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

Q fever is a widespread disease caused by the rickettsia Coxiella burnetii, an obligate intracellular bacteria which man usually acquires through the inhalation of infected dust from subclinically infected animals. Q fever may be acute or chronic. The chronic form mostly presents as endocarditis, which is difficult to diagnose and may ultimately be fatal. Immunocompromised conditions and underlying heart disease are the most important risk factors to consider in cases of Q fever endocarditis. The ultimate diagnosis is based on specific diagnostic tests which include serology, demonstration of C. burnetii in valvular material, isolation of C. burnetii from blood and tissue samples by cell-culture techniques as well as amplification and detection of the bacterial DNA by polymerase chain reaction. Treatment of chronic Q fever endocarditis is complex and requires long-term antibiotic therapy, sometimes associated with heart valve replacement. At the present time neither an optimal antibiotic combination nor the duration of treatment is known and patients with Q fever endocarditis require prolonged follow-up because of the possibility of later relapses.
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PMID:Q fever endocarditis. 924 58

A Rochalimaea-like organism (strain F9251) was isolated from a patient with endocarditis after blood drawn for culture before antimicrobial therapy was subcultured onto blood and chocolate agars and incubated for 2 weeks in 5% CO2. The strain was phenotypically similar to known Rochalimaea species. The cellular fatty acid composition of strain F9251 was close to but distinct from those of the three known Rochalimaea species and was most similar to that of R. vinsonii. Labeled DNA from strain F9251 was 59 to 67% related to DNAs from type strains of the three described Rochalimaea species, and its 16S rRNA gene sequence was 98.9% or more homologous to their 16S rRNA gene sequences. These findings support classification of F9251 as a new Rochalimaea species, for which the name Rochalimaea elizabethae sp. nov. is proposed. The patient infected with the organism had large bacterial vegetations on his aortic valve and was cured with antibiotics and valve-replacement surgery. Recognition of the procedures required to identify this and other Rochalimaea species suggests that clinical laboratories should prolong the incubation times of cultures of blood and tissue from patients with suspected endocarditis, patients with fever of unknown origin, and immunocompromised patients with fever so that the full spectrum of disease caused by these organisms can be recognized.
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PMID:Rochalimaea elizabethae sp. nov. isolated from a patient with endocarditis. 768 47

Streptococcus bovis is a normal inhabitant of the rumen but has been implicated as a causative agent for ruminal lactic acidosis and related problems. While rarely isolated from humans, S. bovis has been identified as a causative agent for endocarditis, meningitis, and septicemia. Recent reports have also suggested a correlation between human colonic carcinoma and increased levels of S. bovis. Identification of S. bovis strains of human origin has been problematic because of variations in results of biochemical tests compared with results for ruminal strains. We have tested a cloned amylase gene from the ruminal strain S. bovis JB1 as a potential DNA probe for rapid and accurate identification of S. bovis strains from all sources. DNAs from strains identified as S. bovis, of both human and ruminal origin, were found to hybridize with the probe under stringent conditions. The probe also hybridized with variants of S. bovis that did not grow on starch. The probe did not hybridize with DNA isolated from other bacteria of human colonic and ruminal origin, including Bacteroides thetaiotaomicron, Bacteroides ruminicola, Butyrivibrio fibrisolvens, and Enterococcus faecalis but did demonstrate hybridization with Streptococcus salivarius.
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PMID:Development of a DNA probe for Streptococcus bovis by using a cloned amylase gene. 769 73

Vegetative valvular endocarditis involving the aortic and, to a lesser extent, mitral valves was diagnosed echocardiographically in a 3-year-old spayed female Labrador retriever. Historically, the dog had been treated with tetracycline hydrochloride and prednisolone for positive seroreactivity to Ehrlichia canis and antinuclear antigens. Although three aerobic and anaerobic blood cultures failed to grow bacteria, blood cultured simultaneously by the lysis centrifugation technique grew a fastidious, gram-negative organism. Despite an initial therapeutic response, the owner elected euthanasia 17 days later. Necropsy confirmed aortic and mitral valvular endocarditis. Bacteria phenotypically similar to Bartonella species were visualized in the heart valve by light and electron microscopy, and Bartonella DNA from a frozen heart valve was amplified by PCR. Subsequent phenotypic and genotypic characterization of the isolate, including biochemical testing, cellular fatty acid analysis, DNA hybridization, and sequencing of the 16S rRNA gene indicated that this organism, which can induce endocarditis in dogs, is a novel Bartonella subspecies containing an insertion sequence unique among currently recognized Bartonella species. The name Bartonella vinsonii subsp. berkoffii subsp. nov. will be proposed for this organism.
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PMID:Endocarditis in a dog due to infection with a novel Bartonella subspecies. 769 33

Four slightly yellow-pigmented, alpha-hemolytic, gram-negative coccobacilli, three from wound specimens and one from multiple blood cultures of a patient with endocarditis, were identified as Neisseria elongata subsp. glycolytica on the basis of their overall biochemical and genetic similarities to this subspecies. These strains resembled N. elongata in their guanine-plus-cytosine contents (55.6 to 57.1 mol%) and in their overall cellular fatty acid profiles, which are characterized by large amounts of 16:0, 16:1 omega 7c, and 18:1 omega 7c fatty acids. Their identities were confirmed by species-level DNA relatedness (hydroxyapatite method) to the type strains of all three N. elongata subspecies. The biochemical profiles and cultural characteristics of these strains resembled those of the type strain of N. elongata subsp. glycolytica except for the production of a weak yellow growth pigment and alpha-hemolysis on sheep blood agar. They differed from N elongata subsp. elongata by the production of catalase, by the production of alpha-hemolysis on sheep blood agar, and by acid production from D-glucose. They differed from N. elongata subsp. nitroreducens by the production of catalase and an inability to reduce nitrate. These studies suggest a pathogenic potential for N. elongata subsp. glycolytica, usually considered to be a transient colonizer in humans.
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PMID:Characterization of Neisseria elongata subsp. glycolytica isolates obtained from human wound specimens and blood cultures. 769 70

DNA probe method is a new bacteriological method for diagnosis of bacteria. The authors tried to apply the method to diagnosis of bacteremia and treatment of infective endocarditis. We could diagnose the patient's illness as bacteremia with this method even when blood cultures are not positive. We suggest that cardiac surgery should be performed in case bacteria is detected repeatedly with DNA probe method. Therefore it is useful for decision whether cardiac surgery for patients with active infective endocarditis should be done or not.
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PMID:[Surgical treatment of infective endocarditis: application of DNA probe method]. 786 38

Bacterial adherence to platelets on the cardiac valve surface is believed to be critical in the induction of infective endocarditis. Recent studies have confirmed that thrombin-activated platelets secrete platelet microbicidal protein (PMP), which can both kill and exert nonlethal antiadherence effects against endovascular pathogens. In the present study, we quantified the influence of antibiotic and/or PMP exposures on in vitro platelet adherence of two Staphylococcus aureus strains, identical by DNA restriction and cell wall protein profiles, that differed in their susceptibility to PMP-induced killing (PMPs or PMPr, respectively). Adherence assays were performed by flow cytometry in the presence of sublethal PMP concentrations (1 to 2.5 micrograms/ml) alone or in combination with ampicillin (AMP) alone, sulbactam (SUL) alone, or AMP plus SUL (AMP-SUL), at levels achievable in serum. Exposure of the PMPs and PMPr S. aureus strains to antibiotics (for 2 h at 37 degrees C) prior to flow cytometry resulted in no substantive changes in the percent adherence to platelets compared with that for S. aureus cells not exposed to antibiotics, except for modestly increased adherence of both PMPs and PMPr cells exposed to AMP-SUL (18.5 and 15.8% increases, respectively). Addition of PMP to antibiotic-S. aureus mixtures (final 30 min) caused a significant decrease in S. aureus adherence to platelets, for both the PMPs and PMPr S. aureus strains, compared with antibiotic exposure alone (e.g., reduction in platelet adherence from 57.9 +/- 8.2% to 12.2 +/- 3.6% for PMPs cells exposed to AMP-SUL and PMP [P = 0.01]). Moreover, addition of PMP following exposure of the PMPs and PMPr strains to AMP-SUL reversed the enhanced bacterium-platelet adherence observed with such antibiotic exposures alone (P < or = 0.005). These data demonstrate that PMP exerts a potent antiplatelet adherence effect which is independent of its microbicidal capacity, rendering S. aureus cells less adherent to platelets in the presence or absence of antibiotics. Reduction of microbial adherence to platelets by PMP alone or with antibiotics provides further insight into the mechanism(s) that may be involved in host defense and antibiotic prophylaxis of infective endocarditis and other endovascular infections.
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PMID:Platelet microbicidal protein alone and in combination with antibiotics reduces Staphylococcus aureus adherence to platelets in vitro. 803 12

We report four cases of infective endocarditis due to nutritionally variant streptococci (NVS) that occurred between 1981 and 1991. Three female and one male patients had underlying heart diseases. Causative organisms showed satellitism to staphylococci. Two strains were identified as S. adjacens and the other two were identified as S. defectivus by DNA-DNA hybridization. All strains had tolerance and one strain had resistance to benzylpenicillin (MIC 4 micrograms/ml). This penicillin-resistant strain also had tolerance to gentamicin. There was no synergism of benzylpenicillin and gentamicin against this strain by a killing curve in vitro. A 11-year-old female patient with infective endocarditis due to this strain, who had a transposition of great arteries, had large vegetations in external conduits by the Rastelli's operation. Some intensive antimicrobial chemotherapies were unsuccessful and a surgical replacement of the conduits must be done in this case. Since infective endocarditis due to NVS is not rare in Japan, NVS should be considered for the causative organisms in culture negative endocarditis.
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PMID:[Microbiological and clinical studies of infective endocarditis due to nutritionally variant streptococci]. 808 48

Immunoblotting sera from cases of Streptococcus mutans or S. sobrinus endocarditis against an extract from S. sobrinus strain MUCOB 263 had identified three immunodominant antigenic bands at 190, 200 and 220 kDa. A lambda ZAPII DNA library was produced from the sheared genomic DNA of S. sobrinus MUCOB 263 and six identical positive clones were identified when this library was screened with serum from a patient with endocarditis caused by a bacterium from the mutans group of streptococci. On subcloning and sequencing, a protein containing 1548 amino acids was identified with a 99.2% homology to the SpaA antigen of S. sobrinus and 68.4% homology to the PAc antigen of S. mutans.
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PMID:Cloning and sequencing the endocarditis immunodominant antigen of Streptococcus sobrinus strain MUCOB 263. 817 20

In the recent clinical trials of teicoplanin therapy of endocarditis caused by Staphylococcus aureus, at least one instance of the emergence of teicoplanin-resistant strains during therapy has been reported (G.W. Kaatz, S. M. Seo, N. J. Dorman, and S. A. Lerner, J. Infect. Dis 162:103-108, 1990). We have confirmed, using conventional electrophoresis of EcoRI-digested chromosomal DNA and pulsed-field gel electrophoresis of SmaI-digested chromosomal DNA, that the resistant strain (12873) (MIC, 16 micrograms/ml) is genetically very similar to the susceptible parent (12871) (MIC, 4 micrograms/ml). Kaatz et al. were able to select spontaneous teicoplanin-resistant mutants (10(-9)), suggesting that a single gene might be involved. We have shown that the mutation is highly stable during growth in the absence of teicoplanin. Using Tn551, we have selected insertion mutants of 12873 that become teicoplanin susceptible. We have examined a number of aspects of cell wall physiology in strains 12871 and 12873 and the teicoplanin-susceptible Tn551 mutants of 12873. 12873 was more susceptible to lysostaphin lysis than 12871 and the susceptible Tn551 derivatives of 12873. Autolysis in phosphate buffer (pH 7.5) and cell wall turnover rates were similar in 12871 and 12873. An analysis of membrane proteins revealed the expression of a ca. 35-kDa protein and increased expression of both polypeptides of penicillin-binding protein (PBP) 2 (PBP2) in 12873 relative to 12871 and the Tn551 mutants of 12873. This increased expression was not related to PBP2', since both strains were susceptible to oxacillin in 2% NaCl (MIC, < or = 0.25 microgram/ml) and cellular DNA from neither strain hybridized with a specific mec gene probe. Two independent Tn551 inserts have been mapped to a ca. 117-kb SmaI fragment of the chromosome. These data suggest the possibility that the mutation resulting in resistance to teicoplanin involves the regulation of expression of both polypeptides of PBP2 and a 35-kDa membrane protein.
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PMID:Teicoplanin-resistant Staphylococcus aureus expresses a novel membrane protein and increases expression of penicillin-binding protein 2 complex. 828 29


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