Whenever a 'new' disease is discovered and the putative agent responsible is isolated, it has been customary to attempt to reproduce the disease in similar animals under controlled experimental conditions. If an identical syndrome is produced, then the agent is considered to be responsible for producing the field disease. As early as 1892, Nocard did just that in relation to bovine pneumonic pasteurellosis (shipping/transit fever). His work however, appears to have escaped the attention of many subsequent workers. In the 1930s many workers attempted to reproduce the disease with crude preparations obtained from either sick or dead animals, but most of them failed. After 1950 several agents (bovine herpes virus 1 [BHV1], parainfluenza-3 virus [PI3] and mycoplasmas) were isolated from cases of shipping fever in North America. These, together with physical stress, were thought to be involved in the aetiology and pathogenesis of the disease, with pasteurellae playing the role of secondary invader. Many experimenters then used multiple agents in different combinations, but their degree of success in reproducing the disease was variable. Greater success was achieved when P haemolytica A1 was given to calves four days after exposure to BHV1. This success, although only moderate, reinforced the concept of the secondary role of pasteurellae. After 1977 however, it became increasingly clear that P haemolytica A1 was capable of causing the disease as a primary pathogen, provided that two conditions were fulfilled. First, the calves had to be susceptible, that is, non-immune, and secondly, P haemolytica A1 in the logarithmic growth phase had to be administered to the trachea or lungs in numbers greater than 5 x 10(9) colony forming units.
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