Even though the prevalence of PCV2 infection is very high and can be 95-100% of the pig population, the incidence of PMWS is typically low, ranging from 5-15% of pigs on affected farms.  Although PCV2 is thought to be the only essential infectious agent, PMWS has been difficult to  reproduce in pigs inoculated only with PCV2.  In a majority of studies, PCV2 alone as inoculum failed to reproduce any pathological changes and/or clinical signs similar to those observed in field cases of PMWS, even though the virus or viral antigens were detected in various tissues.  In a few studies, a low proportion of pigs developed some lesions or clinical signs of PMWS, but few developed all clinical signs and histologic lesions of PMWS, although the virus or viral antigens were detected in various tissues.  Recently, new terminology was introduced and approved by the American Association of Swine Veterinarians (AASV) - Porcine Circovirus ASSOCIATED disease (PCVAD)- used to denote the entire spectrum of diseases that are associated with PCV2 including PMWS, respiratory disease, reproductive failure, diarrheal disease, Porcine Dermatitis Nephritis Syndrome (PDNS), and high mortality in pigs.  In many cases, different co-factors (infectious and non-infectious) are required, along with PCV2, to reproduce clinical signs and lesions in these pigs.  The following pathogens should be considered as differentials  when diagnosing PCVAD in a swine population: Porcine Respiratory and Reproductive Syndrome (PRRS), Swine influenza virus (SIV), Transmissible Gastroenteritis/Porcine Respiratory Corona-virus (TGE/PRCV), Porcine Parvovirus (PPV), pestiviruses, M. hyopneumonia, and Salmonella.  Also, one should take into consideration the history of the animals' on- farm management, vaccination, breed, stress, etc.  PCV2 is infectious to swine, can replicate at a high level in sick animals, is associated with unique lesions and has a significant impact on the swine industry.

   Detection of porcine circovirus types1 and 2, as well as detecting antibodies to PCV, can be accomplished using several testing methods.

Detection of other pathogens is also possible in ADDL upon request.  Cost of tests and submission information can be obtained on ADDL's website - www.addl.purdue.edu - or by calling  (765) 494-7440.

  Confirmation of a diagnosis of PCVAD requires the demonstration of PCV2 in high concentrations within typical lesions.

   For necropsy examination at ADDL, submit   affected live pigs or pigs that have recently died.

    If necropsy is performed onsite, collect serum and the following tissues: several enlarged lymph nodes, tonsil, spleen, kidney, liver, lung (several locations that are representative of all gross lesions observed) and ileum.  Fix one set of tissues in 10% neutral buffered formalin.  Send additional sets of fresh, chilled tissues (1 set each for virology and bacteriology if desired) placed in separate sterile, sealable bags.  When TGE/coronavirus is suspected as a co-factor, also include jejunum and a fecal sample.

  For fixation, parenchymal tissues should be no thicker than 0.5 inches and gut segments approximately 1 inch long and rinsed free of contents prior to placing the tissues in 10% neutral buffered formalin.

  Do not mix lung samples or gut samples with any other tissue in a specimen bag if submitting for viral or bacterial testing.

  Containers should be clearly labeled and all should be shipped chilled to ADDL by 24 hour couriers.  Please do not ship on Friday to avoid degeneration of tissues in a shipping warehouse over the week-end.

-by Dr. Roman Pogranichniy, Head of Virology/Serology and Dr. Greg Stevenson, Head of Pathology

References:

1. Allan, GM, Kennedy, S, McNeilly F, Foster JC, Ellis JA, Krakowka, SJ, Meehan BM and Adair, BM: 1999.  Experimental reproduction of severe wasting disease by coinfection of pigs with porcine circovirus and porcine parvovirus.  J Comp Pathol 121:1-11.

2. Allan GM, McNeilly F, Kennedy S, Daft B, Clarke EG, Ellis JA, Haines DM, Meehan BM, Adair, BM: 1998.  Isolation of porcine circovirus-like viruses from pigs with a wasting disease in the USA and Europe.  J Vet Diagn Invest 1;: 3-10.

3. Clark EG: 1997.  Post-weaning multisystemic wasting syndrome.  Proc AASP Annual Meeting. Pp 499-501.

4. Ellis J, Hassard L, Clark E, Harding J, Allan G, Willson P, Strokappe J, Martin K, McNeilly F, Meehan B, Todd D, Haines D: 1998.  Isolation of circovirus from lesions of pigs with postweaning multisystemic wasting syndrome. Can Vet J39: 44-51

5. Harding J: 1997.  Post-weaning multisystemic wasting syndrome (PMWS): Preliminary epidemiology and clinical presentation.  Proc AASP Ann Meet p. 503.

6. Harding JS, Clark EG: 1997.  Recognition and diagnosing postweaning multisystemic wastingsyndrome (PMWS).  Swine Health and Production 5:201-203.

7. Harms PA, Sorden SD, Halibur PG, Bolin SR, Lager KM, Morozov I, Paul PS: Experimental reproduction of severe disease in CD/CD pigs concurrently infected with type 2 porcine circovirus and porcine reproductive and respiratory syndrome virus.  Vet Pathol 38: 528-539.

8. Kennedy S, Moffett D, McNeilly F, Meehan B, Ellis J, Krakowka S and Allan GM: 2000.  Reproduction of lesions of postweaning multisystemic wasting syndrome by infection of conventional pigs with porcine circovirus type 2 alone or in combination with porcine parvovirus.  J Comp Pathol 122:9-24.

9. Krakowka S, Ellis JA, Meehan B, Kennedy S, McNeilly F, Allan G: 2000.  Viral wasting syndrome of swine: experimental reproduction of postweaning multisystemic wasting syndrome in gnotobiotic swine by coinfection with porcine circovirus 2 and porcine parvovirus.  Vet Pathol 37: 254-263.

10. Opriessnig T, Thacker EL, Yu S, Fenaux M, Meng XJ, Halbur PG: 2004.  Experimental reproduction of postweaning multisystemic wasting syndrome in pigs by dual infection with Mycoplasma hyopneumoniae and porcine circovirus type 2.  Vet Pathol 41: 624-640.

11. Pogranichniy RM, Yoon K-J, Harms PA, Sorden S, Daniels J: 2002.  Case-control study on the association of porcine circovirus type 2 and other swine viral pathogens with postweaning multisystemic wasting syndrome.  14(6):449-456.

12. Pogranichniy RM, Yoon K-J, harms PA, Swenson SL, Zimmerman JJ, Sorden SD: 2000.  Characterization of immune response of young pigs to porcine circovirus type 2 infection.  Viral Immunol 13: 143-153.

13. Sorden SD: 2000.  Update on porcine circovirus and postweaning multisystemic wasting syndrome (PMWS).  Swine Health and Production 8:133-136.

14. Tischer K, Bode L, Peters D, Pociuli S, Germann B: 1995.  Distribution of antibodies to porcine circovirus in swine populations of different breeding farms.  Arch Virol 140:737-743.

15. Tischer I, Gelderblom H, Vettermann W, Koch MA: 1982.  A very small porcine virus with circular single-stranded DNA.  Nature 295:64-66.

16. Rischer I, Mields W, Wolff D, Vagt M, Griem W: 1986.  Studies on epidemiology and pathogenicity of porcine circovirus.  Arch Virol 91: 271-276.

17. Rischer I, Rasch R, Tochtermann G: 1974.  Characterization of papovavirus-and picorna-virus-like particles in permanent pig kidney cell lines.  Zentralbl Bakteriol (Origin A) 226:153-167.