Concept: Infective endocarditis
- Circulation journal : official journal of the Japanese Circulation Society
- Published about 4 years ago
To determine the feasibility of original aortic valve reconstruction (AVRec) for patients with aortic stenosis (AS), 416 consecutive cases were reviewed.Methods and Results:AVRecs for AS were performed for 416 patients from April 2007 through April 2013. All 416 patients were retrospectively reviewed. One hundred and fourteen patients had bicuspid valves and 16 had unicuspid valves. There were 182 men and 234 women. Mean age was 71.2±12.0 years old. On preoperative echocardiography, peak pressure gradient averaged 79.0±33.6 mmHg. Surgical annular diameter was 20.1±2.8 mm. The procedure is based on independent tricuspid replacement by autologous pericardium using original sizing apparatus and template. There was no conversion to prosthetic valve replacement. There were 8 in-hospital mortalities due to non-cardiac cause. On postoperative echocardiography, peak pressure gradient averaged 21.2±10.7 mmHg 1 week after surgery and 14.3±5.0 mmHg 5.5 years after surgery. Four reoperations were done for infective endocarditis. The other 412 patients had less than mild regurgitation. No thrombo-embolic events were recorded. The mean follow-up period was 25.2±17.5 months. Freedom from reoperation was 96.7% with 73-month follow-up.
Pulmonary valve endocarditis is an rare type of infective endocarditis (IE). Streptococcus pneumoniae is a pathogen that is uncommonly associated with IE. A 50 year-old man was referred to us to an incidental echocardiographic finding of a pulmonary valve vegetation. He had a recent admission for drainage of a scrotal abscess from which streptococcus pneumoniae was isolated, complicated by hospital acquired pneumonia and pulmonary embolism. Analysis using Polymerase Chain Reaction of the surgically resected mass revealed signs of 16S rDNA consistent with Streptococcus pneumoniae infection. This is the first confirmed case of pneumococcal pulmonary valve IE presenting entirely asymptomatically in the absence of any known risk factors.
Rothia mucilaginosa is increasingly recognized as an emerging opportunistic pathogen associated with prosthetic device infections. Infective endocarditis is one of the most common clinical presentations. We report a case of R. mucilaginosa prosthetic valve endocarditis and review the literature of prosthetic device infections caused by this organism.
A 69-year-old man, previously independent and with a pre-existing metallic aortic valve, presented with a history of fevers, confusion and malaise and was diagnosed with prosthetic valve endocarditis. Blood cultures taken on presentation grew Streptococcus sanguinis and vegetations were confirmed on transoesophageal echocardiogram. He had had a dental procedure 10 days before presentation but had not received prophylactic antibiotics; he had been receiving antibiotic prophylaxis for dental treatment up until the change in NICE guidelines in 2008. He was treated with high dose antibiotics and was referred for cardiothoracic surgery, but developed a cerebrovascular event, thought to be embolic, and deteriorated and died. Given that the patient had a metallic aortic valve and poor dentition, and therefore was at increased risk of infective endocarditis, should the new guidelines have been followed so rigidly, particularly as American and European guidelines still recommend the use of antibiotic prophylaxis in this patient group?
Animal models of infective endocarditis (IE) induced by high-grade bacteremia revealed the pathogenic role of Staphylococcus aureus surface adhesins and platelet aggregation in the infection process. In humans, however, S. aureus IE possible occurs through repeated bouts of low-grade bacteremia from a colonized site or intravenous device. Here, we used a rat model of IE induced by continuous low-grade bacteremia to explore further the contribution of S. aureus virulence factors in IE initiation.Rats with aortic vegetations were inoculated by continuous intravenous infusion (0.0017 ml/min over 10 h) with 10(6) CFU of Lactococcus lactis pIL253 or recombinant L. lactis expressing individual S. aureus surface proteins (ClfA, FnbpA, BCD or SdrE) conferring different adhesive and platelet aggregation properties. Vegetation infection was assessed 24 h later. Plasma was collected at 0, 2 and 6 h post-inoculation to quantify TNF, IL-1α, IL-1β, IL-6 and IL-10.Compared to infection with strain pIL253 (11%), conferring binding to fibrinogen to L. lactis increased vegetation infection (strain ClfA: 52%; P= 0.007), which further raised with adhesion to fibronectin (strain FnbpA: 75%; P< 0.001). Expression of fibronectin-binding alone was not sufficient to induce IE (strain BCD: 10%). Platelet aggregation increased the risk of vegetation infection (strain SdrE: 30%). Conferring adhesion to fibrinogen and fibronectin favoured IL-1β and IL-6 production.Our results extend, in a model of IE induced by low-grade bacteremia, resembling human disease, the essential role of fibrinogen-binding to initiate S. aureus IE. Triggering platelet aggregation or inflammatory response may contribute to or promote IE development.
This clinical case reports the emergence of a daptomycin-resistant Staphylococcus aureus isolate during daptomycin treatment in a patient with right-sided infective endocarditis who had never been treated with vancomycin.
Infective endocarditis (IE) is a relatively uncommon condition that can present with a variety of noncardiac symptoms, making diagnosis of this condition challenging. Although IE is no longer uniformly fatal as it was in the preantibiotic era, it still has a high mortality rate. The major risk factor for IE, rheumatic fever, has decreased significantly in the industrialized west, but the incidence of IE remains as high as it was in the preantibiotic era. Today, IE has changed from a disease primarily of the young to one of the elderly. The increase in frequency of IE seems to be related to the fact that individuals are now living longer with chronic heart diseases and are having invasive medical procedures performed more often. The 2 main approaches to treating IE are the use of antibiotics and cardiac surgery. This article provides an overview of IE, epidemiology, pathogenesis, clinical manifestations, diagnosis criteria, and treatment options for IE.
Endocarditis of a prosthetic heart valve is a life-threatening condition that is associated with high morbidity and mortality. Perivalvular extension in infective endocarditis includes complications such as periannular or intramyocardial abscesses, pseudoaneurysms and fistulae. The incidence of perivalvular extension ranges from 10 to 30% in native valve endocarditis and 30 to 55% in prosthetic aortic-valve endocarditis. Herein, we describe a case of a 66-year-old man who presented endocarditis of a prosthetic aortic valve complicated by infective pseudoaneurysm with localization next to the right coronary sinus of Valsalva. Moreover, we underscore the importance of the diagnostic imaging tools options and surgical timing.
The aim of this study was to systematically evaluate the incidence of infective endocarditis (IE) in right ventricle-to-pulmonary artery conduits and valves, comparing bovine jugular vein (BJV) valves with all others.
ABSTRACT Infective endocarditis and kidney infections are serious complications of Staphylococcus aureus sepsis. We investigated the role of superantigens (SAgs) in the development of lethal sepsis, infective endocarditis, and kidney infections. SAgs cause toxic shock syndrome, but it is unclear if SAgs contribute to infective endocarditis and kidney infections secondary to sepsis. We show in the methicillin-resistant S. aureus strain MW2 that lethal sepsis, infective endocarditis, and kidney infections in rabbits are critically dependent on high-level SAgs. In contrast, the isogenic strain lacking staphylococcal enterotoxin C (SEC), the major SAg in this strain, is attenuated in virulence, while complementation restores disease production. SAgs' role in infective endocarditis appears to be both superantigenicity and direct endothelial cell stimulation. Maintenance of elevated blood pressure by fluid therapy significantly protects from infective endocarditis, possibly through preventing bacterial accumulation on valves and increased SAg elimination. These data should facilitate better methods to manage these serious illnesses. IMPORTANCE The Centers for Disease Control and Prevention reported in 2007 that Staphylococcus aureus is the most significant cause of serious infectious diseases in the United States (R. M. Klevens, M. A. Morrison, J. Nadle, S. Petit, K. Gershman, et al., JAMA 298:1763-1771, 2007). Among these infections are sepsis, infective endocarditis, and acute kidney injury. Infective endocarditis occurs in 30 to 60% of patients with S. aureus bacteremia and carries a mortality rate of 40 to 50%. Over the past decades, infective endocarditis outcomes have not improved, and infection rates are steadily increasing (D. H. Bor, S. Woolhandler, R. Nardin, J. Brusch, D. U. Himmelstein, PLoS One 8:e60033, 2013). There is little understanding of the S. aureus virulence factors that are key for infective endocarditis development and kidney abscess formation. We demonstrate that superantigens are critical in the causation of all three infections. We show that their association results from both superantigenicity and direct toxic effects on endothelial cells, the latter likely contributing to delayed endothelium healing. Our studies contribute significantly to understanding the development of these illnesses and are expected to lead to development of important therapies to treat such illnesses.