ShapeShapeauthorShapechevroncrossShapeShapeShapeGrouphamburgerhomeGroupmagnifyShapeShapeShaperssShape

PRRSV Enhances PCV2a and PCV2b Replication and Duration of Shedding

by 5m Editor
1 January 2012, at 12:00am

Summary of a paper presented by T. Opriessnig of Iowa State University in the US at the 6th Symposium on Emerging and Re-Emerging Pig Diseases, Barcelona, Spain in June 2011.

Introduction

Several groups have characterised the shedding patterns of PCV2 from pigs experimentally infected with PCV2 and found that PCV2 is shed in nasal and oral secretions as well as in urine and faeces (1). Horizontal transmission of PCV2 via oral-nasal and oral-faecal routes has been suggested as the main mechanism of infection (2) which was further confirmed by a recent experimental study (3).

Co-infections increase the severity of porcine circovirus associated disease (PCVAD) (4). Porcine reproductive and respiratory syndrome virus (PRRSV) infection has been shown to enhance the severity of clinical PCVAD under field and experimental conditions by enhancing PCV2 replication resulting in increased amounts of PCV2 DNA present in the sera of PCV2-PRRSV co-infected groups (4).

Co-infection of PCV2 and PRRSV in pigs is frequently observed in swine herds under field conditions. However, to our knowledge, the effect of PRRSV on PCV2 shedding patterns under controlled experimental conditions has not been investigated to date.

The objectives of this study were to determine if co-infection of piglets with PRRSV and PCV2 has any affect on PCV2 shedding characteristics and if there are differences in shedding patterns between PCV2 subtypes (PCV2a and PCV2b) in co-infected pigs.

Materials and Methods

Twenty-three, two- to six-week-old, PCV2 and PRRSVnaïve pigs were randomly assigned to one of five groups according to Table 1.

Table 1. Experimental design
Group n Inoculation
PCV2 PRRSV
Negative 3 - -
PCV2a-I 5 PCV2a -
PCV2a-PRRSV-CoI 5 PCV2a PRRSV
PCV2b-I 5 PCV2b -
PCV2b-PRRSV-CoI 5 PCV2b PRRSV

PCV2 inoculation was done using PCV2a strain 40895 and PCV2b strain NC16845. For PRRSV inoculation, PRRSV strain VR2385 was utilized. Blood was collected on a weekly basis and tested for presence of anti-PCV2 antibodies by a PCV2 ELISA (5) and for presence of PCV2 DNA (6) and PRRSV RNA by PCR. Oral, nasal and faecal swabs were collected in regular intervals from day post inoculation (dpi) 0 until dpi 70 and tested by quantitative real-time PCR for the presence of PCV2 DNA. All pigs were necropsied at dpi 70.

Results

Negative control pigs remained PCV2 and PRRSV negative for the duration of the study. All pigs infected with PCV2 became infected as evidenced by PCV2 viraemia and seroconversion. There was a significantly (p<0.05) higher load of PCV2a and PCV2b DNA in serum, oral swabs, nasal swabs and faecal swabs in pigs concurrently infected with PCV2 and PRRSV compared to pigs singularly infected with PCV2, further confirming that PRRSV enhances replication and shedding of PCV2. Moreover, PRRSV infection significantly (p<0.05) prolonged the presence of PCV2 DNA in serum and increased the amount of PCV2 DNA in oral and nasal secretions and fecal excretions in the later stages of infection between dpi 28 and 70. Shedding patterns were similar between groups infected with PCV2a and PCV2b, indicating that there was no PCV2 subtype-specific interaction with the PRRSV isolate used in this study.

Discussion

A higher quantity of PCV2a and PCV2b DNA was found in serum, oral swabs, nasal swabs and faecal swabs in pigs concurrently infected with PCV2 and PRRSV compared to pigs singularly infected with PCV2, further confirming that PRRSV enhances replication and shedding of PCV2.

Moreover, PRRSV infection significantly prolonged the presence of PCV2 DNA in serum and several body secretions, thus emphasising the importance of PRRSV control in order to reduce the PCV2 shedding and transmission in the pig population.

References

1. Patterson and Opriessnig, 2010. Animal Health Res Rev 11:217-234.
2. Segalés et al. 2005. Vet Microbiol. 111:223-229.
3. Patterson et al. 2011. Vet Microbiol. in press.
4. Opriessnig et al. 2007. J Vet Diagn Invest. 19:591-615.
5. Nawagitgul et al. 2002. Clin Diagn Lab Immunol. 9:33-40.
6. Opriessnig et al. 2003. Vet Path. 40:521-529.

Further Reading

- You can view the Proceedings of the 6th International Symposium on Emerging and Re-Emerging Pig Diseases by clicking here.


Further Reading

- Find out more information on PMWS by clicking here.


January 2012