Porcine Reproductive and Respiratory Syndrome

Rossow, Kurt

doi:10.1177/030098589803500101

Cited by 487 publications

(353 citation statements)

References 91 publications

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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%

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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Section: Histologic Lesionsmentioning

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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“…Porcine reproductive and respiratory syndrome (PRRS) was first recognized in 1987 in the United States of America and is characterized by reproductive failure in sows and respiratory tract illness in pigs [1,15,23,26]. It became a pandemic disease in North America, Europe, and Asia in the subsequent years [3-6, 16, 31].…”

Section: Introductionmentioning

confidence: 99%

Indian porcine reproductive and respiratory syndrome virus bears discontinuous deletion of 30 amino acids in nonstructural protein 2

et al. 2016

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Since its first outbreak in 2013, porcine reproductive and respiratory syndrome (PRRS) has established as an enzootic disease in pig population of Mizoram state, India. Our previous studies based on phylogenetic analysis of ORF5 and ORF7 gene sequences revealed close relationship of Indian PRRSV with the highly pathogenic variant of PRRSV (HP-PRRSV) of Chinese origin. Despite the control measures, second major outbreak of the disease was recorded in Aizawl district of Mizoram in 2015. The objective of the present study was to examine the origin of PRRSV isolates of 2015 outbreak, identification of deleted region in Nsp2 gene and determination of any genetic variation between 2013 and 2015 isolates of PRRSV. The outbreak was confirmed by the detection of PRRSVspecific antibodies in 57 out of 92 serum samples (61.96 %) and also by RT-PCR in 42 out of 42 necropsy samples (100 %). Nucleotide sequence analysis of Nsp2 coding region of Indian isolates and comparison with reference sequences revealed 90 nucleotides discontinuous deletion further establishes the closeness of Indian PRRSV to Chinese HP-PRRSV. Further, sequence and phylogenetic analysis of ORF5, ORF7 and Nsp2 genes of Indian PRRSV from both 2013 and 2015 revealed that the outbreaks were caused by two different strains of HP-PRRSV closely associated with the Chinese 10 HEB-3 isolate and 07QN isolates of Vietnam origin respectively. The present study confirms that the Indian PRRSV is a highly pathogenic variant of PRRSV and this study serves as the basis for developing practical and effective control measures against this disease.

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“…The causative agent, PRRS virus (PRRSV), is a single-strand positive-sense RNA virus of the order Nidovirales, family Arteriviridae (Rossow, 1998). The disease remains a significant problem worldwide, with a considerable economic impact for affected producers, due to increased mortality, treatment costs, and reduced weight gain and fertility (Neumann et al, 2005).…”

Section: Introductionmentioning

confidence: 99%