Pulmonary Inflammatory and Immunological Responses to Airborne Pathogens: A Review
Influenza and the associated pneumonia is the sixth leading cause of death in the United States. The economic cost in terms of medical dollars and work loss is about $5 billion a year. Deterioration of air quality in the workplace may be caused by microbiological or particulate pollution and such pollution may impair pulmonary defenses sufficiently to enhance the susceptibility to airborne infections such as influenza. Tobacco smoke has been implicated as a disease causing agent even in individuals exposed to second-hand smoke. Ventilation systems in buildings have been implicated in transmission of infectious disease including tuberculosis, measles, smallpox and staphylococcus infections. Carpeting, humidifiers, and flush toilets can harbor bacteria, pollen, fungi, and other allergens. A number of viruses with varying degrees of epidemiologic and pathologic significance may be aerosolized, contribute to air quality deterioration, and cause respiratory disease (Table 1). Influenza viruses are prone to antigenic drift and consequently humoral immunity from previous infections is often only partially effective at preventing disease. The rationale behind vaccinating with a killed or modified live virus vaccine (or prior clinical or subclinical disease) is to stimulate the production of antibodies to certain epitopes on the viral surface. These epitopes are in constant contact with the host blood antibodies and hence are subject to a great deal of selective pressure. This selective pressure tends to favor the emergence of new viral epitopes and hence loss of disease resistance.
KeywordsFunctional Residual Capacity Mucociliary Clearance Respiratory Bronchiole Live Virus Vaccine Malignant Catarrhal Fever
Unable to display preview. Download preview PDF.
- Dunbar, J.R., DeLucia, A.J., Acuff, R.V. and Ferslew, K.E. (1988a). Prolonged, intravenous Paraquat infusion in the rat 1. Failure of coinfused putrescine to attenuate pulmonary paraquat uptake, paraquat-induced biochemical changes or lung injury. Toxicol. Appl. Pharmacol., 94, 207–220.CrossRefGoogle Scholar
- Frank, G.H., Briggs, R.E., and Gillette, K.G. (1986), Colonization of the nasal passages of calves with Pasteurella haemolytica ST1 and regeneration of colonization after experimentally induced viral infection of the respiratory tract. Am. J. Vet. Res., 47, 1704–1707.Google Scholar
- Frank, G. and Smith, P.C. (1983). Prevalence of Pasteurella haemolytica in transported calves. Am. J. Vet. Res., 44, 981–985.Google Scholar
- Gamsu, G., Weintraub, R.M., and Nadel, J.A. (1973). Clearance of tantalum from airways of different caliber in man evaluated by a roentgenographic method. Am. Rev. Respir. Dis., 107, 214–230.Google Scholar
- Grey, C.L. and Thompson, R.G. (1971). Pasteurella haemolytica in the tracheal air of calves. Canad. J. Comp. Med., 35, 121–128.Google Scholar
- Jakab, G.J. (1981). Mechanisms of virus-induced bacterial superinfections of the lung. Clin. Chest. Med., 2, 590–596.Google Scholar
- Markham, R.J.F., Markham, R.J.F., Ramnaraine, M.L.R., and Muscoplat, C.C. (1982). Cytotoxic effects of Pasteurella haemolytica on bovine polymorphonuclear leukocytes and impaired production of chemotoxic factors by Pasteurella haemolytica-infected Alveolar macrophages. Am. J. Vet. Res., 43, 285–288.Google Scholar
- Slocombe, R.F., Malark, J., Ingersoll, R., Derksen, F.J., and Robinson, N.E., (1984). Importance of neutrophils in the pathogenesis of acute pneumonic pasteurellosis in calves. Am. J. Vet. Res., 45, 1757–1763.Google Scholar
- Ettinger, S., (1975). Textbook of Veterinary Internal Medicine. pp.690–695, Saunders Inc., Philadelphia, PA.Google Scholar