Experimental Reproduction of Severe Disease in CD/CD Pigs Concurrently Infected with Type 2 Porcine Circovirus and Porcine Reproductive and Respiratory Syndrome Virus

Abstract

Abstract. Three-week-old cesarean-derived colostrum-deprived (CD/CD) pigs were inoculated with porcine circovirus type 2 (PCV2, n ϭ 19), porcine reproductive and respiratory syndrome virus (PRRSV, n ϭ 13), concurrent PCV2 and PRRSV (PCV2/PRRSV, n ϭ 17), or a sham inoculum (n ϭ 12) to compare the independent and combined effects of these agents. Necropsies were performed at 7, 10, 14, 21, 35, and 49 days postinoculation (dpi) or when pigs became moribund. By 10 dpi, PCV2/PRRSV-inoculated pigs had severe dyspnea, lethargy, and occasional icterus; after 10 dpi, mortality in this group was 10/11 (91%), and all PCV2/ PRRSV-inoculated pigs were dead by 20 dpi. PCV2-inoculated pigs developed lethargy and sporadic icterus, and 8/19 (42%) developed exudative epidermitis; mortality was 5/19 (26%). PRRSV-inoculated pigs developed dyspnea and mild lethargy that resolved by 28 dpi. Microscopic lesions consistent with postweaning multisystemic wasting syndrome (PMWS) were present in both PCV2-and PCV2/PRRSV-inoculated pigs and included lymphoid depletion, necrotizing hepatitis, mild necrotizing bronchiolitis, and infiltrates of macrophages that occasionally contained basophilic intracytoplasmic inclusion bodies in lymphoid and other tissues. PCV2/ PRRSV-inoculated pigs also had severe proliferative interstitial pneumonia and more consistent hepatic lesions. The most severe lesions contained the greatest number of PCV2 antigen-containing cells. PRRSV-inoculated pigs had moderate proliferative interstitial pneumonia but did not develop bronchiolar or hepatic lesions or lymphoid depletion. All groups remained seronegative to porcine parvovirus. The results indicate that 1) PCV2 coinfection increases the severity of PRRSV-induced interstitial pneumonia in CD/CD pigs and 2) PCV2 but not PRRSV induces the lymphoid depletion, granulomatous inflammation, and necrotizing hepatitis characteristic of PMWS.

Longitudinal analysis of acute-phase proteins in saliva in pig farms with different health status

“…Animals were sampled once a week for 6 weeks (from 11 to 17 weeks of age in farms 1 and 3, and from 4 to 10 weeks of age in farm 2) to obtain serum and saliva samples. Selected ages of animals were different in each farm in order to include the period around the expected time of infection, as PCV2 infection typically affects pigs between 8 and 16 weeks of age (Harms et al, 2001), whereas PRRS infection has higher virus replication in animals of 4 to 8 weeks of age (Cho et al, 2006). Animals were vaccinated twice against Mycoplasma hyopneumoniae (Stellamune Mycoplasma, inactivated M. hyopneumoniae NL 1042, Pfizer Animal Health, Madrid, Spain; 1st and 3rd weeks of life) and twice against Aujeszky disease virus (Porcilis Begonia, Intervet, Caracas, Venezuela; at 11 and 14 weeks of age).…”

Reproduction of PMWS in immunostimulated SPF piglets transfected with infectious cloned genomic DNA of type 2 porcine circovirus

“…However, some recent studies have reported reproduction of the complete disease in specific-pathogen-free (SPF) piglets [1], and in cesarean-derived colostrum-deprived piglets [8,19] but with a non-purified preparation of PCV2. Moreover, the lesions were more acute when the PCV2 inoculates were combined with either porcine parvovirus (PPV) [3,21,22] or porcine reproductive and respiratory syndrome virus (PRRSV) [19]. The immunostimulation also influences the PMWS development [4,23,24,30].…”

Detection and Genetic Characterization of Porcine Circovirus 2 Isolates From the First Cases of Postweaning Multisystemic and Wasting Syndrome in Wild Boars in Greece

“…It is possible that the severity of histopathologic lesions was the result of co-infection with PCV2 and PRRSV. In domestic pigs, PCV2 is the primary cause of PMWS, but concurrent PRRSV infection leads to more severe disease forms (Harms et al, 2001).…”