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

Serological parameters were compared in 15 cases of Coxiella burnetii infection comprising 5 cases each of primary Q fever, chronic granulomatous hepatitis, and endocarditis. The diagnosis was made on the basis of clinical history and serology and on the isolation of C. burnetii phase I from biopsy specimens of liver and bone marrow from two patients with granulomatous hepatitis and from the aortic valve vegetations of five patients with endocarditis. The temporal sequences of immunoglobulin levels, rheumatoid factor, and specific antibody responses to phase II and phase I antigens of C. burnetii were evaluated as predictive correlates of the three Q fever entities. Serum levels of immunoglobulin classes G, M, and A were variable in all the entities of Q fever. Increased mean levels (in milligrams per deciliter) of immunoglobulin G (IgG) and IgA were noted with chronic disease in the sera of some patients, whereas IgM levels were not significantly different from normal values. Rheumatoid factor was significantly elevated in chronic disease but not in primary Q fever. The temporal sequence of C. burnetii phase II and phase I antibodies were compared by microagglutination, complement fixation, and indirect microimmunofluorescence tests. All of these serological tests were useful in distinguishing primary from chronic disease. Thus, the ratio of anti-phase II to anti-phase I antibodies was greater than 1, greater than or equal to 1, and less than or equal to 1 for primary Q fever, granulomatous hepatitis, and Q fever endocarditis, respectively. Moreover, the high phase-specific IgA antibody titers in the indirect microimmunofluorescence test were diagnostic for endocarditis.
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PMID:Serological evaluation of O fever in humans: enhanced phase I titers of immunoglobulins G and A are diagnostic for Q fever endocarditis. 688 55

Three patients with visceral Staphylococcal aureus infections, but no evidence of endocarditis, developed signs of acute glomerulonephritis. Renal biopsy in two patients showed a mesangial proliferative glomerulonephritis and mesangial deposits containing IgA, IgG, and C3; autopsy material in a third patient showed acute diffuse proliferative glomerulonephritis. The clinical setting and pathologic findings of our patients with visceral Staphylococcal infection and glomerulonephritis are different than those found in the better-understood syndromes of glomerulonephritis associated with endocarditis or infected ventriculojugular shunts. Our patients provide support for the contention that some cases of primary or idiopathic glomerulonephritis may by caused by Staphylococcal infections.
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PMID:Glomerulonephritis and Staphylococcal aureus infections. 722 84

Two percent polyethylene glycol (PEG) precipitation was found to be a useful method for detecting circulating immune complexes (CIC) and could be used diagnostically to implicate infective endocarditis. Complexes consisting of a least Clq, IgG, and IgA were typically detected in sera from patients with infective endocarditis. Serial studies showed that CIC detection and measurement could be used to monitor clinical progress. Successful clinical improvement was reflected by decreasing CIC levels and the disappearance of rheumatoid factor, and, where increasing amounts of CIC were found, this may indicate situations where treatment was insufficient or inappropriate. There was specific free antibody demonstrable in the serum of six out of nine patients against their own infecting organisms, but attempts to identify the specificity of the complexed antibody as being directed against these organisms or their extracellular products failed. We could not detect any radioactive precipitin arcs, indicative of the free antibody also being in the complex, between the F(ab')2 preparation from the complex and the electrophoresed bacterial antigens in a radio-immunoelectrophoresis system. Eleven out of 13 sera that contained Clq, IgG, and IgA in their complexes also contained rheumatoid factor. Immunisation against the patient's own persisting CIC may explain this phenomenon.
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PMID:Nature of circulating immune complexes in infective endocarditis. 743 Mar 71

We report a patient with a peculiar association of brucella endocarditis, glomerulonephritis, and renal vasculitis, with immunopathological features different from those of endocarditis glomerulonephritis. Renal biopsy revealed moderate diffuse hypercellularity involving the mesangium as well as capillary loops, immunoflurescence revealed no staining for IgG, IgM, IgA, C3, and fibrinogen. The clinical and biochemical evidence of glomerulonephritis disappeared after antibiotic treatment combined with steroid therapy. No similar case has been previously reported in the literature.
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PMID:Brucella endocarditis associated with glomerulonephritis and renal vasculitis. 897 97

The progression of Coxiella burnetii infection to acute or chronic Q fever has been attributed to biological characteristics of the bacterium and to the host immune response. We measured whether serum levels of total and specific subclasses IgA1 and IgA2 could be correlated with the course of disease in acute and chronic Q fever infections, and with the occurrence of endocarditis. In patients with chronic infection, total IgA2 levels were significantly increased. Q-fever-specific IgA1 antibodies were detectable in both acute and chronic infections, but only patients with endocarditis had IgA2 antibodies to C. burnetii phase II antigens. These findings indicate that the measurement of IgA subclasses may be a useful aid in the serological diagnosis of Q fever. Our results reinforce the idea that immunologically mediated host factors are important in the pathogenesis of Q fever and in the disease outcome of this infection.
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PMID:Distribution of IgA subclass response to Coxiella burnetii in patients with acute and chronic Q fever. 968 53

In order to describe the clinical features and the epidemiologic findings of 1,383 patients hospitalized in France for acute or chronic Q fever, we conducted a retrospective analysis based on 74,702 sera tested in our diagnostic center, National Reference Center and World Health Organization Collaborative Center for Rickettsial Diseases. The physicians in charge of all patients with evidence of acute Q fever (seroconversion and/or presence of IgM) or chronic Q fever (prolonged disease and/or IgG antibody titer to phase I of Coxiella burnetii > or = 800) were asked to complete a questionnaire, which was computerized. A total of 1,070 cases of acute Q fever was recorded. Males were more frequently diagnosed, and most cases were identified in the spring. Cases were observed more frequently in patients between the ages of 30 and 69 years. We classified patients according to the different clinical forms of acute Q fever, hepatitis (40%), pneumonia and hepatitis (20%), pneumonia (17%), isolated fever (17%), meningoencephalitis (1%), myocarditis (1%), pericarditis (1%), and meningitis (0.7%). We showed for the first time, to our knowledge, that different clinical forms of acute Q fever are associated with significantly different patient status. Hepatitis occurred in younger patients, pneumonia in older and more immunocompromised patients, and isolated fever was more common in female patients. Risk factors were not specifically associated with a clinical form except meningoencephalitis and contact with animals. The prognosis was usually good except for those with myocarditis or meningoencephalitis as 13 patients died who were significantly older than others. For chronic Q fever, antibody titers to C. burnetii phase I above 800 and IgA above 50 were predictive in 94% of cases. Among 313 patients with chronic Q fever, 259 had endocarditis, mainly patients with previous valvulopathy; 25 had an infection of vascular aneurysm or prosthesis. Patients with endocarditis or vascular infection were more frequently immunocompromised and older than those with acute Q fever. Fifteen women were infected during pregnancy; they were significantly more exposed to animals and gave birth to only 5 babies, only 2 with a normal birth weight. More rare manifestations observed were chronic hepatitis (8 cases), osteoarticular infection (7 cases), and chronic pericarditis (3 cases). Nineteen patients were observed who experienced first a documented acute infection, then, due to underlying conditions, a chronic infection. To our knowledge, we report the largest series of Q fever to date. Our results indicate that Q fever is a protean disease, grossly underestimated, with some of the clinical manifestations being only recently reported, such as Q fever during pregnancy, chronic vascular infection, osteomyelitis, pericarditis, and myocarditis. Our data confirm that chronic Q fever is mainly determined by host factors and demonstrate for the first time that host factors may also play a role in the clinical expression of acute Q fever.
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PMID:Q fever 1985-1998. Clinical and epidemiologic features of 1,383 infections. 1077 10

Antiphospholipid syndrome (APS) is defined by the presence of arterial and venous thromboses, recurrent fetal death, cerebrovascular accidents, hemolytic anaemia, thrombocytopenia and various other manifestations in different organs. APS is a clinical entity that can appear commonly alongside systemic lupus erithemathous on it can occur as a primary disease. The syndrome is defined by the presence of antiphospholipid antibodies in serum, a group of immunoglobulins (IgG, IgM, IgA or an mixture of them) that adopt an hexagonal configuration when they are incubated at 37grades C. In APS, it is rather common to find cardiac lesions such as non-verrucous endocarditis, valvular lesions (especially of the mitral valve), microvascular cardiac disease and more risk of thrombosis at this level, myxomas that could be the cause of a systemic inflammation in relation to the production of antiphospholipid antibodies, intracardiac thrombii and congenital heart disease. We present the case of a woman with APS associated with interauricular communication whose initial diagnosis were pulmonary thromboembolism and cerebrovascular stroke. We were able to diagnose the cardiac abnormality by the use of transesophagic echocardiography. We propose the use of this imaging technique for patients with APS even though the transthoracic Doppler echocardiography was found to be normal. In this way we will be able to rule out cardiac lesions which could also be the cause of embolic manifestations.
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PMID:[Antiphospholipid syndrome. The use of transesophageal echocardiography]. 1458 41

The association of methicillin-resistant Staphylococcus aureus (MRSA) infection with glomerulonephritis (GN) has been well documented in Japan but not in North America. Recently, eight renal biopsies with IgA-predominant or -codominant GN from eight patients with underlying staphylococcal infection, but without endocarditis, were observed at a single institution in a 12-mo period. Renal biopsies were worked up by routinely used methodologies. Eight cases of primary IgA nephropathy were used as controls. Five patients had MRSA infection, one had methicillin-resistant S. epidermidis (MRSE) infection, and two had methicillin-sensitive S. aureus infection. Four patients became infected after surgery; two patients were diabetic and had infected leg ulcers. All patients developed acute renal failure, with active urine sediment and severe proteinuria. Most renal biopsies showed only mild glomerular hypercellularity. Two biopsies had prominent mesangial and intracapillary hypercellularity; one of them (the MRSE-associated case) had large glomerular hyalin thrombi. This patient also had a positive cryoglobulin test. Rare glomerular hyalin thrombi were noted in two other cases. Immunofluorescence showed IgA pre- or codominance in all biopsies. Electron microscopy revealed mesangial deposits in all cases. Five biopsies had rare glomerular capillary deposits as well. In the MRSE-associated GN, large subendothelial electron-dense deposits were present. These cases demonstrate that staphylococcal (especially MRSA) infection-associated GN occurs in the US as well, and a rising incidence is possible. It is important to differentiate a Staphylococcus infection-associated GN from primary IgA nephropathy to avoid erroneous treatment with immunosuppressive medications.
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PMID:Staphylococcus infection-associated glomerulonephritis mimicking IgA nephropathy. 1769 45

Infection by Staphylococcus aureus can result in severe conditions such as septicemia, toxic shock, pneumonia, and endocarditis with antibiotic resistance and persistent nasal carriage in normal individuals being key drivers of the medical impact of this virulent pathogen. In both virulent infection and nasal colonization, S. aureus encounters the host immune system and produces a wide array of factors that frustrate host immunity. One in particular, the prototypical staphylococcal superantigen-like protein SSL7, potently binds IgA and C5, thereby inhibiting immune responses dependent on these major immune mediators. We report here the three-dimensional structure of the complex of SSL7 with Fc of human IgA1 at 3.2 A resolution. Two SSL7 molecules interact with the Fc (one per heavy chain) primarily at the junction between the Calpha2 and Calpha3 domains. The binding site on each IgA chain is extensive, with SSL7 shielding most of the lateral surface of the Calpha3 domain. However, the SSL7 molecules are positioned such that they should allow binding to secretory IgA. The key IgA residues interacting with SSL7 are also bound by the leukocyte IgA receptor, FcalphaRI (CD89), thereby explaining how SSL7 potently inhibits IgA-dependent cellular effector functions mediated by FcalphaRI, such as phagocytosis, degranulation, and respiratory burst. Thus, the ability of S. aureus to subvert IgA-mediated immunity is likely to facilitate survival in mucosal environments such as the nasal passage and may contribute to systemic infections.
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PMID:Structural basis for evasion of IgA immunity by Staphylococcus aureus revealed in the complex of SSL7 with Fc of human IgA1. 1784 12

A severely ill 65-year-old man presented with symptoms of shortness of breath, edema and vasculitidic purpura over his lower extremities. He had severe mitral regurgitation which had not been surgically treated. Hematologic examination demonstrated leukocytosis with profound anemia. Other blood tests revealed impaired renal function, hypoalbuminemia, hypocomplementemia and mixed-type cryoglobulinemia. Urinalysis showed proteinuria, hematuria and pyuria, typical of a nephritic sediment. Renal biopsy indicated diffuse proliferative glomerulonephritis and a "full house" deposition in immunofluorescence study (positive for C3, C4, C1q, IgG, IgA and IgM), resembling the pathologic findings in class IV lupus nephritis. Although subacute bacterial endocarditis was initially suspected owing to a history of a predisposing valvular heart disease, probable vegetation shown by cardiac sonography and a clinical picture suggestive of a chronic infection, it was thought unlikely due to the entire afebrile course and initial sterile blood cultures. However, the blood cultures repeated 2 weeks after admission grew 3 sets of viridans streptococci. Following a course of penicillin and gentamicin treatment, his renal function, anemia and abnormal urine sediments improved gradually. Diffuse proliferative glomerulonephritis is well known to occur in infective endocarditis. However, the "full house" immunostaining in immunofluorescence study has never been reported. This case adds a new entity to the differential diagnosis of "full house" immune complex-related glomerulonephritis and exemplifies the need to maintain a high index of suspicion for underlying infectious disorders when facing glomerulonephritic or vasculitic syndrome.
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PMID:"Full house" proliferative glomerulonephritis: an unreported presentation of subacute infective endocarditis. 1804 78


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