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Lymphocyte alterations in zinc-deficient calves with lethal trait A46
L E Perryman1, D R Leach, W C Davis
1Department of Veterinary Microbiology and Pathology, Washington State University, Pullman 99164-7040.
Veterinary Immunology and Immunopathology
|July 1, 1989
Summary
Genetic zinc deficiency in calves (A46 trait) impairs lymphocyte function and antibody production. This study shows reduced immune cell activity following the onset of zinc deficiency in affected animals.
Area of Science:
- Veterinary Immunology
- Nutritional Immunology
- Genetics
Background:
- Lethal trait A46 (A46) in calves causes genetic intestinal zinc malabsorption.
- Zinc deficiency can severely impact immune system development and function.
- Early identification of immune dysfunction is crucial for affected animals.
Purpose of the Study:
- To investigate the impact of genetic zinc deficiency on lymphocyte populations and functions in calves.
- To determine the timeline of immune alterations following the onset of zinc deficiency in A46 calves.
Main Methods:
- Evaluation of lymphocyte numbers and responses to mitogens (PHA, Con A, PWM) at multiple time points.
- Quantification of CD4+ T-lymphocytes and B lymphocytes.
- Assessment of secondary antibody production against bacteriophage phi X 174.
Main Results:
- Calves with A46 trait exhibited declining plasma zinc levels by 3 weeks, followed by clinical signs.
- Lymphocyte responses to mitogenic stimulation were variably reduced.
- Subnormal CD4+ T-lymphocyte counts and decreased relative B lymphocyte numbers were observed post-deficiency onset.
- Secondary antibody responses were significantly impaired.
Conclusions:
- Calves homozygous for the A46 trait possess normal lymphocyte subpopulations at birth.
- Zinc deficiency resulting from the A46 trait significantly alters lymphocyte activity and immune function.
- This genetic disorder leads to functional immunodeficiency in affected calves.