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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.

Although first identified just 14 decades ago, methicillin-resistant Staphylococcus aureus (MRSA) has undergone rapid evolutionary changes and epidemiologic expansion to become a major cause of nosocomial and community-acquired infections worldwide. Increasing resistance to vancomycin among MRSA strains in conjunction with availability of new antibiotics, including daptomycin and linezolid, have increased treatment choices but made clinical treatment decisions more challenging. This article describes the clinical features and management issues of 2 challenging-to-treat manifestations of MRSA infection, bacteremia and/or endocarditis and osteomyelitis. It also presents a brief review of community-associated MRSA infections and preventive strategies directed against MRSA. Micrococcus, which, when limited in extent and activity, causes acute suppurative inflammation (phlegmon), produces, when more extensive and intense in its action on the human system, the most virulent forms of septicaemia and pyaemia, as well as many forms intermediate between the two extremes. Alexander Ogston, on the organism now known as S. aureus [1]

Over the last decade, the incidence of infective endocarditis (IE) has increased, with a change in the frequency of causative bacteria. Early evidence has substantially demonstrated the crucial role of bacterial interaction with human platelets, with no clear mechanistic characterization in the pathogenesis of IE. The pathogenesis of endocarditis is so complex and atypical that it is still unclear how and why certain bacterial species will induce the formation of vegetation. In this review, we will analyze the key role of platelets in the physiopathology of endocarditis and in the formation of vegetation, depending on the bacterial species. We provide a comprehensive outline of the involvement of platelets in the host immune response, investigate the latest developments in platelet therapy, and discuss prospective research avenues for solving the mechanistic enigma of bacteria–platelet interaction for preventive and curative medicine.

Abstract Background Endocarditis is a rare heart condition with variable clinical expressions in equids. Risk factors for this disease are incompletely understood. Objective Describe risk factors for endocarditis in equids. Animals One hundred and fifty-three equids admitted to Liège University, 9 diagnosed with endocarditis and 144 free from endocarditis but admitted to the hospital with a differential diagnosis including this disease. Methods Retrospective case-control study. Results Equids with endocarditis were significantly younger (mean age = 4.84 ± 5.74 years) than control equids (mean age = 10.8 ± 7.73 years) (P= .01). No sex or breed predisposition was observed. Animals with hyperthermia (odds ratio [OR] = 24.4; confidence interval [CI] = 1.40–428), synovial distension (OR = 13.4; CI = 3.00–59.8), lameness (OR = 6.52; CI = 1.63–26.1), hyperglobulinemia (OR = 26.4; CI = 3.03–229), hypoalbuminemia (OR = 11.4; CI = 1.34–96.8), hyperfibrinogenemia (OR = 9.81; CI = 1.16–82.7), or leukocytosis (OR = 7.12; CI = 1.40–36.4) presented a significantly higher risk of having endocarditis than control horses. The presence of two of the clinical signs mentioned above significantly increased the probability of a diagnosis of endocarditis (P≤ .05). Conclusions and Clinical Importance Age is associated with equine endocarditis. The diagnostic value of certain clinical signs and abnormalities in blood parameters in this disease are described.

Bacterial binding to platelets is a key step in the development of infective endocarditis (IE). Sialic acid, a common terminal carbohydrate on host glycans, is the major receptor for streptococci on platelets. So far, all defined interactions between streptococci and sialic acid on platelets are mediated by serine-rich repeat proteins (SRRPs). However, we identified Streptococcus oralis subsp. oralis IE-isolates that bind sialic acid but lack SRRPs. In addition to binding sialic acid, some SRRP - isolates also bind the cryptic receptor β-1,4-linked galactose through a yet unknown mechanism. Using comparative genomics, we identified a novel sialic acid-binding adhesin, here named AsaA ( a ssociated with s ialic acid a dhesion A), present in IE-isolates lacking SRRPs. We demonstrated that S . oralis subsp. oralis AsaA is required for binding to platelets in a sialic acid-dependent manner. AsaA comprises a non-repeat region (NRR), consisting of a FIVAR/CBM and two Siglec-like and Unique domains, followed by 31 DUF1542 domains. When recombinantly expressed, Siglec-like and Unique domains competitively inhibited binding of S . oralis subsp. oralis and directly interacted with sialic acid on platelets. We further demonstrated that AsaA impacts the pathogenesis of S . oralis subsp. oralis in a rabbit model of IE. Additionally, we found AsaA orthologues in other IE-causing species and demonstrated that the NRR of AsaA from Gemella haemolysans blocked binding of S . oralis subsp. oralis , suggesting that AsaA contributes to the pathogenesis of multiple IE-causing species. Finally, our findings provide evidence that sialic acid is a key factor for bacterial-platelets interactions in a broader range of species than previously appreciated, highlighting its potential as a therapeutic target.

Increasing incidence rates of invasive Streptococcus dysgalactiae subspecies equisimilis (SDSE) infections have been reported worldwide, but the evolutionary mechanisms underlying this development remain elusive. Through prospective surveillance of invasive SDSE infections in western Norway, we observed the emergence of a novel and virulent SDSE genotype, stG62647 . This emm -type, rarely encountered as a cause of invasive disease during 1999–2012, emerged in 2013 as the predominant SDSE-genotype. The stG62647 -infections were associated with an aggressive clinical course, including the occurrence of streptococcal toxic shock syndrome, necrotizing soft-tissue infections and endocarditis. All the invasive stG62647 -isolates were subjected to whole genome sequencing, attempting to explore the genetic events underpinning its epidemicity. Although 10% of the genomes was unique for stG62647 -genotype, notably 18 out of 19 isolates contained a disrupted streptococcal invasive locus ( sil ) due to the insertion of a transposase, IS1548, into the silB -gene. We postulate that the virulence of stG6267 -isolates could be partly attributable to the abrogation of the attenuating control normally exerted by this regulon, although experimental verification was not performed. To the best of our knowledge, this is the first study employing large scale whole genome sequencing to illuminate the genetic landscape of epidemic lineages in SDSE.

In patients with active infective endocarditis (IE), the relationship between timing of surgery and survival is uncertain. The objective was to evaluate clinical characteristics associated with timing of surgery and the association between surgical timing and 6-month survival in complicated, left-sided IE. In a prospective, multicenter, observational registry (The International Collaboration on Endocarditis-PLUS, registry from 2008 to 2012), clinical factors associated with timing of surgery during the index hospitalization were determined among 485 adult patients with definite, complicated, left-sided IE who underwent cardiac surgery during their index hospitalization. The relationship between early surgical intervention (<7 days from admission to surgery center) and outcome after surgery was analyzed. The primary end point of the study was 6-month survival. The median time to surgery from admission to surgical center was 7 (interquartile range 2-15) days. Patients who underwent earlier surgery were more likely transferred to the surgical center (74.2% vs 46.4%, P < .001) and had a lower percentage of preexisting heart failure (before IE diagnosis) (6.0% vs 17.3%, P < .001) but higher rate of acute heart failure (53.2% vs 38.4%, P = .001). Variables independently associated with surgery <7 days from admission were patient transfer, acute heart failure, and nonelective surgical status (C-index = 0.84), but predicted operative risk was not. Cox proportional hazards modeling with inverse probability of treatment weighting found that earlier surgery was associated with a trend toward higher 6-month mortality compared with later surgery (hazard ratio = 1.68, 95% CI 0.97-2.96; P = .065), particularly surgery within 2 days of admission or transfer. Mortality was significantly associated with operative risk and complicated IE, including Staphylococcus aureus infection and presence of abscess. Earlier surgery in IE is strongly associated with acute heart failure and surgical urgency. After adjustment for operative risk and IE complications, earlier surgery <7 days from admission was associated with a trend toward higher 6-month overall mortality compared with surgery later in the index hospitalization.

Background. The prevention of Q fever endocarditis through the use of systematic echocardiography and antibiotic prophylaxis in patients with acute Q fever and valvulopathy has never been validated in a cohort study. Methods. From 2007 to 2012, all patients followed at the French National Referral Center for acute Q fever were included in a cohort study. The prevention of endocarditis included a systematic transthoracic echocardiography (TTE) and a 12-month course of doxycycline and hydroxychloroquine prophylaxis in patients with significant valvulopathy. Transesophageal echocardiography (TEE) was performed in patients with a negative TTE and a rapid rise of phase I immunoglobulin G titers. Results. Seventy-two patients were included with a median follow-up time of 22 months. A valvulopathy was identified in 31 patients (43%), being previously unknown in 24 (33%) and diagnosed only upon TEE or a second TTE in 7 (10%). The major determinants associated with endocarditis were age (hazard ratio [HR], 1.07; 95% confidence interval [CI], 1.006–1.13; P = .03), aortic regurgitation (HR, 10.2; 95% CI, 3.2–32.2; P < .001), and mitral regurgitation (HR, 4.78; 95% CI, 1.4–16.0; P = .01). Antibiotic prophylaxis was highly effective (HR, 0.002; 95% CI, .00–.77; P = .04) for the 31 patients with valvulopathy. Conclusions. Acute Q fever could be associated with an increased prevalence of valvulopathy. The evolution from acute Q fever to endocarditis is associated with age and valvulopathy and can be entirely prevented by antibiotic prophylaxis. Although the name \"chronic Q fever\" suggests otherwise, rapid evolution (<1 month) was observed.

Most previously reported cases involved major axial vessels proximal to the popliteal artery, although rare tibial aneurysms (including 6 peroneal aneurysms) have been reported. 2 One case has been reported of bilateral tibial aneurysms associated with IE and Brucella canis bacteremia. 3 In that report as well as in our case presentation, intraoperative cultures of the aneurysm were negative despite positive blood cultures. A single case report from 2003 describes C. valvarum endocarditis with associated ruptured cerebral artery aneurysm in a 37-year-old male with a congenital bicuspid aortic valve. 4 Different therapeutic options for treatment exist. Endovascular coil embolization with covered stent alone has been reported in the case of a small peroneal aneurysm without signs of compartment syndrome, but the long-term consequences of introducing foreign bodies into known infectious aneurysms are unclear. 2 Intravenous antibiotics should be tailored to the attributable bacterial etiology in all cases.

Background. Staphylococcus aureus causes life-threatening infections, including infective endocarditis, sepsis, and pneumonia, β-toxin is a sphingomyelinase encoded for by virtually all S. aureus strains and exhibits human immune cell cytotoxicity. The toxin enhances S. aureus phenol-soluble modulin activity, and its activity is enhanced by superantigens. The bacteriophage ɸSa3 inserts into the β-toxin gene in human strains, inactivating it in the majority of S. aureus donai groups. Hence, most strains are reported not to secrete β-toxin. Methods. This dynamic was investigated by examining β-toxin production by multiple donai groups of S. aureus, both in vitro and in vivo during infections in rabbit models of infective endocarditis, sepsis, and pneumonia. Results, β-toxin phenotypic variants are common among strains containing ɸSa3. In vivo, ɸSa3 is differentially induced in heart vegetations, kidney abscesses, and ischemie liver compared to spleen and blood, and in vitro growth in liquid culture. Furthermore, in pneumonia, wild-type β-toxin production leads to development of large caseous lesions, and in infective endocarditis, increases the size of pathognomonic vegetations. Conclusions. This study demonstrates the dynamic interaction between S. aureus and the infected host, where ɸSa3 serves as a regulator of virulence gene expression, and increased fitness and virulence in new enivronments.