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

We characterized 22 human clinical strains of Streptococcus bovis by genotypic (16S rRNA gene sequence analysis [MicroSeq]; Applied Biosystems, Foster City, Calif.) and phenotypic (API 20 Strep and Rapid ID32 Strep systems (bioMerieux Vitek, Hazelton, Mo.) methods. The strains, isolated from blood, cerebrospinal fluid (CSF), and urine, formed two distinct 16S ribosomal DNA sequence clusters. Three strains which were associated with endocarditis urinary tract infection (UTI), and sepsis clustered with the S. bovis type strain ATCC 33317 (cluster 1); other closely related type strains were S. equinus and S. infantarius. Nineteen strains clustered at a distance of about 2.5% dissimilarity to the S. bovis type strain (cluster 2) and were associated with central nervous system (CNS) disease in addition to endocarditis, UTI, and sepsis. All strains were distinct from S. gallolyticus. Within cluster 2, a single strain grouped with ATCC strain 43143 (cluster 2a) and may be phenotypically distinct. All the other strains formed a second subgroup (cluster 2b) that was biochemically similar to S. bovis biotype II/2 (mannitol negative and beta galactosidase, alpha galactosidase, beta glucuronidase, and trehalose positive). The API 20 Strep system identified isolates of cluster 2b as S. bovis biotype II/2, those of cluster 1 as S. bovis biotype II/1, and that of cluster 2a as S. bovis biotype I. There was an excellent correlation of biotype and genotype: S. bovis biotype II/2 isolates form a separate genospecies distinct from the S. bovis, S. gallolyticus, and S. infantarius type strains and are the most common isolates in adult males.
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PMID:16S ribosomal DNA sequence analysis distinguishes biotypes of Streptococcus bovis: Streptococcus bovis Biotype II/2 is a separate genospecies and the predominant clinical isolate in adult males. 1128 85

The direct binding of bacteria to platelets may be an important virulence mechanism in the pathogenesis of infective endocarditis. We have previously described Staphylococcus aureus strain PS12, a Tn551-derived mutant of strain ISP479, with reduced ability to bind human platelets in vitro. When tested in an animal model of endocarditis, the PS12 strain was less virulent than its parental strain, as measured by bacterial densities in endocardial vegetations and incidence of systemic embolization. We have now characterized the gene disrupted in PS12 and its function in platelet binding. DNA sequencing, Southern blotting, and PCR analysis indicate that PS12 contained two Tn551 insertions within the clumping factor A (ClfA) locus (clfA). The first copy was upstream from the clfA start codon and appeared to have no effect on ClfA production. The second insertion was within the region encoding the serine aspartate repeat of ClfA and resulted in the production of a truncated ClfA protein that was secreted from the cell. A purified, recombinant form of the ClfA A region, encompassing amino acids 40 through 559, significantly reduced the binding of ISP479C to human platelets by 44% (P = 0.0001). Immunoprecipitation of recombinant ClfA that had been incubated with solubilized platelet membranes coprecipitated a 118-kDa platelet membrane protein. This protein does not appear to be glycoprotein IIb. These results indicate that platelet binding by S. aureus is mediated in part by the direct binding of ClfA to a novel 118-kDa platelet membrane receptor.
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PMID:Clumping factor A mediates binding of Staphylococcus aureus to human platelets. 1129 31

Clinical features of 43 cases of invasive Eikenella corrodens infections diagnosed at National Taiwan University Hospital during a 6-year period (1993-1998) were analyzed. The clinical syndromes included head and neck infection (56%), pulmonary infection (23%), intra-abdominal infection (14%), cutaneous infection (5%), skeletal infection (2%), endocarditis (2%), and pelvic abscess (2%). Nearly two-thirds of the patients (63%) had pre-existing diseases. Malignancy (35%), especially of the head and neck, was the most common underlying illness. More than half of the patients (56%) had associated factors predisposing to invasive Eikenella corrodens infection. Polymicrobial infections occurred in 28 (65%) patients, with two-thirds of the concurrent isolates being streptococci (66%). Five cases were fatal, with four deaths directly attributable to invasive Eikenella corrodens infection. Antimicrobial susceptibility testing and molecular typing were performed on 23 preserved Eikenella corrodens isolates. Antimicrobial susceptibility testing showed that Eikenella corrodens isolates were susceptible to penicillin, amoxicillin, cefoxitin, cefotaxime, cefepime, ciprofloxacin, and imipenem. The isolates were resistant to clindamycin, metronidazole, cephalothin, and cefuroxime. None of the 23 isolates produced beta-lactamase. Random amplified polymorphic DNA patterns of the 23 isolates were different, suggesting that different clones of Eikenella corrodens caused these infections.
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PMID:Clinical features of patients with invasive Eikenella corrodens infections and microbiological characteristics of the causative isolates. 1139 11

Whipple's disease is a rare bacterial infection that may involve any organ system in the body. It occurs primarily in Caucasian males older than 40 years. The gastrointestinal tract is the most frequently involved organ, with manifestations such as abdominal pain, malabsorption syndrome with diarrhea, and weight loss. Other signs include low-grade fever, lymphadenopathy, skin hyperpigmentation, endocarditis, pleuritis, seronegative arthritis, uveitis, spondylodiscitis, and neurological manifestations, and these signs may occur in the absence of gastrointestinal manifestations. Due to the wide variability of manifestations, clinical diagnosis is very difficult and is often made only years or even decades after the initial symptoms have appeared. Trimethoprim-sulfamethoxazole for at least 1 year is usually considered adequate to eradicate the infection. The microbiological diagnosis of this insidious disease is rendered difficult by the virtual lack of culture and serodiagnostic methods. It is usually based on the demonstration of periodic acid-Schiff-positive particles in infected tissues and/or the presence of bacteria with an unusual trilaminar cell wall ultrastructure by electron microscopy. Recently, the Whipple bacteria have been characterized at the molecular level by amplification of their 16S rRNA gene(s). Phylogenetic analysis of these sequences revealed a new bacterial species related to the actinomycete branch which was named "Tropheryma whippelli." Based on its unique 16S ribosomal DNA (rDNA) sequence, species-specific primers were selected for the detection of the organism in clinical specimens by PCR. This technique is currently used as one of the standard methods for establishing the diagnosis of Whipple's disease. Specific and broad-spectrum PCR amplifications mainly but not exclusively from extraintestinal specimens have significantly improved diagnosis, being more sensitive than histopathologic analysis. However, "T. whippelii" DNA has also been found in persons without clinical and histological evidence of Whipple's disease. It is unclear whether these patients are true asymptomatic carriers or whether differences in virulence exist among strains of "T. whippelii" that might account for the variable clinical manifestations. So far, six different "T. whippelii" subtypes have been found by analysis of their 16S-23S rDNA spacer region. Further studies of the pathogen "T. whippelii" as well as the host immune response are needed to fully understand this fascinating disease. The recent cultivation of the organisms is a promising major step in this direction.
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PMID:Whipple's disease and "Tropheryma whippelii". 1143 14

A detailed characterization was performed of the Whipple's disease bacillus, strain Twist-MarseilleT, isolated from the cardiac valve of a patient with Whipple's disease bacillus endocarditis. This strain was isolated and maintained on human embryonic lung fibroblast monolayers, but could not be cultivated in the absence of living eukaryotic cells. Two morphological forms were observed, with differing staining properties; an intracellular form with intact and degenerating bacteria within vacuoles of infected cells and an extracellular form with masses of bacteria embedded in an extracellular matrix. Determination of the DNA G+C content confirmed that it belongs to the high-G+C gram-positive bacteria. Strain Twist-MarseilleT (= CNCM I-2202T) is proposed as the type strain of a new species within a new genus, Tropheryma whipplei gen. nov., sp. nov., that was provisionally created solely on the basis of 16S rRNA gene sequence data.
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PMID:Description of Tropheryma whipplei gen. nov., sp. nov., the Whipple's disease bacillus. 1149 48

The binding of platelets by bacteria is a proposed central mechanism in the pathogenesis of infective endocarditis. Platelet binding by Streptococcus mitis strain SF100 (an endocarditis isolate) was recently shown to be mediated in part by the surface proteins PblA and PblB. The genes encoding PblA and PblB are clustered with genes nearly identical to those of streptococcal phages r1t, 01205, and Dp-1, suggesting that pblA and pblB might reside within a prophage. To address this possibility, cultures of SF100 were exposed to either mitomycin C or UV light, both of which are known to induce the lytic cycle of many temperate phages. Both treatments caused a significant increase in the transcription of pblA. Treatment with mitomycin C or UV light also caused a substantial increase in the expression of PblA and PblB, as detected by Western blot analysis of proteins in the SF100 cell wall. By electron microscopy, phage particles were readily visible in the supernatants from induced cultures of SF100. The phage, designated SM1, had a double-stranded DNA genome of approximately 35 kb. Southern blot analysis of phage DNA indicated that pblA and pblB were contained within the SM1 genome. Furthermore, Western blot analysis of phage proteins revealed that both PblA and PblB were present in the phage particles. These findings indicate that PblA and PblB are encoded by a lysogenic bacteriophage, which could facilitate the dissemination of these potential virulence determinants to other bacterial pathogens.
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PMID:Proteins PblA and PblB of Streptococcus mitis, which promote binding to human platelets, are encoded within a lysogenic bacteriophage. 1155 59

We report the first documented case of endocarditis associated with Bartonella clarridgeiae in any species. B. clarridgeiae was identified as a possible etiological agent of human cat scratch disease. Infective vegetative valvular aortic endocarditis was diagnosed in a 2.5-year-old male neutered boxer. Historically, the dog had been diagnosed with a systolic murmur at 16 months of age and underwent balloon valvuloplasty for severe valvular aortic stenosis. Six months later, the dog was brought to a veterinary hospital with an acute third-degree atrioventricular block and was diagnosed with infective endocarditis. The dog died of cardiopulmonary arrest prior to pacemaker implantation. Necropsy confirmed severe aortic vegetative endocarditis. Blood culture grew a fastidious, gram-negative organism 8 days after being plated. Phenotypic and genotypic characterization of the isolate, including partial sequencing of the citrate synthase (gltA) and 16S rRNA genes indicated that this organism was B. clarridgeiae. DNA extraction from the deformed aortic valve and the healthy pulmonic valve revealed the presence of B. clarridgeiae DNA only from the diseased valve. No Borrelia burgdorferi or Ehrlichia sp. DNA could be identified. Using indirect immunofluorescence tests, the dog was seropositive for B. clarridgeiae and had antibodies against Ehrlichia phagocytophila but not against Ehrlichia canis, Ehrlichia ewingii, B. burgdorferi, or Coxiella burnetii.
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PMID:Aortic valve endocarditis in a dog due to Bartonella clarridgeiae. 1157 71

Culture-negative bacterial endocarditis may be attributed to fastidious microorganisms, prior institution of antibiotic treatment, or both. We describe a case of culture-negative endocarditis in which a modified Steiner stain revealed bacterial structures in the resected heart valve material. Prompted by this finding, broad-range polymerase chain reaction (PCR) amplification of small-subunit ribosomal DNA (16S rDNA) was performed, and Cardiobacterium hominis sequences were detected. This case demonstrates the usefulness of both the Steiner stain and broad-range direct molecular amplification as supplemental diagnostic tools in identification of otherwise unexplained infections.
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PMID:Identification of Cardiobacterium hominis by broad-range bacterial polymerase chain reaction analysis in a case of culture-negative endocarditis. 1186 84

The mechanism of resistance to the streptogramin antibiotics quinupristin and dalfopristin was studied in a Staphylococcus aureus clinical isolate selected under quinupristin-dalfopristin therapy, in four derivatives of S. aureus RN4220 selected in vitro, and in a mutant selected in a model of rabbit aortic endocarditis. For all strains the MICs of erythromycin, quinupristin, and quinupristin-dalfopristin were higher than those for the parental strains but the MICs of dalfopristin and lincomycin were similar. Portions of genes for domains II and V of 23S rRNA and the genes for ribosomal proteins L4 and L22 were amplified and sequenced. All mutants contained insertions or deletions in a protruding beta hairpin that is part of the conserved C terminus of the L22 protein and that interacts with 23S rRNA. Susceptible S. aureus RN4220 was transformed with plasmid DNA encoding the L22 alteration, resulting in transformants that were erythromycin and quinupristin resistant. Synergistic ribosomal binding of streptogramins A and B, studied by analyzing the fluorescence kinetics of pristinamycin I(A)-ribosome complexes, was abolished in the mutant strain, providing an explanation for quinupristin-dalfopristin resistance.
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PMID:Resistance to quinupristin-dalfopristin due to mutation of L22 ribosomal protein in Staphylococcus aureus. 1206 75

Culture-negative endocarditis currently represents a diagnostic challenge for physicians. Traditional methods such as histology, serology, and culture have been improved and new molecular techniques have been developed to improve the detection of difficult-to-culture agents. Serologic tests for the two most frequent etiologic agents, Coxiella burnetii and Bartonella spp, should be performed first because they can usually be identified easily in this way. The sensitivity of culture for intracellular bacteria has been improved by inoculation of samples in shell vials and by the use of novel tissue cell lines. Recently, universal and species-specific primers have been designated to amplify bacterial DNA directly from resected valves, allowing positive identification.
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PMID:Diagnostic methods current best practices and guidelines for identification of difficult-to-culture pathogens in infective endocarditis. 1209 78


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