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Experimental reproduction of PMWS using a 1993 PCV2 Swedish isolate

by 5m Editor
25 February 2002, at 12:00am

By G Allan et al. - Postweaning multisystemic wasting syndrome (PMWS) is now established as a major disease problem in pigs in many countries through out the world. Experimental infections and field studies have indicated that porcine circovirus type 2 (PCV2) is the causal agent of PMWS, although other co-factors, primarily associated with stimulation of the pig immune system, have been shown to be important in the development of disease 3.

In retrospective studies, serum antibodies to PCV2 in pigs have been demonstrated as early as 1974 5 and examination of archived pig tissues has revealed cases of PCV2-associated PMWS as early as 1986. Clearly PMWS is not a new disease and a PCV2 virus has been present in the pig population for some considerable time.

PCV2 antibody has been demonstrated in pigs with and without PMWS, in herds with and without PMWS from countries where PMWS has been reported and not reported. This has led to speculation that an antigenically similar, but mutated, "new" highly virulent PCV2 virus may have recently emerged in PMWS-affected farms and countries.

We wish to present some preliminary findings that may negate this hypothesis.

PMWS has never been reported in the Swedish pig population. In the present study we have isolated a PCV2 virus from a lymph node taken from a PCV2 seropositive pig from Sweden in 1993. The PCV2 virus was isolated following 4 passages in PCV-free PK/15 cells cultures.

This virus was used in an experiment with 3 groups of snatch-farrowed , colostrum-deprived (SFCD) pigs. At 3 days of age, pigs in group A (n = 4) were infected with the Swedish PCV2 (SPCV2) alone, pigs in group B (n = 9) with the SPCV2 and a porcine parvovirus (PPV) and pigs in group C (n = 4) with the PPV alone. All pigs were inoculated by an oral-nasal route, and the 3 groups housed separately. The experiment was terminated at 35 days post infection (PI).

Five of the nine pigs inoculated with SPCV2 +PPV (group B) showed severe clinical signs consistent with PMWS 1.) and were sacrificed at 21-23 days PI. The remaining four inoculates in this group were sacrificed between 30-35 days PI. All nine inoculates in this group had moderate to severe gross lesions consistent with PMWS and an abundance of PCV2 antigen, associated with lesions, as demonstrated by immunostaining of cryostat sections of lymph nodes, liver, spleen, kidney and intestine.

One of the four inoculates in group A, given SPCV2 alone, was found dead at 21 days PI and at necropsy had gross lesions consistent with PMWS. These lesions were associated with an abundance of PCV2 antigen. The remaining 3 inoculates in this group were clinically normal when sacrificed at 35 days PI. All 3 of these inoculates had mild to moderate gross lesions consistent with PMWS and an abundance of PCV2 antigen associated with lesions. In our opinion, based on examination of tissue samples from many experimental infections, these 3 pigs were pre-clinical and would have developed clinical PMWS had the experiment not been terminated.

All piglets in group C, given PPV alone, were clinically normal for the duration of the experiment and no gross lesions were seen at necropsy. No evidence of either environmental or laboratory contamination was observed in the SPCV2-infected pigs and thus it can be concluded that disease reproduction was a result of the pathogenic nature of the SPCV2 inoculum.

Recent studies on the epidemiology of PMWS in England have suggested that the spread of this disease is typical of a new virus infection in a naive population. However, the majority of pigs on PMWS-negative farms have detectable serum antibody levels to PCV2, indicating previous sub-clinical infections. It has been speculated that a new, highly virulent PCV2, is spreading through pig herds in England and elsewhere causing PMWS. Our results suggest that this is not the case. We have demonstrated that a PCV2 virus isolated from a sub-clinically infected pig in a herd with no history of PMWS can cause clinical disease and gross lesions consistent with PMWS in SFCD pigs. These clinical signs were indistinguishable from those obtained following similar experimental infections with PCV2 isolates from pigs with PMWS 1.

In previously reported experimental studies 1, 4, 3, 2, co-infections with other porcine viruses or immunostimulation have been shown to be effective "triggers" for up regulation of PCV2 replication, resulting in earlier and more severe clinical disease. Additionally, field studies have indicated that environmental, husbandry, and/or genetic factors may be important in progression of clinical PMWS 6.

Our preliminary findings with this Swedish PCV2 isolate confirm that PCV2 is the causal agent of PMWS. The results also suggest that the PCV2 virus now causing epidemic PMWS has actually been present in the pig population for some considerable time, without causing significant clinical disease. Why?

Is it possible that changes in the global pig industry that have not been applied in Sweden and other countries where epidemic PMWS is absent, have resulted in up-regulating a sub-clinical PCV2 infection to PMWS?


G. M. Allan, F. McNeilly, B. Meehan, S Kennedy, D Johnston
Veterinary Sciences Division, Department of Agriculture and Rural Development for N Ireland, Stoney Road, Belfast BT4 3SD, N Ireland
J. Ellis
Department of Veterinary Microbiology, University of Saskatchewan, Canada
S. Krakowka
Ohio State University, Ohio, USA
C. Fossum, E Wattrang
Division of Immunology, Dep. of Veterinary Microbiology, BMC P.O. Box 588, SE-751 23 Uppsala, Sweden
P. Wallgren
National Veterinary Institute, SE-751 89 Uppsala, Sweden


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References
1. ALLAN, G. M., KENNEDY, S., MCNEILLY, F., FOSTER, C., ELLIS, J. A., KRAKOWKA, S. J., MEEHAN, B. M. & ADAIR, B. M. (1999) Experimental reproduction of wasting disease and death by co-infection of pigs with porcine circovirs type 2 and porcine parvovirus. Journal of Comparative Pathology 121, 1-11.
2. ALLAN, G. M., MCNEILLY, F., ELLIS, J., KRAKOWKA, S., MEEHAN, B., MCNAIR, I., WALKER, I. & KENNEDY, S. (2000) Experimental infection of CD piglets with PCV2 and PRRSV potentiates PCV2 replication. Archives of Virology 145, 2421-2429.
3. KRAKOWA, S., ELLIS, J. A., MCNEILLY, F., RINGLER, S., RINGS, D. M. & ALLAN G. M. (2001) Activation of the immune system is the pivotal event in the production of wasting disease in pigs infected with PCV2. Veterinary Pathology 38, 31-42.
4. KRAKOWKA, S., ELLIS, J. A., MEEHAN, B., KENNEDY, S., MCNEILLY, F. & ALLAN, G. M. (2000) Viral wasting syndrome of swine: Experimental reproduction of PMWS in gnotobiotic swine by co-infection with PCV2 and PPV. Veterinary Pathology 37, 254-263.
6. MADEC, F., ALBINA, E., CARIOLET, R., HAMON, L., MAHE, D., TRUONG, C., JESTEN, A. & AMENNA, N. (2000) PMWS in the pig: a new challenge for veterinary research and practise. The Pig Journal 45, 69-75.
5. WALKER, I. W., KONOBY, C. A., JEWHURST, V. A., MCNAIR, I., MCNEILLY, F., MEEHAN, B. M., COTTRELL, T. S., ELLIS, J. A. & ALLAN, G. M. (2000) Development and application of a competitive enzyme-linked immunosorbent assay for the detection of serum antibodies to porcine circovirus type 2. Journal of Veterinary Diagnostic Investigations 12, 400-405

This letter was forwarded to us for publication, and is as published in the Pig Veterinary Journal. - 22nd February 2002.