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Biomedical subjects

B Durchfeld

Publications and source records attributed to B Durchfeld.

7 recordsLinked to original sources

Experimental epididymitis due to Chlamydia trachomatis in rats.

A new animal model of epididymitis due to Chlamydia trachomatis was developed. Adult male Wistar rats were inoculated in the vas deferens with C. trachomatis biovar mouse pneumonitis. After infection, C. trachomatis was recovered from the epididymides for up to 90 days. At day 30, organisms were also reisolated from the testes. Clinical findings included enlargement of infected epididymides and concurrent atrophy of the ipsilateral testes. Histological lesions in the epididymides consisted of pyogranulomatous inflammation, abscesses, and spermatic granulomas. Infection of the testis by C. trachomatis was associated with pyogranulomatous changes. In addition, testicular degeneration, characterized by moderate to severe loss of the germinal epithelium, was noted. Chlamydial antigen was detected within epithelial cells, intratubular macrophages, and macrophages in the stroma of the epididymis by immunoperoxidase staining. This rat model of chlamydial epididymitis appears to clinically and histopathologically mimic the human disease. This model offers the opportunity for further studies on the pathogenesis and sequelae of chlamydial epididymitis.

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Intranasal infection of ferrets (Mustela putorius furo) with canine parainfluenza virus.

Immunocompetent and cyclophosphamide-immunosuppressed ferrets were intranasally infected with canine parainfluenza virus (CPIV) and observed for clinical signs, histopathologic lesions, the immunocytochemical demonstration of CPIV antigen in the respiratory tract and scanning electron microscopic alterations of the tracheal epithelium until 36 days post infection (p.i.). In both groups, clinical signs were minimal, restricted to the upper respiratory tract and consisted of cough elicited by tracheal compression between 3 and 7 days p.i. Microscopically, inflammatory and degenerative lesions were observed in the trachea and less frequently in the nasal cavity; bronchiolitis or interstitial pneumonia was not demonstrated. By immunocytochemistry, CPIV antigen was demonstrated in tracheal epithelial cells, whereas nasal cavity, bronchi, bronchioles and lung were devoid of viral antigen. Ferrets given CPIV alone developed a minimal lymphocytic tracheitis with minimal loss of cilia and CPIV antigen was observed only 4 days p.i. 17 days p.i., normal epithelial organization and ciliary reappearance was reestablished. Ferrets treated with cyclophosphamide and infected with CPIV exhibited mild to moderate histological lesions as above with similar scanning electron microscopic changes until 36 p.i. Tracheal lesions consisted of intraepithelial and submucosal infiltration of lymphocytes and macrophages, focal epithelial hyperplasia and multifocal loss of cilia. In addition, mild and transient neutrophilic infiltration was observed. In immunosuppressed ferrets, viral antigen expression was prominent and demonstrated 4 and 8 days p.i. These data suggest that ferrets are susceptible to aerosol CPIV infection.

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In vitro cytopathogenicity and in vivo virulence of two strains of canine parainfluenza virus.

In vivo and in vitro properties of two strains of canine parainfluenza virus (CPIV) were investigated. One strain, designated CPIV(+), induced syncytial giant cell formation and cytolysis in vitro, whereas the second strain, CPIV(-), caused only a mild strand-forming cytopathic effect with few, small syncytial giant cells. Vero cells infected with CPIV(+) or CPIV(-) were 100% positive for CPIV antigen as determined by immunofluorescent staining; however, 100% of CPIV(+) and less than 10% of CPIV(-) infected cells were hemadsorption positive. Sodium dodecyl sulphate-polyacrylamide gel electrophoresis analysis revealed no differences in electrophoretic mobility of viral polypeptides between both strains; however, in CPIV(-), reduced or absent synthesis of the putative HN and F1 proteins was observed. Isopycnic separation of CPIV(+) progeny virions showed a high proportion of viral particles with a buoyant density of 1.18 g/cm3. In contrast, CPIV(-) progeny virions had a heterogeneous density profile ranging from 1.08 to 1.18 g/cm3. Intracerebral infection of six ferrets with CPIV(+) resulted in moderate lymphocytic and histiocytic choroiditis, meningitis, and ependymitis, whereas CPIV(-) infection caused only mild to moderate inflammation. Immunohistologically, CPIV antigen was prominent in ependymal lining cells of the ventricles in CPIV(+)-infected ferrets and was reduced or lacking in CPIV(-)-infected ferrets (n = 6). Sham-injected ferrets (n = 6) did not have histologic lesions and no viral antigen was identified. The present findings suggest that certain changes in the activities of CPIV glycoproteins may lead to alterations of CPIV virulence in vivo.

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Vaccine-associated canine distemper infection in a litter of African hunting dogs (Lycaon pictus).

Four, 57 days old, African hunting dog puppies (Lycaon pictus) from one litter died within three weeks following vaccination with modified-live canine distemper virus (CDV) and killed canine adenovirus type 1, canine parvovirus and Leptospira icterohemorrhagiae and canicola. 18 days post vaccination, the animals developed neurologic disease characterized by episodes of grand mal seizures and circling. Macroscopic, histological and immunohistochemical studies revealed acute systemic CDV infection with acute encephalopathy. Virus isolation attempts using primary dog kidney cells, lung macrophages and Vero cells were negative. Therefore, the question whether the infection was the result of vaccination or natural infection remains open. The benefits and risks regarding the use of modified-live CDV vaccines and killed canine distemper vaccines in exotic carnivores are briefly discussed.

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[Accidental thymus involution in calves].

In 149 necropsied calves (age 0 to 28 days) a reduced thymus was found. The absolute thymus weights varied between 6 and 220 g. The relative thymus weights (applied to bodyweight) were between 0.02 and 0.52% (healthy controls 0.24 to 0.67%). The histological changes resemble those of accidental thymus involution. Corresponding to the duration of the disease and/or loss of body weight of the animals there is an increase of lymphocyte depletion. The accidental thymus involution is presumed to be a morphological expression of a secondary immunodeficiency.

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