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Coinfections

Combinations of pathogens detected in 484 cases of PMWS submitted to the VDL-ISU in 2001-2002 

Porcine Parvovirus (PPV)

Ellis et al. (1999) were the first to reproduce most of the lesions typical of PMWS in gnotobiotic pigs inoculated with filtered cell culture material and filtered lymphoid tissues from pigs with naturally-acquired PMWS. Both PCV2 and PPV and antibodies to these viruses were detected in the experimentally-inoculated pigs. Since then, several groups have demonstrated that colostrum-deprived (CD) pigs dually-inoculated with PCV2 and PPV develop more severe disease and lesions than pigs with singular PCV2 infection (Allan et al., 1999; Kennedy et al., 2000). Krakowka et al. (2000) further confirmed the synergistic effect of PCV2 and PPV in gnotobiotic pigs by reproducing clinical disease and lesions typical of PMWS in coinfected pigs but not in pigs infected with PCV2 or PPV alone. Kim et al. (2003) coinfected twenty-four 28-day-old CD pigs with a Korean PCV2 isolate and PPV and observed clinical PMWS in all pigs. Opriessnig et al. (2004) were able to demonstrate the development of PMWS in conventional SEW pigs coinfected with PCV2 and PPV. The mortality in PCV2/PPV-infected pigs was 6.7%, which is similar to PMWS-associated mortality in affected herds in the US. Hasslung et al. (2005) reproduced PMWS in Swedish and Danish CD pigs concurrently infected with PCV2 and PPV at 3 days of age. Ostanello et al. (2005) coinfected eight 3-week-old conventional pigs confirmed to have passively acquired antibodies to PPV and PCV2 oronasally and intramuscularly with PPV and PCV2. Half of the pigs (4/8) were vaccinated with a commercial APP vaccine at 3 DPI. None or the pigs developed clinical disease and all pigs were necropsied at 42 DPI. It was found that passive immunity against PCV2 can prevent PMWS but it can not prevent subclinical PCV2 infection (Ostanello et al., 2005).

Porcine Reproductive and Respiratory Syndrome Virus (PRRSV)

Allan et al. (2000) inoculated 1- to 2-day-old CD pigs with PCV2 and PRRSV and observed upregulation of PCV2 replication in coinfected pigs. However, the replication and distribution of PRRSV in concurrently infected pigs was not enhanced compared to that observed in single PRRSV infected pigs (Allan et al., 2000). Harms et al. ( 2001) coinfected 3-week-old CDCD pigs at three weeks of age with PCV2 and PRRSV and showed that PCV2-infection increased the severity of PRRSV-induced interstitial pneumonia in CDCD pigs. Rovira et al. (2002) inoculated 5-week-old conventional pigs with PRRSV and seven days later with PCV2 and confirmed that PRRSV infection enhances PCV2 replication. A longer duration of PRRSV viremia and a higher proportion of viremic pigs were observed in the coinfected pigs compared to singular PRRSV infected pigs (Rovira et al., 2002). Chung et al. (2005) coinfected 10-week-old conventional pigs with PRRSV and PCV2 and injected a portion of the pigs with formalin-inactivated Salmonella choleraesuis and complete Freund’s adjuvant one week before inoculation. It was found that PRRSV was significantly upregulated by the Salmonella treatment whereas PCV2 was not (Chung et al., 2005). A recent in vitro study using swine alveolar macrophages found that PCV2-induced interferon-alpha reduced PRRSV infection and PRRSV-associated cytopathic effect (Chang et al., 2005). Subclinical infection of SPF pigs with PCV2 14 days before modified live PRRSV vaccination resulted in significantly (P >0.05) increased PRRSV-induced macroscopic lung lesions after PRRSV challenge (Opriessnig et al. 2006). Evidence of interaction of PCV2 with the attenuated vaccine strain of PRRSV was lacking (Opriessnig et al. 2006).

Mycoplasma hyopneumoniae

Conventional pigs were inoculated intratracheally with M. hyopneumoniae at 4 weeks of age followed by intranasal inoculation with PCV2 at 6 weeks of age (Opriessnig et al., 2004). Four of 17 (23.5%) dual-infected pigs had decreased growth rate and severe lymphoid depletion and granulomatous lymphadenitis associated with high amounts of PCV2-antigen consistent with PMWS. M. hyopneumoniae potentiated the severity of PCV2-associated lung and lymphoid lesions, increased the amount and prolonged the presence of PCV2-antigen, and increased the incidence of PMWS in pigs (Opriessnig et al., 2004).

References:
Allan GM, Kennedy S, McNeilly F, Foster JC, Ellis JA, Krakowka SJ, Meehan BM, Adair BM: Experimental reproduction of severe wasting disease by co-infection of pigs with porcine circovirus and porcine parvovirus. J Comp Path. 121:1-11, 1999

Chang HW, Jeng CR, Liu JJ, Lin TL, Chang CC, Chia MY, Tsai YC, Pang VF: Reduction of porcine reproductive and respiratory syndrome virus (PRRSV) infection in swine alveolar macrophages by porcine circovirus 2 (PCV2)-induced interferon-alpha. Vet Microbiol. 108:167-177, 2005

Chung WB, Chan WH, Chaung HC, Lien Y, Wu CC, Huang YL: Real-time PCR for quantitation of porcine reproductive and respiratory syndrome virus and porcine circovirus type 2 in naturally-infected and challenged pigs. J Virol Methods. 124:11-19, 2005

Ellis J, Krakowka S, Lairmore M, Haines D, Bratanich A, Clark E, Allan G, Konoby C, Hassard L, Meehan B, Martin K, Harding J, Kennedy S, McNeilly F: Reproduction of lesions of postweaning multisystemic wasting syndrome in gnotobiotic piglets. J Vet Diagn Invest. 11:3-14, 1999

Hasslung F, Wallgren P, Ladekjaer-Hansen AS, Bøtner A, Nielsen J, Wattrang E, Allan GM, McNeilly F, Ellis J, Timmusk S, Belák K, Segall T, Melin L, Berg M, Fossum C: Experimental reproduction of postweaning multisystemic wasting syndrome (PMWS) in pigs in Sweden and Denmark with a Swedish isolate of porcine circovirus type 2. Vet Microbiol. 106:49-60, 2005

Harms PA, Sorden SD, Halbur PG, Bolin SR, Lager KM, Morozov I, Paul PS: Experimental reproduction of severe disease in CD/CD pigs concurrently infected with type 2 porcine circovirus and porcine reproductive and respiratory syndrome virus. Vet Pathol. 38:528-539, 2001

Kennedy S, Moffett D, McNeilly F, Meehan B, Ellis J, Krakowka S, Allan GM: Reproduction of lesions of postweaning multisystemic wasting syndrome by infection of conventional pigs with porcine circovirus type 2 alone or in combination with porcine parvovirus. J Comp Path. 122:9-24, 2000

Kim J, Choi C, Chae C: Pathogenesis of postweaning multisystemic wasting syndrome reproduced by co-infection with Korean isolates of porcine circovirus 2 and porcine parvovirus. J Comp Path 128:52-59, 2003

Krakowka S, Ellis JA, Meehan B, Kennedy S, McNeilly F, Allan G: Viral wasting syndrome of swine: experimental reproduction of postweaning multisystemic wasting syndrome in gnotobiotic swine by coinfection with porcine circovirus 2 and porcine parvovirus. Vet Pathol. 37:254-263, 2000

Opriessnig T, Fenaux M, Yu S, Evans RB, Cavanaugh D, Gallup JM, Pallares FJ, Thacker EL, Lager KM, Meng XJ, Halbur PG: Effect of porcine parvovirus vaccination on the development of PMWS in segregated early weaned pigs coinfected with type 2 porcine circovirus and porcine parvovirus. Vet Microbiol. 98:209-220, 2004

Opriessnig T, McKeown NE, Harmon KL, Meng XJ, Halbur PG:Porcine circovirus type 2 infection decreases the efficacy of a modified live porcine reproductive and respiratory syndrome virus vaccine. Clinical and Vaccine Immunology. 13:923-929, 2006

Opriessnig T, Thacker EL, Yu S, Fenaux M, Meng XJ, Halbur PG: Experimental reproduction of postweaning multisystemic wasting syndrome in pigs by dual-infection with Mycoplasma hyopneumoniae and porcine circovirus type 2. Vet Pathol. 41:624-640, 2004

Ostanello F, Caprioli A, Di Francesco A, Battilani M, Sala G, Sarli G, Mandrioli L, McNeilly F, Allan GM, Prosperi S: Experimental infection of 3-week-old conventional colostrum-fed pigs with porcine circovirus type 2 and porcine parvovirus. Vet Microbiol. 108:179-186, 2005

Rovira A, Balasch M, Segalés J, García L, Plana-Durán J, Rosell C, Ellerbrok H, Mankertz A, Domingo M: Experimental inoculation of conventional pigs with porcine reproductive and respiratory syndrome virus and porcine circovirus 2. J Virol. 76:3232-3239, 2002 

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