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The aim of the author was to present conclusions from the results of own examinations and results from literature that will lead to a new and better understanding of the epidemiology and pathogenesis of the enigmatic Bovine herpesvirus 2 (BoHV-2) infection.

The current literature on the BoHV-2 infection was reviewed, and it was concluded that important questions concerning the pathogenesis and ways of transmission within and between herds were still not clarified. It was especially noted that the sensitivity of the tests used for the demonstration of antibodies had generally been much too low, making serological confirmation of infection difficult.

The infection was first seen in Denmark as ulcerative mammillitis (bovine herpes mammillitis, BHM) in September 1980, and up to December 1983, a total of 53 outbreaks were diagnosed. No outbreaks have been confirmed later. The Danish test for neutralizing antibodies was elaborated to show adequately high sensitivity. A herd tested shortly after an outbreak showed that all tested animals, including bull calves up to the age of 14 months, were antibody-positive. All 34 outbreaks in 1980 and 1981 apart from the last one occurred in a limited geographical area, where semen used for artificial insemination (AI) usually came from 2 local AI centers. Some selected bulls from these centers were tested and found antibody-positive.

From the Danish examinations, it was concluded, 1) that all cows showing clinical BHM would be antibody-positive when tested by the highly sensitive Danish test, 2) that the spread in herds to all animals could be explained only as airborne, and 3) that the first spread to Danish herds most likely occurred with semen from AI bull centers.

BoHV-2 is also the cause of the rare pseudo-lumpy skin disease (PLSD), where skin lesions all over the body predominate. PLSD has often been reproduced by intravenous virus inoculations. From the results reported in the literature, it was further concluded (4) that experimental PLSD skin lesions appearing after intravenous inoculation were likely to have been a delayed, adaptive, universal response of the animals to the virus antigen. In consequence, the inflammatory reactions leading to these lesions would be the result of complement activation by the classical pathway, implying that the pathological changes observed clinically were triggered by specific antibodies to the virus at sites of virus propagation. Finally, (5) it was concluded that this explanation would be consistent with the experience that the inflammatory BHM lesions in the skin of teats and udders of cows on the diagnosis of BHM already are antibody-positive.

Furthermore, (6) udder edema aggravates BHM disease, most probably because of the reduced blood circulation resulting in cold skin, which will hamper the removal of the cell-toxic substances formed during the complement activation process. Cold weather causing lowered skin temperature, in particular in hairless areas, during the critical very short period after the production of a sufficient level of reacting antibodies is therefore most likely an essential disease determinant. This will explain why BHM in Europe has predominantly occurred in cold seasons. In cases of BHM, where lesions have appeared only on the teats, a traumatic effect of mechanical milking may have contributed to the development of the clinical picture.

The conclusions may be a valuable contribution to the understanding of skin lesions seen in other diseases caused by dermotropic viruses like herpesviruses and poxviruses.