRV07 is still much more potent than strains such as VR2332, these results may indicate that HP-PRRSV isolates in Asia have attenuated to some degree with time and are on par with higher pathogenic US strains such as SDSU73, which itself a strain that was isolated in association with outbreaks of higher morbidity/mortality known at the time as “atypical” or “acute severe” PRRSV in the US in the late 1990s.
Results indicate that higher amounts of virus were detected in pigs infected with the JXwn06 strain of PRSSV possibly indicating broader replication and dissemination of this virus. The presence of more extensive and disseminated lesions, such as encephalitis (brain inflammation) may explain the increased severity of disease. The increased frequency and quantity of nasal virus shedding of both Asian PRRSV strains suggest they are more transmissible as well. Serum chemistries did not indicate any major organ malfunction was responsible for the severe clinical signs, although they did suggest the pigs were in a severe malnourished state. Pigs infected with JXwn06 also displayed greater measures of immune dysfunction and as a result the frequency and severity of secondary bacterial infections increased with the increasing virulence of PRRSV. Thus secondary infections do appear to play a role in the severity of disease seen with these HP-PRRSV isolates. Furthermore, age influences mortality rates with JXwn06, as mortality in 4 week old pigs was greater than in 7 and 10 week old pigs. Based on experimental results to date severity of disease and mortality rates appear to be dependent on virulence of the PRRSV strain, rate of secondary infection, and age of the pig. The next step is to determine whether intervention methods such as vaccination, antibiotic treatment, or immunomodulators can diminish the devastating effects of these viruses.
Susan Brockmeier, DVM, PhD
Research Veterinary Medical Officer
USDA-ARS-National Animal Disease Center
1920 Dayton Avenue
Ames, IA 50010