Comparative Pathogenicity of Nine US Porcine Reproductive and Respiratory Syndrome Virus (PRRSV) Isolates in a Five-Week-Old Cesarean-Derived, Colostrum-Deprived Pig Model

Halbur, Patrick G.; Paul, P. S.; Meng, Xiang‐Jin; Lum, Melissa A.; Andrews, John J.; Rathje, J. A.

doi:10.1177/104063879600800103

Cited by 222 publications

(212 citation statements)

References 37 publications

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“…These findings may suggest that PRRSV is associated with hypertrophy of pneumocytes, while PCV2 may be associated with necrosis. Hypertrophy and hyperplasia of type II pneumocytes are widely described in pulmonary disease of caesarean-derived, colostrum-deprived (CD/CD) piglets with experimental PRRSV infection (Halbur et al, 1996;Beyer et al, 1998;Harms et al, 2001). Necrotizing bronchiolitis and abundant necrotic debris in the alveolar spaces, associated with a high PCV2 load assessed by immunohistochemistry, were also reported by Drolet et al (2003) and Grau-Roma and Segale´s (2007).…”

Section: Discussionmentioning

confidence: 99%

Immunohistochemical Detection of Aetiological Agents of Proliferative and Necrotizing Pneumonia in Italian Pigs

Morandi

Ostanello

Fusaro

et al. 2010

Journal of Comparative Pathology

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SummaryProliferative and necrotizing pneumonia (PNP) is a form of interstitial pneumonia that occurs in weaning and post-weaning pigs. PNP is characterized by hypertrophy and hyperplasia of type II pneumocytes and coagulative necrosis and granular debris within alveolar spaces. Canadian and European studies suggest that the porcine reproductive and respiratory syndrome virus (PRRSV) and porcine circovirus type 2 (PCV2) are the main causes of the disease, but Aujezsky's disease virus (ADV) and swine influenza virus (SIV) have also been considered as potential aetiological agents. An immunohistochemical study was carried out on the lungs of 28 Italian pigs with PNP in order to evaluate the role of PRRSV, PCV2 and ADV in PNP lesions. PRRSV infection was identified in the lungs of 11 pigs, PCV2 in the lungs of four pigs and coinfection with both viruses in the lungs of eight pigs. Neither virus was detected in the lungs of the remaining five pigs. ADV antigen was not detected in any sample. The principle aetiological agent of PNP in Italy therefore appears to be PRRSV. Coinfection with PRRSV and PCV2 is characterized by more severe microscopical changes in affected lungs.

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Section: Discussionmentioning

confidence: 99%

Immunohistochemical Detection of Aetiological Agents of Proliferative and Necrotizing Pneumonia in Italian Pigs

Morandi

Ostanello

Fusaro

et al. 2010

Journal of Comparative Pathology

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“…PRRSV pigs developed interstitial pneumonia consistent with that previously described for experimental PRRSV inoculation. 18,36 Alveolar septa were infiltrated by lymphocytes, plasma cells, and macrophages, type 2 pneumocytes were hypertrophied and moderately increased in number, and alveolar spaces contained small amounts of necrotic debris (Fig. 8).…”

Section: Histologic Lesionsmentioning

confidence: 99%

“…19 Affected sows had lesions that had previously been associated with PRRS, including lymphohistiocytic interstitial pneumonia, encephalitis, endometritis, myometritis, and lymphoid hyperplasia. 18,36 PRRSV infection was confirmed by demonstration of intralesional viral antigen and/or virus isolation. Sows that died of atypical PRRS also frequently had hepatitis, a lesion that had not been associated with PRRS prior to 1996.…”

mentioning

confidence: 99%

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

et al. 2001

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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.

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“…Total percentage for the entire lung was calculated based on weight proportions of each lung lobe to the total lung volume (45). The final score represents accumulative scores from all lobes originating from same animal (Fig.…”

Section: Generation Of Eight-segmented Siv/606 Expressing H1 and H3mentioning

confidence: 99%

An Eight-Segment Swine Influenza Virus Harboring H1 and H3 Hemagglutinins Is Attenuated and Protective against H1N1 and H3N2 Subtypes in Pigs

Mašić

Pyo

Babiuk

et al. 2013

J Virol

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Swine influenza virus (SIV) infections continue to cause production losses in the agricultural industry in addition to being a human public health concern. The primary method of controlling SIV is through vaccination. The killed SIV vaccines currently in use must be closely matched to the challenge virus, and their protective efficacy is limited. Live attenuated influenza vaccines (LAIV) provide strong, long-lived cell-mediated and humoral immunity against different influenza virus subtypes with no need for antigen matching. Here we report the generation of a new potential LAIV, an eight-segment SIV harboring two different SIV hemagglutinins (HAs), H1 and H3, in the genetic background of H1N1 SIV. This mutant SIV was generated by fusing the H3 HA ectodomain from A/Swine/Texas/4199-2/98 (H3N2) to the cytoplasmic tail, transmembrane domain, and stalk region of neuraminidase (NA) from A/Swine/Saskatchewan/18789/02 (H1N1) SIV. While this H1-H3 chimeric SIV, when propagated in vitro in the presence of exogenous neuraminidase, showed kinetics and growth properties similar to those of the parental wild-type virus, in vivo it was highly attenuated in pigs, demonstrating a great potential for serving as a dual LAIV. Furthermore, vaccination with the H1-H3 virus elicited robust immune responses, which conferred complete protection against infections with both H1 and H3 SIV subtypes in pigs.

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Comparative Pathogenicity of Nine US Porcine Reproductive and Respiratory Syndrome Virus (PRRSV) Isolates in a Five-Week-Old Cesarean-Derived, Colostrum-Deprived Pig Model

Cited by 222 publications

References 37 publications

Immunohistochemical Detection of Aetiological Agents of Proliferative and Necrotizing Pneumonia in Italian Pigs

Immunohistochemical Detection of Aetiological Agents of Proliferative and Necrotizing Pneumonia in Italian Pigs

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

An Eight-Segment Swine Influenza Virus Harboring H1 and H3 Hemagglutinins Is Attenuated and Protective against H1N1 and H3N2 Subtypes in Pigs

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