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)

Isolation of Coxiella Burnetii in the standard laboratory setting is hazardous; therefore most diagnoses are based on retrospective detection of a rising antibody titer to C. burnetti. As a result, this disease is usually undiagnosed or misdiagnosed. Methods for the rapid detection of C. burnetti have now been developed that utilize specific hybridization of labeled DNA probes to nucleic acid in clinical samples. One method detects the presence of C. burnetii 16S ribosomal RNA (rRNA); another uses plasmid sequences. We have developed a probe that detects C. burnetii and one that differentiates between Coxiella strains capable of causing chronic disease and those that cause the acute form. Using these probes, C. burnetii can be identified in blood, urine, and tissue samples. The plasmid-derived probes detect as few as 10(4) organisms and less than 1 ng of Coxiella DNA. A third method differentiates between chronic (endocarditis-causing) strains and those that cause acute Q fever. This method uses the polymerase chain reaction (PCR), in which the target regions of DNA are amplified by iterative cycles of Taq I DNA polymerase chain extension to produce up to a 10(6) amplification of the target sequences. When Southern blotting is used in conjunction with PCR, the test detects as few as 2-9 C. burnetti cells.
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PMID:DNA probes for the identification of Coxiella burnetti strains. 237 70

A method for the rapid detection of Coxiella burnetii and differentiation between strains that cause endocarditis and those that cause acute Q fever is based on the observation that the different strains contain unique plasmid sequences. This method employs the polymerase chain reaction (PCR) and requires knowledge of specific DNA sequences in the region (target) of DNA to be amplified. To detect and differentiate between C. burnetii isolates, two sets of primers are required. The first set was derived from a fragment of plasmid QpH1 which has been detected in all C. burnetii isolates. A second PCR reaction was conducted using primers specific for DNA sequences that are shared only by QpRS plasmid-containing strains of C. burnetii. The first reaction detects the presence of C. burnetii. The second PCR is necessary to determine whether the isolate contains DNA sequences associated with strains causing chronic disease. These procedures detect as few as one to ten organisms.
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PMID:Strategy for detection and differentiation of Coxiella burnetii strains using the polymerase chain reaction. 237 78

Q fever is an zoonosis caused by Coxiella burnetti, the clinical features of which are often nonspecific and self-limited. Involvement of the central nervous system is rare and is usually seen as a complication of endocarditis caused by this rickettsial organism in the chronic disease. Specific neurological manifestations in the course of the acute illness aseptic meningitis, encephalitis, toxic confusional states, extrapyramidal signs, dementia and behavioral disturbances. We describe a patient who developed reversible bilateral abducens nerve paralysis and bilateral optic neuritis in the course of acute Q fever meningoencephalitis.
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PMID:Q fever meningoencephalitis associated with bilateral abducens nerve paralysis, bilateral optic neuritis and abnormal cerebrospinal fluid findings. 261 30

Human rheumatoid factors are antibodies of IgG, IgA, or IgM class that show reactions with antigenic determinants present on other immunoglobulin molecules. The most commonly measured rheumatoid factor relates to the 19S IgM type, which reacts by agglutination of latex particles coated with 7S IgG and is often measured in the standard latex fixation test. Approximately 65 to 70 per cent of patients with rheumatoid arthritis show positive serologic tests for rheumatoid factor; however, a number of other chronic disease conditions are also associated with positive rheumatoid factor reactions, including infective endocarditis, sarcoidosis, leprosy, and other hyperglobulinemic conditions. Although extensive serologic and immunochemical studies have identified a number of specific antigenic structural sites on immunoglobulin molecules that react with rheumatoid factors, recent studies have shown that a certain proportion of such antibodies may show cross-reactivity with DNA-histone complexes as well. It is still not entirely clear how rheumatoid factors fit into the pathogenesis of rheumatoid arthritis itself.
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PMID:Symposium on the immunodiagnosis of rheumatic and related diseases, Part II. Rheumatoid factors. 618 75

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

Between January 1979 and December 1991, we operated on 339 patients for chronic disease of the ascending aorta. The operation was elective in all. Endocarditis and its sequelae have been excluded. Thirty-one patients had a previous operation on the ascending aorta or the aortic valve; 268 patients had aneurysms of the ascending aorta without dissection; 72 had chronic aortic dissections, of whom 33 had a preexistent aneurysm. The patients included 272 men and 67 women. Mean age was 53.58 +/- 7 years. Eight percent of the patients had clinical stigmata of Marfan's disease. A tubular graft replacement was used in 7 patients, a tubular graft and valve replacement in 72 patients, and a composite valve graft replacement with reattachment of the coronary arteries using a 8 mm Dacron graft was performed in 260 patients. Concomitant procedures were used in 74 patients: coronary artery bypass grafts in 25, mitral valve replacement in 9, and aortic arch reconstruction in 40. The 30-day mortality rate was 7.6% (n = 26). For the whole group, multivariate analysis using stepwise logistic regression showed that operative risk factors were concomitant coronary artery bypass grafting, age (increased), aortic valve regurgitation, and previous cardiac surgery. Follow-up was conducted in 303 patients, and risk factors for late mortality were studied. Long-term survival was 59.6% +/- 3.7% at 9 years. It was 67% +/- 3.5% at 9 years for patients without aortic arch reconstruction and 56% +/- 4.5% for patients with aortic arch reconstruction (p = 0.0018). Reoperation was needed in 14 patients. Actuarial freedom from reoperation was 90% +/- 0.2% at 9 years for all the patients. Only one patient with composite valve graft replacement and reattachment of the coronary arteries had required reoperation for problems related to this procedure. This technique is used routinely by our team, especially in patients with large chronic aneurysms, dissected or not, and in those who had previous operations. The long-term results are good.
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PMID:Chronic disease of the ascending aorta. Surgical treatment and long-term results. 793 12

Q fever is caused by a rickettsial microorganism (Coxiella burnetii) harboured in sheep. The highest concentration of organisms are found in birth products. It is a very contagious organism which humans can contract by inhaling aerosolized organisms. Most commonly it leads to an acute 'flu-like illness. Rarely, chronic disease with endocarditis is fatal. Infected patients should be treated with tetracyclines or chloramphenicol. A number of outbreaks have been reported in hospital and research settings. Because of the fear of patients and staff contracting Q fever, Hospital Research Review Boards have increasingly resisted the presence of sheep in medical facilities. The authors have reviewed the circumstances leading to these outbreaks and believe researchers can minimize the risk of Q fever. The most important precautions are to use sheep only from Q fever controlled flocks and, depending on the nature of the research, only male sheep.
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PMID:Minimizing the risk of Q fever in the hospital setting. 816 58

Q fever is a zoonosis with a worldwide distribution with the exception of New Zealand. The disease is caused by Coxiella burnetii, a strictly intracellular, gram-negative bacterium. Many species of mammals, birds, and ticks are reservoirs of C. burnetii in nature. C. burnetii infection is most often latent in animals, with persistent shedding of bacteria into the environment. However, in females intermittent high-level shedding occurs at the time of parturition, with millions of bacteria being released per gram of placenta. Humans are usually infected by contaminated aerosols from domestic animals, particularly after contact with parturient females and their birth products. Although often asymptomatic, Q fever may manifest in humans as an acute disease (mainly as a self-limited febrile illness, pneumonia, or hepatitis) or as a chronic disease (mainly endocarditis), especially in patients with previous valvulopathy and to a lesser extent in immunocompromised hosts and in pregnant women. Specific diagnosis of Q fever remains based upon serology. Immunoglobulin M (IgM) and IgG antiphase II antibodies are detected 2 to 3 weeks after infection with C. burnetii, whereas the presence of IgG antiphase I C. burnetii antibodies at titers of >/=1:800 by microimmunofluorescence is indicative of chronic Q fever. The tetracyclines are still considered the mainstay of antibiotic therapy of acute Q fever, whereas antibiotic combinations administered over prolonged periods are necessary to prevent relapses in Q fever endocarditis patients. Although the protective role of Q fever vaccination with whole-cell extracts has been established, the population which should be primarily vaccinated remains to be clearly identified. Vaccination should probably be considered in the population at high risk for Q fever endocarditis.
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PMID:Q fever. 1051 1

Q fever is a zoonotic disease caused by the bacterium Coxiella burnetii. The most common reservoirs are domesticated ruminants, primarily cattle, sheep, and goats. Humans acquire Q fever typically by inhaling aerosols or contaminated dusts derived from infected animals or animal products. Its highly infectious nature and aerosol route of transmission make C. burnetii a possible agent of bioterrorism. Although up to 60% of initial infections are asymptomatic, acute disease can manifest as a relatively mild, self-limited febrile illness, or more moderately severe disease characterized by hepatitis or pneumonia. It manifests less commonly as myocarditis, pericarditis, and meningoencephalitis. Chronic Q fever occurs in <1% of infected patients, months or years after initial infection. Chronic disease manifests most commonly as a culture-negative endocarditis in patients with valvular heart disease. During 2000-2001, a total of 48 patients who met the case definition of Q fever were reported to CDC. This report describes the case investigations for six of these patients, which indicate that these persons acquired Q fever probably through direct or indirect contact with livestock. To enhance surveillance efforts, health-care providers should report cases of Q fever to state health departments.
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PMID:Q fever--California, Georgia, Pennsylvania, and Tennessee, 2000-2001. 1240 8

Q fever is a zoonosis caused by Coxiella burnetii. Farm animals and pets are the main reservoirs of infection, and transmission to human beings is mainly accomplished through inhalation of contaminated aerosols. This illness is associated with a wide clinical spectrum, from asymptomatic or mildly symptomatic seroconversion to fatal disease. Q fever in children has been rarely reported. We reviewed published work on this topic. Seroepidemiological studies show that children are frequently exposed to C burnetii. However, children are less frequently symptomatic than adults following infection, and may have milder diseases. Using the standard diagnostic criteria, we identified 46 published paediatric cases only. Self-limited febrile illness and pneumonia were the most common manifestations of acute Q fever. Chronic disease manifested as endocarditis and osteomyelitis. A history of exposure to possible sources of infection with C burnetii in a child with a compatible infectious syndrome should prompt testing for Q fever. Studies are required to determine the spectrum of morbidity associated with Q fever during childhood.
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PMID:Q fever in children. 1240 49


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