Chronic Endocarditis Research Articles

Risks factors and prevention of Q fever endocarditis.

Coxiella burnetii causes acute and chronic Q fever. To evaluate the risk factors of development of chronic endocarditis following Q fever and to assess the best preventive therapy, a retrospective study of patients diagnosed as having Q fever during 1985-2000 was conducted. Twelve patients with acute Q fever who developed endocarditis and 102 patients with Q fever endocarditis were included in the study. When compared to 200 control patients with acute Q fever, preexisting valvular disease (P<10(-7)), especially a prosthetic valve (P=.01), were encountered more often among patients with endocarditis. Among patients with valvular defects, we estimate the risk of developing endocarditis to be 39%. A combination of doxycycline plus hydroxychloroquine was better at preventing the development of endocarditis than doxycycline alone (P=.009). Our results should encourage physicians to detect valvular lesions in patients with acute Q fever and to search for acute Q fever in patients with a valvulopathy and unexplained fever. A proper treatment for such patients and a scheduled follow-up should reduce the risk of developing endocarditis.

Minimally invasive video-assisted mitral valve surgery: from Port-Access towards a totally endoscopic procedure.

Right thoracotomy is an alternative to mid-sternotomy for left atrium access. The Port-Access approach is an option that reduces the skin incision and obviates rib spreading. From February 1997 until November 1999, 121 patients underwent mitral valve surgery through a right antero-lateral thoracotomy using the Heartport cardiopulmonary bypass (CPB) system. Mean age was 60 years (31-84). Most patients had normal ejection fractions and were in NYHA Class II or III. Seventy-five patients had valve repair (62%) and 46 (38%) had valve replacement. Pathologies were myxoid (n = 80), rheumatic (n = 30), chronic endocarditis (n = 5), annular dilatation (n = 3), sclerotic (n = 1), ingrowing myxoma (n = 1), and one closure of a paravalvular leak. Two patients had conversion to sternotomy for aortic dissection (one died) with the Endo-Aortic Clamp, and two others for peripheral vascular problems. One patient died at postoperative day 1 after reoperation for failed repair, another with double valve surgery on postoperative day 4 after two revisions for bleeding. Twelve underwent revision for bleeding (10%). Three had prolonged ICU stay for respiratory insufficiency. Two late valve replacements for endocarditis occurred. Echographic control revealed residual insufficiencies (grade 1-2) in two valvular repairs. There were neither paravalvular leaks nor myocardial infarcts. There were no cerebrovascular accidents due to embolic phenomena. Mean ICU and hospital stay were 2.1 and 8.7 days, with a major difference between the first 30 patients and those who followed. Port-Access mitral valve surgery can be a valid alternative to conventional sternotomy and seems to be an important improvement in minimally invasive cardiac surgery.

Video-Assisted Port-Access Mitral Valve Surgery: From Debut To RoutineSurgery. Will Trocar-Port-Access Cardiac Surgery Ultimately Lead to Robotic Cardiac Surgery?

A right thoracotomy is a well-known alternative for midsternotomy to have access to the left atrium. The Port-Access (Heartport, Inc, Redwood City, CA) approach is an invaluable option to avoid cracking of ribs and cartilage. EndoCPB (Heartport, Inc) and Endo-Aortic Clamp (Heartport, Inc) allows installation of the extracorporeal circulation and cardiac arrest from the groin. Videoassistance and shafted instruments help the surgeon to perform the surgery through a 5 x 2-cm port and fulfill the main goals of minimally invasive cardiac surgery, comfort, cosmesis, and fast rehabilitation. From February 1997 to November 1998, 75 patients (40 men/35 women) had either Port-Access mitral valve repair (n = 41) or replacement (n = 33) for a variety of reasons: myxoid degeneration (n = 45), rheumatic disease (n = 21), chronic endocarditis (n = 4), annular dilatation (n = 2), and sclerotic disease (n = 2). One valve was replaced because of an ingrowing myxoma. There was one closure of a paravalvular leak. The mean age was 59.3 years of age (range, 32 to 83 years). Most patients had normal ejection fractions but different grades of mitral valve insufficiency and were in NYHA class II. One 71-year-old patient died after reoperation on postoperative day 1 for failed repair. Two patients had conversion to sternotomy and conventional ECC for repair of a dissected aorta. One patient died, one patient suffered a minor cerebrovascular deficit. Three patients had prolonged intensive care unit (ICU) stays for respiratory insufficiency, 5 patients underwent revision for bleeding. Mean ICU stay was 2.5 days; and mean hospital stay, 9 days (range, 4 to 36). A significant difference between the first 30 and last 38 patients in terms of length of stay in the ICU and the hospital was noticed. Two late mitral valve replacements for chronic endocarditis after repair occurred. One patient had medical therapy for endocarditis after mitral valve replacement. The debut of Port-Access mitral valve surgery may be nerve-racking; the routine is a smooth and sure surgery with maximum comfort, a very discrete scar, and a fast rehabilitation. There were no paravalvular leakages nor myocardial infarctions. Cerebrovascular accidents owing to thromboembolic phenomena, vascular lower limb or wound complications were not seen. Port-Access mitral valve surgery is a very important investment in the future of cardiac surgery. Some learning curve pitfalls were associated with the process of starting this revolutionary technique.

NON‐INPATIENT USE OF TEICOPLANIN

SUMMARYTeicoplanin is a glycopeptide antibiotic which was introduced into clinical use in 1988. Its activity against most Gram‐positive bacteria, including the emergent multiply resistant species, its ease of administration and safety commend its continued use well into the next millennium. The provision of health care in alternative settings such as the home or outpatient clinic has grown in importance, both in Europe and North America. One such service is the provision of parenteral antibiotics for treating a variety of infections in the non‐inpatient setting. This paper aims to review and condense the current published experience of teicoplanin in this setting. Evidence suggests that teicoplanin can be administered effectively using a range of flexible, convenient and safe dosing schedules and is a highly cost‐effective therapeutic option for treating in the non‐inpatient setting many chronic infections, e.g. osteomyelitis and endocarditis, and some acute infections.

Management of brucella endocarditis of a prosthetic valve

A case of chronic brucella endocarditis of a prosthetic valve is reported. The diagnosis of this infection was established by positive blood cultures and high brucella agglutination titre. The patient was successfully managed by combination of medical therapy (consisting of streptomycin, trimethoprim-sulphamethoxazole, rifampin and tetracycline) and surgery.

Most common clinical presentation of Q fever in a province in the north of Spain.

Q fever is a world-wide zoonosis, produced by Coxiella burnetti, a microorganism belonging to the Riskettsiaceae family. Q fever can appear as a non localized feverish disease, as a feverish syndrome with hepatic impairment or as an atypic pneumonia [1, 2]. The form of presentation varies between different geografic areas, thus, feverish form is more prevalent in Australia [3], while the hepatic one is prevalent in France [4] and the pneumonic one in Nova Scotia (Canada) [5]. In order to know which is the most common presentation pattern of Q fever in our area, we have checked all cases diagnosed between 1 January, 1984 and 31 December, 1996, in the province of Soria, situated in northern Spain. A suggestive clinical feature plus antibody detection against Coxiella burnetti were used as diagnostic criteria. The techniques used for serum diagnosis were complement fixation and/or indirect immunofluorescence. Two samples of sera were obtained in all cases, one during the acute phase of the disease, another 2-4 weeks after. Those cases in which seroconversion or a 4-fold antibody titer rise were found, were considered positive. Thirteen cases of Q fever were diagnosed. Patient age at the time of diagnosis ranged from 10 to 41 years old, with a mean age of 26.72 ? 8.05. Of all the Q fever cases, eleven were men and two women. Pneumonia was the most common presentation pattern, counting 10 cases. Another three were a feverish syndrome without any focus and with an intense headache, a feverish form with hepatitis, and a chronic endocarditis. Like in other areas of northern Spain, pneumonia was the most common form of Q fever. Thus, in a group of 60 patients, 75% were pneumonia [6], in a family outbreak of 5 cases, 3 (60%) presented pneumonia [7] and of 492 Q fever cases diagnosed between 1984 and 1991, 265 (54%) had pneumonia [8]. On the other hand, in central and southern regions of Spain, relative prevalence of pneumonia went down, the hepatic form being the most frequent [9, 10]. All our cases presented as an atypical pneumonia with alveolar infiltrate, with cough in four cases and headache in three. Four patients also had chest pain and none had hemoptysis. Only in two cases, contact with animals or derived products could be found as epidemiologic data explaining how the disease was transmitted. Animals infected with C. burnetti are usually the most important source of infection. Man can be infected by aerosol inhalation, or milk or fresh contaminated cheese ingestion [1, 2, 11]. This variability in the form of clinical presentation of Q fever has been related with the presence of different strains of C. burnetti in the different geographic areas and with plasmids that would regulate the virulence of the strains [2]. It has also been postulated that different clinical patterns would be related to different ways of disease transmission. So, in those cases in which C. burnetii is transmitted by milk or dairy products ingestion, both hepatitis and pneumonia can occur, and in those cases in which the organism is acquired by air inhalation, only pneumonia would occur [12].

Is There an Advantage to Repairing Infected Mitral Valves?

Background. The therapy for native mitral valve endocarditis is in evolution. Antibiotics have significantly improved survival rates, but patients with complications of endocarditis may require surgical treatment.Methods. Between January 1985 and December 1995, 146 patients underwent surgical therapy (repair or replacement) for native mitral valve endocarditis. All patients had documented bacterial endocarditis. Univariate and multivariate analyses were performed to determine predictors of hospital death, long-term event-free survival, and probability of repair. Patients were evaluated in three groups: all patients, patients with acute endocarditis, and patients with chronic endocarditis.Results. There were ten hospital deaths (6.8%). Patients undergoing repair had a lower hospital mortality rate (p = 0.008) then those having replacement. Event-free survival was improved after mitral valve repair in the overall group (p = 0.02) and in the group with healed (chronic) endocarditis (p = 0.05). Although the acute endocarditis group demonstrated an improved event-free survival rate after mitral valve repair versus replacement (74% versus 20% at 6 years), this did not reach statistical significance.Conclusions. We conclude that mitral valve repair is preferable to mitral valve replacement when possible, in patients with complications of endocarditis, as repair results in a lower hospital mortality and an improved long-term survival.(Ann Thorac Surg 1997;63:1718–24)

Retrospective survey of chronic Q fever in Japan by using PCR to detect Coxiella burnetii DNA in paraffin-embedded clinical samples.

We used PCR to detect Coxiella burnetii DNA in paraffin-embedded tissues obtained from patients with chronic endocarditis in which the etiological agent had been unknown. On the basis of the published nucleotide sequence of the C. burnetii htpB gene, primers were chosen to produce an amplified fragment of 285 bp. A total of 60 samples from 56 patients were tested for the presence of C. burnetii DNA. Five samples from four patients were found to be positive. All of the amplified DNA fragments possessed a TthHB8I restriction site, as predicted from the published sequence of C. burnetii. In one of the four positive patients, rickettsia-like particles were found in sections of tissue stained by Gimenez's method. This is the first report of chronic Q fever in Japan.

Advances in acquired pediatric heart disease

Acquired heart disease in children may result in significant morbidity and mortality. Advances continue to be made in understanding Kawasaki disease, acute and chronic rheumatic heart disease, infective endocarditis, myocarditis, and dilated cardiomyopathy. The role of superantigens, particularly bacterial toxins, in the pathogenesis of Kawasaki disease continues to be defined. Intravascular ultrasound promises to improve the assessment of coronary arteries in Kawasaki disease. Current recommendations for the long-term management of Kawasaki disease are discussed. Significant changes in the epidemiology of acute rheumatic fever and endocarditis are noted. Updates on the role of echocardiography as well as current therapeutic issues in these diseases are addressed. The application of immunologic and molecular biologic techniques have implicated genetic and immune factors in the pathogenesis of myocarditis and cardiomyopathy. The relationship between viral infection and subsequent dilated cardiomyopathy, as well as the role of autoimmune mechanisms in the pathogenesis of these disorders, remains controversial.

Is plasmid based differentiation ofCoxiella burnetii in ‘acute’ and ‘chronic’ isolates still valid?

Ten human Coxiella burnetii isolates from french patients with acute hepatitis or chronic endocarditis were characterized according to their polymorphism in DNA restriction patterns and differentiated by plasmid-specific PCR. The aim of this investigation was to clarify if the present classification of so called 'acute' and 'chronic' Coxiella burnetii isolates--based on plasmid profile of a so far limited number of partly ancient isolates--could be confirmed with lately isolated organisms of this agent. The data obtained in this investigation indicate that this classification based on C. burnetii plasmid content is no longer justified.

Rapid Growth of Left Ventricular Thrombus Leading to Fatal Heart Failure in Six Hours

A left ventricular (LV) thrombus grew rapidly over chronic endocarditis 2 months after anterior myocardial infarction. Echocardiograms demonstrated a rapidly growing LV thrombus an eventual obstruction. Despite anticoagulant/thrombolytic therapy, the patient died of acute LV failure. Histopathologically, a fresh thrombus overlay thickened endocardium with massive T lymphocyte infiltration over healed infarction.

Endocardite abcédée à Coxiella burnetti avec anévrysme de l'aorte ascendante

The authors report a case of often underdiagnosed condition : chronic fever endocarditis. This case was well documented with serological confirmation and isolation of C. burnetti from aortic valve tissue. Moreover, it was associated with an aortic parietal abcess and aneurysm, complications which are more frequent with C.B. in anatomical statistics.

Comparison of Coxiella burnetii Plasmids to Homologous Chromosomal Sequences Present in a Plasmidless Endocarditis‐Causing Isolatea

Coxiella burnetii is the etiological agent of human Q fever and chronic endocarditis. Different plasmids have been found in C. burnetii isolates and a correlation between disease state and plasmid type has been established. The plasmid QpRS was found in all but four of the endocarditis-causing isolates examined. These four isolates did not contain a detectable plasmid. However, when DNA from the plasmidless isolates is hybridized with 32P-labeled QpRS, homologous sequences are detected. It was hypothesized that plasmid sequences had inserted into the chromosomal DNA of the plasmidless isolate. A cosmid chromosomal gene bank was constructed from one of the plasmidless isolates and a number of clones were obtained. One clone, pEAS137, contained all of the EcoR I fragments with homology to the C. burnetii plasmids plus several non-homologous fragments. The EcoR I fragments in pEAS137 were in the same linear order as present in the chromosome of the plasmidless isolate and were shown to exist as a single contiguous sequence. This information supports the hypothesis that plasmid sequences have inserted into the chromosomal DNA and makes pEAS137 a good candidate for studying the relationships between the plasmids. Initial studies comparing pEAS137 to QpRS and QpH1 suggest that pEAS137 is more closely related to QpRS than to QpH1.

Host Factors in the Severity of Q Fever

The author has reviewed different aspects of the role of immunocompetence in the development of Q fever. Coxiella burnetii lives within the phagolysosomes of infected cells. In animals, the immunosuppression caused by either cortisone or X-irradiation reactivates Q fever. In humans, cases of Q fever are reported in immunocompromised hosts suffering from leukemia, cancer, and human immunodeficiency virus infection (AIDS). Similar data are reported with strict or facultative intracellular parasites living within the phagolysosome. Sporadic publications reported the appearance of auto-antibodies during Q fever which may change the clinical picture of the disease. The pathological findings of hepatitis diagnosed during acute Q fever and those with C. burnetii chronic endocarditis are quite different and may reflect a different immunological response to C. burnetii. These facts emphasize the importance of host factors in the clinical expression and outcome of Q fever.

牛の腫瘍性および炎症性疾患における血清α&lt;SUB&gt;1&lt;/SUB&gt;酸性糖蛋白

The concentrations of serum α1-acid glycoprotein (α1-AGP), sialic acid and mucoprotein were estimated in 145 cattle with neoplastic and inflammatry diseases, and 10 normal cattle. The mean values of serum α1-AGP were 330.5±104.5μg/ml in normal cattle, 897.8±500.8μg/ml in calf type leukemia, 848.3±826.5μg/ml in thymic type leukemia, 1353.2±679.6μg/ml in adult type leukemia, 480.0±353.6gg/ml in skin type leukemia, 4050.0μg/ml in myelocytic leukemia, 702.8±339.4μg/ml in solid tumors, 1065.6±707.4μg/ml in BVD· MD, 1411.8±862.5μg/ml in traumatic pericarditis, 1987.3±1387.1μg/ml in chronic endocarditis, 1471.7±939.5μg/ml in necrotic mastitis and 1107.5±56.4gg/ml in granulocytopathy syndrome.Serum α1-AGP concentration showed a positive correlation with serum sialic acid and mucoprotein concentration. Serum α1-AGP of necrotic mastitis showed a negative correlation with lymphocyte count, and a positive correlation with serum γ-globulin. As a nonspecific marker, measurement of serum α1-AGP was considered to be useful in the diagnosis of bovine leukosis, solid tumors and inflammatory diseases.

Naturally occurring erysipelas in rats.

Erysipelothrix rhusiopathiae was isolated from the main limb joints of two Sprague Dawley rats affected by spontaneous lesions of chronic fibrinopurulent polyarthritis, endocarditis and mycocarditis.

The importance of optic neuritis and retinal haemorrhages in the diagnosis of chronic septic endocarditis

The importance of optic neuritis and retinal haemorrhages in the diagnosis of chronic septic endocarditis

Rupture of a pulmonary artery mycotic aneurysm associated with candidal endocarditis

Candidal endocarditis can develop if candidemia occurs during Swan-Ganz catheterization. Candida endocarditis may persist for many months and is fatal unless the infected valve is resected. Herein is reported the first case of rupture of a mycotic pulmonary artery aneurysm caused by chronic candidal endocarditis. The endocarditis followed Swan-Ganz catheterization and the aneurysm progressed despite appropriate medical and surgical therapy.

Thrombosis and embolism from cardiac chambers and infected valves

In a number of cardiac conditions (acute myocardial infarction, chronic left ventricular aneurysm, dilated cardiomyopathy, infective endocarditis and atrial fibrillation in the absence of valvular disease), the risk of embolism gives cause for concern. Although anticoagulation with warfarin (Coumadin)-derivatives has been shown to be effective in some of these situations, there is no evidence regarding the role of antiplatelet agents. The common factor in the thromboembolic potential of acute myocardial infarction, chronic left ventricular aneurysm and dilated cardiomyopathy is mural thrombus. This can be detected by two-dimensional echocardiography and indium-111 platelet scintigraphy. Although of value in elucidating the natural history of mural thrombus, in most cases, management is not substantially aided by these investigations. In patients with extensive myocardial infarction, particularly anterior infarction, moderate intensity anticoagulation started soon after hospital admission reduces the rate of embolism. After 8 to 12 weeks, embolic risk is low so that anticoagulants can usually be discontinued. Patients with chronic left ventricular aneurysm have a low incidence of embolism; anticoagulation is, therefore, inappropriate. Dilated cardiomyopathy is associated with a high risk of embolism; moderate intensity anticoagulation may be advisable in many such cases. Little information is available regarding the incidence of thromboembolism or the role of antithrombotic therapy in the patient with a diffusely dilated left ventricle due to ischemic heart disease. In native valve infective endocarditis, the risk of hemorrhage is high, and the efficacy of conventional anticoagulants unclear; thus, anticoagulation should not be instituted for the cardiac condition as such. However, in prosthetic valve endocarditis, the risk of embolism seems to be very high, and anticoagulant therapy should be continued, but with great care because there is a substantial risk of cerebral hemorrhage. Atrial fibrillation in patients with valvular heart disease is dealt with in a previous review. Patients with nonvalvular atrial fibrillation are at varying risk of embolism, depending on the etiology of the arrhythmia; trials of antithrombotic therapy are needed for the various subsets of patients. In most elderly patients, the etiology is not known, and their stroke risk is high. The risk of embolism in younger patients with idiopathic atrial fibrillation is so low as to make any antithrombotic therapy unnecessary.(ABSTRACT TRUNCATED AT 400 WORDS)

Cellular Immunity in Q Fever: Specific Lymphocyte Unresponsiveness in Q Fever Endocarditis

Human infection with the rickettsia Coxiella burnetii presents as acute influenza-like primary Q fever, subacute granulomatous hepatitis, or chronic endocarditis with hepatitis. To investigate whether persistent infection is associated with a possible immunologic defect, we tested lymphocyte proliferation specific for Coxiella in vitro in peripheral blood mononuclear cells from patients and controls. All four patients with endocarditis had profound lymphocyte unresponsiveness to Coxiella antigens with normal proliferation to control antigens. Hepatitis and primary Q fever were associated with vigorous responses in vitro to Coxiella antigens. Suppression of lymphocyte unresponsiveness was in part mediated by an antigen-nonspecific, glass-adherent cell. We hypothesize that specific T cell unresponsiveness is an important factor in persistent infection with C. burnetii and offer in vitro lymphocyte stimulation as a more specific diagnostic test to distinguish cases of endocarditis among those with chronic hepatitis due to Q fever.