Vaccination of sows reduces the prevalence of PCV-2 viraemia in their piglets under field conditions.

The objectives of this study were to further understand vertical transmission of porcine circovirus type 2 (PCV-2) and the effect of dam vaccination on PCV-2 viraemia in newborn piglets. Randomly selected sows from each of two breeding herds were designated as non-vaccinated or vaccinated groups. A commercial inactivated PCV-2 vaccine was administered at weaning and 18 days later to half of the sows on each farm. At parturition, colostrum was collected from 70 dams on each farm and postsuckle (Farm 1) or presuckle blood (Farm 2) was collected from five randomly selected piglets per litter. Colostrum samples had an anti-PCV-2 antibody prevalence of 98.5 per cent (135/137) with significantly (P = 0.0039) higher concentrations in vaccinated dams. Among piglets, 43.9 per cent (301/685) were seropositive for PCV-2 and 11.7 per cent (80/686) were PCV-2 DNA-positive. All the PCV-2 DNA-positive samples were further characterised and 28 were PCV-2a, 28 PCV-2b, and five mixed PCV-2a and PCV-2b infection. The prevalence of PCV-2 DNA in piglets was lower (0.7-22.8 per cent) compared with previous studies (44.8-90 per cent) indicating a change in PCV-2 ecology likely due to wide use of vaccination. Under the study conditions, dam vaccination reduced PCV-2 viraemia in the offspring with colostrum access.

Vitamin E and selenium levels are within normal range in pigs diagnosed with mulberry heart disease and evidence for viral involvement in the syndrome is lacking.

Mulberry heart disease (MHD) in pigs is characterized by lesions of acute haemorrhagic myocarditis and myocardial necrosis. The objectives of this study were to determine the levels of vitamin E and selenium and 13 other trace minerals in heart and liver tissues and to determine the prevalence of certain viral infections in heart tissues from MHD-affected and MHD-unaffected pigs and the vitamin E and selenium concentration in feed samples from selected farms with MHD. Based on the pathological examination, 114 pigs were separated into MHD lesion-negative (L-NEG) (n = 57) and MHD lesion-positive (L-POS) (n = 57) groups. Seventy-three samples (40 L-NEG and 33 L-POS) were subjected to chemical analysis, and 66 (32 L-NEG and 34 L-POS) were subjected to PCR detection for viral pathogens. Lower (P < 0.05) levels of myocardial copper, lower (P < 0.05) levels of hepatic magnesium and higher (P < 0.05) levels of myocardial and hepatic sodium were detected in the L-POS cases. Although lower (P < 0.05) levels of hepatic selenium were detected in L-POS group, all were within the normal range. Analysis of feed samples (n = 22) revealed that selenium levels in all the samples were above the legal limit (0.3 ppm) for pigs. Vitamin E levels in all feed samples were above 20 IU/kg. Among the 66 pigs subjected to PCR detection, there were 19, 4, 13, 8, 2 and 1 animals positive for porcine circovirus type 2, porcine reproductive and respiratory syndrome virus, pan-herpes virus, porcine enterovirus, pan-pestivirus and porcine parvovirus, respectively. Clear evidence of viral association with L-POS was lacking.

Experimental reproduction of severe disease in CD/CD pigs concurrently infected with type 2 porcine circovirus and porcine reproductive and respiratory syndrome virus.

Three-week-old cesarean-derived colostrum-deprived (CD/CD) pigs were inoculated with porcine circovirus type 2 (PCV2, n = 19), porcine reproductive and respiratory syndrome virus (PRRSV, n = 13), concurrent PCV2 and PRRSV (PCV2/PRRSV, n = 17), or a sham inoculum (n = 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.

Comparative pathogenicity of nine US porcine reproductive and respiratory syndrome virus (PRRSV) isolates in a five-week-old cesarean-derived, colostrum-deprived pig model.

One hundred forty-six 5-week- old cesarean-derived, colostrum-deprived (CDCD) pigs were inoculated intranasally with 1 of 9 US porcine reproductive and respiratory syndrome virus (PRRSV) isolates. Differences were found in severity of clinical respiratory disease, rectal temperatures (P < or = 0.001), gross lung lesions (P < or = 0.001), and microscopic lung lesions (P < or = 0.05). Gross lung lesions were generally most severe 10 days postinoculation and were distributed primarily in the cranial, middle, and accessory lobes and ventromedial portion of the caudal lung lobes. Mean gross lung lesion scores estimating the percentage of lung affected by pneumonia at 10 days postinoculation ranged from 16.7% +/- 2.8% (mean +/- SEM, n = 10) for isolate ISU-51 to 62.4% +/- 5.7% (n = 10) for isolate ISU-28. Microscopic lung lesions were characterized by hyperplastic and hypertrophied type 2 pneumocytes, septal infiltration by mononuclear cells, and accumulation of necrotic alveolar exudate. Lymph node follicular hyperplasia and focal necrosis was seen with all 9 isolates. This CDCD pig model was useful for demonstration of significant differences in pathogenicity among US PRRSV isolates. This difference in pathogenicity may help explain the variation of severity of clinical disease observed in field outbreaks of porcine reproductive and respiratory syndrome and should provide for meaningful comparison of PRRSV genotypes.

Immunohistochemical identification of porcine reproductive and respiratory syndrome virus (PRRSV) antigen in the heart and lymphoid system of three-week-old colostrum-deprived pigs.

Porcine reproductive and respiratory syndrome virus (PRRSV) antigens were detected by a streptavidin-biotin complex technique in tissues of 3-week-old colostrum-deprived pigs that had been inoculated intranasally with PRRSV and had developed moderate respiratory disease. Moderate, multifocal, tan-colored consolidation of the lungs and severe enlargement of the lymph nodes were noted at necropsy. Severe interstitial pneumonia characterized by type 2 pneumocyte proliferation, septal infiltration with mononuclear cells, and accumulation of macrophages and necrotic cells in alveolar spaces was observed at 4 and 9 days postinoculation. Moderate multifocal perivascular lymphohistiocytic myocarditis was observed at 9 days postinoculation. Marked lymphoid follicular hyperplasia and follicular necrosis in the tonsil, spleen, and lymph nodes was observed. A monoclonal antibody that recognizes a conserved epitope of PRRSV nucleocapsid protein was used as primary antibody for immunohistochemistry. Antigen was readily detected in alveolar macrophages in the lung and in endothelial cells and macrophages in the heart. Macrophages and cells resembling dendritic cells in tonsil, lymph nodes, thymus, and spleen also stained intensely positive for viral antigen. PRRSV appears to replicate primarily within macrophages in the respiratory and lymphoid systems of the pig.