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Host Susceptibility

Madec et al. (2000) found that 42% of the litters in PMWS herds were not affected but 16% of the litters accounted for 54% of the losses. This is indicative of a litter effect and increased susceptibility to PCV2-associated PMWS in some pigs.

A cohort study was conducted to investigate a suspected decreased susceptibility to PCV2-associated disease in Pietrain pigs by manipulating the genetics via artificial insemination on 4 PMWS-affected farms (Rose et al., 2004). Half of the sows were inseminated with Pietrain semen whereas the remaining sows received the semen that was typically used on these farms. The PCV2-associated disease in the Pietrain-offspring did not differ from that observed in other pigs on these farms in terms of PCV2-seroconversion, morbidity, and mortality (Rose et al., 2004).

Allan et al. (2002, 2003) reproduced PMWS in Northern Irish Large White/Landrace pigs experimentally infected with a porcine PCV2 isolate recovered from a clinically normal Swedish Yorkshire pig in 1993. The authors concluded that there is disease potential of PCV2 isolated from regions free of PMWS and that the status of the host and its environment may be an important factor in the development of PMWS (Allan et al., 2002, 2003).

Duroc, Landrace, and Large White pigs were infected intranasally and intramuscularly at 5 to 7 weeks of age with PCV2 (Opriessnig et al., 2006). Clinical disease compatible with PMWS was observed only in the Landrace pigs. Three of 19 Landrace pigs and none of the Duroc or Large White pigs developed severe lymphoid lesions associated with large amounts of intralesional PCV2-antigen typical of PMWS. In this experiment, 23 Duroc pigs (4 sires, 8 dams), 19 Landrace pigs (4 sires, 6 dams), and 21 Large White pigs (4 sires, 6 dams) were inoculated with PCV2. The results suggest a predisposition of the Landrace pigs used in this study to PCV2-induced disease and lesions (Opriessnig et al., 2006).

McIntosh et al. (2005) tested 43 boars for presence of PCV2 DNA in semen. Duroc and Landrace boars were found to be positive for PCV2-DNA in semen whereas Large White and Meishan synthetic breeds were not observed to shed PCV2 DNA.

Zhou et al. (2006) looked at seroprevalence of PCV2 in 46 swine farms in Zhejian, China, and found that 44.83% of all Landrace sows and 64.28% of all Landrace piglets were positive for PCV2-antibodies. The seroprevalence of Landrace sows was higher than that of Yorkshire and Duroc sows.

López-Soria et al. (2004) compared the effect of 3 different genetic boar lines on 2 different Spanish farms on the outcome of general and PCV2-associated postweaning mortality. There was a significant effect of genetics on the expression of PCV2-associated diseases observed on both farms. Pigs with the paternal genetic backgrounds “A” (100% Pietrain) and “B” (50% Large White x 50% Pietrain) showed lower percentages of PCV2-associated disease than those with the paternal genetic background “C” (25% Large White x 75% Duroc). However, due to the limited size of the study, it could not be concluded that the observed effect was due to a particular breed or line, or a particular boar (López-Soria et al., 2004).

Sibila et al. (2005) quantified and compared the PCV2 load in serum of naturally-infected pigs at different ages in two Spanish farms affected by PMWS with three different paternal genetic backgrounds (A=100% Pietrain; B=50% Large White x 50% Pietrain, and C=25% Large Whitex 75% Duroc). PMWS-associated mortality occurred mainly between 9-15 weeks of age and was related with the highest viral loads. A significant relationship between the paternal genetic background C and higher PCV2 viral loads in serum was observed in one farm (Sibila et al., 2005).

References:
Allan G, McNeilly F, Meehan B, McNair I, Ellis J, Krakowka S, Fossum C, Wattrang E, Wallgren P, Adair B: Reproduction of postweaning multisystemic wasting syndrome in pigs experimentally inoculated with a Swedish porcine circovirus 2 isolate. J Vet Diagn Invest. 15:553-560, 2003

Allan GM, McNeilly F, Meehan B, Kennedy S, Johnston D, Ellis J, Krakowka S, Fossum C, Wattrang E, Wallgren P: Reproduction of PMWS with a 1993 Swedish isolate of PCV-2. Vet Rec. 150:255-256, 2002

López-Soria S, Segalés S, Nofrarías M, Calsamiglia M, Ramírez H, Mínguez A, Serrano JM, Marín O, Callén A: Genetic influence on the expression of PCV disease. Vet Rec. 155:504, 2004

Madec F, Eveno E, Morvan P, Hamon L, Blanchard P, Cariolet R, Amenna N, Morvan H, Truong C, Mahé D, Albina E, Jesting A: Post-weaning multisystemic wasting syndrome (PMWS) in pigs in France: clinical observations from follow-up studies on affected farms. Livestock Prod Sci. 63:223-233, 2000

McIntosh KA, Harding JCS, Ellis JA, Appleyard GD: Nested PCR detection and duration of porcine circovirus type 2 in semen collected from naturally infected boars. In: Proc Intern Conf “Animal Circoviruses and Associated Diseases”, Belfast, UK, p 93, 2005

Opriessnig T, Fenaux M, Thomas P, Hoogland MJ, Rothschild M, Meng XJ, Halbur PG: Evidence of breed-dependent differences in susceptibility to porcine circovirus type 2-associated disease and lesions. Vet Pathol. 43:281-293, 2006

Rose N, Abhervé-Guéguen A, Le Diguerher G, Eveno E, Jolly JP, Blanchard P, Oger A, Jestin A, Madec F: Effect de la génétique Piétrain sur l’expression clinique de la maladie de l’amaigrissement du porcelet (MAP): Etude dans 4 élevages naisseuers-engraisseurs. J Rech Porcine Fr 36:339-344, 2004

Sibila M, López-Soria S, Segalés S, Nofrarías M, Ramírez H, Mínguez A, Serrano JM, Marín O, Callén A: PCV2 load dynamics in two PMWS affected farms with three different genetic lines. In: Proc Intern Conf “Animal Circoviruses and Associated Diseases”, Belfast, UK, p 39, 2005

Zhou JY, Chen QX, Ye JX, Shen HG, Chen TF, Shang SB: Serological investigations and genomic characterization of PCV2 isolates from different geographic regions of Zhejiang province in China. Vet Res Commun. 30:205-220, 2006

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