glycogen and Communicable-Diseases

The present study describes light and electron microscopic changes in the liver of Atlantic salmon during the development of infectious salmon anemia (ISA). Atlantic salmon postsmolts weighing 80-100 g were infected by intraperitoneal injections, and liver samples were collected sequentially between day 0 and day 25 post infection (p.i.), with time intervals of 3-4 days. At each collection time, livers from five infected fish and two control fish were examined. Changes involving the perisinusoidal macrophages were observed by transmission electron microscopy, from day 4 p.i. Large vacuoles, containing a fine-granular material with low electron density, accumulated in the cytoplasm. These changes persisted and became more severe throughout the investigation, leading to a considerable increase in the size of the cells. At day 14 p.i., degenerative features of the sinusoidal endothelium were observed. By day 18 p.i., areas of the liver were devoid of a sinusoidal endothelial lining, bringing hepatocytes in direct contact with blood cells. At this stage, the sinusoids were moderately congested. From day 21 p.i., heavy sinusoidal congestion, peliosis hepatis, and degeneration of the hepatocytes were observed. No virus was observed in any of the inhabitant cell types of the liver. Gross and light microscopic changes were first recorded at day 18 p.i., as was a significant decrease in the hematocrit values. By day 25 p.i., characteristic multifocal, confluent, hemorrhagic necroses were present. Results of the present investigation suggest that the liver lesions observed with ISA are not the result of the development of an anemia alone or caused by direct viral damage to hepatocytes. Hepatocellular degeneration succeeded changes in the perisinusoidal macrophages and degeneration of the sinusoidal endothelium. These changes may have impeded the sinusoidal blood flow and hence caused an ischemic hepatocellular necrosis.

Topics: Anemia; Animals; Communicable Diseases; Endothelium; Fish Diseases; Glycogen; Hematocrit; Injections, Intraperitoneal; Liver; Liver Diseases; Microscopy, Electron; Salmon; Tissue Fixation

Quantitative glycogen determinations can be made in single blood and bone marrow cells, using microspectrophotometry or microfluorometry after staining with variants of the periodic acid--Schiff (PAS) reaction. These PAS variant reactions generally do not indicate the presence of non-glycogen PAS-positive substances, known to be prevalent in various hematopoietic cells, possibly due to masking of reactive groups. The specificity of the reaction in blood cells was ascertained by alpha-amylase digestion, which removed more than 95% of the PAS-positive material. Calibration of the PAS reaction was undertaken with a microdroplet model of pure leukocyte glycogen. The glycogen amounts in the droplets were determined by microinterferometry, the droplets were stained with a variant PAS reaction, and the total extinction of the reaction product in the stained droplets was determined by microspectrophotometry. The extinction coefficient (k) was obtained from the equation k equals Etot divided by M where (Etot) is the total extinction as determined by microspectrophotometry and (M) the dry glycogen amount as determined by microinterferometry. The microinterferometric dry mass determinations were calibrated by X-ray absorption in order to obtain the absolute amounts of glycogen. For practical purposes a reference system was made of normal neutrophil leukocytes. The glycogen content in the reference neutrophils was first determined with the micromodel. These neutrophils, now with a known glycogen amount, were stained with the PAS reagents and measured microspectrophotometrically in parallel with cells containing an unknown glycogen amount. Alternatively, the staining was made with a fluorescent PAS reaction, and the glycogen content determined by microfluorometry. Both methods appeared suitable for determining the glycogen content of blood cells from patients with various diseases, though the microfluorometric method was preferable for measurements of small amounts of inhomogeneously distributed glycogen. The mean glycogen content of normal neutrophil leukocytes was found to be 13.6 times 10(-12) g. The content was increased in infectious diseases such as pneumonia and tonisillitis, as well as in polycythemia vera and myelofibrosis, while low amounts were found in untreated chronic myelocytic leukemia. In chronic myelocytic leukemia in remission, the glycogen content of mature neutrophils had completely normalized. Erythroblasts normally do not contain detectable amou

Topics: Autoradiography; Blood Cells; Bone Marrow; Bone Marrow Cells; Communicable Diseases; Diabetes Mellitus; Fluorometry; Glycogen; Glycogen Storage Disease; Histocytochemistry; Humans; Interferometry; Leukemia; Microradiography; Models, Biological; Myocardial Infarction; Neutrophils; Periodic Acid-Schiff Reaction; Polycythemia; Spectrophotometry; Thalassemia; X-Rays

Topics: Animals; Blood; Communicable Diseases; Glycogen; Lactates; Lactic Acid; Lagomorpha; Rabbits; Research; Staphylococcal Infections; Staphylococcus