Date of Award

1981

Document Type

Dissertation

Degree Name

Doctor of Philosophy (PhD)

Abstract

Turpentine-induced inflammation was used as a model for the study of toxic neutrophils in the dog. Changes in the number of circulating toxic neutrophils paralleled changes in clinical signs, body temperature, total leukocyte count, and neutrophil count. Light microscopic appearance of neutrophils from turpentine-injected dogs was similar to toxic neutrophils seen clinically in dogs with severe bacterial or other inflammatory diseases. Ultrastructural studies showed that foamy vacuolation of the cytoplasm was due to irregular, electron-lucent areas which often contained membrane remnants and myelin figures. Increased cytoplasmic basophilia was due to the retention of rough endoplasmic reticulum and polyribosomes in mature toxic neutrophils. Bone marrow studies indicate that dilation of rough endoplasmic reticulum, followed by membrane disruption and degradation led to the formation of electron-lucent areas in mature toxic neutrophils. Morphologic evidence obtained from this study suggests that cytoplasmic immaturity, increased cellular activity, and cell degeneration may be involved in the formation of toxic neutrophils in the dog. In vitro function tests on neutrophils from turpentine-injected dogs showed normal phagocytosis of Staphylococcus aureus, but diminished bactericidal activity after 30 minutes of incubation. The biological significance of this functional defect is uncertain due to the lack of correlation between diminished bactericidal activity and toxic change, body temperature, neutrophil number, or clinical signs.

Pages

124

Share

COinS