- 1 minute, 54 seconds
- Expertise article
- Dürlinger S., Rathkjen PH., Kraft C., Morgenstern R., Knecht C., Zaruba M., Rümenapf T., Ladinig A.
Introduction
Porcine reproductive and respiratory syndrome virus (PRRSV) is responsible for losses in breeding- as well as in growing- pig herds and still has an important economic impact on pig production worldwide. The objectives of the present study were 1) to establish an infection model with the virulent PRRSV-1 isolate AUT 15-33 in weaned piglets to reproduce symptoms comparable to those observed in the field; 2) to assess the efficacy of the MLV vaccine “Ingelvac PRRSFLEX® EU” regarding viral shedding via oral fluids in vaccinated piglets after experimental PRRSV infection with PRRSV strain AUT 15-33 in comparison to non- vaccinated piglets; and 3) to determine if the dose of infection has an influence on the efficacy of the vaccine.
Material and Methods
Non-vaccinated and vaccinated (Ingelvac PRRSFLEX® EU) piglets at four weeks of life (D0) were intranasally infected with a low dose (1x103 TCID50) or a high dose (1x105 TCID50) of PRRSV (AUT 15-33) at study day 28. One additional group of ten vaccinated piglets served as vaccination control group (see Table 1). Serum samples and oral swabs were collected at different time points throughout the study (see Fig. 1) to assess the viremia levels and viral shedding by qRT-PCR. Half of the animals of each group where euthanized and necropsied 14 days post infection (D42) and the remaining animals four weeks later (D70).
Results
Viral load in serum increased in all infected piglets after challenge. A slower increase of viral load in sera was measured in groups infected with the lower dose than in those infected with the higher dose. The viral load of the respective nonvaccinated group increased faster compared to the vaccinated group, but reached similar levels (see Fig. 2).All infected animals shed virus through oral fluids. The vaccinated infected groups shed less virus than the non-vaccinated infected animals. The duration of shedding was shorter in vaccinated pigs than in non-vaccinated pigs (see Fig. 3). There was a significant difference/ a trend towards statistical significance in the Area under the curve (AUC) of viral shedding through oral fluids between the vaccinated and the non-vaccinated groups (p>0.05/ p>0.1).
Conclusion
All infected animals revealed viremia and shed virus via oral fluids post challenge. Nevertheless, vaccinated infected groups shed less virus than the nonvaccinated animals and the duration of shedding was shorter in vaccinated pigs compared to non-vaccinated pigs.