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Query: UMLS:C0014118 (endocarditis)
 15,629 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The authors report a case of endocarditis caused by Candida parapsilosis. To the best of our knowledge, a case has not been described previously in Japan in the English literature. A battery of 8 peroxidase-labeled lectins was tested on sections of paraffin-embedded tissue to determine which lectin could be used in the microscopic diagnosis of C. parapsilosis. One lectin, from Archis hypoaea (PNA) was found to react with C. parapsilosis. On the other hand, C. albicans, Aspergillus, Mucor, and Cryptococcus did not react with A. hypoaea (PNA). On fluorescence microscopic study, C. parapsilosis was not fluorescent, but other fungi were fluorescent when exposed to ultraviolet illumination. Therefore, we propose new procedures for identification of C. parapsilosis in tissue sections using lectin histochemistry and fluorescence microscopy.
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PMID:Endocarditis caused by Candida parapsilosis. 132 23

Eosinophils (EOs) participate in a variety of inflammatory states characterized by endothelial cell damage, such as vasculitis, pneumonitis, and endocarditis. We find that 100 U/ml TNF-alpha/cachectin (TNF), a concentration attainable in the blood of humans with parasitic infestations, stimulates highly purified populations of EOs to damage human umbilical vein endothelial cells (HUVEC), a model of human endothelium. This TNF-dependent EO cytotoxicity is strongly inhibited by heparin and methyprednisolone but unaffected by the platelet-activating factor antagonist BN52012 or scavengers of superoxide anion and H2O2, superoxide dismutase and catalase. However, addition of a physiologically relevant concentration of Br- (100 microM) enhances EO/TNF damage to HUVEC, implicating the possible participation of EO peroxidase (EPO) in the killing mechanism. EOs adherent to FCS-coated plastic wells more than double their production of superoxide anion and the cytotoxic EPO-derived oxidant HOBr when exposed to TNF, showing that TNF activates the respiratory burst of EOs attached to a "physiologic" surface. Unlike PMNs, EOs were not irreversibly activated to kill unopsonized endothelium by previous exposure to TNF, and did not degranulate or upregulate CR3 expression as detected by Mo1 in the presence of 100 U/ml TNF. HUVEC exposed 18 h to TNF were considerably more susceptible to lysis by PMA-activated EOs and reagent H2O2, demonstrating a direct effect of TNF upon endothelium, perhaps through inhibition of antioxidant defenses. These findings suggest that abnormally elevated serum levels of TNF may provoke EOs to damage endothelial cells and thereby play a role in the pathogenesis of tissue damage in hypereosinophilic states.
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PMID:Tumor necrosis factor alpha/cachectin stimulates eosinophil oxidant production and toxicity towards human endothelium. 197 79

Eosinophilic endocarditis is a potentially lethal complication of chronic peripheral blood hypereosinophilia. We hypothesized that eosinophil peroxidase (EPO), an abundant eosinophil (EO) cationic granule protein, promotes eosinophilic endocarditis by binding to negatively charged endocardium, and there generating cytotoxic oxidants. Using an immunocytochemical technique, we demonstrated endocardial deposition of EPO in the heart of a patient with hypereosinophilic heart disease. Because EPO preferentially oxidizes Br- to hypobromous acid (HOBr) rather than Cl- to hypochlorous acid (HOCl) at physiologic halide concentrations, we characterized the Br(-)-dependent toxicity of both activated EOs and purified human EPO towards several types of endothelial cells and isolated working rat hearts. In RPMI supplemented with 100 microM Br-, phorbol myristate acetate-activated EOs, but not polymorphonuclear leukocytes, caused 1.8-3.6 times as much 51Cr release from four types of endothelial cell monolayers as in RPMI alone. H2O2 and purified human EPO, especially when bound to cell surfaces, mediated extraordinarily potent, completely Br(-)-dependent cytolysis of endothelial cells that was reversed by peroxidase inhibitors, HOBr scavengers, and competitive substrates. We further modeled eosinophilic endocarditis by instilling EPO into the left ventricles of isolated rat hearts, flushing unbound EPO, then perfusing them with a buffer containing 100 microM Br- and 1 microM H2O2. Acute congestive heart failure (evidenced by a precipitous decrement in rate pressure product, stroke volume work, aortic output, and MVO2 to 0-33% of control values) ensued over 20 min, which deletion of EPO, Br-, or H2O2 completely abrogated. These findings raise the possibility that EPO bound to endocardial cells might utilize H2O2 generated either by overlying phagocytes or endogenous cardiac metabolism along with the virtually inexhaustible supply of Br- from flowing blood to fuel HOBr-mediated cell damage. By this mechanism, EPO may play an important role in the pathogenesis of eosinophilic endocarditis.
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PMID:Bromide-dependent toxicity of eosinophil peroxidase for endothelium and isolated working rat hearts: a model for eosinophilic endocarditis. 198 18

The potent cytotoxic capacity of eosinophils for parasites and host tissue has in part been attributed to the catalytic action of eosinophil peroxidase (EPO), which preferentially oxidizes Br- to the powerful bleaching oxidant HOBr in buffers that mimic serum halide composition (100 mM Cl-, 20-100 microM Br-, less than 1 microM I-). However, serum also contains 20-120 microM SCN-, a pseudohalide whose peroxidative product, HOSCN, is a weak, primarily sulfhydryl-reactive oxidant. Because of its relative abundance and high oxidation potential, we hypothesized that SCN-, not Br- or I-, is the major substrate for EPO in physiologic fluids. We find that in Earle's buffer (100 mM Cl-) supplemented with 100 microM Br- and varying concentrations of SCN-, HOBr production by activated eosinophils and purified EPO, assayed by conversion of fluorescein to dibromofluorescein, was 50% inhibited (ID50) by only 1 microM SCN-. SCN- also blocked (ID50 10 microM) EPO oxidation of I- to HOI, assayed as iodofluorescein, despite the presence of 100 microM (i.e. grossly supraphysiologic) I-. Thionitrobenzoic acid oxidation kinetics indicate that SCN- is the initial species oxidized by EPO in equimolar mixtures of SCN- and Br- and in human serum. EPO also catalyzed the covalent incorporation of [14C]SCN- into proteins in buffers regardless of Br- concentration and in human serum. Comparing the cytotoxicity of HOSCN and HOBr for host cells, we find that even subphysiologic concentrations of SCN- (3.3-10 microM) nearly completely abrogate the potent Br(-)-dependent toxicity of EPO for 51Cr-labeled aortic endothelial cells and isolated working rat hearts, recently developed models of eosinophilic endocarditis. Thus, HOSCN, hitherto best known as a bacteriostatic agent in saliva and milk, is likely also the major oxidant produced by EPO in physiologic fluids, and the presence of SCN- averts damage to EPO-coated host tissues that might otherwise accrue as a result of HOBr generation. In view of these findings, the potential role of HOSCN in eosinophil killing of parasitic pathogens deserves close examination.
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PMID:Thiocyanate is the major substrate for eosinophil peroxidase in physiologic fluids. Implications for cytotoxicity. 200 37

The antigenic composition of an endocarditis-associated isolate of Streptococcus faecalis was studied by immunoblotting of whole cells and cell walls from sodium-dodecyl sulphate polyacrylamide gels on to nitrocellulose and detection with serum from patients and hyperimmune rabbit serum. A major envelope protein antigen of mol. wt 53 X 10(3) detected with patient's serum was also present in three urinary strains of Str. faecalis and a laboratory strain of Str. faecalis ss. zymogenes but not in Staphylococcus aureus. Other common antigens of Str. faecalis were of mol. wt (10(3)) 65, 63, 56, 49.5, 30 and 21. Two other protein antigens (43 and 37 X 10(3) mol. wt) reacted strongly with asparagus pea lectin-peroxidase conjugate indicating the presence of fucosyl residues. Other lectin-peroxidase conjugates were used to demonstrate the presence of various glycosyl residues on envelope proteins. Growth of Str. faecalis in serum to mimic in-vivo growth conditions in endocarditis infections dramatically altered the antigenic patterns. Only two major antigens of mol. wt (10(3)) 56 and 53 reacted with sera from endocarditis patients. These antigens may, therefore, be of diagnostic or protective potential.
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PMID:Antigenic composition of an endocarditis-associated isolate of Streptococcus faecalis and identification of its glycoprotein antigens by ligand blotting with lectins. 308 28

Actinobacillus actinomycetemcomitans is a fastidious, facultative gram-negative rod associated with endocarditis, certain forms of periodontal disease, and other focal infections. Human neutrophils have demonstrated bactericidal activity against A. actinomycetemcomitans, and much of the oxygen-dependent killing has been attributed to the myeloperoxidase-H2O2-halide system. However, the contribution of other neutrophil components to killing activity is obscure. Lactoferrin, an iron-binding glycoprotein, is a major constituent of neutrophil-specific granules and is also found in mucosal secretions. In this report, we show that human lactoferrin is bactericidal for A. actinomycetemcomitans. Killing activity required an unsaturated (iron- and anion-free) molecule that produced a 2-log decrease in viability within 120 min at 37 degrees C at a concentration of 1.9 microM. Besides exhibiting concentration dependence, killing kinetics were affected by minor variations in temperature and pH. Magnesium, a divalent cation thought to stabilize lipopolysaccharide interactions on the surface of gram-negative organisms, enhanced lactoferrin killing of A. actinomycetemcomitans, while other cations, such as potassium and calcium, had no effect. Our data suggest that lactoferrin contributes to killing of A. actinomycetemcomitans by human neutrophils and that it may also play a significant role in innate secretory defense against this potential periodontopathogen.
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PMID:Killing of Actinobacillus actinomycetemcomitans by human lactoferrin. 341 49

The beneficial effects of polynuclear eosinophils (PE) are well known. However, under certain circumstances, PE can be harmful. The heart is a prime target for PE toxicity which is due to release of basic proteins by eosinophils including major basic protein, cationic protein, and peroxidase. The most common manifestation of PE toxicity is chronic parietal endocarditis (CPE) which regroups two entities: Loeffler's fibroplastic endocarditis and Davies' endomyocardial fibrosis. Loeffler's fibroplastic endocarditis occurs mainly in temperate climates. Patients present high, persistent eosinophil levels similar to those observed in essential hypereosinophilic syndrome (EHS) or Chusid syndrome. Davies' endomyocardial fibrosis occurs in tropical countries where eosinophilic helminthiasis are endemic. The incidence of eosinophilic myocarditis (EM) is low but probably underestimated. EM can be observed in any case involving PE and has been described in many cases of drug-induced atopy, in Churg and Strauss syndrome, and in EHS. The most common cause of death is short-term occurrence of cardiogenic shock or dilated hypokinetic cardiomyopathy. Some patients have been successfully treated by early, intensive corticosteroid therapy and/or heart transplantation. The nosological classification of EM and CPE remains controversial. The two disorders may form a continuum with CPE as the second phase. Other authors have suggested that EM and CPE result from the action of PE on two distinct targets, i.e. endothelial cells for EM and myocytes for CPE. In the future, it may be possible to identify subjects with a predisposition to PE-induced heart disease by studying of genes coding for interleukins (IL-5, IL-4, IL-3) and GM-CSF in the 5q31-q33 region of chromosome 5.
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PMID:[The heart and the eosinophil]. 1041 Mar 66

Wegener's granulomatosis is a systemic vasculitis characterized by necrotizing granulomatous lesions in the upper and lower respiratory tracts, glomerulonephritis and vasculitis involving other organs. Limited forms have been described in which some features of the disease may be absent. Four patients with this disease are being reported with special emphasis on differences in presentation, the ensuing diagnostic problems, and individual outcome. In three, the disease began as a limited form with upper respiratory tract and eye involvement, while in one patient, onset was systemic including affection of the lower respiratory tract. The mean delay from first symptoms to diagnosis was 20 months--much longer for the three limited forms than for the one with systemic onset, in whom the condition was recognized after 2 months following initial misdiagnosis of respiratory and urinary tract infections. One patient developed endocarditis and required aortic valve replacement. Immunofluorescence revealed antineutrophil cytoplasmic antibodies in all, three showing a cytoplasmic pattern and antibodies to proteinase 3, and the fourth a perinuclear pattern and antibodies to myeloperoxidase. Upper respiratory tract biopsies were not specific. Kidney biopsies were performed in all the patients and were crucial for definitive diagnosis and treatment of the disease, which was successful in three patients.
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PMID:Wegener's granulomatosis--a diagnostic challenge. 1102 Sep 56

Secondary vasculitis resulting from unusual pathologic expressions of infections has been described and has important clinical significance. Infectious agents have also been implicated in the pathogenesis of different primary systemic necrotizing vasculitides. Infectious endocarditis is of particular importance in the differential diagnosis of a patient presenting with ANCA associated vasculitis. We report a well-documented case of a patient with recurrent Staphylococcus aureus bacteremia who developed bacterial endocarditis and also fulfilled the Chapel Hill Conference definitions for microscopic polyangiitis. To the best of our knowledge, it is the second case of bacterial endocarditis associated with both pANCA and anti-MPO specificity that fulfilled definitions for systemic necrotizing vasculitis. We emphasize the potential pathogenic role of infection as the trigger factor for the development of systemic vasculitis.
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PMID:Microscopic polyangiitis following recurrent Staphylococcus aureus bacteremia and infectious endocarditis. 1857 83

Infectious endocarditis (IE) is an inflammatory disease of cardiac valves and endocardium of different origin. Subacute IE is a specific form of sepsis associated with the presence of the site of infection in the heart responsible for recurrent septicemia, embolism, and progressive changes in the immune system leading to nephritis, vasculitis, synovitis, and polyserositis. This form develops in response to a low-virulent pathogen (e.g.fungi) or as a result of inefficient antibacterial therapy. A patient is described presenting with fibrous body, aortic and mitral valve infection by the alga Prototheca wickerhamii associated with primary (myeloperoxidase) immunodeficiency. Recent data on diagnostics and treatment of subacute IE are presented.
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PMID:[Subacute infectious endocarditis of unusual etiology: peculiarities of diagnostics and treatment]. 2193 71


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