http://www.loc.gov/mods/v3 http://www.loc.gov/standards/mods/v3/mods-3-2.xsd
histological and ultrastructural study of the pathogenesis of toxic myopathies of avian striated muscle
Toxic myodegeneration of avian striated muscle was studied by giving intraperitoneal injections of plasmocid[6-methoxy-8-(3-diethylaminopropylamino)quinolone] to 15 chickens and oral doses of ground Cassia occidentalis beans to 20 chickens. Samples of peroneus longus muscle (red fibers), pectoralis superficialis muscle (white fibers), and ventricular myocardium were compared by light microscopy of paraffin-embedded and Araldite-embedded tissue and by electron microscopy. The ultrastructural morphology of fibers of the peroneus longus muscle and the pectoralis superficialis muscle form the control birds was similar to that of human Type I and Type II muscle fibers respectively. The initial lesion in plasmocid toxicity was observed in the sarcoplasmic reticulum of skeletal muscle but not cardiac muscle. Filling of the cisternae of the sarcoplasmic reticulum with a finely granular, electron-opaque material apparently was followed by dilation of these organelles with extreme segmental contraction of individual skeletal muscle fibers. The most severe effect was on the fibers of the peroneus longus muscle. In contrast to plasmocid toxicity, the primary lesion of C. occidentalis poisoning was observed in mitochondria of the myocardium. Dilation and fragmentation of mitochondrial cristae was observed initially and fragmentation of external mitochondrial membranes was seen only in a few mitochondria contain fragments of these cristae. Although these two toxic myopathies were manifested by similar microscopic lesions, initial ultrastructural alterations were distinctly different. It was proposed that the inability of the sarcoplasmic reticulum to transport calcium ions out of the cell fluid in plasmocid toxicity and the alteration of oxidative phosphorylation in C. occidentalis poisoning both result in coagulation necrosis and fragmentation of muscle fibers observed in the terminal stages of toxic myodegeneration.
"Submitted to the Graduate College of the Texas A&M University in partial fulfillment of the requirements for the degree of Doctor of Philosophy August 1968".