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Query: UMLS:C0014118 (endocarditis)
15,629 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Infective endocarditis due to fastidious microorganisms is commonly encountered in clinical practice. Some organisms such as fungi account for up to 15% of cases of prosthetic valve infective endocarditis, whereas organisms of the HACEK group (Haemophilus parainfluenzae, H. aphrophilus, and H. paraphrophilus, Actinobacillus actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, and Kingella kingae) cause 3% of community-acquired cases of infective endocarditis. Special techniques are necessary to identify these microorganisms. A history of contact with mammals or birds may suggest infection caused by Coxiella burnetii (Q fever), Brucella species, or Chlamydia psittaci. A nosocomial cluster of postsurgical infective endocarditis may be caused by Legionella species or Mycobacterium species. If risk factors that are commonly associated with fungal infections (cardiac surgical treatment, prolonged hospitalization, indwelling central venous catheters, and long-term antibiotic use) are present, fungal endocarditis is possible. Patients with endocarditis and a history of periodontal disease or dental work in whom routine blood cultures are negative might have infection due to nutritionally variant streptococci or bacteria of the HACEK group. Communication between the microbiologist and the clinician is of crucial importance for identification of these microorganisms early during the course of the infection before complications such as embolization or valvular failure occur. In this article, we review the microbiologic and clinical features of these organisms and provide recommendations for diagnosis and treatment.
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PMID:Infective endocarditis due to unusual or fastidious microorganisms. 917 37

Diagnosis of Chlamydia or Bartonella infections continues to rely mainly on serology. However, serological cross-reactions between members of these genera have recently been described. Sera from eight patients originally diagnosed as having Chlamydia pneumoniae endocarditis reacted with both Chlamydia sp. and Bartonella quintana antigens (microimmunofluorescence technique). Adsorption of sera with B. quintana or C. pneumoniae antigens removed anti-C. pneumoniae antibodies, whereas adsorption with C. pneumoniae antigens did not change antibody titers to B. quintana. Western blot analysis confirmed the presence of cross-reacting antigens and showed antibody patterns in all sera to be compatible with a Bartonella infection. These patients were therefore probably suffering from Bartonella-induced rather than Chlamydia-induced endocarditis. In contrast, sera from 10 patients presumed to be suffering from C. pneumoniae pneumonia did not display anti-B. quintana antibodies, although cross-reacting antigens were revealed by Western blotting. This work highlights the possibility that cases of infective Bartonella endocarditis are erroneously diagnosed as chlamydial infections.
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PMID:Serological cross-reactions between Bartonella and Chlamydia species: implications for diagnosis. 927 3

The authors report a case of tricuspid blood culture-negative endocarditis where serologic investigations showed high titers of antibodies against. Chlamydia pneumoniae, thus suggesting its possible role as the causal agent. The treatment consisted of polymicrobial therapy using ciprofloxacine and doxycycline with favorable response thus avoiding surgical intervention. In all cases of culture-negative endocarditis not responding to classic empiric antibiotics, Chlamydia infection should be suspected. Although rare cases of endocarditis due to Chlamydia pneumoniae have been reported in the literature, to our knowledge, this is the first case of isolated tricuspid valve endocarditis due to this agent to be reported.
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PMID:[Tricuspid endocarditis caused by Chlamydia pneumoniae. Apropos of a case]. 953 44

All series of infective endocarditis had a variable proportion of cases without an etiologic agent because all cultures were negative. New microbiologic techniques have permitted the discovery of the role of many microorganisms in infective endocarditis. C. burnetii is an increasing causative agent of subacute infective endocarditis. In the diagnosis, to the detection of antiphase-I antibodies, immunohistochemical, molecular techniques and cellular cultures have been added. Total cure is difficult to obtain. The combination of doxicicline plus ciprofloxacin for at least 3 years has been proposed as the treatment of choice. Surgery must be reserved for patients with cardiac insufficiency. Less than 2% of cases of acute brucellosis are complicate with infective endocarditis. Infective endocarditis produces serious and rapid valvular destruction with high mortality rates if valve surgery is not performed. For medical treatment at least 3 active agents are required. Bartonella has recently been described as an etiologic agent of infective endocarditis. It mainly affects to homeless people living in poor hygienic conditions. The aortic valve is most commonly involved and, frequently, valve insufficiency requires valve replacement. Blood culture isolation needs long incubation periods. Parenteral nutrition, immunosuppression, wide spectrum antibiotic regimens, intravenous drug addiction and cardiovascular surgery are risk factors previously described in the development of fungal endocarditis. C. albicans and Aspergillus spp. are most frequent etiologic agents. Infective endocarditis should be suspected in any patient with systemic fungal disease. Blood cultures are often negative except for Candida spp. Peripheral emboli and large vegetations are frequent. Mortality is high, antifungal therapy combined with surgery is the treatment of choice. Legionella, Mycoplasma, Chlamydia, Mycobacteria, viruses are potential agents of infective endocarditis, and difficult to diagnose because of special culture requirements. Epidemiological clues, serologic and molecular techniques and blood cultures could identify them.
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PMID:[Infective endocarditis caused by unusual microorganisms]. 965 53

Chlamydia, especially Chlamydia pneumoniae, infection is closely associated with human cardiovascular diseases. Thus far, however, few experimental studies have been carried out to investigate whether natural C. trachomatis infection can induce cardiovascular pathological changes. In this article, we report that pulmonary infection with C. trachomatis mouse pneumonitis strain (MoPn) can induce myocardial and perivascular inflammation and fibrosis in C57BL/6 mice. The pulmonary MoPn infection appeared to be disseminated systemically, because chlamydial antigens were readily detectable in multiple organs including the cardiovascular tissues. In addition, gamma interferon gene knockout mice with a C57BL/6 genetic background showed significant endocarditis and pancarditis characterized by vegetation in aortic valves, interstitial and pericardial inflammatory cellular infiltration, and growth of the organisms in the heart following respiratory tract MoPn infection. The results indicate that C. trachomatis can induce cardiovascular diseases following respiratory tract infection and suggest that murine MoPn respiratory tract infection may be a useful experimental model for investigating cardiovascular diseases caused by chlamydial infection.
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PMID:Chlamydia trachomatis (mouse pneumonitis strain) induces cardiovascular pathology following respiratory tract infection. 1053 Dec 78

A growing amount of epidemiologic, experimental, and clinical evidence has linked infection as a risk factor to variousatherosclerotic diseases including acute myocardial infarction and cerebral infarction. Bacteremic infections with and without endocarditis carry a high risk for both stroke and acute myocardial infarction. During the last decade, chronic bacterial infections such as Chlamydia pneumoniae and dental infections have been associated as risk factors for various atherosclerotic diseases. These chronic bacterial infections are risk factors for acute cardiovascular events, but they may also have some role in the etiopathogenesis of atherosclerotic process itself. There are many known mechanisms that might explain the observed association of infection and atherosclerotic diseases, but it is probable that these mechanisms are complex and multifactorial and probably differ from infection to infection and from patient to patient. Infection theory is by no means against classic risk factor theory in the etiopathogenesis of atherosclerosis. Infection may also act as a synergistic risk factor together with classic risk factors in the development of various atherosclerotic diseases.
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PMID:Role of infections in atherosclerosis. 1053 42

Attributes of Chlamydia pneumoniae of potential importance to a relationship with atherosclerosis are described. Among these are that C. pneumoniae is not new. It is unique. It is a pathogen with which everyone is infected, and it is difficult to treat. It causes immunopathology, myocarditis, and endocarditis and chronicity is a hallmark of Chlamydia infection. Current knowledge of the relation of C. pneumoniae and atherosclerosis comes from observational (e.g., seroepidemiology and tissue studies) and experimental studies. The limitations of the serologic studies of chronic infection are noted as is the conclusive demonstration of an association of C. pneumoniae and atherosclerosis by the repeated and frequent finding of the organism in atherosclerotic tissue. Experimental studies are needed to determine if the association is causal. Such studies should include animal models, basic mechanisms, and secondary prevention antibiotic treatment trials.
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PMID:Background and current knowledge of Chlamydia pneumoniae and atherosclerosis. 1083 24

INJECTABLE SPECTROGRAMIN: Combination regimens using quinupristin/dafopristin with either gentamicin or vancomycin have powerful bactericidal activities (even against quinupristin-resistant strains) against methicillin-resistant Staphylococcus aureus (MRSA) in a model of experimental endocarditis in the rabbit. In clinical trials, quinupristin/dalfopristin is becoming a therapeutic alternative to consider after failure of conventional antistaphylococcal treatments. NEW GENERATION CEPHALOSPORINS: These new cephalosporins, particularly C-3 pyridinium-thiomethyl-cephalosporins, new (3-dithiocarbamoyl) cephalosporins, and a series of new compounds with high affinity for MRSA PLP2a, are particularly active against MRSA and are unaffected by beta-lactamases. A NEW CARBAPENEM: This new antibiotic has a wide bactericidal effect against Gram-positive organisms and is active against MRSA as well as penicillin-resistant S. pneumoniae. NEW FLUOROQUINOLONE DERIVATIVES: In vitro, these new derivatives have been found to be active against MRSA, pneumococci non-sensitive to ciprofloxacin, and Bacteroides fragilis, Mycobacterium tuberculosis, Chlamydia pneumoniae.
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PMID:[Resistance and new antibiotic strategies. New antistaphylococcal antibiotics]. 1115 24

We report a case of aortic valve endocarditis caused by Bartonella henselae. The patient initially presented to a regional hospital with generalized symptoms including lethargy, malaise and decreased appetite. Transthoracic echocardiogram revealed a large vegetation on the aortic valve and he was treated empirically with broad spectrum intravenous antibiotics. Several blood cultures were obtained which all returned negative results and the white blood cell count was normal. He was transferred to our hospital, with persistence of his initial symptoms and additional low-grade fevers. In light of his negative culture results, serological testing for Bartonella and Chlamydia was performed, which gave a positive result for Bartonella henselae. In view of this result and following development of severe aortic valve insufficiency, he underwent an aortic valve replacement and made a good recovery.
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PMID:Aortic valve endocarditis caused by Bartonella henselae: a rare surgical entity. 1180 50

We report on the case of a 54-year-old woman diagnosed as having culture-negative endocarditis (clinical and histopathologic evidence compatible with a recent episode of endocarditis). The responsibility of Chlamydia pneumoniae in this episode of endocarditis was suggested by a serological study and was then confirmed by the positive results of PCR and in situ hybridization tests with aortic and mitral valves tissues. To our knowledge, this is the first case of endocarditis due to C. pneumoniae confirmed by molecular biology-based techniques.
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PMID:Culture-negative endocarditis due to Chlamydia pneumoniae. 1182 6


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