PRRS Compendium Producer Edition - National Pork Board

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References Bush EJ, Corso B, Zimmerman JJ, et al. 1997. Update on the acute PRRS investigative study. Swine Health and Production 7(4):179-180. Christianson WT, Collins JE, Pijoan C, et al. 1991. Swine infertility and respiratory syndrome. Pig Vet J 27:9-12. Christopher-Hennings J, Holler LD, Benfield DA, Nelson EA. 2001. Detection and duration of porcine reproductive and respiratory syndrome virus in semen, serum, peripheral blood mononuclear cells, and tissues from Yorkshire, Hampshire and Landrace boars. J Vet Diagn Invest 13:133-142. Christopher-Hennings J, Nelson EA, et al. 1995. Persistence of porcine reproductive and respiratory syndrome virus in serum and semen of adult boars. J Vet Diagn Invest 7:456-464. Cromwijk W. 1991. The ‘new’ pig disease - further observations in Dutch herds. In: The new pig disease. Porcine reproductive and respiratory syndrome. A report on the seminar/workshop held in Brussels on 29-30 April and organized by the European Commission (Directorate General for Agriculture), pp. 20-27. Dee SA, Joo HS, Polson DD, Marsh WT. 1997. Evaluation of the effects of nursery depopulation on the profitability of 34 pig farms. Vet Rec 140:498-500. Goldberg TL, Weigel RM, Hahn EC, Scherba G. 2000. Associations between genetics, farm characteristics and clinical disease in field outbreaks of porcine reproductive and respiratory syndrome virus. Prev Vet Med 43:293-302. Halbur PG, Sorden SD, Lager KM. 1998. Evaluation of the pathogenecity of “atypical PRRS” virus isolates in caesarean-derived-colostrum-deprived (CDCD) pigs. Proceedings of the International Pig Veterinary Society Congress, p. 136. Hill H. 1990. Overview and history of Mystery Swine Disease (Swine infertility/respiratory syndrome). Proceedings of the Mystery Swine Disease Committee Meeting, Livestock Conservation Institute, Denver, Colorado, pp. 29-31. Hopper SA, White ME, Twiddy N. 1992. An outbreak of blue-eared pig disease (porcine reproductive and respiratory syndrome) in four pig herds in Great Britain. Vet Rec 131:140-144. Hurd HS, Bush EJ, Losinger W, et al. 2001. Outbreaks of porcine reproductive failure: Report on a collaborative field investigation. J Swine Health Prod 9:103-108. Joo HS, Dee SA. 1993. Recurrent PRRS problems in nursery pigs. Proceedings of the Allen D. Leman Swine Conference, pp. 85-86. Keffaber KK. 1989. Reproductive failure of unknown etiology. American Association of Swine Practitioners Newsletter 1:1-10. Lager KM, Halbur PG, Mengeling WL. 1998. Evaluation of the pathogenic effects of an ‘atypical PRRS’ virus isolate in pregnant gilts. Proceedings of the International Pig Veterinary Society Congress, p. 137. Lager KM, Mengeling WL, Brockmeier SL. 1997. Homologous challenge of porcine reproductive and respiratory syndrome virus immunity in pregnant swine. Vet Microbiol 58:113-125. Loula T. 1991. Mystery pig disease. Agri-Practice 12:23-34. Office International des Épizooties (OIE). 1997. World Animal Health in 1996. Part 1. Reports on the Animal Health Status and Disease Control Methods and List A Disease Outbreaks – Statistics, p. 322. Prieto C, Suarez P, Simarro I, et al. 1997. Insemination of susceptible and preimmunized gilts with boar semen containing porcine reproductive and respiratory syndrome virus. Theriogenology 47:647-654. Regula G, Lichtensteiger CA, Mateus-Pinilla NE, et al. 2000. Comparison of serologic testing and slaughter evaluation for assessing the effects of subclinical infection on growth in pigs. J Am Vet Med Assoc 217:888-895. Rossow K, Vaughn E, Nelson E, et al. 1997. Investigation of an abortion storm in a RespPRRS® vaccinated swine herd from SE Iowa. Proceedings of the Allen D. Leman Swine Conference (Research Abstracts), p. 1. Rossow KD, Bautista EM, Goyal SM, et al. 1994. Experimental porcine reproductive and respiratory syndrome virus infection in one-, four-, and 10week-old pigs. J Vet Diagn Invest 6:3-12. Rossow KD, Shivers JL, Yeske PE, et al. 1999. Porcine reproductive and respiratory syndrome virus infection in neonatal pigs characterised by marked neurovirulence. Vet Rec 144:444-448. Rossow KD. 1998. Porcine reproductive and respiratory syndrome. Vet Pathol 35:1-20. Swenson SL, Hill HT, Zimmerman J, et al. 1995. PRRS virus infection in boars: isolation from semen and effect on semen quality. 1995 Research Investment Report. National Pork Producers Council, PO Box 10383, Des Moines, Iowa 50308, pp. 93-96. Swenson SL, Hill HT, Zimmerman JJ, et al. 1994. Excretion of porcine reproductive and respiratory syndrome virus in semen after experimentally induced infection in boars. J Am Vet Med Assoc 204:1943-1948. Thacker BJ. 1992. Serological surveys in a herd before, during, and after an outbreak of SIRS. American Association of Swine Practitioners Newsletter 4:40. Thacker EL, Thacker BJ, Young TF, Halbur PG. 2000. Effect of vaccination on the potentiation of porcine reproductive and respiratory syndrome virus (PRRSV)-induced pneumonia by Mycoplasma hyopneumoniae. Vaccine 18:1244-1252. Thacker EL, Thacker BJ, Young TF, Halbur. 1998. Unpublished data. PAGE 10 PIG 04-01-09
Wills RW, Zimmerman JJ, Yoon K-J, et al. 1997. Porcine reproductive and respiratory syndrome virus: A persistent infection. Vet Microbiol 55:231-240. Yaeger MJ, Prieve T, Collins J, et al. 1993. Evidence for the transmission of porcine reproductive and respiratory syndrome (PRRS) virus in boar semen. Swine Health and Production 1(5):7-9. Chapter - “PRRS Plus” – PRRS Virus Infection in Combination with Other Agents - PG Halbur • • • • • • The severity of PRRS virus infection is often related to its interactions with other concurrent diseases. PRRS virus isolates are known to differ in their ability to cause clinical signs and lesions. The molecular basis for these inherent differences has not been identified and cannot be predicted with our current diagnostic tests. It has been suggested, but not proven, that PRRS virus has a direct immune suppressive effect in the pig. Experimentally, pigs have been subjected to co-infections with PRRS virus and a number of different infectious agents including Streptococcus suis, Haemophilus parasuis, Mycoplasma hyopneumoniae, Pasteurella multocida, Actinobacillus pleuropneumoniae, Salmonella cholerasuis, porcine Circovirus type 2, and swine influenza virus. Generally, co-infections result in much more significant disease than either agent acting alone does. Immunity that develops after infection with a single strain of PRRS virus will frequently not result in protection against other strains of PRRS virus. Laboratory techniques (including genomic sequencing) have not been developed that can accurately predict cross-protection between different strains of PRRS virus. Additionally, the ability of commercial vaccines to protect against a specific field strain of the virus cannot be predicted through laboratory testing. Introduction The clinical manifestations of PRRS virus infection vary from subclinical to severe reproductive failure and/or respiratory disease. Severity of PRRS virus-associated disease may result from interactions among factors involving differences in virulence among PRRS virus isolates, differences in concurrent infections (other viruses and bacteria), genetically-based differences in pig susceptibility, environmental differences from farm to farm, varying management factors among farms (i.e., weaning age, pig flow, gilt acclimatization strategies), level of herd immunity to PRRS virus, and other factors or circumstances. This review will primarily focus on differences in virulence among PRRS virus isolates, the effect of co-infections on the severity of PRRS virus-associated disease, and host genetic susceptibility differences. Although equally important, less documentation is available in the literature on the influence of environment and production style on the manifestation of PRRS virus-associated disease. Differences among PRRS Viruses It is now widely accepted that PRRS virus isolates differ in virulence. In neonatal and growing pigs, PRRS virus isolates vary markedly in the severity of experimentally induced pneumonia (Halbur et al. 1995, 1996a, 1996b; Thanawongnuwech et al., 1998a). Some isolates produce subclinical disease and minimal lesions while others cause severe disease and severe interstitial pneumonia lesions. Differences in virulence among PRRS virus isolates have also been demonstrated in the pregnant female (Mengeling et al., 1994, 1996, 1998; Park et al., 1996). It is widely accepted that PRRS virus isolates differ in genetic and antigenic make-up (Meng et al., 1994, 1995b, 1996a; Meng, 2000). However, a link between specific molecular sequences and the degree of clinical severity among PRRS virus isolates has not yet been identified. At this time, molecular and antigenic characterization of isolates is used as an epidemiological tool rather than a virulence determinant or vaccine selection tool. Viral Pathogenesis The fact that PRRS virus replication occurs in cells of the macrophage lineage is consistent with the idea that PRRS virus leads to immunosuppression (Done and Paton, 1995; Done et al., 1996; Meier et al., 1999; Molitor et al., 1997). However, experimental data has not always supported the perception of a systemic immunosuppressive effect of PRRS virus. It has been proposed that what is perceived as recurrent PRRS infections may be better explained as successive waves of acute infections in susceptible pigs along with infection by opportunistic bacteria (Albina et al., 1998). PAGE 11 PIG 04-01-09
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Page 15 and 16: Dee SA. 1996. The porcine respirato
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Page 23 and 24: virus in Illinois. J Gen Virol 81:1
Page 25 and 26: vidual animals, but anecdotal repor
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Page 29 and 30: toes are capable of mechanical tran
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Page 35 and 36: ting PRRS virus to offspring), then
Page 37 and 38: Dial G, Parsons T. 1989. SMEDI-like
Page 39 and 40: Assays for Detection of PRRS Virus:
Page 41 and 42: during the developmental stage was
Page 43 and 44: then assigned a 3-digit number, e.g
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Page 47 and 48: Thacker BJ. 1992. Serological surve
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Page 51 and 52: several diagnostic laboratories. Se
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Page 55 and 56: Partial depopulation Partial depopu
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virus-infected piglets 2. Change ne
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Dial GD, Hull RD, Olson CL, et al.
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animals will test negative, but inf
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if they test negative (naïve) at 1
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2. 3. 4. Risk of new virus introduc
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ease. The use of MLV PRRS vaccine f
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once with the inactivated vaccine a
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Replacement animals - Only naïve,
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5. 6. therefore, the animals most l
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A biosecurity plan should describe
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to return to the main farm? d. Will
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