Bovine viral diarrhoea

Citation
S. Kecskemeti et I. Kiss, Bovine viral diarrhoea, MAGY ALLATO, 121(6), 1999, pp. 344-348
Citations number
46
Categorie Soggetti
Veterinary Medicine/Animal Health
Journal title
MAGYAR ALLATORVOSOK LAPJA
ISSN journal
0025004X → ACNP
Volume
121
Issue
6
Year of publication
1999
Pages
344 - 348
Database
ISI
SICI code
0025-004X(199906)121:6<344:BVD>2.0.ZU;2-K
Abstract
The infection caused by bovine viral diarrhoea virus (BVDV) usually causes mild clinical symptoms in immunocompetent cattle. When infecting pregnant a nimals, the virus may invade the fetus, causing different pathological chan ges that largely depend on the affected period of gestation. In the first m onth of pregnancy, BVDV infection results in early embryonic death, return to heat, and abortion. Infection of the fetus by a noncythopathogenic strai n of BVDV between the 40th and 120th days of pregnancy leads to the deliver y of persistently infected, immunotolerant animals that are persistently vi raemic and can shed the virus during their whole lifetime. Infection betwee n the 90th and 150th days of pregnancy may produce disorders of the central nervous system and the eyes. In the second half of pregnancy the fetus is able to produce antibodies against the virus. Bulls shed the virus via seme n; in case of acute infection with lower titers and for a shorter period, w hile in case of persistent infections constantly and with a higher titer. A dditionally, infection by BVDV exerts a remarkable suppression on the immun e system of the host. There have been reports of haemorrhagic syndromes acc ompanied by thrombocytopenia, anaemia, haemorrhages, and severe mortality c aused by BVDV. Mucosal disease (MD) may develop in animals persistently inf ected with a non-cythopathogenic BVDV by the superinfection of a cythopatho genic BVDV later on. When the superinfecting virus has a homologous antigen ic structure, MD develops within two or three weeks resulting in high morta lity. If the superinfecting virus is partially heterologous, a humoral immu ne response can be detected against it and the virus disappears from the bl ood, with MD developing weeks or months later. MD does not develop after a superinfection with heterologous cythopathogenic BVDV but rather antibodies are produced against the heterologous virus. Diagnosis of the diseases caused by BVDV is based on the clinical symptoms, pathological and histological alterations and results of laboratory invest igations (demonstration of the presence of the virus, virus antigen or nucl eic acid). Control of BVDV infection is based on the one hand on the prevention of int roduction of the virus and on the other hand, on detection and elimination of persistently infected animals, prevention of transient and persistent in fections by vaccination and hygienic measures, as well as on the prevention of the enrichment of the causative agent on the farm.