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Biomedical subjects

M Vandevelde

Publications and source records attributed to M Vandevelde.

At least 127 records · Page 7Linked to original sources

Immunological and pathological findings in demyelinating encephalitis associated with canine distemper virus infection.

Nine dogs with canine distemper encephalitis (CDE) were examined with immunological techniques including demonstration of antibodies against canine distemper virus (CDV) in the serum and against myelin basic protein (MBP) in serum and in CSF. Mitogen stimulation tests of lymphocytes were also done. The brains were examined pathologically and immunoglobulin and C3 were demonstrated in lesions by means of immunohistological techniques. Six dogs with acute CDE had none or low antibody levels against CDV or MBP, and there was no immunoglobulin in demyelinating lesions. Some of these dogs had depressed lymphocyte mitogen responses. Two dogs with chronic CDE showed recovery of lymphocyte mitogen responses. One of these had a significant antibody response against CDV and MBP in the serum. Both dogs with chronic CDE had very high antibody titers against MBP in the CSF and demyelinating lesions contained immunoglobulin. These results suggest that acute demyelination in CDE is probably due to some direct viral activity and that the progression of demyelination in chronic CDE is associated with a local immune response.

Animals↗

Hereditary neurovisceral mannosidosis associated with alpha-mannosidase deficiency in a family of Persian cats.

Several kittens in a family of Persian cats had a metabolic storage disease. Clinically the disorder was characterized by hepatomegaly, neurological signs and early death. The microscopic lesions consisted of widespread vacuolation of neurons and glial cells in the central nervous system and in liver cells. Electronmicroscopically the lesions consisted of intracytoplasmic accumulation of membrane-bound "empty" vacuoles. In addition to the storage disease, poor myelination of the cerebral white matter was found. The defect was reproduced in breeding trials. On biochemical analysis of brain tissue, deficient function of the enzyme alpha-mannosidase was detected. The clinical and pathological features of mannosidosis in Persian cats were compared to similar defects in other species.

Animals↗

Canine lymphocyte cultures in vitro: evaluation of peripheral blood lymphocyte response to mitogens.

Lymphocytes from dog peripheral blood have been stimulated in vitro with 3 different mitogens (Con A, PHA and PWM). Culture medium was RPMI 1640 enriched with either autologous plasma, fetal calf serum of a newly described defined serum substitute. In such cultures the number of surviving and activated cells was measured by cytofluorometry and the proliferation was assessed by thymidine incorporation. In unstimulated cultures, up to 70% of all cells had disappeared (died) during the first 42 hours of incubation, whereas the number of viable cells was reduced to 50-60% in mitogen stimulated cultures. Of the surviving lymphocytes, between 25-40% of the cells appeared to have an elevated RNA-content (activated or G1 cells). By comparison between thymidine incorporation and number of mitogen induced G1 cells, a very high correlation was found (r=0.92). However, the Slope of the regression line was much lower than expected. The low thymidine incorporation per activated cell was primarily related to the high cell death and a resulting dilution of tritiated thymidine. Indeed, preliminary results suggested that the same thymidine incorporation per G1b cells could be obtained if peripheral blood lymphocytes were washed immediately before pulsing as could be obtained with lymph node cells without washing.

Animals↗

Technical aspects of low 3H-thymidine incorporation by mitogen stimulated canine peripheral blood lymphocytes in vitro.

The value of [3H]-thymidine incorporation as a measurement for mitogen induced proliferation of dog peripheral blood lymphocytes (PBL) has been examined. The cells were cultured in RPMI 1640, enriched with 10% autologous plasma for 48 hours at 37 degrees C, 5% CO2 and 95% relative humidity. Under these conditions a great variability in [3H]-thymidine incorporation was observed. By analysis of CPM and number of activated cells (G1), it was found that comparable number of G1 cells were generated in human and dog PBL. Also, the membrane transport of thymidine was very similar for lymphocytes of the two species. Nevertheless, a low [3H]-thymidine incorporation by dog PBL was frequently seen, and this phenomenon could be related to a release of soluble substance(s) within the cultures. When the cultured cells were washed and resuspended in fresh medium immediately before pulsing, the expected CPM per G1 cell could be obtained. Since it has been described in the literature that macrophages can produce cold thymidine in macrophage enriched lymphocyte cultures, the in vitro response of non-adherent dog PBL was analyzed. Mitogen stimulation of such non-adherent cells resulted in CPM per G1 cells very similar to those obtained with washed cells. Based on these data, it is suggested that the production of cold thymidine might be one of the technical problems related to cultures of lectin stimulated dog PBL in vitro and it should be taken into consideration, if [3H]-thymidine incorporation is used as the only measure of lymphocyte proliferation.

Adult↗

Immunoglobulins in demyelinating lesions in canine distemper encephalitis. An immunohistological study.

The brains of 14 dogs with canine distemper encephalitis were examined with immunohistologic techniques to search for immunoglobulin in demyelinating lesions. Four types of lesions presumably representing a temporal sequence of lesion development were distinguished. Immunohistologic findings included immunoglobulin bearing lymphoid cells, amorphous Ig containing material, immunoglobulin bound to the tissue and immunoglobulin containing macrophages and astrocytes. The humoral immune response was absent or very minimal in acute lesions and very intense in chronic lesions. It was concluded that early demyelination in canine distemper encephalitis occurs in the absence of a local humoral immune response but that this response may aggravate and accelerate myelin destruction in the later stages of the disease.

Acute Disease↗

Dysmyelination in Chow Chow dogs: further studies in older dogs.

The ultrastructure of myelin deficiency in Chow Chow dogs was studied in the spinal cord of a 15-month-old and a 3-year-old animal. It was found that myelination progresses with age in these dogs but is still deficient at the age of 3 years. The findings included axons with thin or uncompacted myelin sheaths, separated from each other by massive astrocytosis, and bizarre myelin formations. Normal numbers of morphologically normal oligodendrocytes were present in the myelin-deficient areas. The disease in these Chow Chow dogs consists of a strongly retarded myelination which is possibly due to a dysfunction or delay in glial maturation.

Animals↗

Non-suppurative encephalomyelitis in cats suggestive of a viral origin.

In 10 of 16 domestic cats with spontaneous non-suppurative encephalomyelitis, lesions were multifocal but relatively few and were considered nonspecific as to cause, although viral agents could not be excluded. Six cats had polioencephalomyelitis or polioencephalitis suggestive of viral infection. The clinical and morphological features are compared with those of previous reports of feline encephalitis possibly of viral origin. Some previously reported epidemiological and serological surveys suggest a possible role for arboviruses.

Animals↗

Necrotizing vasculitis in the central nervous systems of two dogs.

Two dogs with rapidly progressing paralysis had polyarteritis involving medium-sized to large arterioles and small arteries of the spinal meninges. Rupture of structurally weakened vessels caused massive hemorrhage with compression and infarction of the spinal cord. The cause of the vasculitis was not determined.

Animals↗

Immunohistological studies on primary reticulosis of the canine brain.

Brains of 17 dogs with primary reticulosis, and of two with metastatic and one with primary lymphosarcoma, were examined by immunohistologic techniques with antisera against the major immunoglobulin classes of the dog. On the basis of immunoglobulin in tumour cells, two reticuloses were reclassified as primary lymphosarcomas of the brain. The tumour cells in three other dogs with neoplastic reticulosis and in six dogs with microgliomatosis did not contained immunoglobulin. Many cells in inflammatory reticulosis were immunoglobulin-bearing. Although some of these lesions could have been lymphosarcomas, insufficient data were available to ascertain either an inflammatory or a neoplastic nature. It was concluded that some lesions previously classified as reticulosis are in fact primary histiocytic lymphosarcomas of the brain, while others may be true reticulosarcomas.

Animals↗