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Biomedical subjects

B C West

Publications and source records attributed to B C West.

At least 37 records · Page 2Linked to original sources
PubMed1992

Blastomycotic cranial osteomyelitis.

This is the second case report of a temporal bone osteomyelitis caused by Blastomyces dermatitidis, which presented as a chronic serous otitis media. The presenting serous otitis media was refractory to conventional medical and surgical management and progressed to a temporal bone osteomyelitis prior to diagnosis. B. dermatitidis is a rare fungal pathogen that causes a systemic pyogranulomatous disease that primarily manifests itself in the skin, bones, pulmonary, and genitourinary systems. If left untreated it is associated with a high rate of mortality. The otologic presentation of this rare disease is emphasized, while the clinical and therapeutic features are reviewed.

Adult↗
PubMed1988

Leprosy in six isolated residents of northern Louisiana. Time-clustered cases in an essentially nonendemic area.

Northern Louisiana has been essentially free of indigenous leprosy, and now it is not. Six new cases of leprosy have been diagnosed: three in 1986, the other three in 1985, 1983, and 1982, respectively. The patients had been lifelong residents of six scattered rural parishes. Leprosy had never been reported from five of them. No patient had had contact with human leprosy. The patients were white; four were women; the mean +/- SD age at onset was 60.3 +/- 16.4 years (age range, 31 to 80 years); and the mean +/- SD interval to diagnosis was 1.2 +/- 1.4 years. One patient had Hodgkin's disease at the age of 25 years and leprosy at the age of 31 years; another patient had cervical carcinoma. All rural northern Louisiana residents coexist with armadillos (Dasypus novemcinctus), some of which are infected with Mycobacterium leprae, the significance of which is unknown. Hypothetically, exposure to an unknown human case, reactivation of "asymptomatic" leprosy through immunosenescence or immunosuppression, or infection from an environmental source might have occurred. Because the patients lacked contact, travel, residence, and exposure risk factors, the origin of leprosy in the new indigenous cases is noteworthy and is not understood.

Adult↗
PubMed1987

Neutrophil uptake of vaccinia virus in vitro.

We studied human neutrophils for uptake of vaccinia virus. Uptake was determined radiometrically and by electron microscopy. Vaccinia virus was labeled with 14C or 3H, incubated with neutrophils, and quantified in neutrophil pellets in a new radiometric phagocytosis assay. Better results were obtained from assays of [3H]thymidine-labeled virus; uptake increased through 1 hr and then plateaued. Phagocytosis of 3H-labeled Staphylococcus aureus was normal. Uptake of virus was serum dependent. Hexose monophosphate shunt activity was measured by two methods. No 14CO2 from [14C]1-glucose accompanied uptake of vaccinia virus, in contrast to the respiratory burst accompanying bacterial phagocytosis. Electron microscopy showed intact to slightly digested intraphagolysosomal vaccinia virus. Pock reduction assay showed a decrease in viral content due to neutrophils until 6 hr of incubation, when a modest but significant increase was observed. Thus, neutrophil uptake of vaccinia virus is distinguished from bacterial phagocytosis.

Animals↗
PubMed1987

Wegener granulomatosis and trimethoprim-sulfamethoxazole. Complete remission after a twenty-year course.

Wegener granulomatosis was diagnosed in a 42-year-old woman in 1965. Although a regimen of azathioprine and prednisone was helpful, the disease progressed. Cyclophosphamide was added to this regimen in 1969. On three separate occasions her disease relapsed when cyclophosphamide therapy was discontinued. In 1984, she developed cyclophosphamide-resistant disease and drug toxicity. We were able to discontinue cyclophosphamide therapy after a trimethoprim-sulfamethoxazole regimen that was begun in February 1985 led to rapid improvement, a fall in the erythrocyte sedimentation rate, and a complete remission. Her 22-year survival is the longest one reported. Because patients with Wegener granulomatosis sometimes respond to trimethoprim-sulfamethoxazole, this therapy deserves careful study and implies that Wegener granulomatosis is an as yet unidentified infection.

Blood Sedimentation↗
PubMed1986

Blastomycotic meningitis.

A difficult and tragic case of central nervous system blastomycosis is presented as the basis for a review of the diagnostic criteria required to establish this diagnosis and to present a scheme for the diagnosis and therapy of chronic meningitis. The diagnosis in our case was complicated by preexisting inadequately treated tuberculosis; a prepontine mass; and a cervical intradural, extramedullary, circumferential mass. This exceptional case of chronic basilar meningitis with cervical myelopathy was caused by Blastomyces dermatitidis.

Adult↗
PubMed1986

Chédiak-Higashi syndrome neutrophils are characterized by the absence of both normal azurophilic granules.

Neutrophils from two Chédiak-Higashi syndrome brothers were isolated, suspended in heparinized sucrose, lysed, and filtered. The granule-rich filtrate was centrifuged on a sucrose gradient (rho = 1.287-1.10 g/ml) at a mean force of 95,000g for 4 hours. The gradients contained one band at rho = 1.18 g/ml (band C) which was broader than normal and lacked normal bands A, rho = 1.22 g/ml, and B, rho = 1.20 g/ml. Gradient fractions were assayed for enzyme activities and protein. No marker enzymes identified densities normally occupied by bands A and B, and of the enzymes measured, only lysozyme showed peak activity with band C. Thus, only normal specific granules were present. Two azurophil granules, normally present and separable, were absent. Also identified was eosinophil granule peroxidase at rho = 1.24 g/ml (band E). Alkaline phosphatase, not a granule marker, was twice normal at the normal density, rho = 1.14-1.15 g/ml, consistent with an increase in unidentified membranes. A lysate gradient suggested that the giant azurophilic granules were rho = 1.25-1.27 g/ml. These neutrophils contain blue-grey or slate-grey giant granules, which are not truly azurophilic or basophilic, but should continue to be identified as azurophilic to conform to the convention making "azurophilic" and "peroxidase-positive" synonymous. The eosinophils contain normal eosinophil granules as well as giant inclusion granules. In contrast, neutrophils are deficient in both normal azurophilic granules.

Adult↗
PubMed1986

Niridazole-induced red/brown urine pigment is associated with increased urinary beta-glucuronidase excretion and a bladder site of formation.

Niridazole caused red/brown urine pigment in a man during treatment for Schistosoma mansoni infection. The urine pigment has been observed during niridazole treatment of schistosomiasis, but has not been documented during treatment of other diseases. Urinary beta-glucuronidase (EC 3.2.1.31) concentration increased proportionately to the amount of red/brown pigment in the urine. Concurrently, sterile pyuria developed. The duration of the time urine was in the bladder was directly related to the concentration of beta-glucuronidase and to the intensity of the red/brown urine color, there being much more in infrequently than in frequently voided urine specimens. Pigment development appears to occur in the bladder. The associated and possibly contributing components appear to be niridazole or one of its metabolites, beta-glucuronidase from the kidneys or from urinary granulocytes, and possibly a schistosomal factor. Given time, this combination generated the red/brown pigment.

Adult↗
PubMed1985

Heparin inhibition of human neutrophil and eosinophil-enriched leukocyte acid beta-glycerophosphatase.

Heparin inhibited acid beta-glycerophosphatase (EC 3.1.3.2) from human blood leukocytes, eosinophil-enriched leukocytes, and neutrophils. The inhibition interfered in the hydrolysis of phosphorus from glycerophosphate, not in the formation or detection of colored complexes of phosphomolybdate in the second or color development step in two conventional assays. Heparin inhibited human hypereosinophilic syndrome leukocyte homogenate enzyme activity according to the equation: activity equals 0.946 - 0.087 ln heparin (units/assay) when heparin was varied from 1 to 100 units per assay. At 100 units of heparin per assay, 51% of the original activity remained. Enzyme activity was less in neutrophils than in eosinophils; moreover, the inhibition of neutrophil homogenate by heparin was considerably less than that seen in the eosinophil-enriched leukocyte preparations. In neutrophil homogenates containing 100 units of heparin per assay, 77.1% of activity without heparin was retained. When neutrophil lysates were utilized, less inhibition was observed: e.g., at 1 unit of heparin per assay, 91.7% enzyme activity was retained and at 1000 units, 76.2%; here, activity equals 0.289 - 0.007 ln heparin. The data allowed more precise consideration of the inhibition of acid beta-glycerophosphatase by heparin, and, while confirming quantitatively the greater content of acid beta-glycerophosphatase in eosinophil-enriched leukocyte preparations than in neutrophil preparations, provide experimental support for an acid beta-glycerophosphatase in human eosinophils, which is different from that in human neutrophils. It is more highly susceptible to heparin inhibition than acid beta-glycerophosphatase in human neutrophils from which it is apparently distinct.

Acid Phosphatase↗
PubMed1984

Human neutrophil N-acetyl-beta-D-glucosaminidase: granule localization. Further evidence for two azurophil granules.

The heterogeneity of human neutrophil granules, particularly of azurophil granules, defined as peroxidase containing, was examined by measuring N-acetyl-beta-D-glucosaminidase in fractions of isopycnic sucrose gradients of such granules. Neutrophil granules were prepared from normal human blood, monodispersed in heparinized sucrose, and centrifuged by established methods. N-Acetyl-beta-D-glucosaminidase was previously shown to be exquisitely sensitive to small amounts of heparin; paradoxically, larger amounts restore activity. The inhibition is reversed with protamine. N-Acetyl-beta-D-glucosaminidase activity had its peak at density 1.20 gm/ml (band B) and a lesser peak at density 1.22 gm/ml (band A). Mean specific enzyme activity was 899 +/- 217 nmol p-nitrophenol released per minute per milligram protein in gradient fraction 12 (band B), and 507 +/- 149 nmol p-nitrophenol released per minute per milligram protein in fraction 8 (band A) (p less than 0.01), which correlated in part to the significantly higher protein content in band A. These specific activities are 31-fold and 17-fold greater, respectively, then mean neutrophil lysate specific activity of 28.8 +/- 7.0 nmol p-nitrophenol released per minute per milligram protein, indicating a considerable concentration of granule enzyme activity in these gradient bands. The gradient distribution of N-acetyl-beta-D-glucosaminidase is nearly identical to that of myeloperoxidase and beta-glucuronidase, thus providing another enzyme marking the existence of two populations of azurophil granules, separable by density. Of total gradient enzyme activity, the mean percentage distribution of N-acetyl-beta-D-glucosaminidase in the pellet was 0.3%. Because the mean percentage of total gradient activity in the pellet was on an order of magnitude higher for myeloperoxidase (4.7%), beta-glucuronidase (3.7%), lysozyme (3.9%), and protein (2.8%), our data suggest that N-acetyl-beta-D-glucosaminidase has a possibly unique site within or an affinity to one or both of the two populations of azurophilic granules that is distinct from that for myeloperoxidase and beta-glucuronidase.

Acetylglucosaminidase↗
PubMed1983

Human neutrophil N-acetyl-beta-D-glucosaminidase: heparin inhibition.

To determine N-acetyl-beta-D-glucosaminidase (EC 3.2.1.30) in human neutrophil granules separated by a method requiring heparin, the inhibition of this enzyme by heparin was studied. Neutrophils were purified from blood of five donors by modifications of the Hypaque-Ficoll and dextran separation methods resulting in a suspension which was 96% neutrophils. Neutrophil lysates were assayed for N-acetyl-beta-D-glucosaminidase by measuring the amount of p-nitrophenol released from p-nitrophenyl-N-acetyl-beta-D-glucosaminide. The reaction showed first-order kinetics with regard to enzyme concentration. Triton X-100, 0.1% v/v, enhanced enzyme activity. Heparin was shown to reduce neutrophil lysate N-acetyl-beta-D-glucosaminidase to a specific activity of 46% at a heparin concentration of 2 units per assay and to 43% (maximal inhibition) at 17 and 50 units of heparin per assay. Substantially higher heparin concentrations partially restored the inhibited activity, the maximal restoration being a return to 80% of the original activity at 1700 units of heparin per assay. Protamine sulfate was assessed for its ability to restore N-acetyl-beta-D-glucosaminidase activity in the presence of heparin. At 1.0 mg/10 units of heparin, protamine restores enzyme activity to its heparin-free activity. These studies of human neutrophil N-acetyl-beta-D-glucosaminidase demonstrate: (1) specific enzyme activity is 28.8 +/- 7.0 nmole p-nitrophenol released per minute per milligram of protein or 1.7 +/- 0.5 nmole p-nitrophenol released per minute per 10(6) neutrophils; (2) heparin rapidly but finitely inhibits enzyme activity at very low concentrations and paradoxically restores it toward normal at high concentrations; and (3) protamine sulfate restores enzyme activity inhibited by heparin.

Acetylglucosaminidase↗
PubMed1983

Inguinal abscess caused by Rhizopus rhizopodiformis: successful treatment with surgery and amphotericin B.

Rhizopus rhizopodiformis has seldom been isolated from human mucormycosis. We report the first subcutaneous abscess to be caused by this fungus. It occurred in a diabetic man and presented as an inguinal mass, suggestive of a hernia, superficial to his cadaveric renal transplant. The fungus was readily isolated from pus inoculated onto blood and chocolate agars after a short incubation. The patient was cured by surgical drainage and treatment with 2.0 g of intravenous amphotericin B. Complete identification of such isolates is recommended.

Abscess↗
PubMed1982

Five-year follow-up of a man with subcutaneous mycetomas caused by Microsporum audouinii.

A black man with subcutaneous mycetomas caused by Microsporum audouinii was treated by a combination of griseofulvin, 18.5 g of amphotericin B, excisional surgery, and later, ketoconazole, resulting in a satisfactory arrest or cure of the clinical illness. Complications of therapy included residual impaired renal function and a change in hair color from black to a rust brown color. The continued use of the term mycetoma to describe such lesions is justified.

Adult↗