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

(1) Neurologic complications remain a significant problem in bacterial endocarditis. Of 218 patients with endocarditis, 84 (39%) had a neurologic complication and 58% of these 84 patients died. In contrast, the mortality rate was only 20% among those endocarditis patients without neurologic complications. (2) Of the neurologic complications, cerebral embolism is the most frequent and important. An embolic stroke occurred in 37 (17%) of our patients, with 30 of these patients dying. Emboli are important not only in terms of the direct morbidity and mortality they cause via cerebral infarction, but also because of their role in the causation of mycotic aneurysms, brain abscesses, and abnormal CSF formulae. (3) Cerebral emboli are particularly common in patients with mitral valve infection, and in patients with infection due to virulent organisms, particularly S. aureus and enteric gram-negative bacilli. (4) Mycotic aneurysms occur more frequently in the course of acute endocarditis rather than late in the course of subacute disease. Management of angiographically demonstrated mycotic aneurysms is dependent upon the presence or absence of hemorrhage, the anatomic location of the aneurysm, and the clinical course of the patient. Healing of mycotic aneurysms can occur during the course of effective antimicrobial therapy, thus obviating the need for neurosurgical intervention in all such patients. (5) Macroscopic brain abscess is a rare complication of bacterial endocarditis. Miliary microscopic abscesses are more common than larger abscesses, particularly in patients with acute disease and miliary infection in other organs of the body. (6) Focal seizures occur most commonly in endocarditis patients with acute embolic disease; generalized seizures are of diverse etiologies, with metabolic factors being most important. Penicillin neurotoxicity should be considered in patients with impaired renal function who are receiving high dose penicillin. (7) With the exception of hemorrhagic complications, lumbar puncture results tend to reflect the nature of the infecting organism rather than the nature of the neurologic complication. Endocarditis due to virulent organisms such as S. aureus is usually associated with a purulent CSF formula while nonvirulent organisms, such as viridans streptococci, susually have aseptic or normal CSF formulae.
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PMID:Neurologic complications of bacterial endocarditis. 58 Jul 94

Nonbacterial thrombotic endocarditis is the most prevalent endocarditis at autopsy. It is a clinically important cause of arterial embolisation. Often it is observed in association with malignancy (mainly gastrointestinal adenocarcinomata), severe infections and other fulminant acute disease processes. A deranged or damaged valvular surface and clotting disorders are important pathogenic factors. The valvular vegetations are pathologically characterized by a bland, fibrin-platelet thrombus; they usually affect the mitral and aortic valve. Neurologic events are the most common clinical manifestations, but any organ may be involved by emboli. The association of venous and arterial thromboses and pulmonary thromboembolism underscores the pathogenetic role of hypercoagulability in the development of nonbacterial thrombotic endocarditis. The clinician must be a vigilant observer in order to make the antemortem diagnosis. If possible, the underlying process should be treated; anticoagulation therapy with heparin sometimes is helpful.
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PMID:[Nonbacterial thrombotic endocarditis. Case report and literature review]. 132 12

The diagnosis of Q fever endocarditis cannot be made by bacterial cultures and necessitates serological identification of specific antibodies to Coxiella burnetii which stimulates mainly the production of anti-phase II antibodies during the acute disease, but primarily anti-phase I antibodies in endocarditis. Indirect microimmunofluorescence allows rapid detection of specific IgA, IgG and IgM. The results of serological analyses of 191 acute cases of Q fever were compared with those of 8 cases of Coxiella burnetii endocarditis. All sera were evaluated by complement fixation and microimmunofluorescence tests. The highest titre differences between primary Q fever and Q fever endocarditis were observed with anti-phase I IgA and IgG antibodies measured by microimmunofluorescence followed by anti-phase I antibodies measured by complement fixation tests. Antiphase I IgG and IgM titres were consistently higher than anti-phase II titres in endocarditis. The reverse is true in acute Q fever. In addition, anti-phase I IgA appeared to be diagnostic for Coxiella burnetii endocarditis. Accordingly we recommend the testing of these specific IgA, IgG, and IgM by microimmunofluorescence in cases of culture-negative endocarditis. These tests could also prove useful for following the development of Coxiella burnetii endocarditis in patients under treatment.
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PMID:Serological diagnosis of Q fever endocarditis. 354 13

Q fever is a zoonosis with a worldwide distribution with the exception of New Zealand. The disease is caused by Coxiella burnetii, a strictly intracellular, gram-negative bacterium. Many species of mammals, birds, and ticks are reservoirs of C. burnetii in nature. C. burnetii infection is most often latent in animals, with persistent shedding of bacteria into the environment. However, in females intermittent high-level shedding occurs at the time of parturition, with millions of bacteria being released per gram of placenta. Humans are usually infected by contaminated aerosols from domestic animals, particularly after contact with parturient females and their birth products. Although often asymptomatic, Q fever may manifest in humans as an acute disease (mainly as a self-limited febrile illness, pneumonia, or hepatitis) or as a chronic disease (mainly endocarditis), especially in patients with previous valvulopathy and to a lesser extent in immunocompromised hosts and in pregnant women. Specific diagnosis of Q fever remains based upon serology. Immunoglobulin M (IgM) and IgG antiphase II antibodies are detected 2 to 3 weeks after infection with C. burnetii, whereas the presence of IgG antiphase I C. burnetii antibodies at titers of >/=1:800 by microimmunofluorescence is indicative of chronic Q fever. The tetracyclines are still considered the mainstay of antibiotic therapy of acute Q fever, whereas antibiotic combinations administered over prolonged periods are necessary to prevent relapses in Q fever endocarditis patients. Although the protective role of Q fever vaccination with whole-cell extracts has been established, the population which should be primarily vaccinated remains to be clearly identified. Vaccination should probably be considered in the population at high risk for Q fever endocarditis.
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PMID:Q fever. 1051 1

The mortality observed in pacemaker endocarditis may be high when all the components of the device are not withdrawn. Few studies have reported the posterior morbidity once the acute disease is resolved. Herein we present a patient who developed superior vena cava thrombosis, obstruction of thoracic duct and chylothorax after the initial episode of endocarditis. The evolution of the patient illustrates the late complications of isolated antibiotic treatment of pacemaker endocarditis, the poor results obtained with temporal oral anticoagulation in the management of superior vena cava thrombosis in the presence of retained intravascular foreign material, the excellent, prolonged initial response of chylothorax to conservative measures with anticoagulation and diet, relapse of chylothorax related to the increase in arterial pulmonary pressure, the absence of response at this time to the dietary measures and the successful treatment with video-assisted thoracic surgery to treat chylothorax without the morbidity of the large surgical procedures.
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PMID:[Chylothorax as a late complication of pacemaker endocarditis]. 1118 15

Q fever is a zoonotic disease caused by the bacterium Coxiella burnetii. The most common reservoirs are domesticated ruminants, primarily cattle, sheep, and goats. Humans acquire Q fever typically by inhaling aerosols or contaminated dusts derived from infected animals or animal products. Its highly infectious nature and aerosol route of transmission make C. burnetii a possible agent of bioterrorism. Although up to 60% of initial infections are asymptomatic, acute disease can manifest as a relatively mild, self-limited febrile illness, or more moderately severe disease characterized by hepatitis or pneumonia. It manifests less commonly as myocarditis, pericarditis, and meningoencephalitis. Chronic Q fever occurs in <1% of infected patients, months or years after initial infection. Chronic disease manifests most commonly as a culture-negative endocarditis in patients with valvular heart disease. During 2000-2001, a total of 48 patients who met the case definition of Q fever were reported to CDC. This report describes the case investigations for six of these patients, which indicate that these persons acquired Q fever probably through direct or indirect contact with livestock. To enhance surveillance efforts, health-care providers should report cases of Q fever to state health departments.
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PMID:Q fever--California, Georgia, Pennsylvania, and Tennessee, 2000-2001. 1240 8

Despite progress in the management of infective endocarditis, delays in diagnosis or prior antimicrobial treatment may adversely influence the symptom duration and outcome. The duration of symptoms in patients with infective endocarditis was studied in 683 cases among 653 patients with 703 episodes of the disease; patients were hospitalized within 10 days of symptom onset in 169 (24.7%) cases. Antimicrobial therapy before hospital admission was administered to 257 (36.5%) patients. Overall mortality was 25.6%. Symptom duration was longer when antimicrobials were administered before diagnosis (58.8+/-78.1 vs. 44.8+/-54.9 days), when vegetations were detected on echocardiogram (53.5+/-68.2 vs. 38.8+/-47.3) and among patients admitted before 1990 (42.3+/-67.1 vs. 54.2+/-62.4 days). Symptom duration was shorter in patients with prosthetic valve endocarditis (26.8+/-34.2 vs. 59.3+/-71.6 days). In 54 (26.5%) episodes of prosthetic valve endocarditis, patients had symptoms for more than 30 days. Staphylococcus aureus was the most frequent agent among patients with symptoms up to 10 days (41.2%) and Streptococcus among those with symptoms over 20 days (53.9%). Symptom duration did not significantly differ in regard to medical (51.3+/-69.2 days) or surgical (46.7+/-55.7 days) treatment. Mortality increased as symptom duration decreased and was highest for patients who experienced symptoms for less than 10 days (36.1%). In some patients medical care may be delivered relatively late in the course of infective endocarditis. Administration of antibiotics previous to hospital admission increased duration of symptoms, and cardiac valve prosthesis, staphylococcal infection and death were associated with more acute disease.
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PMID:Duration of symptoms in patients with infective endocarditis. 1272 6

The study of 1527 autopsies showed that in 2% of cases the cause of death was Infective Endocarditis (IE) (acute in the absolute majority), mostly not diagnosed due to fulminant disease or to the short hospital stay and in some cases not correctly treated. Sepsis was correctly diagnosed in 12 patients (9 of whom were i.v. drug addicts) and was not identified in 14 patients (12 of whom had acute disease) who were diagnosed as suffering from CNS disease or pneumonia. Systematic autoptic study of patients with or without IE appears to be a very useful method to determine correctly IE mortality.
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PMID:[Infective endocarditis in a series of 1527 autopsies: clinical-pathology correlations]. 1275 29

Coxiella burnetii causes acute Q fever in humans and occasional chronic infections that typically manifest as endocarditis or hepatitis. Isolates associated with acute disease were found to be distinct from a group of chronic disease isolates by a variety of biochemical parameters and in a guinea pig fever model of acute disease, suggesting a difference in virulence potential. We compared antigenic polypeptides among C. burnetii isolates and found an immunodominant 28-kDa protein in acute group isolates but not in chronic group isolates (T. Ho, A. Hotta, G. Q. Zhang, S. V. Nguyen, M. Ogawa, T. Yamaguchi, H. Fukushi, and K. Hirai, Microbiol. Immunol. 42:81-85, 1998). In order to clone the adaA gene, the N-terminal amino acid sequence of adaA was determined and a 59-bp fragment was amplified from Nine Mile phase I DNA by PCR. The putative gene fragment was used to screen a lambda ZAP II genomic DNA library, and an open reading frame expressing a 28-kDa immunoreactive protein was identified. Sequence analysis predicted a gene encoding an approximately 28-kDa mature protein with a typical signal sequence. The adaA (acute disease antigen A) gene was detected in acute group C. burnetii isolates but not identified in chronic group isolates by PCR and Southern blotting. A typical signal peptide was predicted in adaA, and specific antibody to adaA reacted with the purified membrane fraction of acute group isolates by Western blotting, suggesting that adaA is exposed on the outer surface of C. burnetii. adaA was overexpressed in pET23a as a fusion protein in Escherichia coli to develop anti-recombinant adaA (anti-radaA) specific antibody, which recognized a approximately 28-kDa band in acute group isolates but not in chronic group isolates. In addition, immunoblotting indicates that radaA reacted with sera derived from animals infected with acute group isolates but did not react with sera from animals infected with chronic group isolates. These results support the idea that an adaA gene-targeted PCR assay and an radaA antigen-based serodiagnostic test may be useful for differential diagnosis of acute and chronic Q fever.
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PMID:Identification and characterization of an immunodominant 28-kilodalton Coxiella burnetii outer membrane protein specific to isolates associated with acute disease. 1573 Oct 54

Coxiella burnetii is an obligate intracellular bacterium that causes a worldwide zoonosis, Q fever, and can be misused as a biological warfare agent. Infection in animals (coxiellosis) is mostly persistent. Infection in humans is often asymptomatic, but it can manifest as an acute disease (usually a self-limited flu-like illness, pneumonia, or hepatitis) or as a chronic form (mainly endocarditis, but also hepatitis and chronic fatigue syndrome). C. burnetii infection in pregnant women may result in abortions, premature deliveries, and stillbirths. Infection in nature is maintained and transmitted by ticks as the principal vector and reservoir. Cattle, sheep, and goats are the most important source of human infections. Humans contract C. burnetii infection mostly by aerosol in contact with contaminated environs, wind playing an important factor in spreading the infection. The wide distribution of C. burnetii contributes to a high resistance of its extracellular small cell variant to environmental conditions. Its intracellular large cell variant, adapted to survive under harsh conditions of phagolysosomes, enables long-term survival and persistence of C. burnetii, namely in monocytes/macrophages. Host factors such as underlying disease and cell-mediated immunity play a decisive role in the clinical expression of C. burnetii infection. Complete genome analysis of C. burnetii will certainly contribute to better understanding of the pathogenesis of C. burnetii infection and will improve Q fever diagnosis and immunoprophylaxis.
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PMID:Coxiella burnetii infection. 1648 1


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