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Biomedical subjects

E M Chester

Publications and source records attributed to E M Chester.

10 recordsLinked to original sources

Comparative serological evaluation of 10 Blastomyces dermatitidis yeast phase lysate antigens from different sources.

Yeast phase lysate antigens from 10 isolates of Blastomyces dermatitidis (dog, ERC-2 and T-58; T-27, polar bear; woodpile, ER-3; bat lung, 48938; human, B5929, B5895, B5896, B5931, and CAPP) from different geographical regions, in addition to a Histoplasma capsulatum (G217B) lysate preparation were compared with respect to their reactivity against serum specimens from dogs, rabbits and humans positive for blastomycosis using an indirect enzyme-linked immunosorbent assay. In addition, the lysate antigens were also assayed against histoplasmosis-positive human serum samples to study their cross-reactivity. Variable results were obtained with T-58 and T-27 exhibiting the greatest reactivity. We also noticed that the lysate did not react consistently to serum samples across species with lesser reactivity evidenced when testing dog sera. Finally, T-58 gave the highest cross-reactivity with histoplasmosis-positive sera. The study may prove valuable in the development of antigen candidates for blastomycosis serodiagnosis.

Animals↗

Blastomyces dermatitidis lysate antigens: antibody detection in serial serum specimens from dogs with blastomycosis.

Yeast phase lysate antigens prepared from different isolates of Blastomyces dermatitidis (T-58, dog-Tennessee; T-27, polar bear-Tennessee; ERC-2, dog-Wisconsin; ER-3, woodpile-Wisconsin) were compared with respect to the detection of antibodies (indirect enzyme-linked immunosorbent assay-ELISA, peroxidase system) in 126 serial serum specimens (pre-treatment, 30 and 60 days post-treatment with itraconazole) from 42 dogs with diagnosed blastomycosis. Mean absorbance values observed with the four lysate antigens at the three treatment intervals ranged from the most reactive to the least reactive as follows: T-58 (0.270, 0.210, 0.136); T-27 (0.209, 0.156, 0.096); ER-3 (0.189, 0.144, 0.089) and ERC-2 (0.158, 0.129, 0.080). Even though variations in reactivity were evidenced, the lysates prepared from isolates from various geographical regions and sources were all efficacious as antigens for the immunodiagnosis of canine blastomycosis.

Animals↗

Retinal abnormalities associated with anemia.

The incidence of clinically apparent retinal changes in 35 anemic patients and 35 age- and sex-matched control subjects was studied. Retinal photographs of all subjects were obtained. From these, all vascular and extravascular retinal lesions were noted. No retinal abnormalities were observed in the control subjects. Seven (20%) of the anemic patients exhibited extravascular lesions. There was no relationship detected between the occurrence of these changes and the severity or the cause of the anemia. Employing the assumption that true venous length for a given net distance traveled correlates with the degree of venous tortuosity, venous length over a standard radial distance from the optic disc was assessed with a curvometer. A significant negative correlation was determined between venous length and the level of hematocrit, thereby implying that retinal venous tortuosity is directly related to severity of anemia.

Adolescent↗

Optic atrophy in experimental vitamin B12 deficiency in monkeys.

The clinical findings and pathological changes of the visual pathway of vitamin B12 deficient monkeys have been described. The cellular morphology and counts of the peripheral blood and bone marrow remained normal during the study (nine deficient, three controls: one still alive in each group). Visual impairment was noted in all seven of the deficient animals that were evaluated by clinical observations. Ophthalmoscopic examination disclosed optic atrophy in six of the seven deficient monkeys. Degeneration of the visual pathway was demonstrated by pathological examination in eight of the deficient group of nine (one is still alive). Loss of ganglion cells was noted in the maculae of two of three deficient animals with completed studies. In the three control animals there were neither visual disturbances nor ophthalmoscopic changes and in two animals autopsies disclosed no lesions in the visual pathways. The third animal is still alive and well.

Animals↗

An ultrastructural study of subacute combined degeneration of the spinal cord in vitamin B12-deficient rhesus monkeys.

Prolonged deprivation of vitamin B12 in rhesus monkeys produced changes in the central nervous system that were indistinguishable topographically and histologically from those of human subacute combined degeneration. Ultrastructural studies of early lesions of the spinal cord disclosed a degeneration of myelin characterized by separation of myelin lamellae and formation of intramyelinic vacuoles, leading eventually to complete destruction of myelin sheaths. At a later stage, there was degeneration and loss of axons, and marked gliosis. The theories of pathogenesis of subacute combined degeneration are reviewed in the light of these observations.

Animals↗

Hypertensive encephalopathy: a clinicopathologic study of 20 cases.

The clinical and pathologic findings in 20 patients with hypertensive encephalopathy were reviewed. The dominant central nervous system (CNS) symptoms were altered state of consciousness and severe headache. Nausea, vomiting, and visual disturbances were less common. Seizures and focal signs were infrequent. The changes seen were invariably accompanied both by the characteristic ophthalmoscopic alterations of malignant hypertension and by uremia. The neuropathologic changes consisted of severe vascular alterations (fibrinoid necrosis of arterioles, thrombosis of arterioles and capillaries), and of parenchymal lesions (microinfarcts, petechial hemorrhages) secondary to the vascular lesions. The vascular changes were not confined to the brain but were diffuse, affecting the eyes, kidneys, and other organs. In the CNS the brainstem was most severely affected. Cerebral edema was not observed, even in those patients who had increased cerebrospinal fluid pressure and papilledema.

Adult↗

Neuropathology of experimental vitamin B12 deficiency in monkeys.

We have produced severe vitamin B12 deficiency in rhesus monkeys by feeding them a defined experimental diet under controlled conditions. Five years after institution of the deficient diet, the morphology and counts of peripheral blood and bone marrow are normal. Gross visual impairment appeared in five of the monkeys between 33 and 45 months after the institution of the vitamin B12 deficient diet. Subsequently, in three of the visually impaired animals, a gradually progressive spastic paralysis of their hind limbs developed. Autopsies of six deficient animals showed degeneration of the peripheral visual pathway in all and of white matter in the spinal cord in four. Degeneration of several cranial nerve roots was found in four monkeys and a mild diffuse degeneration of cerebral white matter in four. The lesions in all affected parts of the central nervous system were bilaterally symmetrical and were indistinguishable from those due to B12 deficiency in the human. No abnormalities were found in one B12 supplemented control animal.

Animals↗