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Biomedical subjects

W Baumgärtner

Publications and source records attributed to W Baumgärtner.

At least 73 records · Page 4Linked to original sources
PubMed1996

Multiple peripheral nerve sheath tumors in the small intestine of a horse.

Multiple neurofibromas, schwannomas, and hyperplastic enteric plexuses were observed in the distal jejunum and ileum of a 6-year-old pinto gelding. The animal was presented because of an acute episode of colic. Three meters of distal small intestine, partially incarcerated in the epiploic foramen, were surgically removed. Numerous tumor nodules up to 10 mm in diameter were found adjacent to a Meckel's diverticulum, predominantly located in the subserosa of a hypertrophic segment. Histologically, tumors were well demarcated and composed of interlacing fascicles formed by spindloid cells. Adjacent enteric plexuses were hyperplastic. Immunohistochemically, all tumors were positive for vimentin and S-100. Desmin immunoreactivity was only observed in larger tumors (> 500 microns). Glial fibrillary acid protein was demonstrated nearly exclusively in smaller ones. Immunostaining for neurofilament was restricted to entrapped ganglion cells. Based on conventional light microscopic examination and immunohistochemical evaluation, the lesion was diagnosed as multiple benign peripheral nerve sheath tumors in the small intestine.

Animals↗
PubMed1996

[A case of necrotizing meningoencephalitis in a pug dog (pug dog encephalitis--PDE)].

A three-year-old female pug dog was euthanized because of recurrent seizures. Pathological examination revealed severe multifocal necrosis confined to the cerebrum. Histologically, areas of malacia of different stages, with prominent gitter cell infiltration were observed. Furthermore, there was severe rarefication resulting in cavities separated by tissue bridges and blood vessels. In the adjacent tissue and in the meninges a moderate to severe non-purulent meningoencephalitis was evident. The lesions are consistent with those reported for pug dog encephalitis (PDE). In the present paper, the first case of PDE in Germany is described and an overview of the clinical symptoms, the neuropathological findings of this etiologically unknown disease, the differential diagnoses and the possible pathogenesis is given.

Animals↗
PubMed1995

Distemper in wild carnivores: an epidemiological, histological and immunocytochemical study.

Brain tissue from 236 wild carnivores, 146 mustelids and 90 foxes, originating from the same geographical area in southwest Germany was collected over a 2 year period between May 1989 and May 1991 and studied for the presence of canine distemper virus (CDV) antigen by immunohistochemistry. CDV antigen was found in the brains of 54 (37%) mustelids, predominantly in the cerebellar grey matter. Interestingly, no CDV infection was observed in foxes. An increasing number of CDV infections among mustelids was noted between November 1989 and November 1990, peaking in summer 1990. Histological brain lesions, demonstrated only in 45% of the CDV positive mustelids, were characterized by non-purulent encephalitis predominantly in the cerebrum and focal vacuolation of the cerebellar white matter, whereas demyelination was only rarely observed. Histological and immunocytochemical CNS findings indicate an early stage of distemper infection in these mustelids and the high percentage of CDV positive animals together with the seasonal prevalence are suggestive of a CDV epizootic among mustelids.

Animals↗
PubMed1995

Metaphyseal bone lesions in young dogs with systemic canine distemper virus infection.

Bone lesions, restricted to the metaphyses of long bones, were observed in young dogs with systemic distemper following experimental and spontaneous infection. Canine distemper virus (CDV) antigen was found immunocytochemically in hematopoietic marrow cells, osteoclasts, osteoblasts and rarely in osteocytes. In experimentally infected dogs, viral antigen was demonstrated in the metaphysis between 5 and 36 days after infection. Associated lesions, characterized by necrosis of osteoclasts, persistence of primary spongiosa and atrophy and necrosis of osteoblasts and marrow cells, were mild and most prominent between 8 and 32 days postinfection. Metaphyseal osteosclerosis (MO) of the long bones, varying from mild to severe, was observed macroscopically in 8 (19%) out of 42 dogs with spontaneous distemper. Affected animals were between 3 and 6 months of age and belonged mainly to the large breeds. In these animals, MO was characterized histologically by persistence of primary spongiosa, loss of bone marrow cells and necrosis of osteoclasts and bone marrow cells varying from mild to severe. Summarized, CDV-associated bone lesions were only transient and there were no indications of viral persistence in bones of dogs experimentally infected with CDV. Although no clinical signs related to the bones were observed, the present study reveals that infection of metaphyseal bone cells is common in young dogs with systemic distemper and occurrence of viral antigen in these cells results in defects in bone modelling.

Animals↗
PubMed1995

Round cell sarcomas of possible myelomonocytic origin localized at the lip of aged dogs.

Four round cell tumors, situated at the lip of dogs older than 4 years of age, which could not be further classified, were examined light and electron microscopically, immunocytochemically and in part functionally and cytochemically. Immunocytochemically they were positive for vimentin, but negative for cytokeratin, desmin, neurofilament, synaptophysin, S-100 protein, neuron specific enolase, lysozyme, IgG and a pan-T-cell marker. Cell lines were established from two malignant neoplasms. In vitro, neoplastic cells had morphological, functional and cytochemical properties of myelomonocytic cells. A tumor cell-specific polyclonal rabbit antiserum reacted immunocytochemically positive with primary and recurrent tumors and metastases of the original and the three other round cell tumors. Immunoblotting demonstrated a main band with approximately 65-75 kDa. All four tumors were present in aged dogs and metastasized. They most likely represent a distinct group of malignant tumors among the canine round cell tumors.

Aging↗
PubMed1995

Histologic and immunocytochemical characterization of canine distemper-associated metaphyseal bone lesions in young dogs following experimental infection.

The proximal metaphyses of the humerus of weanling gnotobiotic dogs experimentally infected with canine distemper virus (CDV) were investigated histologically and immunocytochemically between 4 and 41 days after infection. Viral antigen was demonstrated in hematopoietic marrow and bone cells at postinfection day (PID) 5 and PID 7, respectively. Between PID 8 and 27, CDV antigen was abundantly present in marrow cells, osteoclasts, and osteoblasts and less frequently in osteocytes. Immunopositive cells in both osseous tissues and bone marrow declined between PID 29 and PID 36 and were absent by PID 41. Chondrocytes of the growth plate were negative for viral antigen throughout the observation period. In bone, viral antigen was more frequently observed in bone cells of the primary spongiosa than in the secondary spongiosa. There was a strong correlation between occurrence of CDV antigen and osseous changes. Associated metaphyseal bone lesions were mild and most prominent between PID 8 and PID 32. Lesions consisted of necrosis of osteoclasts, which was associated with subsequent persistence of the primary spongiosa (growth retardation lattice). Atrophy and necrosis of osteoblasts and marrow cells were also noted. Infection of metaphyseal bone cells appears to be common in young dogs with experimental systemic distemper. Bone cell infection is preceded by infection of marrow cells, and infected bone cells may experience degeneration and necrosis. This subtle viral effect may result in defects in bone modeling in CDV-infected dogs.

Animals↗
PubMed1995

[Detection of distemper virus N protein RNA in the brain of dogs with spontaneous distemper encephalitis using a digoxigenin-labeled, double-stranded DNA probe for in situ hybridization].

A digoxigenin-labelled dsDNA-probe of 287 basepairs length complementary to the nucleoprotein-gene of canine distemper virus (CDV) was generated by the polymerase-chain-reaction. The dsDNA-probe hybridized specifically with base sequences of 8 different CDV strains, whereas no hybridization was observed with a porpoise and a canine parainfluenza virus and only a weak signal was obtained with measles virus. In formalin-fixed, paraffin-embedded brain sections of 35 immunohistologically CDV antigen positive dogs with spontaneous distemper encephalitis CDV-RNA could be detected in 25 cases by in situ hybridization. The reason for the lack of RNA detection in some immunohistologically positive dogs may be due to the low stability of DNA-RNA-hybrids. Degradation of RNA by RNAses or diffusion out of autolysed cells can not be excluded.

Animals↗
PubMed1994

Characterization of a reovirus isolate from a rattle snake, Crotalus viridis, with neurological dysfunction.

A virus isolate from the brain of a rattle snake with central nervous system (CNS) symptoms was identified as a reovirus. The isolate did not agglutinate pig erythrocytes and was not neutralized by antisera against avian reovirus S1133 and mammalian reovirus type 3. The cytopathic effect in Vero cells was characterized by formation of syncytial giant cells. Electrophoretic analysis of the genome revealed 10 segments of dsRNA. The isolate displayed characteristics distinct from avian and mammalian reoviruses.

Animals↗
PubMed1994

Valvular endocarditis occurs as a part of a disseminated Coxiella burnetii infection in immunocompromised BALB/cJ (H-2d) mice infected with the nine mile isolate of C. burnetii.

BALB/cJ (H-2d) mice were injected intraperitoneally (ip) with cyclophosphamide 2 days after ip inoculation with Coxiella burnetii Nine Mile, phase I. Ten days after infection, disseminated microabscesses, granulomas, and microthrombi were observed in most organs, including spleen and liver, and in bone marrow. In addition, endocarditis of the atrioventricular and semilunar valves, characterized by macrophages and neutrophils, was present. At the same time, C. burnetii antigen was found in most organs and in cardiac valves, aorta, and pulmonary artery, mainly within macrophages, neutrophils, and endothelial cells. C. burnetii-specific IgG antibodies were detected 150 days after infection but not in the early phase of infection. Cardiac valves were devoid of C. burnetii antigen and without residual lesions at 150 days. These findings offer the possibility for further studies on the pathogenesis of C. burnetii-associated valvular endocarditis and show that acute strains of C. burnetii can cause endocarditis as a part of a disseminated infection in the immunocompromised host.

Animals↗
PubMed1993

Restricted expression of viral surface proteins in canine distemper encephalitis.

Sixteen dogs with naturally occurring acute and chronic canine distemper virus (CDV) encephalitis were examined immunohistochemically for the presence of the five major CDV-specific proteins in the central nervous system. Monoclonal antibodies (mAbs) directed against two, three, four and five epitopes of the nucleo- (N), phospho- (P), fusion (F), and hemagglutinin (H) protein, respectively, and a polyclonal monospecific antibody recognizing the matrix (M) protein were used. Both core proteins and their epitopes, three F protein epitopes and the M protein were demonstrated in all animals examined. A fourth F protein epitope was found only in 13 animals. The H-2 and H-3 epitope of the H protein were detected in 15, the H-1 and H-5 epitope in 14, and the H-4 epitope in 3 animals. All viral proteins were observed in the same types of brain cells including neurons and astrocytes. The N and P protein were demonstrated in nucleus, cytoplasm and cell processes, whereas M, H and F protein were observed in the cytoplasm only and rarely in cell processes. In addition, the M protein was detected occasionally in the nucleus of neurons and reactive astrocytes. Intralesional distribution of CDV-specific proteins varied between core and surface proteins. In acute and subacute lesions without associated inflammation, expression of the M, H and F protein was only slightly diminished compared to the N and P protein. However, plaques with severe inflammation were either devoid of viral antigen or exhibited N- and P protein-specific immunoreactivity exclusively at the periphery, whereas expression of surface proteins was severely reduced or absent. These results are suggestive of restricted synthesis of CDV envelope proteins in acute, and more prominent in chronic, distemper encephalitis.

Animals↗
PubMed1993

In vivo and in vitro expression of canine distemper viral proteins in dogs and non-domestic carnivores.

The occurrence of the nucleo-, phospho-, matrix, fusion, and hemagglutinin proteins of the canine distemper virus (CDV) was investigated immunocytochemically in the brains of 3 dogs, 6 stone martens, 1 polecat, and 1 weasel. In addition, viral protein expression was studied in primary brain cell cultures of the 3 dogs after co-cultivation with Vero cells. Immunohistochemically, only minor differences, restricted to the H-4 epitope, were noted between the various species and CDV isolates. The data presented indicate that the mustelid virus is antigenically not distinct from the canine morbillivirus.

Animals↗
PubMed1993

Spread and distribution of Coxiella burnetii in C57BL/6J (H-2b) and Balb/cJ (H-2d) mice after intraperitoneal infection.

Spread and distribution of Coxiella burnetii were investigated immunocytochemically and antigen dissemination was correlated with light microscopic alterations in Balb/cJ (H-2d) and C57BL/6J (H-2b) mice. Intraperitoneal inoculation of C. burnetii resulted in a self-limiting systemic infection. Gross findings consisted of hepatosplenomegaly and histological lesions were characterized by microabscesses and granulomas in numerous organs including spleen, liver, mesentery, bone marrow, lymph nodes, pancreas, heart and uterus. In addition, splenic lymphoid depletion, venous microthrombi and reduction of bone marrow cells were observed. Coxiella burnetii antigen was demonstrated immunocytochemically in the aforementioned organs, especially in spleen, liver and most of all in the bone marrow. Coxiella antigen was detected in macrophages, macrophage precursor cells, and occasionally endothelial cells. Numerous C. burnetii antigen-positive cells were observed between 5 and 12 days post-infection; thereafter, the amount of C. burnetii antigen decreased rapidly. Immunopositivity was detectable until 30 and 44 days post-infection in the bone marrow of Balb/cJ and C57BL/6J mice, respectively. Severity of histological lesions was associated with presence and clearance of C. burnetii antigen. Specific IgM antibodies were detected 4 days after infection and IgG seroconversion was noticed 7 to 10 days post-infection. Coxiella burnetii-specific IgM and IgG antibodies were still present 150 days after infection. Significant strain-specific differences in the antibody response were not found. The findings demonstrate systemic spread of C. burnetii, especially to bone marrow, spleen and liver, and antigen distribution was closely correlated with the appearance and degree of histological lesions.

Animals↗
PubMed1993

Immunocytochemical demonstration of Coxiella burnetii antigen in the fetal placenta of naturally infected sheep and cattle.

Coxiella burnetii antigen was demonstrated immunocytochemically in the placental tissues of aborted fetuses from four cows and two ewes and from one full-term calf. Antigen was observed in cytoplasmic vacuoles of trophoblasts, especially along the base of the chorionic villi. Positive trophoblasts were of normal size or exhibited striking cytoplasmic enlargement. Antigen was also demonstrated in neutrophils, degenerated cells and extracellularly in the intervillous spaces. The chorioallantoic connective tissue, allantoic surface and fetal tissues were devoid of C. burnetii antigen. Ovine placentas showed strong coxiella-specific staining and histological lesions characterized by moderate to severe, multifocal, necrotizing and purulent inflammation. In bovine placentas, the number of immunopositive cells varied from few to moderate and changes were mild or absent. Placental vasculitis consisting of infiltrating mononuclear cells, neutrophils or eosinophils was observed in both of the ovine and two of the bovine fetuses. In addition, a few intravascular thrombi were observed in one ovine and one bovine placenta. Thus the ovine coxiellosis cases were associated with an abundant accumulation of C. burnetii antigen and with severe necrotizing purulent placentitis, whereas in bovine coxiellosis the lesions were mild or absent and the number of organisms demonstrated immunocytochemically was much smaller. These results suggest a relation between species, lesion severity and weight of infection.

Animals↗
PubMed1992

Canine distemper infection associated with acute nervous signs in dogs.

Eight vaccinated dogs suddenly developed progressive ataxia, paresis or paralysis of short duration. A histopathological examination revealed a non-suppurative meningoencephalitis suggestive of a viral infection, and immunohistochemical examination confirmed the presence of canine distemper virus antigen in five of the dogs. Distemper had not been suspected from the clinical examination of the dogs.

Acute Disease↗
PubMed1992

Histological and immunocytochemical characterization of Coxiella burnetii-associated lesions in the murine uterus and placenta.

The fetoplacental units and the postgravid uterus of BALB/cJ (H-2d) mice inoculated intraperitoneally with Coxiella burnetii (Nine Mile isolate, phase I) on day 6 of pregnancy were examined histologically and immunocytochemically at 1 to 160 days postinoculation. Clinically, abortions, stillbirths, and perinatal deaths were observed. Histological lesions in the placenta were characterized by severe necrosis of the decidua basalis and the labyrinth, fibrinoid degeneration of decidual vessels, and microthrombosis. Pyometra and endometritis at the sites of previous placental attachment, characterized by ulceration, central necrosis, and moderate cellular infiltration consisting of neutrophils and macrophages, were observed postpartum. Pups sacrificed at the age of 9 days exhibited interstitial pneumonia with few granulomas and granulomatous hepatitis and splenitis. Immunocytochemically, antigen-bearing cells were first detected in the decidua 9 days postconception, and single immunopositive cells were detected in the fetal placenta 4 days later. Thereafter, until abortion or parturition, abundant accumulation of C. burnetii antigen was observed in the maternal and fetal compartments of the placenta. Up to 28 days postinoculation, many immunopositive cells were demonstrated at the sites of previous placental attachment, whereas the adjacent endometrium contained only a few antigen-positive cells. C. burnetii antigen was demonstrated in decidual cells, trophoblasts, and macrophages and extracellularly within the sinuses of the labyrinth and in the uterine lumen but not in granulated metrial gland cells. Fetuses in utero and aborted, stillborn, or perinatally dying offspring were immunocytochemically negative for C. burnetii antigen; however, pups killed 9 days after birth showed lesion-associated positive immunoreaction in the lung, liver, and spleen. The present study shows that infection with C. burnetii during pregnancy results in uncontrolled growth of the organism in the murine uteroplacental unit and that associated lesions are characterized by necrosis of placental tissues, fibrinoid degeneration of decidual vessels, and microthrombosis.

Animals↗
PubMed1992

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.

Animals↗