Innate Immunology of Bovine Respiratory Disease
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Derscheid, Rachel
Roth, James
Roth, James
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Abstract
Pneumonia is a leading cause of loss to the cattle industry in the United States and Europe. Of cattle diseases, it has the greatest economic impact. Respiratory pathogens can cause serious outbreaks of acute pneumonia in neonatal, weaned and growing calves. Chronic infection leads to debilitation, decreased performance, and culling in older animals. The means to enhance effective and non-injurious immune responses are needed because of the high incidence of pneumonia in cattle, ubiquity of respiratory pathogens, the increasing frequency of antibiotic resistance, and the general expectation by consumers for producers to use antibiotics less frequently. The lung has a wide array of both innate and adaptive immune responses to airborne particulates, vapors, and microbial pathogens. Vaccines can effectively enhance resistance to some pathogens, but not all. More recently, additional attention has been given to innate immune responses and method/regimens that increase innate immune activity. Despite advances in managerial practices, vaccines, and clinical therapies, pneumonia remains a widespread problem and methods to enhance host resistance to pathogen colonization and pneumonia are needed.
There are a variety of factors and conditions that pre-dispose cattle to pneumonia. Cattle have anatomic and cellular differences from humans and other species and are managed in groups/ herds all of which increases susceptibility to microbial pathogens. This review highlights the basic innate immune response of the respiratory tract and newer developments in the understanding of adaptive immune responses of the bovine respiratory tract placing special emphasis on features unique to cattle.
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This is a manuscript of an article published as Ackermann, Mark R., Rachel Derscheid, and James A. Roth. "Innate immunology of bovine respiratory disease." Veterinary Clinics: Food Animal Practice 26, no. 2 (2010): 215-228. doi: 10.1016/j.cvfa.2010.03.001. Posted with permission.