Submitted to: Avian Pathology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 7/5/2010
Publication Date: 9/2/2010
Citation: Li, G., Lillehoj, H.S., Lee, K.Y., Park, M.S., Jang, S.I., Pages, M., Bauchan, G.R., Gay, C.G., Ritter, D., Bautista, D., Siragusa, G.R. 2010. Immunopathology and Cytokine Responses in Commercial Broiler Chickens with Gangrenous Dermatitis. Avian Pathology. 39(4):255-264. Interpretive Summary: Gangrenous dermatitis (GD) is caused by the Gram-positive spore-forming anaerobic bacilli Clostridium perfringens (CP) type A and C. septicum (CS). Although the underlying causes for GD is not fully known, both CP and CS are known to contribute to disease pathology associated with GD. According to the United States Animal Health Association’s Committee on Transmissible Diseases of Poultry and other Avian Species, GD has consistently ranked as a top priority disease for the poultry industry in recent years. In this report, ARS scientists working together with scientists from University of Delaware Extension Service, Mountaire Farms and Danisco Laboratory investigated host-pathogen immunobiology in a field outbreak of GD in the Eastern Shore farms in MD. Host immune response of birds showing typical disease symptoms and pathological lesions (GD-like birds) was compared to that of chickens lacking clinical symptoms (GD-free birds). The results showed abnormal immune responses of GD-affected birds compared to GD-free birds in many aspects of immune responses including lymphocyte subpopulations, cytokine secretion profile and tissue immunohistology. The results of this study represent the first detailed description of host immunopatholgy associated with a field GD outbreak. This study will facilitate the development of logical management strategy and vaccines against GD infection.
Technical Abstract: Gangrene dermatitis (GD) is an emerging disease of increasing economic importance in poultry that results from infection by Clostridium septicum and C. perfringens (CP) type A. Lack of a reproducible disease model has been a major obstacle in understanding the immunopathology of GD. To gain better understanding of host-pathogen interactions in GD infection, we evaluated various immune parameters in two groups of birds from a recent commercial outbreak of GD, the first showing typical disease symptoms and pathological lesions (GD-like birds) and the second lacking clinical symptoms (GD-free birds). Our results revealed that GD-like birds showed (1) reduced T- and B-cell mitogen-stimulated lymphoproliferation, (2) higher levels of serum nitric oxide and a-1-acid glycoprotein, (3) greater numbers of K55+, K1+, CD8+, and MHC class II+ intradermal lymphocytes, and increased K55+, K1+, CD8+, TCR1+, TCR2+, Bu1+, and MHC class II+ intestinal intraepithelial lymphocytes, and (4) increased levels of mRNAs encoding proinflammatory cytokines and chemokines in skin compared with GD-free chickens. These results provide the first evidence of altered systemic and local (skin and intestine) immune responses in GD pathogenesis in chickens.