Title page for ETD etd-12232009-020526


Type of Document Master's Thesis
Author Grasman, Keith A.
URN etd-12232009-020526
Title Effects of lead ingestion on the immune function in quail
Degree Master of Science
Department Wildlife Sciences
Advisory Committee
Advisor Name Title
Scanlon, Patrick F. Committee Chair
Elgert, Klaus D. Committee Member
Kirkpatrick, Roy L. Committee Member
Vaughan, Michael R. Committee Member
Keywords
  • Quails
Date of Defense 1992-03-05
Availability restricted
Abstract

Wild birds can be exposed to high concentrations of lead caused by spent lead shot and industrial waste. The immunosuppressive effects of lead have been demonstrated in laboratory mammals, but little research has been conducted in birds. Because immunocompetence is important for survival, the effects of acute lead exposure on immune function in 2 quail species, Japanese quail (Cotumix coturllix) and northern bobwhites (Colinus virginianus), were investigated. In preliminary experiments, intubation with lead shot produced inconsistent doses within treatment groups. Both quail species exhibited poor antibody responses after immunization with sheep erythrocytes. In a third experiment, male Japanese quail were dosed with 100 or 400 ppm lead in drinking water for 7 days. Quail were fed either laying mash or com. Some quail were treated with corticosterone as a positive control Lead enhanced the loss of body mass caused by com. Lead-induced mortality was observed only in quail fed com. There was marginal evidence that lead increased the heterophil to lymphocyte ratio in quail fed com. Com decreased the cell-mediated immune response to an intradermal injection of phytohemagglutinin. Corticosterone suppressed cell-mediated immunity more than lead. The primary total antibody response to chukar (Alectoris graeca chukar) erythrocytes was significantly suppressed in lead-dosed quail fed com. Lead also reduced the secondary total antibody and IgG responses in the low lead/com group. The most pronounced effect of lead on immune function was a suppression of antibody responses in groups that exhibited clinical lead poisoning.

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