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Author(s): Halbur, Pat and Tanja Opriessnig
Publication Date: January 1, 2006
Reference: Carthage Veterinary Service Ltd. 16th Annual Swine Conference
Country: United States

Summary:

Symptoms of PCVAD include: gross lesions; microscopic lesions; hallmark lymphoid lesions; immunohistochemistry; main confirmatory test; serology; ELISA, IFA; PCR; quantitative, nested, multiplex; virus isolation; sequencing; and antigen capture ELISA.
An assessment was done on boars using ELISA or IFA to determine PCV2 status because naïve incoming boars may represent a risk. Producers must consider exposing naïve boars to PCV2, either by Vaccination or PCV2 positive (by PCR or Antigen Capture ELISA) feces from resident boars 5 weeks prior to bringing them into the main stud. In order to assess the breeding herd use ELISA or IFA to determine PCV2 status. Naïve incoming gilts may represent a risk. Consider exposing naïve gilts to PCV2 by vaccination or planned exposure (fecal feedback, mummified fetus feedback, cull sow exposure). In order to assess the nursery or finisher pigs confirm that PCVAD is a problem by histopath and IHC; use ELISA or IFA to determine when maternal antibodies wane and to determine when seroconversion occurs; do PCR on pooled serum (or saliva) to further define time of infection; do some PCV2 sequencing so you have a historical record of the system. If morbidity and mortality are unusually high, use sequencing to determine if the PCV2 in the system has changed. PCV2 isolates that are genetically highly homologous may differ in virulence. These differences may explain differences in clinical manifestation of PCV2 associated diseases. An experiment was done to determine the effects of host genetics on susceptibility to PCV2-associated disease and lesions. It was concluded that 3/19 (15.8%) Landrace pigs developed PMWS whereas none of the Duroc or Large White pigs developed PMWS. There was significantly more severe lymphoid depletion in tonsils and lymph nodes of Landrace pigs. The Landrace pigs used in this study appear to be predisposed to PCV2-associated lymphoid depletion and PMWS. Reproduction of severe disease and lesions typical of PMWS in CDCD pigs co-infected with PCV2 and PRRSV resulted in a 90% mortality in coinfected group, no mortality in singular PRRSV group and less severe disease and lesions in PCV2 only group (40% mortality). PCV2 and PPV coinfected conventional SEW pigs had increased incidence and severity of clinical signs characteristic of PMWS. There was also a significantly higher incidence and more severe lymphoid depletion observed in coinfected pigs. The PCV2 coinfection Model characterized severe disease by coughing, dyspnea, lethargy and decreased growth. Dual infected pigs had significantly more severe lung lesions and a significantly higher number of genomic copies of PCV2 in sera at 14 and 21 DPI. They also had more severe lymphoid depletion and higher amounts of PCV2 antigen in lungs and lymphoid tissues. A field trial looked for evidence for immune stimulation induced progression of PCV2 infection to PMWS. They found PMWS in 42.9% of the vaccinated pigs versus 10.7% in the group treated with normal saline. This work provides evidence that the efficacy of PRRSV vaccines can be decreased when administered to PCV2- infected pigs. Based on field evidence, we suspect that PCV2 infection may similarly decrease the efficacy of other vaccines administered between 6-14 weeks of age. The use and the appropriate timing of M. hyo vaccination is an effective tool in reducing the production losses associated with PCV2 and M. hyo-induced respiratory disease complex. Another experiment confirmed that the use of CTC (Aureomycin®) in the feed for 2-4 weeks at an approximate dose of 22 mg/kg body weight is a highly effective tool in reducing the production losses associated with PCV2- and M. hyoinduced respiratory disease complex. In order to control PCV2-Asscociated Diseases confirm PMWS/PCV2 by histopath, IHC; identify and control concurrent viral infections; minimize effects of M. hyo. with commercial vaccines and/or antimicrobials; aggressively treat other bacterial coinfections; determine if there is an association of increased PCV2-induced disease with the use of certain vaccines or timing of vaccination; use anti- inflammatory drugs; pulsing the group with spray dried plasma protein; pull sick pigs; focus on decreasing stress and improving pig comfort; use effective disinfectants (Virkon-S) between groups; consider a change in pig genetics; and use PCV2 vaccines. These are all ideas that will help control the outbreak of PCV2 in swine barns.

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