Abstract

Scabies is one of the leading causes of morbidity in pigs worldwide. Limited data are available regarding the role of immune reactions in the development of porcine scabies. The aim of this study was to investigate key pro-inflammatory cytokines (IL-1, TNF-α), soluble variant of adhesion molecule ICAM-1 and mite-mediated apoptosis of peripheral leukocytes in 20 pigs with scabies, in addition to 10healthy controls. The pigs with at least three typical clinical signs and found positive for Sarcoptes scabiei var. suis in microscopy were recruited for the present study. IL-1 acted as the major pro-inflammatory cytokine as serum IL-1 concentrations showed significantly (p<.05) higher levels (7-fold increase) in cases than in controls. The minor cytokine TNF-α was 4-fold higher during scabies, and its mean serum concentration was significantly increased (p<.05) in cases when compared to healthy controls. Soluble ICAM-1levels were significantly higher (p<.05) in all the pigs of infested group compared with the controls. The percentage of apoptotic and necrotic leukocytes was found to be significantly higher (p<.05) in scabies positive pigs as compared to the healthy controls. It is concluded that systemic elevation in pro-inflammatory cytokines IL-1 and TNF-α, shedding of soluble ICAM-1 variant in peripheral blood and increased rate of host-cell apoptosis in peripheral leukocytes might be implicated in the immunopathology of naturally acquired porcine scabies.

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call

Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.