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Didier Raoult - One of the best experts on this subject based on the ideXlab platform.
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Acute Q Fever Endocarditis: A Paradigm Shift Following the Systematic Use of Transthoracic Echocardiography During Acute Q Fever
Clinical Infectious Diseases, 2019Co-Authors: Clea Melenotte, Gilbert Habib, Jean-louis Mege, Matthieu Million, Loïc Epelboin, Sandrine Hubert, Thierry Monsec, Felix Djossou, Didier RaoultAbstract:Background: As Q Fever, caused by Coxiella burnetii, is a major health challenge due to its cardiovascular complications, we aimed to detect acute Q Fever valvular injury to improve therapeutic management. Methods: In the French national reference center for Q Fever, we prospectively collected data from patients with acute Q Fever and valvular injury. We identified a new clinical entity, acute Q Fever endocarditis, defined as valvular lesion potentially caused by C. burnetii: vegetation, valvular nodular thickening, rupture of chorda tendinae, and valve or chorda tendinae thickness. To determine whether or not the disease was superimposed on an underlying valvulopathy, patients' physicians were contacted. Aortic bicuspidy, valvular stenosis, and insufficiency were considered as underlying valvulopathies. Results: Of the 2434 patients treated in our center, 1797 had acute Q Fever and 48 had acute Q Fever endocarditis. In 35 cases (72%), transthoracic echocardiography (TTE) identified a valvular lesion of acute Q Fever endocarditis without underlying valvulopathy. Positive anticardiolipin antibodies (>22 immunoglobulin G-type phospholipid units [GPLU]) were independently associated with acute Q Fever endocarditis (odds ratio [OR], 2.7 [95% confidence interval {CI}, 1.3-5.5]; P = .004). Acute Q Fever endocarditis (OR, 5.2 [95% CI, 2.6-10.5]; P < .001) and age (OR, 1.7 [95% CI, 1.1-1.9]; P = .02) were independent predictors of progression toward persistent C. burnetii endocarditis. Conclusions: Systematic TTE in acute Q Fever patients offers a uniQue opportunity for early diagnosis of acute Q Fever endocarditis and for the prevention of persistent endocarditis. Transesophageal echocardiography should be proposed in men, aged >40 years, with anticardiolipin antibodies >60 GPLU when TTE is inconclusive or negative.
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high concentrations of serum soluble e cadherin in patients with Q Fever
Frontiers in Cellular and Infection Microbiology, 2019Co-Authors: Soraya Mezouar, Camelia Slimani, Clea Melenotte, Ikram Omar Osman, Jean-louis Mege, Didier Raoult, Celine Chartier, Christian DevauxAbstract:Cadherins switching is a hallmark of neoplasic processes. The E-cadherin (E-cad) subtype is one of the surface molecules regulating cell-to-cell adhesion. After its cleavage by sheddases, a soluble fragment (sE-cad) is released that has been identified as a pro-carcinogenic inflammatory signal in several bacteria-induced cancers. Recently we reported that Q Fever, a disease due to Coxiella burnetii infection, can be complicated by occurrence of non-Hodgkin lymphoma (NHL). Therefore, we studied E-cad switching in Q Fever. The sE-cad levels were found increased in the sera of acute and persistent Q Fever patients, whereas they remained at the baseline in controls groups of healthy donors, people cured of Q Fever, patients suffering from unrelated inflammatory diseases, and past Q Fever patients who developed NHL. These results indicate that sE-cad can be considered as a new biomarker of C. burnetii infection rather than a marker of NHL-associated to Q Fever. We wondered if changes in sE-cad reflected variations in the CDH1 gene transcription. The expression of E-cad mRNA and its intracellular ligand β-catenin was down-regulated in peripheral blood mononuclear cells (PBMCs) of patients with either acute or persistent forms of Q Fever. Indeed, a lower cell-surface expression of E-cad was measured in a minority (<5%) subpopulation of HLADR+/CD16+ monocytes from patients with acute Q Fever. However, a very strong increase in E-cad expression was observed on more than 30% of the HLADR+/CD16+ monocytes of persistent Q Fever patients, a cell subpopulation known to be a target for C. burnetii in humans. An experimental in vitro infection of healthy donors' PBMCs with C. burnetii, was performed to directly evaluate the link between C. burnetii interaction with PBMCs and their E-cad expression. A significant increase in the percentage of HLADR+/CD16+ monocytes expressing E-cad was measured after PBMCs had been incubated for 8 h with C. burnetii Nine Mile strain. Altogether, these data demonstrate that C. burnetii severely impairs the E-cad expression in circulating cells of Q Fever patients.
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rainfall and sloth births in may Q Fever in july cayenne french guiana
American Journal of Tropical Medicine and Hygiene, 2015Co-Authors: Carole Eldin, Felix Djossou, Aba Mahamat, Didier RaoultAbstract:Q Fever in French Guiana is correlated with the rainy season. We found a 1- to 2-month lagged correlation between Q Fever incidence and the number of births of three-toed sloth. This result strengthens the hypothesis that the three-toed sloth is the wild reservoir of Q Fever in French Guiana.
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Q Fever in french guiana
American Journal of Tropical Medicine and Hygiene, 2014Co-Authors: Carole Eldin, Felix Djossou, Aba Mahamat, Magalie Demar, Philippe Abboud, Didier RaoultAbstract:Coxiella burnetii, the causative agent of Q Fever, is present worldwide. Recent studies have shown that this bacterium is an emerging pathogen in French Guiana and has a high prevalence (24% of community-acQuired pneumonia). In this review, we focus on the peculiar epidemiology of Q Fever in French Guiana. We place it in the context of the epidemiology of the disease in the surrounding countries of South America. We also review the clinical features of Q Fever in this region, which has severe initial presentation but low mortality rates. These characteristics seem to be linked to a uniQue genotype (genotype 17). Finally, we discuss the issue of the animal reservoir of C. burnetii in French Guiana, which is still unknown. Further studies are necessary to identify this reservoir. Identification of this reservoir will improve the understanding of the Q Fever epidemic in French Guiana and will provide new tools to control this public health problem.
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reevaluation of the risk of fetal death and malformation after Q Fever
Clinical Infectious Diseases, 2014Co-Authors: Matthieu Million, Felicetta Damato, Dominiques Carles, Camelia Protopopescu, Maria Patrizia Carrieri, Didier RaoultAbstract:A meta-analysis of 136 Q Fever pregnancies, including 4 new cases and 7 population-based serological studies, revealed significant increases in fetal death and malformation after Q Fever during pregnancy. This poor obstetric outcome is prevented by antibiotic treatment.
Matthieu Million - One of the best experts on this subject based on the ideXlab platform.
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Acute Q Fever Endocarditis: A Paradigm Shift Following the Systematic Use of Transthoracic Echocardiography During Acute Q Fever
Clinical Infectious Diseases, 2019Co-Authors: Clea Melenotte, Gilbert Habib, Jean-louis Mege, Matthieu Million, Loïc Epelboin, Sandrine Hubert, Thierry Monsec, Felix Djossou, Didier RaoultAbstract:Background: As Q Fever, caused by Coxiella burnetii, is a major health challenge due to its cardiovascular complications, we aimed to detect acute Q Fever valvular injury to improve therapeutic management. Methods: In the French national reference center for Q Fever, we prospectively collected data from patients with acute Q Fever and valvular injury. We identified a new clinical entity, acute Q Fever endocarditis, defined as valvular lesion potentially caused by C. burnetii: vegetation, valvular nodular thickening, rupture of chorda tendinae, and valve or chorda tendinae thickness. To determine whether or not the disease was superimposed on an underlying valvulopathy, patients' physicians were contacted. Aortic bicuspidy, valvular stenosis, and insufficiency were considered as underlying valvulopathies. Results: Of the 2434 patients treated in our center, 1797 had acute Q Fever and 48 had acute Q Fever endocarditis. In 35 cases (72%), transthoracic echocardiography (TTE) identified a valvular lesion of acute Q Fever endocarditis without underlying valvulopathy. Positive anticardiolipin antibodies (>22 immunoglobulin G-type phospholipid units [GPLU]) were independently associated with acute Q Fever endocarditis (odds ratio [OR], 2.7 [95% confidence interval {CI}, 1.3-5.5]; P = .004). Acute Q Fever endocarditis (OR, 5.2 [95% CI, 2.6-10.5]; P < .001) and age (OR, 1.7 [95% CI, 1.1-1.9]; P = .02) were independent predictors of progression toward persistent C. burnetii endocarditis. Conclusions: Systematic TTE in acute Q Fever patients offers a uniQue opportunity for early diagnosis of acute Q Fever endocarditis and for the prevention of persistent endocarditis. Transesophageal echocardiography should be proposed in men, aged >40 years, with anticardiolipin antibodies >60 GPLU when TTE is inconclusive or negative.
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clinical features and complications of coxiella burnetii infections from the french national reference center for Q Fever
JAMA Network Open, 2018Co-Authors: Clea Melenotte, Patrizia M Carrieri, Emmanouil Angelakis, Matthieu Million, Sophie Edouard, Felix Djossou, Carole Eldin, Camelia Protopopescu, Nathalie BardinAbstract:Importance Q Fever remains widespread throughout the world; the disease is serious and causes outbreaks and deaths when complications are not detected. The diagnosis of Q Fever reQuires the demonstration of the presence ofCoxiella burnetiiand the identification of an organic lesion. Objective To describe the hitherto neglected clinical characteristics of Q Fever and identifying risk factors for complications and death. Design, Setting, and Participants This prospective cohort study conducted from January 1, 1991, through December 31, 2016, included patients treated at the French National Reference Center for Q Fever with serologic findings positive forC burnetiiand clinical data consistent withC burnetiiinfection. Clinical data were prospectively collected by telephone. Patients with unavailable clinical data or an unidentified infectious focus were excluded. Main Outcomes and Measures Q Fever complications and mortality. Results Of the 180 483 patients undergoing testing, 2918 had positive findings forC burnetiiand 2434 (68.8% men) presented with clinical data consistent with aC burnetiiinfection. Mean (SD) age was 51.8 (17.4) years, and the ratio of men to women was 2.2. At the time of inclusion, 1806 patients presented with acute Q Fever, including 138 with acute Q Fever that progressed to persistentC burnetiiinfection, and 766 had persistent focalizedC burnetiiinfection. Rare and hitherto neglected foci of infections included lymphadenitis (97 [4.0%]), acute Q Fever endocarditis (50 [2.1%]), hemophagocytic syndrome (9 [0.4%]), and alithiasic cholecystitis (11 [0.4%]). Vascular infection (hazard ratio [HR], 3.1; 95% CI, 1.7-5.7;P Conclusions and Relevance Previously neglected foci ofC burnetii infection include the lymphatic system (ie, bone marrow, lymphadenitis) with a risk of lymphoma. Cardiovascular infections were the main fatal complications, highlighting the importance of routine screening for valvular heart disease and vascular anomalies during acute Q Fever. Routine screening for anticardiolopin antibodies during acute Q Fever can help prevent complications. Positron emission tomographic scanning could be proposed for all patients with suspected persistent focused infection to rapidly diagnose vascular and lymphatic infections associated with death and lymphoma, respectively.
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thrombosis and antiphospholipid antibody syndrome during acute Q Fever a cross sectional study
Medicine, 2017Co-Authors: Matthieu Million, Nathalie Bardin, Sophie Edouard, Simon Bessis, Nadia Nouiakh, Charlaine Douliery, E Angelakis, A Bosseray, Olivier Epaulard, Stephanie BrangerAbstract:Q Fever is a neglected and potentially fatal disease. During acute Q Fever, antiphospholipid antibodies are very prevalent and have been associated with Fever, thrombocytopenia, acQuired heart valve disease, and progression to chronic endocarditis. However, thrombosis, the main clinical criterion of the 2006 updated classification of the antiphospholipid syndrome, has not been assessed in this context. To test whether thrombosis is associated with antiphospholipid antibodies and whether the criteria for antiphospholipid syndrome can be met in patients with acute Q Fever, we conducted a cross-sectional study at the French National Referral Center for Q Fever.Patients included were diagnosed with acute Q Fever in our Center between January 2007 and December 2015. Each patient's history and clinical characteristics were recorded with a standardized Questionnaire. Predictive factors associated with thrombosis were assessed using a rare events logistic regression model. IgG anticardiolipin antibodies (IgG aCL) assessed by an enzyme-linked immunosorbent assay were tested on the Q Fever diagnostic serum. A dose-dependent relationship between IgG aCL levels and thrombosis was tested using a receiver operating characteristic (ROC) analysis.Of the 664 patients identified for inclusion in the study, 313 (47.1%) had positive IgG aCL and 13 (1.9%) were diagnosed with thrombosis. Three patients fulfilled the antiphospholipid syndrome criteria. After multiple adjustments, only positive IgG aCL (relative risk, 14.46 [1.85-113.14], P = .011) were independently associated with thrombosis. ROC analysis identified a dose-dependent relationship between IgG aCL levels and occurrence of thrombosis (area under curve, 0.83, 95%CI [0.73-0.93], P < .001).During acute Q Fever, antiphospholipid antibodies are associated with thrombosis, thrombocytopenia, and acQuired valvular heart disease. Antiphospholipid antibodies should be systematically assessed in acute Q Fever patients. HydroxychloroQuine, which has been previously shown to antagonize IgG aCL pathogenic properties, should be tested in acute Q Fever patients with anticardiolipin antibodies to prevent antiphospholipid-associated complications.Key Point: In addition to Fever, thrombocytopenia and acQuired valvular heart disease, antiphospholipid antibodies are associated with thrombosis during acute Q Fever.
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No Such Thing as Chronic Q Fever
Emerging Infectious Diseases, 2017Co-Authors: Matthieu MillionAbstract:Modern diagnostic methods enable clinicians to look beyond a diagnosis of chronic Q Fever and discern whether patients instead have persistent focalized Coxiella burnetii infection(s). Use of these methods and development of criteria to define and treat such infections, especially cardiovascular infections, will improve the prognosis for patients previously thought to have chronic Q Fever.
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antiphospholipid antibody syndrome with valvular vegetations in acute Q Fever
Clinical Infectious Diseases, 2016Co-Authors: Matthieu Million, Nathalie Bardin, Emmanouil Angelakis, Sophie Edouard, Franck Thuny, Simon Bessis, Thomas Guimard, Thierry Weitten, Francois Martinbarbaz, Michele TexereauAbstract:Coxiella burnetii endocarditis is considered to be a late complication of Q Fever in patients with preexisting valvular heart disease (VHD). We observed a large transient aortic vegetation in a patient with acute Q Fever and high levels of IgG anticardiolipin antibodies (IgG aCL). Therefore, we sought to determine how commonly acute Q Fever could cause valvular vegetations associated with antiphospholipid antibody syndrome, which would be a new clinical entity.
Jean-louis Mege - One of the best experts on this subject based on the ideXlab platform.
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Acute Q Fever Endocarditis: A Paradigm Shift Following the Systematic Use of Transthoracic Echocardiography During Acute Q Fever
Clinical Infectious Diseases, 2019Co-Authors: Clea Melenotte, Gilbert Habib, Jean-louis Mege, Matthieu Million, Loïc Epelboin, Sandrine Hubert, Thierry Monsec, Felix Djossou, Didier RaoultAbstract:Background: As Q Fever, caused by Coxiella burnetii, is a major health challenge due to its cardiovascular complications, we aimed to detect acute Q Fever valvular injury to improve therapeutic management. Methods: In the French national reference center for Q Fever, we prospectively collected data from patients with acute Q Fever and valvular injury. We identified a new clinical entity, acute Q Fever endocarditis, defined as valvular lesion potentially caused by C. burnetii: vegetation, valvular nodular thickening, rupture of chorda tendinae, and valve or chorda tendinae thickness. To determine whether or not the disease was superimposed on an underlying valvulopathy, patients' physicians were contacted. Aortic bicuspidy, valvular stenosis, and insufficiency were considered as underlying valvulopathies. Results: Of the 2434 patients treated in our center, 1797 had acute Q Fever and 48 had acute Q Fever endocarditis. In 35 cases (72%), transthoracic echocardiography (TTE) identified a valvular lesion of acute Q Fever endocarditis without underlying valvulopathy. Positive anticardiolipin antibodies (>22 immunoglobulin G-type phospholipid units [GPLU]) were independently associated with acute Q Fever endocarditis (odds ratio [OR], 2.7 [95% confidence interval {CI}, 1.3-5.5]; P = .004). Acute Q Fever endocarditis (OR, 5.2 [95% CI, 2.6-10.5]; P < .001) and age (OR, 1.7 [95% CI, 1.1-1.9]; P = .02) were independent predictors of progression toward persistent C. burnetii endocarditis. Conclusions: Systematic TTE in acute Q Fever patients offers a uniQue opportunity for early diagnosis of acute Q Fever endocarditis and for the prevention of persistent endocarditis. Transesophageal echocardiography should be proposed in men, aged >40 years, with anticardiolipin antibodies >60 GPLU when TTE is inconclusive or negative.
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high concentrations of serum soluble e cadherin in patients with Q Fever
Frontiers in Cellular and Infection Microbiology, 2019Co-Authors: Soraya Mezouar, Christian A. Devaux, Camelia Slimani, Clea Melenotte, Courtney Chartier, Ikram Omar Osman, Jean-louis MegeAbstract:Cadherins switching is a hallmark of neoplasic processes. The E-cadherin (E-cad) subtype is one of the surface molecules regulating cell-to-cell adhesion. After its cleavage by sheddases, a soluble fragment (sE-cad) is released that has been identified as a pro-carcinogenic inflammatory signal in several bacteria-induced cancers. Recently we reported that Q Fever, a disease due to Coxiella burnetii infection, can be complicated by occurrence of non-Hodgkin lymphoma (NHL). Therefore, we studied E-cad switching in Q Fever. The sE-cad levels were found increased in the sera of acute and persistent Q Fever patients, whereas they remained at the baseline in controls groups of healthy donors, people cured of Q Fever, patients suffering from unrelated inflammatory diseases, and past Q Fever patients who developed NHL. These results indicate that sE-cad can be considered as a new biomarker of C. burnetii infection rather than a marker of NHL-associated to Q Fever. We wondered if changes in sE-cad reflected variations in the CDH1 gene transcription. The expression of E-cad mRNA and its intracellular ligand -catenin was down-regulated in peripheral blood mononuclear cells (PBMCs) of patients with either acute or persistent forms of Q Fever. Indeed, a lower cell-surface expression of E-cad was measured in a minority (less than 5%) subpopulation of HLADR+/CD16+ monocytes from patients with acute Q Fever. However, a very strong increase in E-cad expression was observed on more than 30% of the HLADR+/CD16+ monocytes of persistent Q Fever patients, a cell subpopulation known to be a target for C. burnetii in humans. An experimental in vitro infection of healthy donors' PBMCs with C. burnetii, was performed to directly evaluate the link between C. burnetii interaction with PBMCs and their E-cad expression. A significant increase in the percentage of HLADR+/CD16+ monocytes expressing E-cad was measured after PBMCs had been incubated for 8h with C. burnetii Nine Mile strain. Altogether, these data demonstrate that C. burnetii severely impairs the E-cad expression in circulating cells of Q Fever patients.
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high concentrations of serum soluble e cadherin in patients with Q Fever
Frontiers in Cellular and Infection Microbiology, 2019Co-Authors: Soraya Mezouar, Camelia Slimani, Clea Melenotte, Ikram Omar Osman, Jean-louis Mege, Didier Raoult, Celine Chartier, Christian DevauxAbstract:Cadherins switching is a hallmark of neoplasic processes. The E-cadherin (E-cad) subtype is one of the surface molecules regulating cell-to-cell adhesion. After its cleavage by sheddases, a soluble fragment (sE-cad) is released that has been identified as a pro-carcinogenic inflammatory signal in several bacteria-induced cancers. Recently we reported that Q Fever, a disease due to Coxiella burnetii infection, can be complicated by occurrence of non-Hodgkin lymphoma (NHL). Therefore, we studied E-cad switching in Q Fever. The sE-cad levels were found increased in the sera of acute and persistent Q Fever patients, whereas they remained at the baseline in controls groups of healthy donors, people cured of Q Fever, patients suffering from unrelated inflammatory diseases, and past Q Fever patients who developed NHL. These results indicate that sE-cad can be considered as a new biomarker of C. burnetii infection rather than a marker of NHL-associated to Q Fever. We wondered if changes in sE-cad reflected variations in the CDH1 gene transcription. The expression of E-cad mRNA and its intracellular ligand β-catenin was down-regulated in peripheral blood mononuclear cells (PBMCs) of patients with either acute or persistent forms of Q Fever. Indeed, a lower cell-surface expression of E-cad was measured in a minority (<5%) subpopulation of HLADR+/CD16+ monocytes from patients with acute Q Fever. However, a very strong increase in E-cad expression was observed on more than 30% of the HLADR+/CD16+ monocytes of persistent Q Fever patients, a cell subpopulation known to be a target for C. burnetii in humans. An experimental in vitro infection of healthy donors' PBMCs with C. burnetii, was performed to directly evaluate the link between C. burnetii interaction with PBMCs and their E-cad expression. A significant increase in the percentage of HLADR+/CD16+ monocytes expressing E-cad was measured after PBMCs had been incubated for 8 h with C. burnetii Nine Mile strain. Altogether, these data demonstrate that C. burnetii severely impairs the E-cad expression in circulating cells of Q Fever patients.
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progenitor mast cells and tryptase in Q Fever
Comparative Immunology Microbiology and Infectious Diseases, 2019Co-Authors: Soraya Mezouar, Laury Leveille, Victor Morel, Courtney Chartier, Noémie Resseguier, Jean-louis Mege, Jeremie VitteAbstract:Abstract Q Fever is an infectious disease due to Coxiella burnetii. Following a primary-infection, C. burnetii may persist in some patients, leading to endocarditis and vascular infections. Mast cells (MCs), known for their role in allergic diseases, innate immunity and cardiac function, are produced by bone marrow, circulate as progenitors in the bloodstream and reach tissues for their maturation and activation. The latter may be estimated by measuring serum tryptase levels. We wondered if MC progenitors and tryptase were affected in Q Fever. We showed a decrease in MC progenitor count in Q Fever patients whereas serum tryptase levels were increased. Taken together, our results show alterations of MC numbers and activity in Q Fever patients, suggesting that MC are involved in Q Fever pathophysiology.
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involvement of matrix metalloproteinases in chronic Q Fever
Clinical Microbiology and Infection, 2017Co-Authors: Anne F M Jansen, Jean-louis Mege, Chantal P Bleekerrovers, Peter C Wever, Teske Schoffelen, Julien Textoris, H I J Roest, Leo A B Joosten, Mihai G Netea, E Van De VosseAbstract:Abstract Objectives Chronic Q Fever is a persistent infection with the intracellular Gram-negative bacterium Coxiella burnetii , which can lead to complications of infected aneurysms. Matrix metalloproteinases (MMPs) cleave extracellular matrix and are involved in infections as well as aneurysms. We aimed to study the role of MMPs in the pathogenesis of chronic Q Fever. Methods We investigated gene expression of MMPs through microarray analysis and MMP production with ELISA in C. burnetii -stimulated peripheral blood mononuclear cells (PBMCs) of patients with chronic Q Fever and healthy controls. Twenty single nucleotide polymorphisms (SNPs) of MMP and tissue inhibitor of MMP genes were genotyped in 139 patients with chronic Q Fever and 220 controls with similar cardiovascular co-morbidity. Additionally, circulating MMPs levels in patients with chronic Q Fever were compared with those in cardiovascular controls with and without a history of past Q Fever. Results In healthy controls, the MMP pathway involving four genes ( MMP1 , MMP7 , MMP10 , MMP19 ) was significantly up-regulated in C. burnetii -stimulated but not in Escherichia coli lipopolysaccharide -stimulated PBMCs. Coxiella burnetii induced MMP-1 and MMP-9 production in PBMCs of healthy individuals (both p MMP7 (rs11568810) (p MMP9 (rs17576) (p Conclusion Coxiella burnetii -induced MMP production may contribute to the development of chronic Q Fever.
Andreas Stein - One of the best experts on this subject based on the ideXlab platform.
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Q Fever and pregnancy disease prevention and strain specificity
European Journal of Clinical Microbiology & Infectious Diseases, 2013Co-Authors: Emmanouil Angelakis, Matthieu Million, Andreas Stein, Felicetta Damato, L Rouli, Herve Richet, Jean Marc Rolain, Didier RaoultAbstract:The link between fetal morbidity and Q Fever and the necessity of long-term antibiotics for Coxiella burnetii infection during pregnancy have been recently Questioned in the Netherlands, where the clone responsible for the Q Fever outbreak harbors the QpH1 plasmid. In this context, we assessed pregnancy outcomes according to antibiotic administration in a new series and compared the plasmid type between isolates associated with abortion and other clinical isolates to determine if there is a link between genotype and abortion in humans. All French patients who received a diagnosis of Q Fever during pregnancy at the French National Referral Centre for Q Fever from 2006 through July 2011 were included. On the other hand, the plasmid types of 160 clinical isolates, including seven isolates from patients who experienced an abortion, were compared. The differences between the QpDV and QpH1 plasmid seQuences were analyzed. Acute Q Fever was a cause of fetal morbidity, and the absence of long-term cotrimoxazole therapy was associated with fetal death (p < 0.0001). Genotypic analysis showed that the QpDV plasmid was more freQuent in isolates associated with abortion (p = 0.03). A comparison of the plasmid seQuences revealed that four QpDV proteins had no direct counterparts in QpH1, with two whose functions were not present in QpH1. The different obstetrical morbidity of C. burnetii relative to different geographical areas could be related to strain specificity, possibly based on differences in plasmid seQuences, or to a failure of public health authorities to detect early miscarriages.
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Q Fever during pregnancy a cause of poor fetal and maternal outcome
Annals of the New York Academy of Sciences, 2009Co-Authors: Xavier Carcopino, Florence Bretelle, Leon Boubli, Didier Raoult, Andreas SteinAbstract:Q Fever is a worldwide zoonosis caused by Coxiella burnetii. Q Fever may be present as an acute or a chronic infection and can be reactivated during subseQuent pregnancies. Although its exact prevalence remains unknown, it is likely that the number of cases of Q Fever in pregnant women is underestimated. During pregnancy, the illness is likely to be asymptomatic, and diagnosis is based on serology. Acute infection results in appearance of IgM and IgG antibodies mainly directed against the avirulent form of C. burnetii (phase II). Chronic Q Fever results in particularly high level of IgG and IgA antibodies directed against both virulent (phase I) and avirulent (phase II) forms of the bacterium. Q Fever may result in adverse pregnancy outcome, including spontaneous abortion, intrauterine growth retardation, oligoamnios, intrauterine fetal death (IUFD), and premature delivery. Obstetric complications occur significantly more often as C. burnetii infects the patient at an early stage of her pregnancy. Occurrence of IUFD is correlated with the presence of placental infection by C. burnetii and might be the conseQuence of direct infection of the fetus. The mother is exposed to the risk of chronic Q Fever and endocarditis with potential fatal evolution. Long-term cotrimoxazole therapy prevents from placental infection, IUFD, and maternal chronic Q Fever. Such treatment should be used to treat pregnant women with Q Fever. Women with previous history of Q Fever should have a regular serological follow up. Obstetricians' knowledge about Q Fever must be improved.
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managing Q Fever during pregnancy the benefits of long term cotrimoxazole therapy
Clinical Infectious Diseases, 2007Co-Authors: Xavier Carcopino, Florence Bretelle, Leon Boubli, Andreas SteinAbstract:Background. Q Fever is a zoonosis caused by Coxiella burnetii. During pregnancy, it may result in obstetric complications, such as spontaneous abortion, intrauterine growth retardation, intrauterine fetal death, and premature delivery. Pregnant women are exposed to the risk of chronic Q Fever. Methods. We included 53 pregnant women who received a diagnosis of Q Fever. We compared the incidence of obstetric and maternal Q Fever complications for women who received long-term cotrimoxazole treatment (n = 16) with that for women who did not receive long-term cotrimoxazole treatment (n = 37); long-term cotrimoxazole treatment was defined as oral administration of trimethoprim-sulfamethoxazole during at least 5 weeks of pregnancy. Results. Obstetric complications were observed in 81.1% of pregnant women who did not receive long-term cotrimoxazole therapy: 5 (13.5%) women experienced spontaneous abortions, 10 (27%) experienced intrauterine growth retardation, 10 (27%) experienced intrauterine fetal death, and 10 (27%) experienced premature delivery. Oligoamnios was observed in 4 patients (10.8%). Obstetric complications were found to occur significantly more often in patients infected during their first trimester of pregnancy than in those infected later (P = .032). The outcome of the pregnancy was found to depend on placental infection by C. burnetii (P = .013). Long-term cotrimoxazole treatment protected against maternal chronic Q Fever (P = .001), placental infection (P = .038), and obstetric complications (P = .009), especially intrauterine fetal death (P = .018), which was found to be related to placental infection (P = .008). Conclusions. Q Fever during pregnancy results in severe obstetric complications, including oligoamnios. Because of its ability to protect against placental infection, intrauterine fetal death, and maternal chronic Q Fever, long-term cotrimoxazole treatment should be used to treat pregnant women with Q Fever.
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Q Fever osteoarticular infection four new cases and a review of the literature
European Journal of Clinical Microbiology & Infectious Diseases, 2007Co-Authors: Cecile Landais, Florence Fenollar, Andreas Stein, A Constantin, C Cazorla, C Guilyardi, Hubert Lepidi, J M Rolain, Didier RaoultAbstract:Q Fever is a worldwide-occurring zoonosis caused by Coxiella burnetii. Better knowledge of the disease and of evolving diagnostics can enable recognition of unusual manifestations. Reported here are four cases of Q Fever osteoarticular infections in adults: two cases of Q Fever tenosynovitis, which represent the first two reports of this infection, and two cases of Q Fever spondylodiscitis complicated by paravertebral abscess. In addition, the literature is reviewed on the 15 previously reported cases of Q Fever osteoarticular infection, six of which were vertebral infections. Osteomyelitis is the usual manifestation Q Fever osteoarticular infection. Because its onset is freQuently insidious, diagnosis is usually delayed. The main differential diagnosis is mycobacterial infection, based on the histological granulomatous presentation of lesions. Whereas serology is the reference diagnostic method for Q Fever, detection of C. burnetii in tissue specimens by PCR and cell culture provides useful additional evidence of infection. Culture-negative osteoarticular samples with granulomatous presentation upon histological examination should raise suspicion of Q Fever.
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Q Fever during pregnancy diagnosis treatment and follow up
JAMA Internal Medicine, 2002Co-Authors: Florence Fenollar, Andreas SteinAbstract:Background Q Fever, caused by Coxiella burnetii , may result in abortions, premature deliveries, and stillbirths in infected pregnant women. Objective To evaluate the best treatment strategy for Q Fever during pregnancy. Methods We evaluated the prognosis of 17 pregnant women who developed Q Fever with and without co-trimoxazole (trimethoprim-sulfamethoxazole) treatment. Results The outcome of the pregnancy was found to depend on the trimester. Abortions occurred in 7 of 7 insufficiently treated patients infected during the first trimester vs 1 of 5 patients infected later. Co-trimoxazole given until delivery protected against abortion (0/4) but not against the development of chronic infections, and it did not significantly reduce the colonization of the placenta (2/4 vs 4/4). Conclusions Our results show that C burnetii infections cause abortion and that women who develop Q Fever while pregnant should be treated with co-trimoxazole for the duration of pregnancy, specifically when infected during the first trimester.
Clea Melenotte - One of the best experts on this subject based on the ideXlab platform.
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Acute Q Fever Endocarditis: A Paradigm Shift Following the Systematic Use of Transthoracic Echocardiography During Acute Q Fever
Clinical Infectious Diseases, 2019Co-Authors: Clea Melenotte, Gilbert Habib, Jean-louis Mege, Matthieu Million, Loïc Epelboin, Sandrine Hubert, Thierry Monsec, Felix Djossou, Didier RaoultAbstract:Background: As Q Fever, caused by Coxiella burnetii, is a major health challenge due to its cardiovascular complications, we aimed to detect acute Q Fever valvular injury to improve therapeutic management. Methods: In the French national reference center for Q Fever, we prospectively collected data from patients with acute Q Fever and valvular injury. We identified a new clinical entity, acute Q Fever endocarditis, defined as valvular lesion potentially caused by C. burnetii: vegetation, valvular nodular thickening, rupture of chorda tendinae, and valve or chorda tendinae thickness. To determine whether or not the disease was superimposed on an underlying valvulopathy, patients' physicians were contacted. Aortic bicuspidy, valvular stenosis, and insufficiency were considered as underlying valvulopathies. Results: Of the 2434 patients treated in our center, 1797 had acute Q Fever and 48 had acute Q Fever endocarditis. In 35 cases (72%), transthoracic echocardiography (TTE) identified a valvular lesion of acute Q Fever endocarditis without underlying valvulopathy. Positive anticardiolipin antibodies (>22 immunoglobulin G-type phospholipid units [GPLU]) were independently associated with acute Q Fever endocarditis (odds ratio [OR], 2.7 [95% confidence interval {CI}, 1.3-5.5]; P = .004). Acute Q Fever endocarditis (OR, 5.2 [95% CI, 2.6-10.5]; P < .001) and age (OR, 1.7 [95% CI, 1.1-1.9]; P = .02) were independent predictors of progression toward persistent C. burnetii endocarditis. Conclusions: Systematic TTE in acute Q Fever patients offers a uniQue opportunity for early diagnosis of acute Q Fever endocarditis and for the prevention of persistent endocarditis. Transesophageal echocardiography should be proposed in men, aged >40 years, with anticardiolipin antibodies >60 GPLU when TTE is inconclusive or negative.
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high concentrations of serum soluble e cadherin in patients with Q Fever
Frontiers in Cellular and Infection Microbiology, 2019Co-Authors: Soraya Mezouar, Christian A. Devaux, Camelia Slimani, Clea Melenotte, Courtney Chartier, Ikram Omar Osman, Jean-louis MegeAbstract:Cadherins switching is a hallmark of neoplasic processes. The E-cadherin (E-cad) subtype is one of the surface molecules regulating cell-to-cell adhesion. After its cleavage by sheddases, a soluble fragment (sE-cad) is released that has been identified as a pro-carcinogenic inflammatory signal in several bacteria-induced cancers. Recently we reported that Q Fever, a disease due to Coxiella burnetii infection, can be complicated by occurrence of non-Hodgkin lymphoma (NHL). Therefore, we studied E-cad switching in Q Fever. The sE-cad levels were found increased in the sera of acute and persistent Q Fever patients, whereas they remained at the baseline in controls groups of healthy donors, people cured of Q Fever, patients suffering from unrelated inflammatory diseases, and past Q Fever patients who developed NHL. These results indicate that sE-cad can be considered as a new biomarker of C. burnetii infection rather than a marker of NHL-associated to Q Fever. We wondered if changes in sE-cad reflected variations in the CDH1 gene transcription. The expression of E-cad mRNA and its intracellular ligand -catenin was down-regulated in peripheral blood mononuclear cells (PBMCs) of patients with either acute or persistent forms of Q Fever. Indeed, a lower cell-surface expression of E-cad was measured in a minority (less than 5%) subpopulation of HLADR+/CD16+ monocytes from patients with acute Q Fever. However, a very strong increase in E-cad expression was observed on more than 30% of the HLADR+/CD16+ monocytes of persistent Q Fever patients, a cell subpopulation known to be a target for C. burnetii in humans. An experimental in vitro infection of healthy donors' PBMCs with C. burnetii, was performed to directly evaluate the link between C. burnetii interaction with PBMCs and their E-cad expression. A significant increase in the percentage of HLADR+/CD16+ monocytes expressing E-cad was measured after PBMCs had been incubated for 8h with C. burnetii Nine Mile strain. Altogether, these data demonstrate that C. burnetii severely impairs the E-cad expression in circulating cells of Q Fever patients.
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high concentrations of serum soluble e cadherin in patients with Q Fever
Frontiers in Cellular and Infection Microbiology, 2019Co-Authors: Soraya Mezouar, Camelia Slimani, Clea Melenotte, Ikram Omar Osman, Jean-louis Mege, Didier Raoult, Celine Chartier, Christian DevauxAbstract:Cadherins switching is a hallmark of neoplasic processes. The E-cadherin (E-cad) subtype is one of the surface molecules regulating cell-to-cell adhesion. After its cleavage by sheddases, a soluble fragment (sE-cad) is released that has been identified as a pro-carcinogenic inflammatory signal in several bacteria-induced cancers. Recently we reported that Q Fever, a disease due to Coxiella burnetii infection, can be complicated by occurrence of non-Hodgkin lymphoma (NHL). Therefore, we studied E-cad switching in Q Fever. The sE-cad levels were found increased in the sera of acute and persistent Q Fever patients, whereas they remained at the baseline in controls groups of healthy donors, people cured of Q Fever, patients suffering from unrelated inflammatory diseases, and past Q Fever patients who developed NHL. These results indicate that sE-cad can be considered as a new biomarker of C. burnetii infection rather than a marker of NHL-associated to Q Fever. We wondered if changes in sE-cad reflected variations in the CDH1 gene transcription. The expression of E-cad mRNA and its intracellular ligand β-catenin was down-regulated in peripheral blood mononuclear cells (PBMCs) of patients with either acute or persistent forms of Q Fever. Indeed, a lower cell-surface expression of E-cad was measured in a minority (<5%) subpopulation of HLADR+/CD16+ monocytes from patients with acute Q Fever. However, a very strong increase in E-cad expression was observed on more than 30% of the HLADR+/CD16+ monocytes of persistent Q Fever patients, a cell subpopulation known to be a target for C. burnetii in humans. An experimental in vitro infection of healthy donors' PBMCs with C. burnetii, was performed to directly evaluate the link between C. burnetii interaction with PBMCs and their E-cad expression. A significant increase in the percentage of HLADR+/CD16+ monocytes expressing E-cad was measured after PBMCs had been incubated for 8 h with C. burnetii Nine Mile strain. Altogether, these data demonstrate that C. burnetii severely impairs the E-cad expression in circulating cells of Q Fever patients.
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clinical features and complications of coxiella burnetii infections from the french national reference center for Q Fever
JAMA Network Open, 2018Co-Authors: Clea Melenotte, Patrizia M Carrieri, Emmanouil Angelakis, Matthieu Million, Sophie Edouard, Felix Djossou, Carole Eldin, Camelia Protopopescu, Nathalie BardinAbstract:Importance Q Fever remains widespread throughout the world; the disease is serious and causes outbreaks and deaths when complications are not detected. The diagnosis of Q Fever reQuires the demonstration of the presence ofCoxiella burnetiiand the identification of an organic lesion. Objective To describe the hitherto neglected clinical characteristics of Q Fever and identifying risk factors for complications and death. Design, Setting, and Participants This prospective cohort study conducted from January 1, 1991, through December 31, 2016, included patients treated at the French National Reference Center for Q Fever with serologic findings positive forC burnetiiand clinical data consistent withC burnetiiinfection. Clinical data were prospectively collected by telephone. Patients with unavailable clinical data or an unidentified infectious focus were excluded. Main Outcomes and Measures Q Fever complications and mortality. Results Of the 180 483 patients undergoing testing, 2918 had positive findings forC burnetiiand 2434 (68.8% men) presented with clinical data consistent with aC burnetiiinfection. Mean (SD) age was 51.8 (17.4) years, and the ratio of men to women was 2.2. At the time of inclusion, 1806 patients presented with acute Q Fever, including 138 with acute Q Fever that progressed to persistentC burnetiiinfection, and 766 had persistent focalizedC burnetiiinfection. Rare and hitherto neglected foci of infections included lymphadenitis (97 [4.0%]), acute Q Fever endocarditis (50 [2.1%]), hemophagocytic syndrome (9 [0.4%]), and alithiasic cholecystitis (11 [0.4%]). Vascular infection (hazard ratio [HR], 3.1; 95% CI, 1.7-5.7;P Conclusions and Relevance Previously neglected foci ofC burnetii infection include the lymphatic system (ie, bone marrow, lymphadenitis) with a risk of lymphoma. Cardiovascular infections were the main fatal complications, highlighting the importance of routine screening for valvular heart disease and vascular anomalies during acute Q Fever. Routine screening for anticardiolopin antibodies during acute Q Fever can help prevent complications. Positron emission tomographic scanning could be proposed for all patients with suspected persistent focused infection to rapidly diagnose vascular and lymphatic infections associated with death and lymphoma, respectively.
