Infectious bovine rhinotracheitis in Great Britain in the period 1970 to 1986

Abstract

Bovid herpesvirus 1 (BHV1) causes a variety of disease syndromes in cattle world -wide. The biology of the virus is reviewed with emphasis on clinical disease, epidemiology and the role of viral latency, the physical, genetic and antigenic make -up of the virus, experimental respiratory disease (infectious bovine rhinotracheitis - IBR), the immune response of cattle and its exploitation in diagnostic tests. An analysis was made of the epidemiology of BHV1 infection in Great Britain, using diagnostic data from Veterinary Investigation Centres and the Central Veterinary Laboratory. There was a marked seasonal incidence, with IBR occurring mainly in winter and fetopathy in summer. There was a dramatic increase in IBR incidence in the late 1970s. Estimates of the prevalence of seropositive cattle showed a rising trend over the period 1970 -1986.Restriction endonuclease fingerprinting of the DNA of BHV1 showed that early British isolates (from both IBR and genital disease) were all of genotype 2 along with the prototype American genital strain. More recent isolates, since 1977, are predominantly of genotype 1 resembling the prototype IBR strains from America. This supports the view that genotype 1 viruses were imported to Britain during the 1970s.Four British isolates of genotype 1 virus and two of genotype 2 were used in a series of experimental calf inoculations. All six strains produced a febrile upper respiratory and ocular disease. A score system was used to quantify the clinical responses. Statistical analysis indicated that genotype 1 viruses were more virulent than genotype 2, and calves inoculated with genotype 1 excreted significantly more virus. For both genotypes of virus, the calves showed clinical resistance to subsequent challenge with the opposite genotype. In the primary infections, an early serological IgM response peaked on days 12-14 after inoculation. IgG1 and IgG2 were first detected on days 9 or 10 with a marked rise in IgG1 between days 10 and 15. Secondary rises in IgG antibodies occurred following challenge exposure and also after reactivation of latent virus by the administration of dexamethasone.Comparisons were made of the diagnostic tests for BHV1 infection. Antigen-detection methods were specific and sensitive although they could not equal the sensitivity of virus isolation. Direct immunofluorescent labelling of cells extracted from the nasal mucus or the use of reverse passive haemagglutination to detect soluble antigen in secretions, were the simplest techniques which offered high sensitivity. A. number of enzyme immunossays for cytological labelling or the detection of soluble antigen were evaluated but their technical complexity led to increased opportunities for test error. In contrast, enzyme linked immunosorbent assay proved a flexible and reliable tool for serological diagnosis. The parameters of an IgG assay were determined so as to enable its use in a variety of diagnostic applications. Preliminary studies suggested that an IgM capture assay using monoclonal antibodies was of potential diagnostic value as an indicator of recent infection.