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D Seidler

Publications and source records attributed to D Seidler.

32 records · Page 2Linked to original sources
PubMed1975

[Experimental erysipelas in different species as a model for systemic connective tissue disease. I. Systemic vascular processes during organ manifestation (author's transl)].

INTRODUCTION: The similarities between erysipelas in animals and rheumatic diseases in man have been discussed since the work of Nieberle (1931). The present work sets out to investigate the course of organ manifestations in pigs, rats, and mice using germ-free or specific pathogen-free experimental animals. Particular consideration will be given to the initial systemic vascular processes as well as to the significance of the erysipelas antigen. MATERIAL AND METHODS: In several experiments, a total of 166 pigs--partly gnotobiotic or specific pathogen-free animals--37 specific pathogen free Wistar rats and 57 albino mice were orally and/or parenterally infected with standardized erysipelas strains of serotype B. Clinical examination post infection were carried out with the EKG and by x-raying the joints of the extremities. All large parenchymatous organs, as well as heart valves, aorta and synovia were examined histologically in paraffin sections. In mice and rats, joints of the extremities were embedded in toto in metracrylate. Besides various histological staining methods, histochemical reactions were used to demonstrate mucopolysaccharides and fibrin. The myocardium, central nervous system and synovia of several joints were examined with the electron microscope. In the pig, immunohistological methods demonstrating the presence of fibrin, complement and IgG, as described by Seidler et al. (1971) and Trautwein et al. (1972), were used. RESULTS: The most important changes in joints, heart valves heart musculature and blood vessels occur during the early bacteriemic phase. A distinct sticking effect develops in the mouse 3.5 hours p.i., in the rat 24 hours p.i., and in the pig 36 hours p.i. Simultaneously, hyaline thrombi occur in capillaries and venules; these are seen as parallel, loosely-packed fibrin fibers in the electron microscope. With the aid of immunofluorescence fibrin, IgG and complement C3 can also be demonstrated here. Exudates rich in fibrin develop parallel to the microthrombosis. In pigs and rats vascular and myocardial necroses develop to 3 days p.i. The mice do not survive the 3rd p.i. 39% of the pigs showed edema and mesenchymal activation of varying intensity in the heart valves between the 3rd and 8th day p.i. Besides the insudation of the valves, endocardial thromboses developed in 80% of the mice. Endocarditis, aand in addition large aortic thromboses were recognized in more than 50% of the rats. As early as the 4th day p.i., coagulopathy, angionecrosis and exudation led to acute arthritic symptoms..

Animals↗
PubMed1975

[Experimental erysipelas in different species as a model for systemic connective tissue disease. II. The chronic phase with special reference to polyarthritis (author's transl)].

INTRODUCTION: In part I of this paper (Schulz et al., 1975) it was shown that in the initial phase of experimental erysipelas a transition from the vascular processes to a systemic connective tissue reaction can be demonstrated in different species. It is the purpose of this paper to describe the chronic phase of the disease with special emphasis on polyarthritis. MATERIALS AND METHODS: 12 spontaneously diseased and 22 experimentally infected pigs were used in experiments to study the pathogenesis of the disease. In addition, 74 Wistar rats and 148 Sprague-Dawley rats were used in the experiments. All experimental animals were specific-pathogen-free and were parenterally infected with the standardized E. insidiosa serotype B strain T 28. The observation period for the pigs was up to 2 years, for the rats up to 11 months. The methods used for pathohistological and electron microscopical studies are described in part I. Immunihistological studies were carried out on synovial tissue with peroxidase-conjugates of goat-anti-pig-IgG, goat-anti-pig-IgM, pig-collagen, E. insidiosa-homogenate and heat-aggregated-pig-IgG. Furthermore, goat-anti-pig-IgG and rabbit-anti-pig-C3 conjugated with FITC were used. Passive hemagglutination tests and Latex agglutination test (Singer and Plotz) were performed to demonstrate rheumatoid factors and collagen antibodies. RESULTS: Polyarthritis occurred in pigs between the 4th and 10th day p.i. and between the 4th and 8th day p.i. in nearly 100% of the infected rats. Fibrinous exudation, proliferation and destruction with pannus formation are marked in most of the joints examined during the first three months. Fibrosis begins 30 days p.i. in the rats' joints and is most severe in both species between the 5th and 8th month. 3 types of lining cells may be differentiated electron microscopically: A (M) cells, B (F) cells and an intermediate form which is found in both species most frequently. Swelling of the endothelial cells together with constriction of the lumen and thickening of the basal membrane occurs in the capillaries. DISCUSSION: A comparison of chronic erysipelas polyarthritis in pigs and rats with rheumatoid arthritis of men reveals many morphological and immunological similarities between the two diseases. Systemic connective tissue activation manifests itself in organs predilected for rheumatic changes, such as heart valves, endocardium and joints. The possible prepetuation of the processes by specific or nonspecific immunomechanisms or by deposits of fibrin is discussed. In addition, experimental erysipelas is reproducible in nearly 100% of the animals given one single subcutaneous application of one defined bacteria strain. Therefore too, erysipelas is suited as an animal model for human rheumatic diseases.

Animals↗
PubMed1975

[Neuraminidase neutralizing antibodies in pigs with chronic Erysipelothrix rhusiopathiae infection (author's transl)].

Investigating sera from pigs with chronic E. rhusiopathiae infection relative gamma-globulin values, agglutination titers, and neuraminidase-neutralizing humoral antibodies were determined at the 12th and 15th, 11th and 14th, and 3rd and 6th month after infection. We found increasing gammaglobulin values and increasing neuraminidase neutralizing antibodies but decreasing agglutination titers. Few animals don't have antibodies against neuraminidase and died during the observation period. Furthermore immunodiffusion test demonstrated precipitating lines of antibodies against living E. rhusiopathiae cells and active neuraminidase. No or very weak bands were observed against heat killed cells and heat-inactivated enzyme.

Agglutinins↗
PubMedDate not supplied

[Immunopathology and pathogenesis of chronic erysipelas polyarthritis of swine].

Several immuno-pathological aspects of polyarthritis following experimental infection with erysipelas in pigs were studied for two years. Aseptic and specifically pathogenfree animals were infected subcutaneously and intravenously-intraarticularly with living erysipeals bacteria (erysipelothrix rhusiopathiae) of serotype B. After an initial febrile phase a progressive polyarthritis and disco-spondylitis developed. Some animals also developed thrombo-endocarditis. Hypergammaglobulinemia and high titers of specific antibodies were observed during the whole experimental period. Antiglobulin factors, however, were not detected in the serum or the synovium. In some animals collagen antibodies were demonstrated in synovial tissue. Bacterial examination of the synovium showed that erysipelas bacteria were present in arthritic joints for months. Living erysipelas bacteria were isolated 24 months after the experimental infection from synovial tissue of two pigs. The polyarthritis was characterised by exudates rich in fibrin, villous proliferation, pannus formation, cartilage erosions, and peri-articular fibrosis. IgG and specific erysipelas antibodies were demonstrated in plasma cells from synovial tissue by immuno-histological methods. The findings emphasize the morphological resemblance of the erysipelas induced chronic polyarthritis in pigs to human rheumatoid arthritis.

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