[The changing picture of bacterial endocarditis--infectious endocarditis].
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Infectious endocarditis sometimes causes coronary embolism which induces acute myocardial infarction. A 59-year-old man was admitted to our hospital with a diagnosis of acute myocardial infarction accompanied by left ventricular free wall rupture and papillary muscle rupture. We perfomed mitral valve replacement combined with repair of left ventricular free wall rupture. The anterior mitral leaflet had perforation and vegetation, which suggested that acute myocardial infarction was caused by septic embolus originated from infectious endocarditis in this case.
Infectious endocarditis (IE) develops following bacteremic episodes during which bacteria may attach to sterile thrombotic vegetations. Such thrombotic vegetations result from the deposition of platelets and fibrin on lesioned endothelium. These sterile vegetations are the most susceptible to infection in the left side of the heart, since this localization is found in as much as 80% of the patients with IE. Any circulating bacterial or mycotic organism may induce endocarditis, but streptococci are most often responsible, possibly because of their high capacity to adhere to thrombotic vegetations. The host cell defenses apparently cannot penetrate the dense network of platelet and fibrin in the vegetation, and humoral immunity (antibodies and complement) are of no help against gram-positive cocci. Thus, the infected vegetation has been compared to a localized agranulocytic focus, permitting the survival of infection and allowing bacteria to be released freely and continuously into the circulation (hence the constant bacteremia, a hallmark of IE). In the subacute and chronic evolution of IE, the clinical findings are mainly due to immunization of the host against the infecting microbe, resulting in antigen-antibody-complex-mediated vasculitis, and in nonspecific symptoms. Only positive blood cultures at this stage will confirm the clinical suspicion of endocarditis. Embolism may occur in any organ and falsify the diagnosis because of focal signs. Local complications of IE are the major cause of mortality in this disease, and are due to valve perforation, paravalvular abscesses, cardiac metastatic abscesses etc. If these complications occur early in the course of IE, the course may be acute.(ABSTRACT TRUNCATED AT 250 WORDS)
Infectious endocarditis was diagnosed in four patients, men aged 18, 44, 35 and 22; the bacteria involved were Streptococcus viridans, Eikenella corrodens, Staphylococcus aureus and Streptococcus mutans, respectively. In all patients mycotic aneurysms were observed which had led to seemingly unrelated neurological or abdominal complaints. In one patient an aneurysm of the A. cerebri media resolved in two years, another patient died following fatal bleeding of a ruptured aneurysm in the A. hepatica propria. Mycotic aneurysms may be found in all parts of the body. This complication is often diagnosed too late because it is not considered.
Out of 242 patients treated for systemic lupus erythematosus (SLE) in Novosibirsk for 15 years, valvular lesions and endocarditis were diagnosed in 41(16.9%) patients. Combination of Libman-Sax endocarditis (LSE) with infectious endocarditis (IE) was observed in three patients (two women, one man, age 18-40 year). SLE ran a subacute course in one woman, an acute one--in the other. LSE emerged early in SLE in two patients. All the patients had polyorganic lupus pathology, lupus nephritis with nephrotic syndrome (morphological class IV). Two patients had mitral valve disease, one patient--mitral-aortic disease. The rise of secondary IE was seen after massive immunosuppressive therapy. The diagnosis of secondary IE was made after SLE duration for 10-36 months. At IE diagnosis, all the patients had high titers of blood antiphospholipid antibodies. IE was of staphylococcal origin in two patients and candidosis-induced in one patient. In SLE with IE there was thromboembolic syndrome. LSE and IE have related aspects which should be regarded in clinical practice: possible "IE mask" in LSE, risk of secondary IE in about 10% of LSE patients, prophylactic measures necessary to prevent IE in hemodynamically prominent forms of LSE.
BACKGROUND: Infectious endocarditis can lead to embolic arterial retinal occlusions. Which therapy is indicated? RESULTS: A 33-year-old man suddenly became blind in his left eye as the result of a central retinal artery occlusion (CRAO). This occurred during high-dosage treatment for infectious endocarditis that had been diagnosed 3 weeks earlier. The echocardiogram showed distinct vegetation and an abscess on the aortic valve. The CRAO together with the ultrasound findings was considered an absolute indication for surgery of the aortic valve. During this emergency operation, a 2 cm deep abscess cavity was found between the mitral and aortic valves. After removal of the abscess, together with the infected valve, a prosthetic valve was inserted. Following the operation, the patient made an uneventful recovery. The antibiotic treatment was continued for several months. The left eye remained sightless. No recurrence of infectious endocarditis occurred during the follow-up of 2 1/4 years. A branch retinal arterial occlusion occurred in the right eye of a 35-year-old man who had suffered from chronic infectious endocarditis for several months. Insufficiency of more than one valve had been diagnosed on several occasions. The patient, a drug-addict, had refused surgical treatment on each occasion. After 3 months, the right eye became completely blind owing to CRAO. Following high-dosage treatment with antibiotics, the infectious endocarditis was healed. The right eye remained blind. One year later the patient died. CONCLUSION: Retinal arterial occlusion of embolic origin in a patient with infectious endocarditis is an indication for immediate medical and/or surgical treatment. This is of particular importance if there is ultrasound evidence of an abscess in the valve area.
A 40-year-old female had a history of fever, arthralgia, proteinuria, and dyspnea on effort twenty years ago, and was diagnosed as SLE, renal failure, and aortic regurgitation. She also suffered from pyelonephritis and sepsis due to the infection of E. coli. Preoperative examination revealed non-active phase of SLE. Echocardiography and aortography showed massive aortic regurgitation and operation was recommended. Operative findings showed fresh vegetation on the aortic leaflets, and aortic valve replacement (Tekna-Edwards 19 mm) was performed. Histological findings of the vegetation showed Libman-Sacks endocarditis and infectious endocarditis. Predonisolone was infused intravenously to prevent the acute deterioration of SLE after the operation. She was discharged from the hospital three weeks after the operation.
INTRODUCTION: Splenic involvement in the course of endocarditis consists in either splenic infarct or abscess. Pathophysiological examinations suggest the existence of a continuum between the two types of lesion. Signs and symptoms are usually poor or aspecific. Current incidence and diagnostic methods are rarely reported in recent medical literature. EXEGESIS: We report a retrospective study conducted from a questionnaire that was circulated to nine French medical units. Two hundred and twenty five patients with infectious endocarditis according to Duke university criteria were included in the study. The existence of splenic lesions was investigated in 153 patients (68%). Splenic involvement was documented in 35 patients. Diagnostic methods were: abdominal echography (n = 77), abdominal CT scan (n = 40), and both techniques (n = 36). The incidence of splenic lesions was 9%, 35% and 36%, respectively. Among patients investigated using both diagnostic techniques, splenic abnormalities were detected by CT scan in 13 cases and by echography in six cases. Splenic abscess was suspected in nine patients by combining suggestive clinical course and radiological abnormalities, but was definitively evidenced in only four patients (surgery, n = 2, post-mortem examination, n = 2) presenting with large lesions (> or = 8 cm) associated with aortic endocarditis. All other 26 cases were categorized as splenic infarcts; however, diagnosis was confirmed in only two cases (surgery n = 1, autopsy n = 1). CONCLUSION: These data suggest that: 1) the incidence of splenic involvement during endocarditis is approximately 35%, 2) CT scan is probably superior to echography for spleen screening, and 3) incidence of abscess requiring specific surgery is very low, inferior to 2%.
Infective endocarditis, resulting from deposition of circulating microorganisms during a period of bacteremia on damaged endothelial heart valves, remains a serious disease. Its overall incidence did not decline in recent years, 24 cases/year/million inhabitants, in France. This can be explained by a modification of the type of underlying cardiac conditions with regression of rheumatic fever and increase of degenerative heart diseases, prosthetic valves and mitral valve prolapse. The risk of bacterial seeding on a damaged valve remains difficult to evaluate, the highest risk being for patients with prosthetic valve, previous infective endocarditis and cyanotic congenital heart disease. A case-control study, done in 1991, confirmed that procedures are risk factors for infective endocarditis and that the multiplicity of procedures increases the risk. A French consensus conference on the prophylaxis of infective endocarditis has updated the recommendations for antibiotic prophylaxis. Two groups of cardiac patients were identified, based on the incidence and the severity of endocarditis occurring in patients with these conditions, 1) patients considered at risk which require specific prophylaxis, and 2) patients considered non at risk which do not require antibiotic prophylaxis. Procedures which require antibiotic prophylaxis are dental procedures and specific gastrointestinal and urologic procedures. As complex protocols are associated with poor compliance by practitioners and patients, the jury has aimed for simplicity and feasibility.
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Secondary hypertrophic osteoarthropathy occurred in a patient with subacute endocarditis. Chest x-ray in this smoker with ethylic cirrhosis showed a pulmonary opacity. Clinical signs of osteoarthropathic inflammation resolved with antibiotics before surgical cure of the aortic insufficiency. The diagnosis was retained on the basis of outcome after antibiotic therapy and the absence of any other etiology, notably bronchogenic cancer. Endocarditis or infectious endarteritis should be entertained in case of hypertrophic osteoarthropathy in patients with an infectious syndrome. Pathogenic hypotheses are discussed. In congenital cardiopathies, intrapulmonary shunts, megacaryocytes and activation of the vascular-platelet endothelium unit may be involved. Bacterial factors and platelet aggregation could play a role in initiating hypertrophic osteoarthropathy in patients with infectious endocarditis.
Microbe-induced (infectious) endocarditis is an endovascular infection, caused mainly by bacteria, of cardiovascular structures. The major predilection site are the native heart valves, but involvement of implanted intracardiac foreign material is increasingly being seen. The mortality rate of infectious endocarditis depends on clinical factors and the causal agent, but also on the time of the establishment of the diagnosis and the initiation of appropriate treatment. In Germany, the current mortality rate ranges up to 18%. Between January 2003 and July 2004, with the aim of improving patient care and thus the outcome of this condition, a guideline commission worked out recommendations for the diagnosis, treatment and management of the disease for the use of general practitioners and hospital physicians, in particular microbiologists, infectiologists, cardiologists and cardiac surgeons. The basis for this guideline was the systematic search through the literature of the European guideline. On the 16th and 28th of June 2004, the entire guideline was formerly approved in a nominal group process.
BACKGROUND: Many studies in the literature have warned of the need for investigation of colonic lesions among patients, especially elderly ones, who have bacteremia and/or endocarditis from Streptococcus bovis. Bacteremia and infectious endocarditis from Streptococcus bovis may be related to the presence of neoplastic lesions in the large intestine and hepatic disease. AIM: This report describes a patient who presented infectious endocarditis from Streptococcus bovis associated with colonic carcinoma and tubular-villous adenomas. CONCLUSIONS: The finding of this bacterium among patients with septicemia and/or endocarditis is also related to the presence of villous or tubular-villous adenomas in the large intestine. For this reason, complete and detailed investigation of the large intestine must be performed in patients with infectious endocarditis, even in the absence of intestinal symptoms. An increased incidence of this condition or hepatic dysfunction has been reported among patients with infectious endocarditis from Streptococcus bovis. Patients with infectious endocarditis from Streptococcus bovis and normal colonoscopy may be included in the group at risk for developing colonic cancer. The knowledge that there is an association between endocarditis from Streptococcus bovis and carcinoma of the colon has important clinical implications. If the lesion can be discovered at an early stage, curative resection may become possible.
The clinical and immunological 8-year follow-up of a 45-year old female with hypereosinophilic syndrome and cardiac involvement of Löffler's fibroplastic endocarditis which was complicated by infective endocarditis during immunosuppressive treatment is presented. All 3 stages of the disease were documented by clinical and histologic data: stage 1 by biopsy proven eosinophilic myocarditis and arteritis, stage 2 with Berlin blue positive parietal thrombosis, and the fibrotic features of stage 3 both by fibrosis in the latest biopsies and by echocardiography. It was remarkable, however, that this classic clinical case of Löffler's endocarditis lacked a few serological markers postulated to be found regularly, e.g., a positive staining for the cationic protein and major ribonucleases. Instead, the patient demonstrated all the immunological features of autoreactive myocarditis with cytolytic, complement fixing antimyolemmal antibodies. After an initial loading dose of 120 mg prednisolone per day for 6 weeks (11/1986), the steroid dosage was reduced to 40 mg (12/1986) and diminished to 15 mg/day in 1988 to 1989. Finally, the patient was on 4 mg prednisolone per day for almost 4 years. In 1987, azathioprine was added in the dose of 150 mg/day for 6 weeks. In 3/1994 the patient developed infective endocarditis with streptococcus sanguis and presented with dyspnoea. By echocardiography a large floating structure was diagnosed on the anterior mitral leaflet and the left atrium was enlarged by severe mitral regurgitation. Infective endocarditis was successfully treated with antibiotics, but mitral regurgitation made valve replacement obligatory.
OBJECTIVE: To analyze the epidemiology, diagnosis, clinical aspects causes and evolution of infectious endocarditis. METHODS: The patients analyzed were treated at the University Hospital of the Faculdade de Medicina of Ribeirão Preto-USP and had a diagnosis of infectious endocarditis defined by Duke's criteria, which classifies infectious endocarditis as native, prosthetic valve or that occurring in intravenous drug users. RESULTS: One hundred and eighty episodes of infectious endocarditis in 168 patients were observed. Echocardiograms in 132 (73.3%) provided a diagnosis of infectious endocarditis in 111 (84%) patients; mitral valves were affected in 55 (30.5%), tricuspid valves in 30 (16.6%) and the aortic valve in 28 (15.5%) patients. Hemocultures were performed in 148 (93.8%) episodes of IE. The most commonly isolated infectious organisms were Staphylococcus aureus in 46 (27.2%) patients and Streptococcus viridans in 27 (15.9%). Complications occurred in 116 (64.4%) patients and 73 (40.5%) of the patients died. CONCLUSION: The general profile of the observed infectious endocarditis was similar to that reported in studies performed in other countries and included users of intravenous drugs. The high degree of mortality observed is not compatible with progress in diagnosis and treatment of infectious endocarditis and is probably due to the absence of diagnostic suspicion. The high frequency of fatal cases of septicemia (45.1% of deaths) in the patients studied indicates that unnoticed cases of infectious endocarditis had only been diagnosed at necropsy.
PURPOSE: Histologic examination of valve samples is considered as the gold standard for the diagnosis of infectious endocarditis. Molecular tools are also very promising for patients with negative-culture endocarditis. Thus, we studied the contribution of valvular histology, culture, and 16S rRNA PCR amplification plus sequencing to the diagnosis of infectious endocarditis in patients undergoing valve surgery. SUBJECTS AND METHODS: We performed culture, histological examination, and broad-range PCR amplification plus sequencing on valve samples taken from 127 patients with infectious endocarditis and from 118 patients without endocarditis. The sensitivity and specificity of these tests for the diagnosis of endocarditis in patients undergoing valve surgery were studied. RESULTS: The sensitivity of PCR was of 61% (64/105) whereas that of histological examination was of 63% (62/98) and that of valve culture was of only 13% (14/105). All 68 positive PCR results considered reliable according to an interpretation scheme were from patients with infectious endocarditis, resulting in a 100% (118/118) specificity of the interpreted molecular approach. The specificity of histology was also of 100% (118/118) when using stringent criteria (ie, presence of vegetation, microorganisms, and/or valvular inflammation with mainly polymorphonuclear cells). PCR identified an etiological agent in 38% (5/13) of definite blood culture-negative infectious endocarditis. CONCLUSION: We show that valvular histology with stringent criteria is the gold standard for the diagnosis of infectious endocarditis. Broad-range amplification of 16S rRNA gene is indicated for infectious endocarditis of unknown etiology, whereas valve culture is of limited sensitivity.
Using a new computer program SPHERE, amikacin concentrations have been computed at various layers of simulated endocardial vegetations. Inputs are the computed serum (central compartment) concentrations of either population pharmacokinetic models or of individualized patient-specific models utilizing Bayesian fitting to data of doses given and measured serum levels, using the USC*PACK PC Clinical Programs. The vegetation is modeled as an isotropic homogeneous sphere. Fick's second law of radial diffusion was applied to compute the in situ antibiotic concentrations. Examination of factors affecting concentrations in vegetations shows that in situ peak concentrations are less when the vegetation is larger, and when the antibiotic dose, serum concentrations and diffusivity are all less. The results show that early and aggressive treatment of infectious endocarditis is required with high doses of concentration-dependent antibiotics, such as aminoglycosides, to achieve the desired high peak serum levels and to reach effective concentrations deep inside the vegetations.
Infectious endocarditis (IE) is an uncommon condition carrying a relatively high mortality and morbidity. Two epidemiological studies, undertaken eight years apart, provide data allowing an appreciation of changes in the epidemiological and clinical profiles of IE. They show a progressive increase in the age of patients affected by IE and a decrease in percentage of IE on native pathological valves and valvular prostheses, compensated by the increase in incidence of IE occurring in patients with no known underlying cardiac disease. Moreover, there has been a change in microbiological profile, with the emergence of Streptococcus bovis and increase in staphylococcal IE, a decrease in IE due to oral streptococci and an improvement in microbiological diagnosis with negative blood cultures. Finally, from the therapeutic point of view, surgery is used more frequently and at an earlier stage of the disease. The global mortality of IE at the end of the initial hospital period remains 16%.