header shadow

PCV2 Vaccines

Company
Name

Ingelvac®
CircoFLEX™

Suvaxyn PCV2® One Dose Circumvent™ PCV Circovac®
Antigen PCV2 expressed in incativated Baculovirus Inactivated PCV1-2 Chimera PCV2 expressed in incativated Baculovirus
Inactivated PCV2
Dose

1 ml IM

Single dose

2 ml IM

Single dose

2 ml IM

Two injections 3 weeks apart

2 ml IM

Primary vaccination: Two injections 3-4 weeks apart, at least 2 weeks before mating

Revaccination: One injection at each gestation, at least 2-4 weeks before farrowing

Licensed for: Healthy pigs 3-weeks and older Healthy pigs 4-weeks and older Healthy pigs 3 weeks and older

Healthy female breeding age pigs
 

Available

United States
Canada

United States United States
Canada

Canada
Europe

CONTROL OF PCVAD

Good Management Practices

Control of Coinfections

 

Serotherapy

General Info

Research

Control

Diagnosis

Factors

PCVAD

Molecular Organization

Pathogenesis

Host Range

Epidemiology

Related Links

There is substantial and increrasing evidence that PCV2 vaccines will be useful in controlling PCVAD. Vaccination of sows with an inactivated oil-adjuvanted PCV2-vaccine (CIRCOVAC®; Merial Inc.) in field conditions in Europe was beneficial in reducing the PCV2 circulation and shedding in the first weeks of life, and also in improving the pig health after experimental PCV2 challenge at 3- 4 weeks of age (Charreyre et al., 2005). Eleven gilts free of PCV2-antibodies were vaccinated with the PCV2-vaccine intramuscularly at 5 and 2 weeks before breeding and again at 2 weeks before farrowing. A group of 22 piglets born to 4 vaccinated gilts and a group of 22 piglets born to unvaccinated control gilts were inoculated with PCV2 intranasally at 3-4 weeks of age. Seroconversion was observed in piglets born to seronegative dams. PCV2 DNA in serum and mesenteric lymph nodes was significantly (P = 0.00002) lower in piglets born to unvaccinated dams. In another field efficacy study, 3 groups of piglets were selected on farm and brought to the research facility. Group 1 pigs (n = 12) were born to unvaccinated sows, group 2 pigs (n = 10) were born to sows that had been vaccinated once with the PCV2-vaccine 2 weeks before farrwowing, and group 3 pigs (n = 11) were from a different farm and free of antibodies to PCV2. All piglets were infected intranasally with PCV2 at 25-47 days of age. Piglets born to non-vaccinated sows had a rise in PCV2 antibodies, whereas the PCV2-antibodies decayed in the pigs born to vaccinated sows. Lymph nodes were grossly unremarkable in this group whereas the lymph nodes were enlarged in the two other groups. During field efficacy studies of the PCV2 vaccine conducted in Germany and France it was found that there was a rise in PCV2 antibody level in the breeder herds concurrently with a decrease in PMWS rates in the pigs originating from the farms (Charreyre et al., 2005).

Pogranichniy et al. (2004) tested two inactivated US-PCV2 isolate preparations (ultraviolet irradiation or chemical inactivation) in the CDCD PCV2 PRRSV coinfection model and in the CDCD PCV2 KLH model using 57 piglets randomly assigned to 6 groups. Vaccination was done at 7 days of age and again 2 weeks later. PRRSV inoculation was done at 7 days of age. KLH with incomplete Freund’s adjuvant was infected at 21 and 27 days of age. At 24 days of age, the pigs were inoculated with PCV2. After PCV2 inoculation, the mortality in the vaccinated pigs was 20% whereas it was 70% in the non-vaccinated pigs implying that vaccination against PCV2 can be effective (Pogranichniy et al., 2004).  

It has been demonstrated that a chimeric PCV1-2 virus (with the immunogenic capsid gene of PCV2 cloned into the backbone of PCV1) induces an antibody response to PCV2 capsid protein and is attenuated in pigs (Fenaux et al., 2003). The attenuated chimeric PCV1-2 induced protective immunity to wild-type PCV2 challenge in pigs (Fenaux et al., 2004). A total of 48 SPF pigs were randomly and equally assigned to 4 groups of 12 pigs each. Pigs in group 1-3 were vaccinated with the chimeric PCV1-2 and pigs in group 4 were not vaccinated and served as controls. At 42 days post vaccination, all pigs were challenged intranasally and intramuscularly with wild-type pathogenic PCV2. Mild-to-severe lymphoid depletion and histiocytic replacement were detected in lymphoid tissues in the majority of nonvaccinated group 4 pigs but in only a few vaccinated group 1-3 pigs (Fenaux et al., 2004)

Blanchard et al. (2003) found the ORF2 protein to be a major immunogen, inducing protection in a prime-boost protocol. Thirty-five, 25-day-old SPF pigs were divided into 5 groups of seven piglets. Groups 1-4 piglets received an intramuscular injectin of DNA plamid preparation followed by a second injection 2 weeks later. Pigs were challenged intratracheally and intramuscularly with PCV2 10 days after the second injection. As evaluated by growth parameters, clinical signs and seroconversion, the pigs were protected against a PCV2 challenge after vaccination. In a second trial, sixty-four 4-week-old SPF pigs were divided into eight groups with eight pigs in each group. Piglets received either in intramuscular DNA injection or a intramuscular infection of baculovirus-expressed protein followed by a booster injection 2 weeks later. The piglets were inoculated with PCV2 11 days after second injection. The results indicated that protection induced by a subunit vaccine was even better than the one induced by a DNA vaccine, since PCV2 replication was completely inhibited (Blanchard et al. 2003).

Seven week old female Balb/c mice were vaccinated with a DNA-based vaccine against PCV2 structural protein on 0, 30, and 52 days and seroconverted to PCV2 (Kamstrup et al., 2004). The authors cloned a 768 bp fragment of the capsid protein of a Danish PCV2 isolate into the vector pcDNA1.1/V5-His/TOPO. The plasmid DNA was coated onto gold particles and used for particle mediated DNA vaccination. After 2 vaccinations, all mice had seroconverted to PCV2. A PCV2 challenge was not done in this study (Kamstrup et al., 2004).

References:

Blanchard P, Mahé D, Cariolet R, Keranflec'h A, Baudouard MA, Cordioli P, Albina E, Jestin A: Protection of swine against post-weaning multisystemic wasting syndrome (PMWS) by porcine circovirus type 2 (PCV2) proteins. Vaccine. 21:4565-4575, 2003

Charreyre C, Bésème S, Brun A, Bublot M, Joisel F, Lapostolle B, Sierra P, Vaganay A: Protection of piglets against a PCV2 experimental challenge by vaccinating gilts with inactivated adjuvanted PCV2 vaccine. In: Proc Intern Conf “Animal Circoviruses and Associated Diseases”, Belfast, UK, 26-30, 2005

Fenaux M, Opriessnig T, Halbur PG, Elvinger F, Meng XJ:A chimeric porcine circovirus (PCV) with the immunogenic capsid gene of the pathogenic PCV type 2 (PCV2) cloned into the genomic backbone of the nonpathogenic PCV1 induces protective immunity against PCV2 infection in pigs. J Virol. 78:6297-6303, 2004

Fenaux M, Opriessnig T, Halbur PG, Meng XJ: Immunogenicity and pathogenicity of chimeric infectious DNA clones of pathogenic porcine circovirus type 2 (PCV2) and nonpathogenic PCV1 in weanling pigs. J Virol. 77:11232-11243, 2003

Kamstrup S, Barfoed AM, Frimann TH, Ladekjær-Mikkelsen AS, Bøtner A: Immunization against PCV2 structural protein by DNA vaccination of mice. Vaccine. 22:1358-1361, 2004

Pogranichnyy RM, Yoon KJ, Yaeger M, Vaughn E, Stammer R, Roof M: Efficacy of experimental inactivated PCV2 vaccines for preventing PMWS in CDCD pigs. In: Proc Am Assoc Swine Vet. Des Moines, Iowa. 35:443-444, 2004