Effect of Timing of Vaccination with a Commerically Available Bacterin on PCV2-Associated Lesions - By T Opriessnig, Iowa State University and XJ Meng, Virginia Polytechnic and State University - Vaccines play an important role to minimize economic losses associated with diseases such as mycoplasmal pneumonia. On the other hand, several groups have recently demonstrated that vaccination with commercially available Mycoplasma hyopneumoniae (M. hyo.)

Introduction and Objectives

bacterins enhance clinical signs (wasting, reduced average daily gain) and macroscopic (enlarged lymph nodes) and microscopic lesions (lymphoid depletion and granulomatous inflammation of lymphoid tissues and other organ systems) associated with porcine circovirus type 2 (PCV2) infections (1, 2, 3). Our group recently demonstrated enhanced PCV2 replication manifest as significantly longer PCV2 viremia, a higher copy number of PCV2 antigen, and an increased severity of lymphoid depletion in segregated early weaned pigs vaccinated with Actinobacillus pleuropneumoniae and M. hyo. bacterins. In that experiment the pigs were vaccinated two weeks prior to and again on the day of PCV2 infection (4).

The objective of this study was to investigate if there is an effect of timing of vaccination on PCV2 replication and disease manifestation. The goal was to give practitioners the information necessary to choose the best point in time to use M. hyo. vaccines in herds with PCV2- associated diseases.

Material and Methods

Seventy-eight pigs were randomly assigned to 8 groups of 9-10 pigs each. A portion of the pigs (groups 1-7) were vaccinated with a commercially available M. hyo bacterin (M+PAC®; Schering-Plough Animal Health, Inc.) either as a two dose regime (groups 1-4) or as single dose regime (groups 5-6) at different time points in relationship to PCV2 inoculation (Table 1).

PCV2 inoculation was done at eight weeks of age. Groups 1-7 pigs received 5ml of PCV2 isolate ISU-40895 (5), passage 6 at a dose of 105.1 TCID50 intranasally. Group 8 pigs served as the non-vaccinated, non-PCV2-infected control group. Pigs were evaluated daily for clinical signs and weighed in weekly intervals. Necropsy was performed for all pigs 42 days post PCV2 inoculation (DPI). Samples from lymphoid tissues, spleen, tonsil, thymus, kidney, lung, liver, heart, and intestine were evaluated microscopically in a blinded fashion for presence and severity of lesions.

Results and Discussion

Clinical signs were limited to mild respiratory disease and macroscopic lesions to enlargement of lymph nodes in the PCV2-infected pigs. None of the vaccinated or unvaccinated pigs developed clinical PMWS in this model. Microscopically, PCV2-infection was characterized by mild-to-moderate lymphoid depletion and granulomatous inflammation in lymph nodes (significantly [p<0.05] more severe in groups 1, 4, 5, and 6 compared to groups 2, 3, 7, and 8), mild-to-moderate lymphohistiocytic hepatitis (significantly [p<0.05] more severe in group 1, 4, and 5 pigs compared to group 2, 7, and 8 pigs), mild-to-moderate lymphohistiocytic myocarditis (significantly [p<0.05] more severe in group 4 pigs compared to group 1, 2, 3, 7, and 8 pigs), and mild focal-to-diffuse interstitial pneumonia (significantly [p<0.05] more severe in group 4, 5, and 6 pigs compared to group 2, 7, and 8 pigs).

At 14 DPI, pigs in groups 1, 4, and 5 had significantly (p<0.05) higher PCV2 genomic copy numbers in sera compared to non-vaccinated group 7 pigs as determined by quantitative real-time PCR. The results of this study indicate a trend towards no-to-minimal PCV2-associated lesions when pigs are vaccinated 4-2 weeks prior to expected PCV2 exposure. Based on the results, producers with recurrent PCV2-associated disease should consider determining the approximate time of PCV2 infection and placing vaccines 4-2 weeks prior to this time.

Acknowledgments

This study was funded by the Iowa Healthy Livestock Initiative and by a grant from Schering-Plough Animal Health, Inc.

References

1. Allan GM, et al. 2000. Vet Rec 147:170-171.
2. Allan GM, et al. 2001. Pig J 48:34-41.
3. Kyriakis SC, et al. 2002. J Comp Path 126:38-46.
4. Opriessnig T, et al. 2003. Vet Pathol 40:521-529.
5. Fenaux M, et al. 2002. J Virol 76:541-551.