Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0014118 (endocarditis)
 15,629 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The indirect immunofluorescence antibody test is currently the method of choice for Q-fever laboratory diagnosis. It permits the detection of IgG-, IgM-, and IgA-specific antibodies against the two phases of Coxiella burnetii. Sera from 20 cases of C. burnetii infection have been examined. Only total IgG against phase II were detected in cryptic infections. In acute Q-fever cases, the appearance of total IgG antibodies against phase I was a sign of aggravation, while IgM titers remained low. In subacute cases of Q-fever, anti-phase-I IgG titers were equal to or higher than anti-phase-II titers, and IgM against both phases were produced over a long time. Particularly high IgM titers were found in cases of granulomatous hepatitis. IgA antibodies against phase I were found in cases of Q-fever endocarditis, although the two cases that died had few or no IgA antibodies, despite very high IgG and IgM titers.
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PMID:Immunofluorescence serology. A tool for prognosis of Q-fever. 389 27

The obligate intracellular bacterium Coxiella burnetii is the etiological agent of acute Q-fever and chronic endocarditis in humans and of several zoonotic infections. The DNA from a variety of these disease isolates was compared for homology to the plasmid QpH1, found in the Nine Mile strain. Three patterns of homology were found in these isolates, i.e., one pattern identical to that of QpH1, one common to several endocarditis isolates and goat abortion isolates, and one common to the remaining group of endocarditis isolates. Plasmid DNA from the endocarditis-abortion isolate group, designated QpRS, was mapped by restriction enzyme analysis and compared with QpH1. These data show that QpRS was 2 to 3 kilobase pairs larger, contained DNA not found in QpH1, but was not generated from QpH1 by a single insertional event. Isolation of plasmid DNA from the second endocarditis group of isolates was not successful and may indicate that the plasmid has integrated into the chromosome. This analysis provides the first clear evidence that differences exist between C. burnetii isolates which cause various diseases, indicating that different C. burnetii strains may have unique virulence characteristics.
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PMID:Correlation of plasmid type and disease caused by Coxiella burnetii. 403 Jan 4

Seven patients are described in whom chronic Q fever was detected by serology (Coxiella burneti phase I antibody titre greater than 1:200) during routine screening at admission for cardiac catheterisation. None had clinical evidence of endocarditis, hepatitis or other foci of infection. Three of the patients were kept under observation without antibiotic treatment for periods of six, 18 and 20 months. In two patients of this group, cardiac tissue was obtained at operation and in one patient seroconversion following guinea-pig inoculation indicated the presence of Coxiella burneti infection. Four patients were given antibiotic treatment when Q fever was confirmed by serology. Courses of antibiotic treatment with a combination of two drugs were maintained for four to six years and in three of these patients phase I antibody titres fell to very low levels with no appearance of overt infection. The fourth patient died after resection of an aortic aneurysm, seven months after starting antibiotic treatment. Cases reported in the literature indicate that while endocarditis is the most common manifestation of chronic Q fever, the infection can persist at other sites. Of the seven cases of subclinical chronic Q fever reported here, the infection was localised in only one. Patients with this subclinical form of infection pose the therapeutic dilemma of whether or not they should receive antibiotic treatment.
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PMID:Subclinical chronic Q fever. 408 Sep 56

The case-history of a 7-year-old boy with endocarditis, myocarditis and pericarditis, possibly caused by Coxiella burnetii (Q-fever), is presented. As far as we know only one case of Q-fever endocarditis in a child is previously described in literature. That child had, contrary to our patient, a pre-existing valve abnormality. Q-fever was diagnosed after demonstration of a significant rise in titer of the antibodies against Coxiella burnetii in both the IgM and the IgG fractions. IgA antibodies, indicative for an endocarditis, were also demonstrated.
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PMID:[Coxiella burnetii as a possible cause of endocarditis in a 7-year old boy]. 408 71

Endocarditis was recorded in 92 (11%) of 839 confirmed Q-fever infections reported for the Communicable Disease Report by laboratories between 1975 and 1981; Q-fever endocarditis accounted for approximately 3% of all cases of endocarditis reported. Two-thirds of the 92 reports were of men, and in both men and women endocarditis affected mainly young and middle-aged adults. Only one-third of Q-fever endocarditis patients were noted to have an underlying heart-valve lesion. There were also 30 reports of chronic Q-fever infection, and in 10 the primary clinical feature was liver disease. The laboratory data do not support the view that Q-fever endocarditis is a rare compilation of Coxiella burnetii infection, and the condition may be considerably underdiagnosed. Joint veterinary and medical investigations should be undertaken to establish the natural history of Coxiella burnetii infection in the U.K. in order to formulate policies for prevention of acute and chronic infection.
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PMID:Q-fever endocarditis in England and Wales, 1975-81. 612 19

The application of an indirect ELISA for detection of IgM and IgG antibodies against Coxiella burnetii in five Q fever patients--among them one with endocarditis and one with hepatitis--is described. In the acute phase of infection, within a few days after onset of clinical symptoms, a significant rise of IgM antibodies could be detected. It was followed by a rise of IgG in the second and third week. In chronic Q fever endocarditis, IgM antibodies persisted over a period of nine months. High IgM and low IgG values indicated acute infection, while in convalescent sera the IgM/IgG relationship was vice versa. In a comparative investigation with complement fixation (CF) test it could be shown that CF antibodies were associated exclusively with immunoglobulin G. IgM separated from IgG by gel chromatography did not fix complement. So, the CF test does not appear to be suitable for detection of antibodies against Coxiella in the early stages of the disease. Because of the persistence of IgG antibodies over a longer period of time, sole detection of a titer against the agent is insufficient for diagnosis of current disease, if not a rise or fall in titer can be detected in a second serum sample. Using the sensitive ELISA technique, a diagnosis is usually possible with one serum sample--in connection with history and clinical investigation--by differentiation of IgM and IgG antibodies.
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PMID:[Serodiagnosis of human Q-fever--demonstration of non-complement binding IgM antibodies in the enzyme-linked immunosorbent assay (ELISA)]. 633 14

Antimyolemmal antibodies can be demonstrated in sera of patients with coxsackie B, influenza, mumps and Q-fever perimyocarditis, in sera of patients with postpericardiotomy and postinfarction syndromes, in part of the sera of patients with endocarditis and in some patients with dilated heart disease most likely due to secondary immunopathogenesis after perimyocarditis. Antimyolemmal antibodies in titres greater than 1: 40 are complement fixing and cytolytic when added to cultures of vital myocytes. In vitro cardiocytolysis indicates that humoral effector mechanisms could also play a pathogenetic role in vivo. In vitro antibody dependent and independent cellular cytotoxicity of patients lymphocytes against isolated cardiocytes could not be observed in perimyocarditis and postmyocarditic cardiomyopathy. It could be demonstrated, however, in patients with postpericardiotomy syndrome and in some patients with dilated cardiomyopathies. Immunological investigations are therefore not only of diagnostic significance but have widened our knowledge of the etiology and pathogenesis of perimyocardial diseases. Furthermore they are helpful in the follow-up and prognosis of patients with protracted perimyocardial affections.
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PMID:[Secondary immunopathogenesis of cardiac diseases]. 637

Since the introduction of effective antimicrobial therapy, the leading cause of death in patients with infective endocarditis is no longer sepsis but, rather, congestive heart failure. The mortality is higher in patients with severe heart failure due to infective endocarditis who are treated with medical therapy only than in those who additionally undergo cardiac valve replacement. The mortality is also higher in patients with severe heart failure due to aortic infective endocarditis (40 to 93%) than in those with heart failure due to mitral infective endocarditis (17 to 66%). In patients with and in those without infective endocarditis, surgical intervention can be carried out with comparable mortality not only for aortic valve replacement (9 vs 8.4%) but also overall for valve replacement (10 vs 12%). In patients with class IV heart failure, overall mortality of valve replacement was higher (17%) than in patients with class II (8%) or class III heart failure (7%) and, similarly, comparable with that of matched groups of patients without infective endocarditis. In patients with class IV disability, the mortality of valve replacement was higher in those with active infective endocarditis (19%) than in those with inactive infective endocarditis, possibly due to a higher incidence of sudden onset of severe aortic regurgitation and myocardial abscess. No patient with valve replacement for inactive infective endocarditis developed prosthetic valve endocarditis; a single case of prosthetic valve endocarditis occurred in a patient with active infective endocarditis. In general, early surgical intervention is preferable to procrastination in the management of patients with progressive or severe heart failure due to infective endocarditis. Although, in at least 70% of patients, blood cultures may be rendered sterile within one week of initiation of appropriate antimicrobial therapy, patients with infective endocarditis due to staphylococci, multiply-resistant gram-negative bacilli, fungi, Q-fever or those with myocardial abscess or multiple relapses may require surgical intervention. While the overall incidence of clinically apparent emboli has been reported to be as high as 30%, in a ten-year observation period at the Mayo Clinic, the rate was 5.6%. Patients with echocardiographic evidence of large or mobile vegetations and those with infective endocarditis cause by microorganisms associated with a high risk of embolization such as slow-growing fastidious gram-negative bacilli, fungi (especially Aspergillus) and nutritionally-variant viridans streptococci should be considered candidates for surgery irrespective of a history of emboli.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Cardiac valve replacement in patients with active infective endocarditis. 666 78

Cell-mediated immunity is clearly the critical host defense mechanism against human Coxiella burnetii infection (Q fever); the role of specific antibody is unclear. By using a mouse macrophage tumor cell line, J774, persistently infected with C. burnetii phase I organisms, in a standard 51Cr-release cytotoxicity assay, we explored the possibility that antibody-dependent cellular cytotoxicity may be immune mechanism in Q fever. After 16 h of incubation in the presence of immune sera from Q fever hepatitis or endocarditis patients, nonimmune human peripheral blood effector cells specifically lysed infected J774 target cells; no 51Cr release was seen in the presence of nonimmune sera or uninfected target cells. An effector/target ratio of at least 5:1 was required, and monocytes were more efficient effector cells than lymphocytes. Cytotoxicity was blocked by preincubation of effector cells with purified aggregated human immunoglobulin G, indicating the role of Fc receptor-bearing effector cells. Two nonphagocytic lymphoid tumor cell targets, passively coated with C. burnetii, did not induce substantial immune-specific cytolysis, suggesting that bystander lysis does not explain the observation of specific lysis. Although antibody-dependent cellular cytotoxicity may participate in primary defense, alternatively, it may facilitate the dissemination of C. burnetii or surreptitiously participate in granuloma formation.
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PMID:Antibody-dependent cellular cytotoxicity of Coxiella burnetii-infected J774 macrophage target cells. 669 Apr 2

Sixteen patients with serologically proven Q-fever infection are reviewed. Fifteen had significantly raised antibody titres to both phase I and phase II Coxiella burneti antigens, indicating persistent or chronic infection. One patient, a premature infant who died, had raised phase II titres only, but is included together with the mother who had chronic Q-fever and was the presumed source of infection. Chronic Q-fever infection has previously been regarded as virtually synonymous with Q-fever endocarditis, but only seven of the patients in this survey had evidence of valvular endocarditis. In those who did, the infection had arisen on prosthetic valves or those affected by rheumatic or syphilitic heart disease. One patient had inexorably progressive destruction of an infected congenitally bicuspid aortic valve. Eight patients had infections associated with extra-valvular sites and several of these associations have not been previously described. These include extreme prematurity with perinatal death, possibly following transplacental infection, the sudden infant death syndrome (SIDS), multiple lower limb emboli from endocarditis of an abdominal aortic dacron graft, and colonization of ventricular endocardium following left ventricular myotomy/sub-aortic diaphragm resection. The current concept that chronic Q-fever is invariably associated with endocarditis is therefore untenable and the indications for phase I antibody screening should be extended to include patients other than those under investigation for 'culture-negative' endocarditis, for example those with unusual osteomyelitis of vertebrae.
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PMID:Chronic or fatal Q-fever infection: a review of 16 patients seen in North-East Scotland (1967-80). 687 20


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