Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0014118 (endocarditis)
 15,629 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 47-year-old man was hospitalized in May, 1990, because of breathlessness and continuous fever which appeared about 4 weeks after he had had his periodontic tooth removed in December, 1989. He had been diagnosed as having ventricular septal defect (VSD) at the age of 6 years. When he was hospitalized, he was in a condition of class IV by NYHA classification, with a white blood cell count of 17,300/mm3, an increase in CRP, a red blood cell sedimentation rate of 108 mm/hr, and positive alpha-streptococcus in blood culture. His cardiothoracic ratio was 64% with signs of pulmonary congestion on a chest X-ray film. Echocardiography revealed the presence of VSD and huge vegetations on the tricuspid, mitral and aortic valves. He was considered to have active infective endocarditis (AIE) which had presumably been provoked by VSD and the tooth removal. Penicillin G at a daily dose of 20 million units and gentamicin at a daily dose of 80 mg were intravenously administered to treat the alpha-streptococcus infection for about 4 weeks. Furosemide was used for congestive heart failure. Since, although his cardiac function appeared to have been improved, the signs and symptoms of the infection persisted, triple valve replacement for the tricuspid, mitral and aortic valves and patch closure of the VSD were performed 4 weeks after the hospitalization. The operation revealed inflammatory lesions extending from the endocardium of the right ventricle to the mitral valves through the VSD, and huge vegetations on the tricuspid, mitral and aortic valves. The operation was successful and the inflammatory areas gradually disappeared.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of ventricular septal defect associated with active infective endocarditis which was successfully treated by triple valve replacement and ventricular septal defect patch closure]. 174 71

The serum protein binding, extravascular diffusion and urinary excretion of pefloxacin were studied in rabbits. The effect of furosemide on the urinary excretion of pefloxacin was investigated. In an experimental model of Escherichia coli endocarditis, diffusion into heart valves and infected vegetations and bactericidal effect of pefloxacin were also studied. We observed a serum protein binding of 25%. Extravascular concentrations found were within the range of the minimal inhibitory concentrations for most susceptible strains. Pefloxacin appeared to be reabsorbed by renal tubules (fractional excretion: 61 +/- 21%). Furosemide significantly increased the renal excretion of pefloxacin through a tubular process. We observed a good penetration of pefloxacin into normal heart valves and infected vegetations. Pefloxacin reduced the colony counts in infected vegetations after seven im injections of the drug (given as 15 mg/kg/12 h).
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PMID:Pefloxacin in rabbits: protein binding, extravascular diffusion, urinary excretion and bactericidal effect in experimental endocarditis. 638 75

The penicillinase-resistant penicillins (methicillin, oxacillin, nafcillin) have been the mainstay of antibiotic therapy for S. aureus septicaemia and endocarditis. In experimental rabbit S. aureus endocarditis, these three antibiotics were equally effective. There has been no prospective comparative clinical studies to determine the relative effectiveness of these antibiotics. In experimental rabbit S. aureus endocarditis, cephalothin and cefazolin are less effective than methicillin and nafcillin. The results of therapy with cephalosporins in patients with S. aureus endocarditis are variable. Clindamycin therapy of S. aureus endocarditis has been associated with clinical relapse. Vancomycin has been used to treat S. aureus septicaemia and endocarditis with good results. Fusidic acid has been used in combination with another effective drug in treating S. aureus septicaemia and endocarditis. Although the combination of a cell-wall acting antibiotic with an aminoglycoside has been shown to have an enhanced anti-staphylococcal activity in vitro and in animal studies, there is no evidence that such a combination reduces morbidity or mortality clinically. Rifampin in combination with a cell-wall acting antibiotic is antagonistic against S. aureus in vitro and in experimental endocarditis in rabbits. The use of such a combination has not shown consistent benefits clinically. The clinical importance of tolerance (MBC/MIC greater than or equal to 32) of cell-wall acting antibiotics to S. aureus is not clear. It appears not to be important in animal studies. Cephalosporins appear not to be effective in the treatment of methicillin-resistant S. aureus infections. The treatment of choice of sepsis and endocarditis due to such strains is vancomycin which is effective against all strains of methicillin-resistant S. aureus.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A general survey of antibiotic treatment of staphylococcal septicaemia and endocarditis. 658 52

The usefulness of fusidic acid, alone or combined with vancomycin, was investigated for the therapy of experimental endocarditis caused in rabbits by a methicillin-resistant strain of Staphylococcus aureus. In vitro killing curves showed an indifferent interaction between the two antibiotics. In vivo, vancomycin alone was as effective as a vancomycin-fusidic acid combination (P < 0.05 versus control animals). No resistance to fusidic acid emerged during combination therapy. Fusidic acid alone was not effective. Resistance emerged in 5 of 12 animals treated with fusidic acid alone and was responsible for antibacterial failure. Fusidic acid alone was effective (P < 0.001) and did not select resistant strains if therapy was started when animals retained a smaller inoculum. We concluded that the vancomycin-fusidic acid combination exhibited no advantage over vancomycin alone in this model.
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PMID:Fusidic acid alone or in combination with vancomycin for therapy of experimental endocarditis due to methicillin-resistant Staphylococcus aureus. 828 35