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Results for “Phagocyte Bactericidal Dysfunction”

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At least 253 records · Page 14Linked to original sources
PubMed1988

Neonatal Job's syndrome featuring a vesicular eruption.

A newborn infant who developed a vesicular eruption, clinically indistinguishable from herpetic lesions, eventually developed the classic features of Job's syndrome. The initial ares of involvement included the hands and feet, then the scalp, face, and suprapubic skin. The clear, tense vesicles varied only slightly in size and appeared as isolated, grouped, or confluent lesions on inflamed skin. Many eventually became umbilicated. The more typical eczematous component appeared over the course of the next several months. Although the child initially had an elevated white blood cell count and eosinophilia, his IgE level did not become dramatically elevated until after 1 year of age. Job's syndrome should be considered as part of the differential diagnosis of a vesicular eruption in the newborn.

Chronic Disease↗
PubMed1976

Pseudomonas cepacia pneumonia in a child with chronic granulomatous disease and selective IgA deficiency.

A 6 1/2 year-old boy with chronic granulomatous disease (CGD) and selective IgA deficiency developed a chronic progressive pneumonia which failed to respond to several conventional combinations of antimicrobial therapy. On lung biopsy, Pseudomonas cepacia was obtained in pure culture, sensitive to chloramphenicol, tetracycline, kanamycin and nalidixic acid. With specific therapy, he slowly recovered. P. cepacia has not been previously described as a cause of persistent pneumonia in immunodeficient children. The occurrence of CGD and selective IgA deficiency together is a very rare combination of immunodeficiencies.

Child↗
PubMed1976

A case of impaired chemotaxis and lymphocyte transformation.

The report describes the clinical syndroms of a 14-year-old boy which suffered from recurrent infections since early infancy. The clinical and general laboratory findings were similar to "the granulomatous disease of childhood" as described by Bridges et al. (8). The following serum factors were determined: Immunoglobulins, complement factors, isoagglutinins. The following assays with normal or patient's granulocytes were done: Chemotactic activity, nitroblue-tetrazolium test, bactericidal assay, fungicidal assay, myeloperoxidase, monocytes fungicidal assay. Immunological studies include kinetics of phytohaemagglutinin response, effect of serum of the patient on lymphocytic reactivity in vitro and skin tests. The following results were obtained: 1) Assays with normal or patient's granulocytes showed an impaired chemotatic activity, when serum of the patient was added. There was strong indication by treatment of the patient with plasma infusions, that the chemotactic defect is a serum dependent factor. 2) It could be demonstrated that the patient's serum also inhibited the response of lymphocytes to tuberculin and phytohaemagglutinin. Therefore the patient report focuses attention upon the possibility of serum related abnormalities that may influence granulocytic as well as lymphocytic functions leading to recurrent bacterial, fungal and viral infections.

Adolescent↗
PubMed1976

Acute disseminated phycomycosis in a patient with impaired neutrophil granulocyte function.

A 13-year-old girl with no previously known predisposing disease developed phycomycosis involving the left lung, pleura and shoulder, the left side of the neck, the left thigh, the kidneys and the brain. Prolonged amphotericin B therapy resulted in clinical improvement, but the disease was wide-spread when the patient died 5 months after debut of symptoms from a subarachnoid haemorrhage due to fungal destruction of the basilar artery. During hospitalization, a marked reduction in the bactericidal activity of circulating neutrophil granulocytes was repeatedly demonstrated and the endotoxin stimulated nitroblu tetrazolium test was negative. Together with the demonstration of granuloma formation and the accumulation of lipid-laden histiocytes in the spleen, lymph nodes, bone marrow and the thymus, these findings indicate that the patient had a less severe form of chronic granulomatous disease.

Adolescent↗
PubMed1977

Kinetics of phagocytosis and intracellular killing of Candida albicans by human granulocytes and monocytes.

The study of the phagocytosis and intracellular killing of Candida albicans by granulocytes and monocytes has been hampered by the budding and pseudomycelium formation of this yeast during a relatively short incubation period at 37 degrees C and by the similar density of candida cells and phagocytes, which makes differential centrifugation impossible. In the present study, C. albicans was used after 5 days of preculture at 30 degrees C, after which the number of candida cells remained constant during incubation at 37 degrees C for 90 min. On this basis, phagocytosis and intracellular killing were limited to a period of 60 min. Phagocytosis of C. albicans by granulocytes and monocytes was measured with a hemocytometer, the number of extracellular candida being a measure of the ingestion of these microorganisms. After 60 min, 96% of the candida cells were ingested by normal human granulocytes and monocytes. This process was dependent on the opsonin concentration and temperature and was inhibited by mono-iodoacetic acid. Heat-inactivated serum was less active than fresh serum, reflecting the role of complement factors with respect to opsonization. Intracellular killing was measured by a microbiological assay. After 60 min of incubation of phagocytes together with C. albicans and serum, human granulocytes and monocytes killed 58 and 50% of the ingested candida, respectively. This process was inhibited by phenylbutazone. Phagocytes from patients with chronic granulomatous disease showed impaired intracellular killing.

Candida albicans↗
PubMed1978

Allosteric transformation of reduced nicotinamide adenine dinucleotide (phosphate) oxidase induced by phagocytosis in human polymorphonuclear leukocytes.

We used sensitive isotopic and fluorometric assay procedures to investigate reduced nicotinamide adenine dinucleotide (phosphate) [NAD(P)H]oxidation in a particulate fraction derived from normal and chronic granulomatous disease leukocytes. Granules isolated from normal resting cells showed allosteric kinetics with regard to oxidation of either NADH or NADPH, so that no enzyme activity was observed at physiological concentrations of substrate. If the granules were isolated from cells that had previously phagocytized zymosan, normal hyperbolic kinetics were obtained, so that activity could now be observed at low levels of substrate. The activity towards NADPH was always substantially greater than that towards NADH at any given concentration of substrate. This alteration in kinetics with phagocytosis was not observed with the other granule enzymes, acid phosphatase or beta-glucuronidase, and thus appeared to be specific for the reduced pyridine nucleotide oxidase(s). In contrast, granules isolated from cells of patients with chronic granulomatous disease showed allosteric kinetics regardless of whether they were obtained from resting or phagocytizing cells, so that NADPH oxidation was not measurable at physiological concentrations of substrate. This defect in the oxidation of NADPH by granules isolated from phagocytizing chronic granulomatous disease cells was observed over the pH range of 4.0 to 7.0. These data suggest that initiation of the respiratory burst by pahgocytosis normally requires an allosteric transformation in a reduced pyridine nucleotide oxidase, which in turn allows expression of enzymatic activity at physiological concentrations of substrate. The defect in chronic granulomatous disease appears to lie in an inability to achieve this transformation, and the enzyme remains in the inactive, allosteric form.

Acid Phosphatase↗
PubMed1971

Reduced germination of Clostridium botulinum type A spores in vitro by polymorphonuclear leukocytes from chronic granulomatous disease.

Leukocytes from two patients with chronic granulomatous disease of childhood (CGD) and from one female carrier were examined for their capacity to induce germination of Clostridium botulinum type A spores in vitro. Normal human leukocytes induced germination of C. botulinum spores to the same extent as guinea pig neutrophils. Germination was depressed by more than half when cells from CGD patients were used. A noticeable, but less severe, abnormality was present in leukocytes from a female carrier for this X-linked trait. CGD leukocytes are defective in cellular production of H(2)O(2), and the latter is known to be effective in inducing germination of clostridial spores. Lysozyme is also known to be effective in spore germination and is present in CGD leukocytes in normal amounts. The posibility that C. botulinum spores require a mechanism which sensitizes them to the action of H(2)O(2) and lysozyme is raised, and it is suggested that the methodology used in this work measures a defect of such a mechanism in CGD leukocytes.

Animals↗
PubMed1974

Role of peroxide in phagocytic killing of pneumococci.

Two mutants of a pneumococcus type I with diminished peroxide production were selected from a population of nitrosoguanidine-treated cells. White cells of normal patients killed the mutant pneumococci as well as the otherwise isogenic wild-type strain. In patients studied with chronic granulomatous disease, however, the peroxide-poor strain was killed far less well than the wild type. These studies indicate that the removal of a peroxide-generating system in the phagocytic vacuole specifically brings forth the killing defect in chronic granulomatous disease.

Animals↗
PubMed1975

Association of Pseudomonas cepacia with chronic granulomatous disease.

Pseudomonas cepacia was recovered from a number of infected sites in three patients with chronic granulomatous disease of childhood. The organisms were identified on the basis of their oxidative utilization of a variety of carbohydrates and their positive beta-galactosidase and oxidase activities. They were resistant to most antimicrobial agents and moderately susceptible to chloramphenicol. Peripheral blood leukocytes isolated from two siblings with chronic granulomatous disease, including one of the patients in this series, failed to kill P. cepacia in vitro. Prolonged prophylactic and antimicrobial therapy may well have played a significant role in the colonization and infection of these patients with P. cepacia.

Blood Bactericidal Activity↗
PubMed1981

A polymorph bactericidal defect and a lupus-like syndrome.

We describe a child with primary defect of polymorph bacterial killing associated with systemic lungs erythematosus. We suggest that her autoimmune disease results from chronic bacterial antigen stimulation and propose a hypothetical model linking immunodeficiency with autoimmunity.

Blood Bactericidal Activity↗