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)

Q fever is an infectious disease caused by Coxiella burnetii, an obligate intracellular microorganism that inhabits monocytes/macrophages. The dysregulated production of TNF-alpha in Q fever endocarditis has been associated with defective killing of C. burnetii by patient monocytes. As soluble receptors for TNF-alpha (TNF-R55 and TNF-R75) regulate TNF-alpha activity, we investigated their release by monocytes in Q fever. Spontaneous and C. burnetii-stimulated release of TNF-R75, but not of TNF-R55, was up-regulated in patients with ongoing endocarditis compared with controls. The increase in TNF-R75 release was related to the activity of Q fever endocarditis, since TNF-R75 release was similar in patients with cured endocarditis and controls. While spontaneous release of TNF-R75 by monocytes from patients with ongoing Q fever endocarditis occurred without changes in its membrane expression, C. burnetii increased the surface expression of TNF-R75. In addition, TNF-R75 transcripts were increased in resting and C. burnetii-stimulated monocytes from patients with ongoing endocarditis. On the other hand, TNF-R75 release was not related to TNF-alpha secretion. These results indicate that the modulation of TNF-R75 is a critical feature of the pathophysiology of Q fever endocarditis.
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PMID:The 75-kD tumour necrosis factor (TNF) receptor is specifically up-regulated in monocytes during Q fever endocarditis. 1093 Nov 45

Coxiella burnetii, an obligate intracellular bacterium, is the agent of Q fever. The chronic form of the disease is associated with the overproduction of interleukin-10 and deficient C. burnetii killing by monocytes. We hypothesized that the replication of C. burnetii inside monocytes requires a macrophage-deactivating cytokine such as interleukin-10. In the absence of interleukin-10, C. burnetii survived but did not replicate in monocytes. C. burnetii replication (measured 15 days) was induced in interleukin-10-treated monocytes. This effect of interleukin-10 is specific since transforming growth factor beta1 had no effect on bacterial replication. C. burnetii replication involves the down-modulation of tumor necrosis factor (TNF) release. First, interleukin-10 suppressed C. burnetii-stimulated production of TNF. Second, the addition of recombinant TNF to interleukin-10-treated monocytes inhibited bacterial replication. Third, the incubation of infected monocytes with neutralizing anti-TNF antibodies favored C. burnetii replication. On the other hand, deficient C. burnetii killing by monocytes from patients with chronic Q fever involves interleukin-10. Indeed, C. burnetii replication was observed in monocytes from patients with Q fever endocarditis, but not in those from patients with acute Q fever. Bacterial replication was inhibited by neutralizing anti-interleukin-10 antibodies. As monocytes from patients with endocarditis overproduced interleukin-10, the defective bacterial killing is likely related to endogenous interleukin-10. These results suggest that interleukin-10 enables monocytes to support C. burnetii replication and to favor the development of chronic Q fever.
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PMID:Interleukin-10 stimulates Coxiella burnetii replication in human monocytes through tumor necrosis factor down-modulation: role in microbicidal defect of Q fever. 1125 92

Coxiella burnetii causes acute and chronic Q fever. To evaluate the risk factors of development of chronic endocarditis following Q fever and to assess the best preventive therapy, a retrospective study of patients diagnosed as having Q fever during 1985-2000 was conducted. Twelve patients with acute Q fever who developed endocarditis and 102 patients with Q fever endocarditis were included in the study. When compared to 200 control patients with acute Q fever, preexisting valvular disease (P<10(-7)), especially a prosthetic valve (P=.01), were encountered more often among patients with endocarditis. Among patients with valvular defects, we estimate the risk of developing endocarditis to be 39%. A combination of doxycycline plus hydroxychloroquine was better at preventing the development of endocarditis than doxycycline alone (P=.009). Our results should encourage physicians to detect valvular lesions in patients with acute Q fever and to search for acute Q fever in patients with a valvulopathy and unexplained fever. A proper treatment for such patients and a scheduled follow-up should reduce the risk of developing endocarditis.
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PMID:Risks factors and prevention of Q fever endocarditis. 1143 95

Whipple's disease is a systemic infection sometimes associated with cardiac manifestations. Recently, there has been an increase in the number of reported cases of Whipple's endocarditis. The purpose of our study was to describe this entity. Data from 35 well-described cases of Whipple's endocarditis were collected and compared with those of blood culture-positive endocarditis, Q fever endocarditis, and Bartonella endocarditis. Some patients with generalized Whipple's disease presented with cardiac involvement, among other symptoms. Others presented with a nonspecific, blood culture-negative endocarditis with no associated symptoms. In comparison with cases of endocarditis due to other causes, congestive heart failure, fever, and previous valvular disease were less frequently observed in the cases of Whipple's endocarditis. Without examination of the excised valves, the diagnosis of infective endocarditis could not have been confirmed in most cases. Treatment is not well established. Whipple's endocarditis is a specific entity involving minor inflammatory reactions and negative blood cultures, and its incidence is probably underestimated.
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PMID:Whipple's endocarditis: review of the literature and comparisons with Q fever, Bartonella infection, and blood culture-positive endocarditis. 1156 70

Up to now no Q fever endocarditis (caused by rickettsia Coxiella burnetii) has been diagnosed in Poland. Potential endocarditis caused by Coxiella burnetii strains can be related to a group of strains present in Poland or sensitivity of Polish Population. The aim of the study was to estimate frequency of Q fever endocarditis is patients of National Institute of Cardiology and to characterize Coxiella burnetii strains and correlation between frequency of Q fever endocarditis and the group of strains. In all patients infective endocarditis and valvular heart disease were diagnosed. In all cases vegetations on TTE or TEE and negative blood cultures were confirmed. No fungal antigens or elevated anti-Candida and anti-Aspergillus antibodies were found. Serological investigations as far as it concerns C. burnetii antibodies were negative in all cases. No Coxiella burnetii infection were found in patients with infective endocarditis and negative blood cultures in the National Institute of Cardiology. However due to high probability of occurrence of such an infection in Poland further investigations in other centers would be useful.
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PMID:[Attempt of estimation of Q fever endocarditis frequency in Poland]. 1176 82

A case of Q fever endocarditis was diagnosed in a patient with no sign of active endocarditis by performing PCR targeting eubacterial 16S rDNA on the resected mitral valve. The diagnosis was confirmed by detection of high levels of anti-Coxiella burnetti antibodies, positive immunohistologic analysis of the valve tissue with specific antibodies and culture of C. burnetti from the valve tissue. As this patient had an unexplained aggravation of valve dysfunction, we recommended routine serologic testing for C. burnetti to allow the diagnosis of Q fever endocarditis at a very early stage.
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PMID:Clinically and histologically silent Q fever endocarditis accidentally diagnosed by PCR. 1195 25

Endocarditis is a rare but severe complication of Q fever, an infectious disease caused by the intracellular pathogen Coxiella burnetii. Heart involvement is the most common clinical presentation of chronic Q fever, and it occurs almost invariably in patients with previous valvular disease or artificial valves, and in the immunocompromised host. The optimal treatment of Q fever endocarditis is still today debated, and recommended duration of treatment varies from one year to one's lifespan. A case of chronic Q fever endocarditis is described in a patient with biological prosthetic aortic valve and aortic homograft, successfully treated with doxycycline and chloroquine for 2 years.
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PMID:Doxycycline and chloroquine as treatment for chronic Q fever endocarditis. 1221 21

Q fever manifests as primary infection or acute Q fever and may become chronic in patients with underlying valvulopathy. Because Coxiella burnetii infection depends on host response, we measured tumor necrosis factor (TNF), interleukin (IL)-6, IL-12, and IL-10 in patients with different clinical presentations of acute Q fever. Compared with control subjects, patients with uncomplicated acute Q fever exhibited increased release of the 4 cytokines. Their amounts were higher in patients with hepatitis than in patients with fever or pneumonia. In patients with valvulopathy, who exhibited the highest risk of chronic evolution, the amounts of TNF and IL-10 were higher than in patients without valvulopathy. TNF production was specifically enhanced in patients who developed Q fever endocarditis. These results show that acute Q fever is associated with cytokine overproduction. Persistent TNF amounts were associated with the occurrence of endocarditis in patients with valvulopathy, and that may be a marker of chronic evolution of Q fever.
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PMID:Dysregulation of cytokines in acute Q fever: role of interleukin-10 and tumor necrosis factor in chronic evolution of Q fever. 1266 Sep 42

Coxiella burnetii (C.b.) is a strictly intracellular, Gram-negative bacterium. It causes Q fever in humans and animals worldwide. The animal Q fever is sometimes designated "coxiellosis". This infection has many different reservoirs including arthropods, birds and mammals. Domestic animals and pets, are the most frequent source of human infections. Q fever may appear basically in two forms, acute and chronic (persistent). The latter form of Q fever in animals is characteristic by shedding C.b. into the environment during parturition or abortion. Human Q fever results usually from inhalation of contaminated aerosols originating mostly from tissue and body fluids of infected animals. Q fever may appear in humans either in an acute form accompanied mainly by fever (pneumonia, flu-like disease, hepatitis) or in a chronic form (mainly endocarditis). Diagnosis of Q fever is based on isolation of the agent in cell culture, its direct detection, namely by PCR, and serology. Detection of high phase II antibodies titers 1-3 weeks after the onset of symptoms and identification of IgM antibodies are indicative to acute infection. High phase I IgG antibody titers >800 as revealed by microimmunofluorescence offer evidence of chronic C.b. infection. For acute Q fever, a two-weeks-treatment with doxycycline is recommended as the first-line therapy. In the case of Q fever endocarditis a long-term combined antibiotic therapy is necessary to prevent relapses. Application of Q fever vaccines containing or prepared from phase I C.b. corpuscles should be considered at least for professionally exposed groups of the population. Infections caused by C.b. are spread worldwide and may pose serious and often underestimated health problems in human but also in veterinary medicine. Though during the last decades substantial progress in investigation of C.b. has been achieved and many data concerning this pathogen has been accumulated, some questions, namely those related to the pathogenesis of the disease, remain open.
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PMID:Q fever--still a query and underestimated infectious disease. 1269 56

Q fever, a worldwide zoonosis caused by Coxiella burnetii, has many manifestations in humans. Endocarditis is the most serious complication of Q fever. Animal models are limited to acute pulmonary or hepatic disease and reproductive disorders. An appropriate experimental animal model for Q fever endocarditis does not yet exist. In this study, severe combined immunodeficient (SCID) mice infected with C. burnetii showed persistent clinical symptoms and died, whereas immunocompetent mice similarly infected became asymptomatic and survived. The SCID mice examined in this study had severe chronic lesions in their primary organs: the heart, lung, spleen, liver, and kidney. The heart lesions of the SCID mice were similar to those in humans with chronic Q fever endocarditis: they had focal calcification and expanded macrophages containing C. burnetii. The 50% lethal dose of C. burnetii in SCID mice was at least 10(8) times less than that in immunocompetent mice. The SCID mouse is highly susceptible to C. burnetii, and the immunodeficiency of the host enhances the severity of Q fever. This animal model could provide a new tool for the study of chronic Q fever and Q fever in immunodeficient hosts.
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PMID:SCID mouse model for lethal Q fever. 1287 53


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