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)

Immediate attention must be given to the respiratory system of the heroin abuser; then he should be given naloxone HCl. Search for evidence of use of additional drugs, which may compound problems. Pulmonary edema, aspiration pneumonia and pulmonary embolization are the most common complications. Infections, particularly endocarditis, and cardiac arrhythmia also occur with heroin overdose. Hepatitis is common. Treatment must include not only attention to the presenting symptoms but also referral to a rehabilitation center when possible.
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PMID:Treating heroin overdose. 112 10

The first report of prosthetic valve endocarditis due to a nutritionally variant streptococcus is presented. A 21-year-old woman developed persistent fever within one week of mitral valve replacement. Prosthetic valve dysfunction developed necessitating valve replacement. Cultures of blood and the excised prosthetic valve using routine media were negative; Streptococcus mitior grew as satellite colonies around Staphylococcus aureus and in beef heart infusion broth supplemented with 0.001% pyridoxine HCl. Treatment with penicillin G and streptomycin for six weeks was curative. Nutritionally variant streptococci should be considered in patients with prosthetic valve endocarditis and negative routine cultures.
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PMID:Case report: prosthetic valve endocarditis due to a nutritionally variant streptococcus. 400 33

Actinobacillus actinomycetemcomitans is an oral bacterium which is being encountered with increasing frequency in infective endocarditis. This organism occurs in high numbers in periodontitis lesions of patients with localized juvenile periodontitis (periodontosis). It is present infrequently, and only in low numbers in most other individuals. Its common resistance to penicillin, erythromycin and vancomycin represents a clinical problem in patients at risk of developing endocarditis after dental treatment. However, the high activity of tetracyclines against A. actinomycetemcomitans may be useful in prophylactic endocarditis considerations by allowing a suppression of the organism prior to the institution of recommended prophylactic protocols. In this study, we determined the effect of systemic tetracycline-HCl therapy (1 gm/day) on the oral A. actinomycetemcomitans population in five localized juvenile periodontitis patients who were heavily infected with the organism. A. actinomycetemcomitans could not be detected in samples of subgingival and supragingival dental plaque and cheek mucosal surfaces following 14 days of administration of systemic tetracycline. The organism was still undetectable 3 weeks after therapy but it reappeared at a few oral sites at week 8 post-treatment. On the basis of this data, it is proposed that the prophylactic endocarditis therapy of patients with high numbers of penicillin-resistant A. actinomycetemcomitans include a two-stage approach: first, the systemic administration of tetracycline for 14 days, and second, institution of a conventional prophylactic protocol during the time of dental treatment.
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PMID:Suppression of penicillin-resistant oral Actinobacillus actinomycetemcomitans with tetracycline. Considerations in endocarditis prophylaxis. 657 27

The ability to aggregate human platelets was examined for five Lactobacillus rhamnosus strains and five Lactobacillus paracasei subsp. paracasei strains isolated from patients with infective endocarditis (IE), 25 laboratory isolates from the same two species, and 14 strains from five other oral species, namely Lactobacillus acidophilus, Lactobacillus fermentum, Lactobacillus oris, Lactobacillus plantarum and Lactobacillus salivarius. Amongst the L. rhamnosus strains, platelets were aggregated by all five IE strains and 8/16 laboratory strains. For the L. paracasei subsp. paracasei strains, the respective numbers were 2/5 and 2/9. Aggregation also occurred with 11/14 strains of the other five species; each species was represented. The optimal ratio of bacteria to platelets for aggregation was approximately 1:1, and there was considerable variation in the lag phase that preceded aggregation, depending on the source of the platelets. Overall, the lag phase varied between 0.25 +/- 0.1 and 20.4 +/- 3.2 min and the percentage aggregation ranged between 70 +/- 2.6 and 104 +/- 13.5%. Confirmation that aggregation was being observed came from studies with five strains on the inhibitory effects of EDTA, dipyridamole, apyrase, imipramine, acetylsalicylic acid and quinacrine. Inhibition of aggregation by L. rhamnosus strains by the peptide arginine-glycine-aspartic acid-serine (RGDS) further indicated a role for fibronectin and/or fibrinogen. Pronase treatment of cells for 1 h and extraction of bacterial surface components with 0.1 M-Tris/HCl (pH 8.5) at 37 degrees C for 1 h stopped aggregation in 8/9 IE strains. Extracted surface proteins (200 micrograms) completely inhibited platelet aggregation by 8/9 of the homologous strains.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The aggregation of human platelets by Lactobacillus species. 812 21