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Biomedical subjects

G Trautwein

Publications and source records attributed to G Trautwein.

At least 109 records · Page 6Linked to original sources
PubMed1977

Spontaneous glomerulonephritis in dogs. I. Classification and immunopathology.

A morphological study of kidneys of 101 dogs with and without clinical signs of renal disease was done. In 90% of the dogs there was morphologic evidence of glomerulopathy. Types of glomerulonephritis were: membranous, 26 cases (with spikes, six cases; without spikes, 20 cases); membranoproliferative, 30 cases (with mesagial proliferation, nine cases; with mesangial sclerosis, 21 cases); mesagial-proliferative, 16 cases; and mesangial-sclerosing, 19 cases. There was no linear immunofluorescence indicative of autoantibodies to the glomerular basement membrane. Membranous glomerulonephritis with spikes was associated with coarse subepithelial deposits of IgG and C3. Membranous glomerulonephritis without spikes often had a linear fluorescence pattern of C3. In membranoproliferative glomerulonephritis, there were subendothelial deposits of IgG and C3, and frequently C3 deposits were within the mesangium. Mesagial deposits of C3 were frequently found in kidneys with mesangial-proliferative and mesagial-sclerosing glomerulonephritis and glomeruli that histologically appeared normal.

Animals↗
PubMed1977

Spontaneous glomerulonephritis in dogs. II. Correlation of glomerulonephritis with age, chronic interstitial nephritis and extrarenal lesions.

A morphologic study of 103 dogs, including two with renal amyloidosis, showed that different types of diffuse glomerulonephritis are correlated with different age groups. Membranous and membranoproliferative glomerulonephritis were more common in middle-aged and older animals, whereas mesangial lesions were found predominantly in younger dogs and considered to be early glomerular changes. Glomerulonephritis largely occurred independently of interstitial nephritis. The incidence of interstitial lesions was 71%. Chronic interstitial nephritis was rare in dogs under 1 year old. Glomerulonephritis did not seem to induce interstitial nephritis. Glomerulonephritis occurred not only in kidneys with severe interstitial damage, but also in those with slight damage. The indicated that glomerulonephritis occurred independently of interstitial nephritis. In end-stage kidneys with severe fibrosis, mesangial changes seemed to predominate.

Age Factors↗
PubMed1977

[Experimental infection of mice, gerbils, and rats with mycoplasms from canine pericardium and cardial value (author's transl)].

Mycoplasms isolated from heart valves (A. laidlawii (A 42 Hzbtl)) and pericardium (M. canis (A 56 Hzkl)) of dogs were investigated for infectivity of rats, mice and gerbils (Meriones unguiculatus). In mice the species M. spumans (PG 13), M. maculosum (PG 15), M. edwardii (PG 24) and M. molare (H 542) were investigated too. The mycoplasmas were inoculated by oral, subcutaneous, intravenous and intraperitoneal route. Intraperitoneally the mycoplasmas were given without and with complete and incomplete Freund adjuvants. The injected Mycoplasmas did not produce any disease and could not be reisolated from rats and gerbils. From mice A. laidlawii (A 42 Hzbtl), M. canis (A 56 Hzkl) and M. edwardii (PG 24) could be reisolated after intraperitoneal administration in emulsion with complete and incomplete Freund adjuvants. Whereas M. canis (A 56 Hzkl) and M. edwardii (PG 24) could be reisolated from lung, liver and spleen only, A. laidlawii (A 42 Hzbtl) was present in heart muscle too. In histological investigations the mice which got A. laidlawii (A 42 Hzbtl) intraperitoneally with complete Freund adjuvants showed focal lymphocytic infiltrations in the myocardium.

Acholeplasma laidlawii↗
PubMed1975

[Pathogenesis of aleutian mink disease. VII. Chronic hepatitis with bile duct proliferation].

Aleutian disease is a chronic persistent viral infection of mink characterized by hypergammaglobulinema, generalized plasmacytosis, sclerosing glomerulonephritis, polyarteritis, and plasma cell hepatitis with bile duct proliferation. The development of hepatic lesions was studied both light- and electron-microscopically in mink experimentally infected with Aleutian disease virus. Fifteen normal and 99 mink experimentally infected with Aleutian disease virus were used. Experimental mink were killed in intervals from 3 weeks to 23 months after infection, and liver sections were processed for both light- and electron-microscopic studies. Experimentally infected mink developed portal and intralobular lymphocytic and plasmacytic infiltrates in the liver 3 weeks after infection. Four to five weeks after infection there was evidence of early bile duct proliferation that began as an outgrowth of the portal bile ducts. Three to five months after infection a marked bile duct proliferation was present in some of the portal triads and adjacent liver lobules; but there was no tendency of these lesions to progress into biliary cirrhosis. Ultrastructural characteristics of proliferating bile duct cells were marked deformation, formation of multiple cell layers, reduction in the number of microvilli and desmosomes, and infiltration of the epithelial cells by lymphoid cells and plasmacytes. The hepatic lesions either develop by direct virus stimulation or by the deposition of virus-antibody complexes.

Aleutian Mink Disease↗