Epidemiology and pathogenesis of the Bovine herpesvirus 2 infection. (Summary)
Bovine herpesvirus 2 (BoHV-2) is most probably spread among cattle by the respiratory route. There are no indications of a transmission by insects or milking machines.
If clinical disease occurs, it appears in two different forms as either pseudo-lumpy skin disease (PLSD) or bovine herpes mammillitis (BHM), but no differences in pathogenicity of virus strains from PLSD and BHM outbreaks have been found. Both manifestations were recorded in Africa, before the infection was diagnosed in Europe, where it has appeared almost exclusively as BHM. Here, the infection was probably first spread to herds in a region with semen from artificial insemination centres. Later, spread between herds with both acutely and latently infected animals seems to have occurred.
PLSD must be the outcome of a generalized infection, where skin lesions appear as the result of an inflammation process at sites of virus propagation caused by complement activation, which again is triggered by the action of specific antibody to BoHV-2 (complement activation by the classical pathway). This implies that lesions do not appear, until antibody has been produced.
Naturally occurring clinical cases of BHM have regularly been found antibody-positive in the very early stage of disease when examined by a test of acceptable sensitivity. BHM lesions may therefore similarly be explained as the outcome of a generalized infection, where inflammatory lesions appear late in the course of the infection at sites of virus propagation immediately after the initial formation of specific antibody. Complement activation by the classical pathway will explain the sudden appearance of multiple lesions characteristic of PLSD - and of BHM, when several lesions develop.
Tissue damage caused by the inflammatory reactions seems to be aggravated by - or even dependent on - low skin temperature and the associated reduced blood circulation (and in some cases of BHM probably also by a traumatic influence of milking machines) during the first short period after complement activation. This may explain (1) why udder lesions have developed especially in animals with udder oedema, (2) why clinical outbreaks in Europe have been seen predominantly in the autumn, when the cows were still at pasture during the daytime, and (3) why no skin reactions are observed in most cases of natural infection.
July 2011, Viggo Bitsch
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