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Maternal antibody, vaccination and reproductive failure in dogs with parvovirus infection
Author(s) -
GOODING G. E.,
ROBINSON W. F.
Publication year - 1982
Publication title -
australian veterinary journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.382
H-Index - 59
eISSN - 1751-0813
pISSN - 0005-0423
DOI - 10.1111/j.1751-0813.1982.tb15997.x
Subject(s) - vaccination , parvovirus , virology , antibody , medicine , immunology , biology , virus
Summary. The maternal antibody (MAb) titre to canine parvovirus (CPV) was determined on consecutive serums from 39 puppies in 7 litters. Vaccination with inactivated CPV was performed at a variety of ages and the response of the puppies determined. Transfer of MAb was demonstrated in 71% (5/7) of the litters and persisted for up to 10 weeks in some litters. MAb titres of >20 precluded a vaccination response by puppies. Sixty‐ one per cent (8/13) of puppies responded to vaccination when the MAb titre was <20. However, no anamestic response occurred and in some cases a decrease in antibody titre was observed following a second vaccination. During an outbreak of canine parvovirus enteritis (CPE) in the kennel, 33 puppies developed clinical signs of enteritis. Of these puppies 85% (28) had MAb titres of <80 at the onset of clinical signs. Fifty per cent (4/8) of the puppies which responded to vaccination developed CPE, whereas 100% (5/5) of those that did not respond to vaccination developed CPE. The results indicate that MAb may persist for up to 10 weeks and puppies with MAb in the titre range >20 to <80 do not respond to vaccination but are still susceptible to infection. It is also apparent that a significant minority of puppies with MAb <20 do not respond to vaccination. An examination of the breeding records of the kennel for the 7 year period 1973–1981 demonstrated a sudden decrease in reproductive efficiency during and subsequent to 1978. This coincided with the recognition of cases of CPV infection in the kennel. It is suggested that further investigation is required into the possible role of CPV in reproductive failure. The authors would like to thank H. Findlay, P. Hinchliffe, G. Griffiths and S. MacPhail for technical assistance and Dr G. Wilcox and R. Flower for helpful discussion and advice.