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

Two colonial variants of Staphylococcus epidermidis were isolated from the valvular tissue of a patient with native valve endocarditis. In addition to differing in colonial morphology, the two variants differed in hemolysis on blood-containing media, in adherence capacity, and in the expression of certain enzymes. Under suitable conditions, both variants were themselves capable of phenotypic variation, although they differed in the rate at which variants were generated. The variants yielded identical profiles on restriction endonuclease analysis of plasmid DNA and pulsed-field gel electrophoresis of whole-cell DNA. This report suggests a possible role for phenotypic variation in coagulase-negative staphylococcal virulence. Congo red agar would be an excellent medium for studying the contribution of variation to the virulence of these organisms.
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PMID:Phenotypic variation of Staphylococcus epidermidis isolated from a patient with native valve endocarditis. 140 Oct 3

This study examines a series of phenotypic variants of Staphylococcus epidermidis that were generated from a pair of parent variants, isolated from valvular tissue of a patient with prosthetic valve endocarditis. The variants were initially classified by examining their colonial morphology on Congo red agar. In addition to differences in Congo red binding and colonial morphology, they differed in the expression of several surface components and enzymes. Despite these phenotypic differences, all variants had the same restriction endonuclease profile of plasmid DNA. Examination of a collection of clinical isolates demonstrated that phenotypic variation is a common property of S. epidermidis. The ability to express different combinations of surface components and enzymes could contribute to the virulence of S. epidermidis strains by enabling these organisms to colonize a range of diverse environments.
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PMID:A study of phenotypic variation of Staphylococcus epidermidis using Congo red agar. 146 27

During the last few years, among nosocomial pathogens, Acinetobacter spp. have given rise to an increasing number of nosocomial infections. Acinetobacter strains are widely distributed in nature; in hospitals, the human skin is the likely source for most outbreaks of hospital infections. The organism has been frequently found in the inanimate environment, especially in moist situations and it has been isolated from various types of opportunistic infections (septicaemia, endocarditis, meningitis, pneumonia, skin and wound sepsis and urinary tract infection). For epidemiological studies, various typing methods such as biotyping, bacteriocin typing and serology have been developed. More recently electrophoretic patterns of cell-envelope proteins and plasmid analysis have proved useful in differentiating outbreak strains. Antibiogram typing may be useful but the antibiotic resistance of Acinetobacter spp. has changed rapidly within the last few years and thus antibiotyping must be complemented by other typing systems. New methods such as electrophoretic analysis of isoenzymes, definition of plasmidotype profiles or restriction endonuclease digestion of chromosomal DNA are under investigation.
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PMID:Hospital infection with Acinetobacter spp.: an increasing problem. 167 90

A single strain of Staphylococcus epidermidis caused an outbreak of postoperative wound infections and endocarditis during a 6-month period. Infections caused by the epidemic strain developed more frequently in valve surgery patients than in those undergoing coronary artery bypass graft surgery (P = .03) and occurred only in patients operated on by surgeon A. None of 17 members of the cardiac surgery team carried the epidemic strain in their anterior nares, axillae, or inguinal folds. Hand cultures were performed on 8 surgical personnel, and only surgeon A carried the epidemic strain on his hands. Isolates from cardiac surgery patients, bypass pump blood cultures, and the hands of the implicated surgeon all had identical antimicrobial susceptibility patterns, plasmid profiles, and EcoRI restriction endonuclease digest patterns. In the 24 months after control measures were implemented, no infections caused by the epidemic strain occurred among open heart surgery patients. The findings suggest that the common-source outbreak of infections among cardiac surgery patients was due to carriage of a strain S. epidermidis on the hands of a cardiac surgeon.
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PMID:A common-source outbreak of Staphylococcus epidermidis infections among patients undergoing cardiac surgery. 217 23

The clinical findings relating to 11 patients in Hong Kong (HK) and to 43 patients described elsewhere, all with Streptococcus zooepidemicus septicaemia, are reviewed. There was a particular association with cardiovascular disease (27%) with seven cases of endocarditis, three of abdominal aortic aneurysm and two of deep venous thrombosis. Associations not previously reported included two cases of pharyngitis and two patients with persistent post-operative fever. The overall mortality was 22%. Both human and porcine strains of S. zooepidemicus from HK did not hydrolyse aesculin in contrast to the aesculin-positive biotypes reported previously. HK strains also had very mucoid colonies and capsules of hyaluronic acid were seen in electron micrographs. Samples of chromosomal DNA, extracted by means of HindIII restriction endonuclease, of strains from human beings and pigs were identical. The MIC of penicillin for all strains was less than or equal to 0.03 mg/l but the MBC for all was greater than 32 mg/l. Penicillin alone is generally sufficient for cure but combination with an aminoglycoside may be indicated in seriously ill patients. In our locality, pigs were incriminated as a possible source of human infection whereas consumption of contaminated dairy products is important elsewhere.
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PMID:Streptococcus zooepidemicus (Lancefield group C) septicaemia in Hong Kong. 227 71

Clinical blood isolates from sequential episodes of endocarditis occurring over a six-month period of time in an addict were investigated. The pathogens were Streptococcus sanguis II, Streptococcus mitis, and a nutritionally deficient (variant) streptococcus. The authors determined the DNA relatedness of these isolates by antibiograms, plasmid profiles, chromosomal endonuclease restriction digestions, and dot blot DNA-DNA hybridization analyses. The S. sanguis II and nutritionally deficient streptococcal strain had similar antibiograms being resistant to penicillin; neither produced beta-lactamase. No plasmids were found. The restriction endonuclease chromosomal digestion patterns of these isolates were unique and epidemiologically unrelated to each other. Dot blot DNA-DNA hybridizations, using the nutritionally deficient streptococcal DNA as the probe, showed homology to the preceding clinical isolates, S. sanguis II and S. mitis, at 15.4% and 45.1% hybridization levels, respectively. The nutritionally deficient streptococcus was only 4.2% homologous to a S. mitis ATCC strain and another nutritionally deficient streptococci isolate. Therefore, this patient had endocarditis with three distinct streptococcal strains.
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PMID:Molecular analysis of viridans and nutritionally deficient (variant) streptococci causing sequential episodes of endocarditis in a patient. 271 64

The prevalence of colonization of patients in a cardiac surgery unit with gentamicin-resistant, coagulase-negative staphylococci increased from 20% to 68% over a period of four years. Gentamicin resistance was found to be plasmid associated and transmissible from wild-type coagulase-negative staphylococcal donors to a Staphylococcus aureus recipient by filter mating (conjugative). These plasmids were present in isolates from 50 (74%) of 69 individuals examined. This figure included isolates from colonized patients, colonized staff, and patients with prosthetic valve endocarditis. A common restriction-endonuclease digestion pattern (pG02; 50 kilobases) was seen in only 19 (38%) of the 50 conjugative plasmids. However, filter hybridization, restriction-endonuclease mapping, and transposon insertional mutagenesis showed that representatives of the other 10 restriction-endonuclease digestion patterns were physically related to pG02 over greater than 80% of their genome, with differences largely due to deletions or insertions of DNA in three areas, and that their gentamicin-resistance genes were identical. Molecular analysis may be required to ascertain the physical similarity among phenotypically and epidemiologically related plasmids.
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PMID:Molecular epidemiology of transmissible gentamicin resistance among coagulase-negative staphylococci in a cardiac surgery unit. 298 34

An exfoliatin B-producing strain of Staphylococcus aureus was isolated from two adults with typical staphylococcal scalded skin syndrome (SSSS). One patient developed desquamation after a local staphylococcal infection of the hand, and the other developed exfoliation after nosocomially acquired staphylococcal endocarditis. Neither patient was immunocompromised, had evidence of renal insufficiency, or manifested other potential risk factors for SSSS. Purified toxin, isolated from the causative organisms, produced a Nikolsky sign in neonatal mice. The toxins were shown to be exfoliatin B by biochemical and immunologic methods and heretofore had been described only in children with SSSS. Analysis of plasmid DNAs from both strains revealed a 23-megadalton plasmid with identical restriction endonuclease digestion fragments. One isolate belonged to phage group II (3B/3C/6/7/47/54/55), whereas the other isolate belonged to phage groups I and III (7/29/52/52A/53/54/80). The observation that a non-phage group II exfoliatin-producing strain of S. aureus may produce SSSS in adults indicates the need to better define the diagnostic criteria for SSSS. Immunocompetent adults may remain susceptible to some strains of exfoliatin B-producing S. aureus.
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PMID:Staphylococcal scalded skin syndrome in two immunocompetent adults caused by exfoliatin B-producing Staphylococcus aureus. 313 45

Species of the genus Rochalimaea, recently renamed Bartonella, are of a growing medical interest. Bartonella quintana was reported as the cause of trench fever, endocarditis, and bacillary angiomatosis. B. henselae has been implicated in symptoms and infections of human immunodeficiency virus-infected patients, such as fever, endocarditis, and bacillary angiomatosis, and is involved in the etiology of cat scratch disease. Such a wide spectrum of infections makes it necessary to obtain an intraspecies identification tool in order to perform epidemiological studies. B. vinsonii, B. elizabethae, seven isolates of B. quintana, and four isolates of B. henselae were studied by pulsed-field gel electrophoresis (PFGE) after restriction with the infrequently cutting endonucleases NotI, EagI, and SmaI. Specific profiles were obtained for each of the four Bartonella species. Comparison of genomic fingerprints of isolates of the same species showed polymorphism in DNA restriction patterns, and a specific profile was obtained for each isolate. A phylogenetic analysis of the B. quintana isolates was obtained by using the Dice coefficient, UPGMA (unweighted pair-group method of arithmetic averages), and Package Philip programming. Amplification by PCR and subsequent sequencing using an automated laser fluorescent DNA sequencer (Pharmacia) was performed on the intergenic spacer region (ITS) between the 16 and 23S rRNA genes. It was found that each B. henselae isolate had a specific sequence, while the B. quintana isolates fell into only two groups. When endonuclease restriction analysis of the ITS PCR product was done, three enzymes, TaqI, HindIII, and HaeIII, allowed species identification of Bartonella spp. Restriction fragment length polymorphism after PCR amplification of the 16S-23S rRNA gene ITS may be useful for rapid species identification, and PFGE could be an efficient method for isolate identification.
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PMID:Inter- and intraspecies identification of Bartonella (Rochalimaea) species. 858 46

Thrombin-induced platelet microbicidal protein (tPMP) exerts potent in vitro microbicidal activity against pathogens commonly found in the bloodstream, including Staphylococcus aureus, Staphylococcus epidermidis, and Candida albicans. Localized platelet release of tPMP may be important in defense against infections involving the vascular endothelium caused by tPMP-susceptible organisms. In contrast, pathogens capable of surviving in the presence of tPMP could then exploit the platelet as an adhesive surface for attachment to damaged endothelium. To examine these hypotheses, we derived a tPMP-resistant (tPMP(r)) C. albicans strain from its tPMP-sensitive (tPMP(s)) parental strains were equivalent in vitro as assessed by genotyping (electrophoretic karyotype and restriction endonuclease analysis of genomic DNA), biotyping, germination, platelet aggregation, adherence to vascular endothelial cells, and growth characteristics. In addition, the tPMP(r) phenotype was stable following multiple in vitro and in vivo passages. We then investigated the in vivo relevance of tPMP susceptibility on endovascular infection using a rabbit model of endocarditis and hematogenous dissemination. Rabbits with transaortic catheters (n = 15 in each group) were challenged with either the tPMP(s) or tPMP(r) C. albicans strain. All rabbits developed C. albicans-induced endocarditis, as determined by the presence of infected vegetations. In rabbits challenged with tPMP(s) strain (P < 0.001). These results were seen in the absence of differences in either initial adherence of strains to cardiac valves or vegetation weights. Furthermore, although these C. albicans strains induced equivalent rates and extent of hematogenous renal infection, only the tPMP(r) strain disseminated hematogenously to the spleen (15 of 15 rabbits) versus 0 of 15 [tpmp(s) strain]; P < 0.0001). Thus, tPMP(r) C. albicans caused more-severe endocarditis and produced greater metastatic sequelae than the tPMP(s) counterpart.
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PMID:Resistance to platelet microbicidal protein results in increased severity of experimental Candida albicans endocarditis. 860 4


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