Ipvs2014 02 mortensen et al.-pcv2 circulation control in danish fatteners abs...
Aasv2014 daresta et al. comparative pcv2 fetal protection-poster
1. Vaccine-related protection against PCV2 fetal
infection in conventional gilts
M. Daresta, DVM, V. Felice, DVM, S. Panarese, DBS, C. Bianco, DVM, M.L. Bacci, DVM,
M. Dottori, DVM, P. Bonilauri, DBS, D. Lelli, DVM, G. Sarli, DVM, F. Ostanello, DVM
INTRODUCTION
PCV2 is involved in reproductive failure in swine that includes clinical and subclinical forms2. Clinical form is characterized by early termination of pregnancy,
increased numbers of mummified foetuses, still born or weak-born piglets, microscopic lesions within foetal tissues (heart, liver or lymphoid tissues) and PCV2
antigen or PCV2 DNA within foetal tissues2. In contrast, subclinical PCV2 in utero infection is identified by the detection of PCV2 DNA or specific antibodies in
foetal tissues, pre-suckling serum or foetal thoracic fluid without the presence of microscopic lesions or indication of reproductive failure2.
For these reasons, it is important to collect data on the protective role of PCV2 vaccination against this two clinical entities.
MATERIALS AND METHODS
Four groups of conventional gilts:
- Group VAI (n=6): vaccinated with a commercial inactivated PCV2
vaccine licensed for sows and piglets, 2mL, twice 4 weeks apart, IM;
- Group VBI (n=6): vaccinated with a commercial vaccine based on a
ORF2 capsid protein expressed in a baculovirus system and licensed
for use in piglets, 1 mL, twice 4 weeks apart, IM;
- Group NVI (n=6): non-vaccinated;
- Group CTR (n=3): non-vaccinated and non-infected controls.
Both types of vaccines were administered in gilts at 120 &150 days of life.
After syncronization/superovulation protocol, VAI, VBI and NVI groups
were inseminated with a double (24h apart) dose of PCV2-negative
semen spiked with a PCV2b strain isolated in a PMWS outbreak in Italy.
CTR gilts were fecundated with a double dose of PCV2-free semen.
Days
post-AI
Control
CTR
PCV2 infected
RESULTS
In the VAI group 4 out of 6 gilts were pregnant, in VBI 3 out of 6, in NVI 3 out of 6 and in CTR 2 out of 3, from which were collected 23, 19, 33 and 15 foetuses,
respectively and the corresponding placenta membranes and amniotic fluid. No difference in dam antibody titre or vireamia was evidenced among groups.
In the experimentally infected animals, compared to NVI, gilts of the VAI group showed a significantly (P<0.05) lower proportion of positivity in foetuses (VAI
21.74% vs NVI 48.48%) but not in amniotic fluid (VAI 17.39% vs NVI 33.33%) and placentas (VAI 73.91% vs NVI 72.73%), while in VBI group the percentages
of samples positive to PCV2 genome were significantly higher (P<0.05) in amniotic fluid (VBI 68.42% vs NVI 33.33%), placentas (VBI 100% vs NVI 72.73%)
but not in foetuses (VBI 36.84% vs NVI 48.48%).
Comparing the two vaccinated groups, the difference between the proportion of samples positive to PCV2 genome in amniotic fluid (VAI 17.39% vs VBI
68.42%), placentas (VAI 73.91% vs VBI 100%) was found significant but not in foetuses (VAI 21.74% vs VBI 36.84%).
Vaccination was found to be successful in reducing PCV2-associated reproductive failure and
improving sow performance under field conditions1. However the effect of sow vaccination on
foetal PCV2 infection in utero needs to be investigated because in PCV2-associated reproductive
failure, as well as the clinical form, also the subclinical in utero foetal infection must be
considered. For now, only data mainly addressed to demonstrate the role of vaccination on the
clinical PCV2-associated reproductive failure are available. However, it is at least equally
important to evaluate the protective effect of vaccination against the subclinical reproductive
failures.
In the present experimental conditions with a very severe challenge, vaccination with a
commercial inactivated PCV2 vaccine licensed for sows and piglets (vaccine A) did not eliminate
but significantly reduced the risk of foetus infection. Considering the most common way of foetus
infection through the foetal membranes/fluids, the protective role of the two vaccines against the
subclinical form of PCV2-associated reproductive failure does not seem to be similar. The lowest
proportion of placentas and amniotic fluid infected in VAI compared to VBI groups may explain the
lowest foetal positivity to PCV2 in this group of gilts compared to NVI animals.
100%
90%
80%
70%
60%
50%
40%
30%
20%
10%
0%
bc
a
b b b
a
Foetuses Amniotic
fluid
Placenta
Percentage of PCR-positive samples
1. Madson DM et al, . Effect of Porcine Circovirus Type 2 (PCV2) Vaccination of the Dam on PCV2 Replication In Utero. Clin and Vac Immunology, 2009; 16:830–834
2. Madson DM, Opriessnig T. Effect of porcine circovirus type 2 (PCV2) infection on reproduction: disease, vertical transmission, diagnostics and vaccination. Anim Health Res Rev 2011;
12:47-65.
3. Sarli G et al., Reproduction in porcine circovirus type 2 (PCV2) seropositive gilts inseminated with PCV2b spiked semen Acta Vet Scand 2012, 54:5.
Samples
(analysis)
Vaccine A
VAI
Vaccine B
VBI
Non vaccinated
NVI
0
artificial
insemination
PCV2 free
semen
10 ml
PCV2 spiked semen
10 ml
103.9TCID50/ml
Weekly blood
samplings
(serology , PCR)
29 Ultrasonography
55 Euthanasia of pregnant sows
Fetuses: heart,
liver, spleen ;
placenta,
amniotic fluid,
(PCR)
DISCUSSION AND CONCLUSION
REFERENCES
Table 1. Experimental design
Figure 1. PCR results.
a,b,c: different letters mean statistical difference, p<0.05
CTR
IVA
IVB
INV
ab
a
c
a a
c