Protective effect of inactivated bovine herpesvirus-1 in calves experimentally infected with bovine herpesvirus-1 and Pasteurella haemolytica.
The protective effect of an inactivated whole-virion bovine herpesvirus-1 (BHV-1) immunising inoculum, without adjuvant, against viral-bacterial respiratory disease was studied in three experimental treatment groups of five calves each. One group was boosted 14 days after the first vaccination and at this time the second group received their initial inoculation. Seven days later, calves were challenged with BHV-1 in aerosol and four days after this challenge all calves were exposed to Pasteurella haemolytica A1 in aerosol. Among the three groups, differences in rectal temperature responses four days after viral challenge (P less than 0.01) did not relate to protection. However the main response variable, viral-bacterial pneumonia, was reduced in boosted calves (P less than 0.05).
Impairment of pulmonary homeostatic and antimicrobial defence mechanisms by infectious bovine rhinotracheitis and parainfluenza-3 virus infections
In calves, infectious bovine rhinotracheitis and parainfluenza-3 viruses caused significant inhibition of the macrophage chemi1uminescence reaction. Similar effects were observed due to parainf1uenza-S virus in guinea-pigs. Beta-adrenergic receptors in both macrophages and airway smooth muscle were disrupted by virus infection. The viruses caused marked hyperreactivity in airway smooth muscle and in mast cell histamine release. Hyperreactivity may be a factor in bovine virus infection and may predispose to opportunistic secondary bacterial colonization. Levamisole and verapamil prevent some of the virus-induced responses. These drugs may be useful in the management of secondary bacteria pneumonia.
Pharmacological abnormality in bronchial asthma and the role of respiratory pathogens.
Upper respiratory tract infection has frequently been shown to precipitate or exacerbate the asthmatic condition and to increase airway reactivity to bronchospastic agents. The hypothesis first proposed by Szentivanyi suggested a beta-adrenoceptor deficiency in the pulmonary system in bronchial asthma leading to an alteration in the autonomic control of the airways in favour of excessive alpha-adrenergic and cholinergic bronchoconstrictor influence. Experimental exposure of isolated leukocytes and airway smooth muscle of laboratory animals and man with respiratory pathogens, e.g. influenzae virus, rhinovirus and Haemophilus influenzae has caused impaired pharmacological modulatory responses to isoprenaline, histamine (H2) and PGE, resulting in increased cellular release of inflammatory mediators and enhanced muscle contraction. Szentivanyi's hypothesis may now be extended to include impairment due to respiratory infection of other hormonal mechanisms responsible for bronchodilatation; i.e. histamine H2-receptor, PGE receptor and possibly non-adrenergic of "purinergic" receptor stimulation. Thus, the hypothesis of "pharmacological abnormality in bronchial asthma and the role of respiratory pathogens' has been discussed using experimental evidence.