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The data on infective endocarditis after transcatheter aortic valve implantation (TAVI) is scarce and limited to case reports and case series in the literature. It is the need of the hour to analyze the available data on post-TAVI infective endocarditis from the available literature. The objectives of this systematic review were to evaluate the incidence of infective endocarditis after transcatheter aortic valve implantation, its microbiological profile and clinical outcomes. It will help us to improve the antibiotic prophylaxis strategies and treatment options for infective endocarditis in the context of TAVI. EMBASE, Medline and the CENTRAL trials registry of the Cochrane Collaboration were searched for articles on infective endocarditis in post-TAVI patients till October 2018. Eleven articles were included in the systematic review. The outcomes assessed werethe incidence of infective endocarditis, its microbiological profile andclinical outcomes including major adverse cardiac event (MACE), net adverse clinical event (NACE), surgical intervention and valve-in-valve procedure. The incidence of infective endocarditis varied from 0%-14.3% in the included studies, the mean was3.25%. The average duration of follow-up was 474 days (1.3 years). Enterococci were the most common causative organism isolated from 25.9% of cases followed by Staphylococcus aureus (16.1%) and coagulase-negative Staphylococcus species (14.7%). The mean in-hospital mortality and mortality at follow-up was 29.5% and 29.9%, respectively. The cumulative incidence of heart failure, stroke and major bleeding were 37.1%, 5.3% and 11.3%,respectively. Only a single study by Martinez-Selles et al. reported arrhythmias in 20% cases. The septic shock occurred in 10% and 27.7% post-TAVI infective endocarditis patients according to 2 studies. The surgical intervention and valve-in-valve procedure were reported in 11.4% and 6.4% cases, respectively. The incidence of post-TAVI infective endocarditis is low being 3.25% but it is associated with high mortality and complications. The most common complication is heart failure with a cumulative incidence of 37.1%. Enterococciare the most common causative organism isolated from 25.9% of cases followed by Staphylococcus aureus in 16.1% of cases. Appropriate measures should be taken to prevent infective endocarditis in post-TAVI patients including adequate antibiotics prophylaxis directed specifically against these organisms. PROSPERO registration number CRD42018115943.

Forensic pathologists often encounter cases of acute subdural hematoma (SDH) due to trauma, whereas those attributable to endogenous causes are rare. Here, we report a case of the latter type in a 42-year-old man who was found dead at home after several months of fever and malaise. Postmortem computed tomography (PMCT) and autopsy were undertaken to clarify the cause of death. PMCT images revealed a fatal SDH and a localized hyper-density area in the right parietal lobe; macroscopic and microscopic examinations revealed SDH due to rupture of a mycotic aneurysm (MA) associated with meningitis. The PMCT images also indicated thickening and calcification of the mitral valve, while autopsy demonstrated infective endocarditis (IE). In addition, PMCT demonstrated a low-density area in the spleen, which was shown to be a splenic abscess at autopsy. PMCT also demonstrated tooth cavities. Based on the findings of autopsy, the cause of death was considered to be SDH due to rupture of the MA resulting from meningitis with IE and splenic abscess. Although PMCT was unable to clarify the significance of any individual feature, a retrospective review of the PMCT images might have suggested IE, bacteremia, or ruptured MA leading to SDH. This case suggests that, instead of interpreting individual features demonstrated on PMCT images, integrated interpretation of overall PMCT findings might provide clues for identifying causes of death, despite the fact that PMCT lacks diagnostic accuracy for infectious diseases such as IE and meningitis.

Streptococcus gordonii and Streptococcus sanguinis belong to the Mitis group streptococci, which mostly are commensals in the human oral cavity. Though they are oral commensals, they can escape their niche and cause infective endocarditis, a severe infection with high mortality. Several virulence factors important for the development of infective endocarditis have been described in these two species. However, the background for how the commensal bacteria, in some cases, become pathogenic is still not known. To gain a greater understanding of the mechanisms of the pathogenic potential, we performed a comparative analysis of 38 blood culture strains, S . sanguinis ( n  = 20) and S . gordonii ( n  = 18) from patients with verified infective endocarditis, along with 21 publicly available oral isolates from healthy individuals, S . sanguinis ( n  = 12) and S . gordonii (n  = 9). Using whole genome sequencing data of the 59 streptococci genomes, functional profiles were constructed, using protein domain predictions based on the translated genes. These functional profiles were used for clustering, phylogenetics and machine learning. A clear separation could be made between the two species. No clear differences between oral isolates and clinical infective endocarditis isolates were found in any of the 675 translated core-genes. Additionally, random forest-based machine learning and clustering of the pan-genome data as well as amino acid variations in the core-genome could not separate the clinical and oral isolates. A total of 151 different virulence genes was identified in the 59 genomes. Among these homologs of genes important for adhesion and evasion of the immune system were found in all of the strains. Based on the functional profiles and virulence gene content of the genomes, we believe that all analysed strains had the ability to become pathogenic.

Infective endocarditis (IE) is frequently caused by Staphylococcus aureus (S. aureus) and most commonly affects the aortic valve. Early diagnosis and treatment initiation are challenging because the involved immunological processes are poorly understood due to a lack of suitable in vivo models. To establish a novel reproducible murine IE model, based on ultrasound-guided wire injury (WI) induced endothelial damage. IE was established by inducing endothelial damage via ultrasound-guided wire injury followed by bacterial challenge with S. aureus using 104-6 colony-forming units (CFU) 24h to 72h after wire injury. Cross-sections of valvular leaflets were prepared for scanning electron microscopy (SEM) and immunofluorescence microscopy to visualize valvular invasion of macrophages, neutrophils, and S. aureus. Bacterial cultivation was carried out from blood and valve samples. Systemic immune response was assessed using flow cytometry. Wire injury induced endothelial damage was observed in all mice after wire-injury in SEM imaging. We reliably induced IE using 105 (85%) and 106 (91%) CFU S. aureus after wire injury. Aortic regurgitation was more prevalent in wire injury mice after bacterial challenge. Mice undergoing bacterial challenge responded with significant neutrophilia and elevated pro-inflammatory cytokines in the blood. Immunofluorescence staining revealed significantly increased immune cell accumulations using our proposed model compared to controls. Echocardiography and ex vivo histological staining demonstrated consistent infective endocarditis induction in our new model, combining a wire injury-induced endothelial damage and S. aureus administration. Further exploration of the initial immune cell response and biomarker expression could potentially identify indicators for early IE diagnosis and novel treatment targets.

Background. The impact of early valve surgery (EVS) on the outcome of Staphylococcus aureus (SA) prosthetic valve infective endocarditis (PVIE) is unresolved. The objective of this study was to evaluate the association between EVS, performed within the first 60 days of hospitalization, and outcome of SA PVIE within the International Collaboration on Endocarditis–Prospective Cohort Study. Methods. Participants were enrolled between June 2000 and December 2006. Cox proportional hazards modeling that included surgery as a time-dependent covariate and propensity adjustment for likelihood to receive cardiac surgery was used to evaluate the impact of EVS and 1-year all-cause mortality on patients with definite left-sided S. aureus PVIE and no history of injection drug use. Results. EVS was performed in 74 of the 168 (44.3%) patients. One-year mortality was significantly higher among patients with S. aureus PVIE than in patients with non–S. aureus PVIE (48.2% vs 32.9%; P = .003). Staphylococcus aureus PVIE patients who underwent EVS had a significantly lower 1-year mortality rate (33.8% vs 59.1%; P = .001). In multivariate, propensity-adjusted models, EVS was not associated with 1-year mortality (risk ratio, 0.67 [95% confidence interval, .39–1.15]; P = .15). Conclusions. In this prospective, multinational cohort of patients with S. aureus PVIE, EVS was not associated with reduced 1-year mortality. The decision to pursue EVS should be individualized for each patient, based upon infection-specific characteristics rather than solely upon the microbiology of the infection causing PVIE.

Background. Blood culture-negative endocarditis (BCNE) may account for up to 31% of all cases of endocarditis. Methods. We used a prospective, multimodal strategy incorporating serological, molecular, and histopathological assays to investigate specimens from 819 patients suspected of having BCNE. Results. Diagnosis of endocarditis was first ruled out for 60 patients. Among 759 patients with BCNE, a causative microorganism was identified in 62.7%, and a noninfective etiology in 2.5%. Blood was the most useful specimen, providing a diagnosis for 47.7% of patients by serological analysis (mainly Q fever and Bartonella infections). Broad-range polymerase chain reaction (PCR) of blood and Bartonella-specific Western blot methods diagnosed 7 additional cases. PCR of valvular biopsies identified 109 more etiologies, mostly streptococci, Tropheryma whipplei, Bartonella species, and fungi. Primer extension enrichment reaction and autoimmunohistochemistry identified a microorganism in 5 additional patients. No virus or Chlamydia species were detected. A noninfective cause of endocarditis, particularly neoplasic or autoimmune disease, was determined by histological analysis or by searching for antinuclear antibodies in 19 (2.5%) of the patients. Our diagnostic strategy proved useful and sensitive for BCNE workup. Conclusions. We highlight the major role of zoonotic agents and the underestimated role of noninfective diseases in BCNE. We propose serological analysis for Coxiella burnetii and Bartonella species, detection of antinuclear antibodies and rheumatoid factor as first-line tests, followed by specific PCR assays for T. whipplei, Bartonella species, and fungi in blood. Broad-spectrum 16S and 18S ribosomal RNA PCR may be performed on valvular biopsies, when available.

Treatment failure in biofilm-associated bacterial infections is an important healthcare issue. In vitro studies and mouse models suggest that bacteria enter a slow-growing/non-growing state that results in transient tolerance to antibiotics in the absence of a specific resistance mechanism. However, little clinical confirmation of antibiotic tolerant bacteria in patients exists. In this study we investigate a Staphylococcus epidermidis pacemaker-associated endocarditis, in a patient who developed a break-through bacteremia despite taking antibiotics to which the S. epidermidis isolate is fully susceptible in vitro. Characterization of the clinical S. epidermidis isolates reveals in-host evolution over the 16-week infection period, resulting in increased antibiotic tolerance of the entire population due to a prolonged lag time until growth resumption and a reduced growth rate. Furthermore, we observe adaptation towards an increased biofilm formation capacity and genetic diversification of the S. epidermidis isolates within the patient. Staphylococcus epidermidis is a frequent cause of medical implant-associated biofilm infections. Here, studying a patient with pacemaker-associated endocarditis, the authors report in-host evolution of S. epidermidis leading to phenotypes exhibiting increased biofilm formation and antibiotic tolerance.

Background. Infective endocarditis (IE) is a serious complication of Staphylococcus aureus bacteremia (SAB). There is limited clinical evidence to guide use of echocardiography in the management of SAB cases. Methods. Baseline and 12-week follow-up data of all adults hospitalized at our institution with SAB from 2006 to 2011 were reviewed. Clinical predictors of IE were identified using multivariable logistic regression analysis. Results. Of the 757 patients screened, 678 individuals with SAB (24% community acquired, 56% healthcare associated, and 20% nosocomial) met study criteria. Eighty-five patients (13%) were diagnosed with definite IE within the 12 weeks of initial presentation based on modified Duke criteria. The proportion of patients with IE was 22% (36/166) in community-acquired SAB, 11% (40/378) in community-onset healthcare-associated SAB, and 7% (9/136) in nosocomial SAB. Community-acquired SAB, presence of cardiac device, and prolonged bacteremia (≥72 hours) were identified as independent predictors of IE in multivariable analysis. Two scoring systems, day 1 (SAB diagnosis day) and day 5 (when day 3 culture results are known), were derived based on the presence of these risk factors, weighted in magnitude by the corresponding regression coefficients. A score of ≥4 for day 1 model had a specificity of 96% and sensitivity of 21%, whereas a score of <2 for day 5 model had a sensitivity of 98.8% and negative predictive value of 98.5%. Conclusions. We propose 2 novel scoring systems to guide use of echocardiography in SAB cases. Larger prospective studies are needed to validate the classification performance of these scoring systems.

Infective endocarditis (IE), an infection of the cardiac endothelium, is associated with significant morbidity and mortality. IE cases vary substantially based on their valvular involvement, both in terms of risk factors and severity. This study describes patient characteristics and outcomes associated with valvular involvement in IE. Data for this multicenter, retrospective study were obtained from electronic medical chart review of adult patients hospitalized for their index admission for IE between January 2014- January 2018 in the Appalachian region, USA. Descriptive summary statistics are presented by valvular involvement: (1) Left-sided Infective Endocarditis (LSIE): aortic/mitral valve; (2) Right-sided Infective Endocarditis (RSIE): tricuspid/pulmonary valve; and (3) Bilateral Infective Endocarditis (BLIE): right and left-sided. Multivariable logistic regression analysis examined the association of valvular involvement with intensive care unit (ICU) admission. Overall, 726 patients with IE were included in this retrospective study that provides a novel analysis of IE valvular involvement, highlighting how patient characteristics, comorbidities, substance use behaviors, and clinical outcomes differ across LSIE, RSIE, and BLIE presentations. Drug use, the presence of one or two comorbidities, and bilateral or left-sided valve involvement were independently associated with increased odds of ICU admission. Notably, patients with BLIE experienced a greater clinical burden, requiring more frequent specialist consultations, increased use of pain management services, higher mortality, and a higher rate of surgical interventions. BLIE represents a clinically distinct IE subgroup characterized by dual vulnerabilities: high-risk substance use behaviors associated with RSIE, and medical complexity typically seen in LSIE. Our findings underscore the importance of including BLIE as a distinct category in future epidemiological and clinical investigations of endocarditis valvular involvement.

Infective Endocarditis (IE) and Sepsis are two closely related infectious diseases, yet their shared pathogenic mechanisms at the transcriptional level remain unclear. This research gap poses a barrier to the development of refined therapeutic strategies and drug innovation. This study employed a collaborative approach using both microarray data and single-cell RNA sequencing (scRNA-seq) data to identify biomarkers for IE and Sepsis. It also offered an in-depth analysis of the roles and regulatory patterns of immune cells in these diseases. We successfully identified four key biomarkers correlated with IE and Sepsis, namely CD177, IRAK3, RNASE2, and S100A12. Further investigation revealed the central role of Th1 cells, B cells, T cells, and IL-10, among other immune cells and cytokines, in the pathogenesis of these conditions. Notably, the small molecule drug Matrine exhibited potential therapeutic effects by targeting IL-10. Additionally, we discovered two Sepsis subgroups with distinct inflammatory responses and therapeutic strategies, where CD177 demonstrated significant classification value. The reliability of CD177 as a biomarker was further validated through qRT-PCR experiments. This research not only paves the way for early diagnosis and treatment of IE and Sepsis but also underscores the importance of identifying shared pathogenic mechanisms and novel therapeutic targets at the transcriptional level. Despite limitations in data volume and experimental validation, these preliminary findings add new perspectives to our understanding of these complex diseases.