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Culture-independent genome sequencing of Coxiella burnetii from a native heart valve of a Tunisian patient with severe infective endocarditis.

ABSTRACT: We report draft genome of a Coxiella burnetii strain sequenced from the native valve of a patient presenting with severe endocarditis in Tunisia. The genome could be sequenced without a cellular or axenic culture step. The MST5 strain was demonstrated to be closely related to the published reference genome of C. burnetii CbuK_Q154.

SUBMITTER: Delaloye J

PROVIDER: S-EPMC5701788 | biostudies-literature | 2018 Jan

REPOSITORIES: biostudies-literature

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Culture-independent genome sequencing of Coxiella burnetii from a native heart valve of a Tunisian patient with severe infective endocarditis.

Delaloye J J Pillonel T T Smaoui M M Znazen A A Abid L L Greub G G

New microbes and new infections 20171010

We report draft genome of a Coxiella burnetii strain sequenced from the native valve of a patient presenting with severe endocarditis in Tunisia. The genome could be sequenced without a cellular or axenic culture step. The MST5 strain was demonstrated to be closely related to the published reference genome of C. burnetii CbuK_Q154. ...[more]

PMID: 29201381

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Molecular detection of Coxiella burnetii in heart valve tissue from patients with culture-negative infective endocarditis.

Project description:Coxiella burnetii is a common cause of blood culture-negative infective endocarditis (IE). Molecular detection of C burnetii DNA in clinical specimens is a promising method of diagnosing Q fever endocarditis. Here, we examined the diagnostic utility of Q fever polymerase chain reaction (PCR) of formalin-fixed heart valve tissue from patients with blood culture-negative IE who underwent heart valve surgery. Clinical and laboratory data of patients with blood culture-negative IE who underwent heart valve surgery during a 6-year period and for whom biopsy tissues were available were reviewed retrospectively. Blood culture-positive IE patients who underwent heart valve surgery within the last 3 years were used as controls. Heart valve samples were cultured and also subjected to histological examination and PCR for Q fever, brucellosis, and bartonellosis. Data from 20 patients with blood culture-negative IE and 20 with blood culture-positive IE were analyzed. Eight cases of blood culture-negative IE were PCR-positive for C burnetii (40%; 95% confidence interval, 19-64). No specimen was PCR-positive for brucellosis or bartonellosis. Histologically, 4 of 8 specimens with a positive Q fever PCR result were characterized by clusters of multinucleated giant cells without a fibrin ring. None of 20 patients with blood culture-negative IE received anti-Coxiella antibiotic therapy due to lack of clinical suspicion. Six-month mortality was higher in the Q fever PCR-positive group than in the Q fever PCR-negative group [38% (3/8) vs 0% (0/12), P = .049). Of the 20 patients with blood culture-positive IE, none yielded a positive Q fever PCR result for valve tissue. Approximately 40% of patients with culture-negative IE who received heart valve surgery were PCR-positive for Q fever; patients without clinical suspicion suffered high mortality. These data suggest that Q fever IE in patients with culture-negative IE is often missed in routine clinical practice.

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Bartonella spp. and Coxiella burnetii Associated with Community-Acquired, Culture-Negative Endocarditis, Brazil.

Project description:We evaluated culture-negative, community-acquired endocarditis by using indirect immunofluorescent assays and molecular analyses for Bartonella spp. and Coxiella burnetii and found a prevalence of 19.6% and 7.8%, respectively. Our findings reinforce the need to study these organisms in patients with culture-negative, community-acquired endocarditis, especially B. henselae in cat owners.

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Cardiac pseudoaneurysm as a complication of native mitral valve infective endocarditis.

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Molecular diagnosis of Coxiella burnetii in culture negative endocarditis and vascular infection in South Korea.

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A structured approach to native mitral valve infective endocarditis: Is repair better than replacement?

Project description:ObjectivesMitral valve repair in native active infective endocarditis is technically challenging. The survival benefit over valve replacement is poorly established and possibly absent because of the high risk of repair failure and reoperation. In this study, we explore the results of our structured approach in these patients.MethodsBetween January 2000 and January 2017, 149 patients underwent surgery for native mitral infective endocarditis. Among them, 97 (66%) patients underwent valve repair and 52 (34%) underwent valve replacement. Our structured approach consisted of early surgery, radical resection of infected tissue, liberal use of prosthetic materials and 'patch' repair techniques. A critical assessment of expected repair durability was made intraoperatively and repair was not performed if concerns of long-term durability existed. To study the effects of valve repair on overall survival, landmark analysis was performed.ResultsIn-hospital mortality was 15.4% (14 repair vs 9 replacement patients; P = 0.642). There were no residual infective endocarditis cases or early reoperations. On Cox proportional hazards analysis, valve replacement was not inferior to repair within 1-year post-surgery [hazard ratio (HR) 1.134, 95% confidence interval (CI) 0.504-2.540; P = 0.76]. Beyond 1 year post-surgery, replacement was associated with decreased survival (HR 2.534, 95% CI 1.002-6.406; P = 0.049). There were no differences in freedom from recurrent infective endocarditis (P = 0.47) and mitral valve reintervention (P = 0.52).ConclusionsActive mitral valve endocarditis remains a complex disease with significant early and late morbidity and mortality. A structured approach allows valve repair in two-thirds of patients. Clinical results could be improved by focussing on early surgery, prior to extensive valve destruction, to enable durable repairs and improve late outcomes.

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Ruptured mitral valve abscess with mitral incompetence in culture negative infective endocarditis: case report.

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Diagnostic value of harmonic transthoracic echocardiography in native valve infective endocarditis: comparison with transesophageal echocardiography.

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Infective endocarditis caused by Neisseria elongata on a native tricuspid valve and confirmed by DNA sequencing.

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Association of Novel Streptococcus sanguinis Virulence Factors With Pathogenesis in a Native Valve Infective Endocarditis Model.

Project description:Streptococcus sanguinis (S. sanguinis) is an abundant oral commensal which can cause disseminated human infection if it gains access to the bloodstream. The most important among these diseases is infective endocarditis (IE). While virulence phenotypes of S. sanguinis have been correlated to disease severity, genetic factors mediating these phenotypes, and contributing to pathogenesis are largely uncharacterized. In this report, we investigate the roles of 128 genes in virulence-related phenotypes of S. sanguinis and characterize the pathogenic potential of two selected mutants in a left-sided, native valve IE rabbit model. Assays determining the ability of our mutant strains to produce a biofilm, bind to and aggregate platelets, and adhere to or invade endothelial cells identified sixteen genes with novel association to these phenotypes. These results suggest the presence of many uncharacterized genes involved in IE pathogenesis which may be relevant for disease progression. Two mutants identified by the above screening process - SSA_1099, encoding an RTX-like protein, and mur2, encoding a peptidoglycan hydrolase - were subsequently evaluated in vivo. Wild type (WT) S. sanguinis reliably induced cardiac vegetations, while the SSA_1099 and mur2 mutants produced either no vegetation or vegetations of small size. Splenomegaly was reduced in both mutant strains compared to WT, while pathology of other distal organs was indistinguishable. Histopathology analyses suggest the cardiac lesions and vegetations in this model resemble those observed in humans. These data indicate that SSA_1099 and mur2 encode virulence factors in S. sanguinis which are integral to pathogenesis of IE.

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