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Parvovirus Antibodies in Vaccinated Gilts ¨C HI versus ELISA tests
Still parvovirus infections are responsible for economical losses is swine `production`. Vaccination is possible, but does the vacciantion lead to protective antibody titers? A very interesting new study from Finland.

This study was conducted to determine the antibody response for porcine parvovirus (PPV) of 39 gilts in field conditions after vaccination.

Gilts from four herds endemically infected with PPV were injected twice with a commercial vaccine of inactivated PPV and Erysipelothrix rhusiopathiae.

The PPV antibodies were analysed both with haemagglutination inhibition (HI) and enzyme-linked immunosorbent assay (ELISA) in order to study the agreement between these methods.

The possible association between high-antibody titres and reproductive failure (repeat breeding, culling for infertility, ¡Ü6 piglets born alive) was also investigated. In these study herds, endemically infected by PPV, most gilts (84.6%) had not seroconverted by the age of 6 months.

On-field vaccination resulted in a consistent increase of humoral immunity not exceeding the antibody level of 1 : 512 in the majority of gilts in all herds examined.

The agreement between ELISA and HI tests was moderate (Spearman`s ¦Ñ = 0.87, ¦Ê = 0.63). The seroconversion over the level >1 : 512 by mid-pregnancy was not associated with reproductive failure.



Source: Oravainen, J, Hakala, M, Rautiainen, E, Veijalainen, P, Heinonen, M, Tast, A, Virolainen, JV & Peltoniemi, OAT (2006): Parvovirus Antibodies in Vaccinated Gilts in Field Conditions ¨C Results with HI and ELISA tests. In:
Reproduction in Domestic Animals 41 (1), 91-93.




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BOVINE

Zinc Deficiency-Like Syndrome in Fleckvieh Calvesmembers
Zinc deficiency-like (ZDL) syndrome is an inherited defect of Fleckvieh calves, with striking similarity to bovine hereditary zinc deficiency (BHZD). However, the causative mutation in a phospholipase D4 encoding gene (PLD4) shows no connection to zinc metabolism. The objectives of this study were to describe clinical signs, laboratory variables, and pathological findings of ZDL syndrome and their utility to differentiate ZDL from BHZD and infectious diseases with similar phenotype.

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