Consequences of Infective Endocarditis, And the Effective of Antibiotics Treatments: Review

Transcription

1 Consequences of Infective Endocarditis, And the Effective of Antibiotics Treatments: Review 1 Nasser Mohammed Abdullah Alshahrani, 2 Abdullah Saad Judaya Alshahrani, 3 Fayez abdulrahman fayez alshahrani, 4 Saeed Faleh Saeed Al Shahrani, 5 Abdullah saad amer alshahrani, 6 Abdulrahman Mubarak Abdulrahman Albishi, 7 Abdualla Mohammed A Alshahrani, 8 Abdulraheem Ali Alzahrani Abstract: Staphylococcus aureus is the most common organism. Approximately 30% of those having bacteremia with staphylococcus will develop endocarditis. This review was aimed to discuss the complications following infective endocarditis, and also overview the proper antibiotics treatment, and how effective could be this option of treatment over other options, we also indented to overview the risk factors and epidemiology of infective endocarditis in most evidence based review. We searched, with English language restrictions, and only human subject articles following electronic databases; PubMed, MEDLINE and EMBASE for any relevant article, whether was it reviews or randomized controlled studies or systematic reviews discussing infective endocarditis from the time of databases inception to December We used the term infective endocarditis for the Mesh keyword. Date last search performed was December, Optimal antibiotic recommending for enterococcal IE requires that MICs of penicillin, amoxicillin, aminoglycosides, and glycopeptides be determined. When the strain shows only low level resistance to aminoglycoside, advised therapy is a combination of high dose β lactam ( million units/day penicillin or 200 mg/kg/day amoxicillin) plus gentamicin for 4-6 weeks. The aminoglycoside element ought to be administered in two or three equally divided doses; this suggestion is based on outcomes of speculative studies. When it comes to high level resistance to gentamicin, cross resistance may be expected with all other aminoglycosides, other than often streptomycin Keywords: Staphylococcus aureus, infective endocarditis, MICs of penicillin, amoxicillin, aminoglycosides. 1. INTRODUCTION In developed countries, the occurrence of infective endocarditis (IE) varies from 3 to 9 cases per annually, and it is twice as common in males (1,2,3). Staphylococcus aureus is the most common organism. Approximately 30% of those having bacteremia with staphylococcus will develop endocarditis (4). Patients with valvular abnormalities, such as prostheses, mitral regurgitation (MR), or aortic stenosis or with endocardial damage from distributing particulate matter as from intravenous (IV) drug use, are at the greatest risk of contracting endocarditis. Indeed, some 75% of patients with IE have structurally abnormal hearts (4). In addition to host factors, IE advancement likewise overwhelmingly includes microorganisms that have certain attributes, such as platelet aggregating abilities. Staphylococcus and Streptococcus species are the most typical etiologic agents of IE, owing in part to this capacity (4). Capability of the microbe to activate platelets creates an environment conducive to vegetation formation and in theory supports the use of antiplatelet agents in the management of disease. However, studies of antiplatelet usage in neurological complications of endocarditis have had negative or neutral results (5,6). IE is more common in guys than ladies (7), and is more typical with increasing age (8). The mean age of IE patients has increased over time, from under 30 years in the pre-antibiotic age (9) to nearly 60 years in 1990s (10). In the elderly, IE is more often related to intracardiac prosthetic devices and bacteria from the gastrointestinal system (11). In a big observational accomplice study, IE most commonly included the mitral valve just (approximately 40% of patients), Page 861

2 followed by the aortic valve only (36% of patients), followed by multivalvular disease (10,12). Right-sided valves are rarely affected except among injection drug users. The pulmonic valve is least most likely to be associated with IE. Structural heart problem is a risk factor for IE because it leads to turbulent blood circulation. About 75% of patients who establish IE have underlying structural heart problem (13). In the past, rheumatic heart disease with mitral stenosis was the most typical valvular problem in patients with IE. Recently, the most typical predisposing lesions are mitral regurgitation, aortic valve disease (stenosis and regurgitation), and congenital heart disease (14,15). Mitral valve prolapse is a risk factor for IE, primarily when regurgitation is present (16). OBJECTIVE: This review was aimed to discuss the complications following infective endocarditis, and also overview the proper antibiotics treatment, and how effective could be this option of treatment over other options, we also indented to overview the risk factors and epidemiology of infective endocarditis in most evidence based review. 2. METHODOLOGY We searched, with English language restrictions, and only human subject articles following electronic databases; PubMed, MEDLINE and EMBASE for any relevant article, whether was it reviews or randomized controlled studies or systematic reviews discussing infective endocarditis from the time of databases inception to December We used the term infective endocarditis for the Mesh keyword. Date last search performed was December, We supplemented the search with references from articles reviewed and correspondence with other researchers, including experts in the field. When a reference was deemed potentially suitable for inclusion, a full-text copy was obtained and reviewed according to our study criteria which are obvious in the objective of this study. Epidemiological overview: 3. RESULTS & DISCUSSION The epidemiological profile of infective endocarditis (IE) has altered dramatically over the last few years (17). When a disease impacting young people with previously well identified valve disease mostly rheumatic disease IE is now impacting older patients, a significant percentage of whom has no previously known valve disease and develop IE as the result of health care associated treatments (18). The occurrence of IE differs from nation to country, which may show more methodological differences in surveys than true occurrence variations. In an epidemiologic study performed in Sweden from 1984 to 1988 the incidence of IE was 5.9 episodes/ person years after adjusting for both age and sex (19). Throughout a comparable period, the overall occurrence of IE was 9.29 episodes/ person years in the Philadelphia city, which was up to 5.02 episodes/ person years when cases involving intravenous drug users were excluded (20). In the 1990s, French private investigators carried out two epidemiologic surveys in three areas of France that represented about 25% of the entire French population. In 1991 their survey discovered the unrefined occurrence to be 2.24 episodes/ person years, which increased to 2.43 episodes/ person years after change for age and sex (21). Complications of Infective endocarditis and their management: Encephalopathy: Encephalopathy is a typical issue of IE that need to trigger more workup. Encephalopathy might be secondary to systemic insults such as fever, azotemia, electrolyte disturbances, or hypercarbia or point to underlying main nerve system participation through ischemic stroke, hemorrhage, cerebral abscess, or meningitis as gone over subsequently (22). Severe ischemic stroke is the most typical neurological issue of IE, manifesting scientifically in 20% to 40% of patients with IE (23,24,25). Asymptomatic ischemia acknowledged by neuroimaging studies occurs in another 30% to 40% of patients (23,26). Thus, ischemic stroke may be most likely than not in patients with IE. There are some scenarios where the risk of cerebral ischemia is more likely. Anterior mitral valve leaflet endocarditis provides the greatest risk (27). Second, left-sided endocarditis is connected with a much higher risk of stroke than right-sided IE. Third, S aureus infection, before or less than 1 week after initiation of antibiotics, increases the likelihood of stroke. The system of acute cerebral ischemia in IE is likely embolic. Ischemic strokes in IE most frequently occur in the middle cerebral artery territory (Figure 1) (27). Page 862

3 Figure 1: Stroke complicating endocarditis. Axial diffusion-weighted imaging (left) and T2 fluid-attenuated inversion recovery (FLAIR) imaging (right) of a 64-year-old female with a history of severe mitral regurgitation who presented with confusion 2 weeks after a dental procedure. Imaging shows a large right middle cerebral artery territory embolic infarct. The patient was found to have Streptococcus mitis bacteremia and mitral valve endocarditis. Vessel imaging was patent, and she underwent successful valve repair 2 weeks after antibiotics were started. (27) Management of stroke in the setting of IE varies from that of stroke due to noninfective mechanisms insofar as anticoagulation and antiplatelet agents are contraindicated, a minimum of acutely (27). Assessment of cardiac function may reveal a sign for valvular surgical intervention, and stroke complicating IE can affect the timing of this, as talked about further on. Thrombolytic therapy with recombinant tissue plasminogen activator (r-tpa) or related agents has not been well studied in IE-related stroke. In the biggest case series (28), 4 patients having IE presented with ischemic stroke and were treated with thrombolysis. All 4 established hemorrhage after IV r-tpa, 3 of whom passed away. For this reason and due to bad results with intense anticoagulation, r-tpa might increase the risk of bleeding in these patients. The management distinctions to other kinds of ischemic stroke posture a prospective medical problem in the circumstance where stroke is the presenting sign of IE. If a patient appears with a stroke that is amenable to thrombolytic treatment, antiplatelet representatives, or anticoagulation, one might unintentionally use a thrombolytic drug in a patient with occult endocarditis, therefore precipitating disastrous results (28). Cerebral microhemorrhage is significantly acknowledged as a silent issue of endocarditis (26,29) and recently has been implicated in anticipating obvious hemorrhage (30). Cerebral microhemorrhage has actually been detected in 57% of cases with IE, typically situated cortically and with approximately about 8 microbleeds per patient (26). The proposed system is that of infective vasculitis (31) although this is speculative. Furthermore, although there is no information linking the existence of microhemorrhage to later on overt hemorrhage when antiplatelet agents or anticoagulants are used, there could be an increased risk in this setting. Antibiotic prophylaxis to prevent infective endocarditis: Infective endocarditis is a unusual however serious and typically life threatening condition. The pathogenesis of infective endocarditis comprises of an intricate series of events (32). Anatomic localization of infection is identified by the adherence of microorganisms to various sites (33). The coincidence in between bacterial infection and endocarditis was described prior to the turn of 20th century (34). Studies have shown that oral procedures are trigger factors for few cases of endocarditis (35,36). A poor condition of the gum health is a considerable risk factor (37). Lockhart reported more incidence of infective endocarditis following dental extraction and periodontal surgical treatment (38). Ottent et al reported that bacteremia was associated with 74% of patients following tooth extraction (39). Antibiotic prophylaxis not just acts by destroying bacteria, however also by preventing bacterial adherence (40). It is shown in high risk oral procedures in patients with pre-existing high rate cardiac disorders (42). The basic program includes high dosages of amoxicillin in adults and children, one hour prior to the oral treatment. 2 g of oral amoxicillin must be given to grownups prior to the oral procedure beginning (43). Dajani et al have reported that 2g of amoxicillin offers a number of hours of antibiotic coverage (44). Clindamycin is recommended in patients adverse beta- lactamics (45). Furthermore, finest results have actually been attained by use of clindamycin in treating odontogenic infections (46). Vancomycin and streptomycin are used prophylactically for prevention of infective endocarditis in patients with prosthetic heart valves. If the proper antibiotic is Page 863

4 not chosen (47), prophylactic failure is possible to occur in patients with congenital heart disease. The neglect to administer antibiotic prophylaxis for dental treatments may lead to SBE and will result in worst consequences for the patient. Cunha et al documented a comparable case which, resulted in a cerebral vascular accident, embolic occlusion of the leg, and mitral valve replacement (48). On the other hand, a decrease of 78.6% in prescribing antibiotics was seen after the unveiling of NICE guideline (49). The French agency for Health Product Health Safety advices against or contraindicates oral facial surgery, bone surgery, periodontal surgery, root canal treatment in these patients except under emergency situation situations, as these patients are prone to high risk of infection (50). Clinical effectiveness of antibiotic treatment of IE: The intravenous route for antibiotic administration is the very best because it provides optimum bioavailability. A lot of antibiotics are administered as brief infusions (30 minutes). There are some exceptions, nevertheless. Since of the risk of seizures secondary to the high serum concentrations achieved with periodic infusion, penicillin G is normally administered continually. One to two hour infusions of vancomycin enhance the tolerability of the drug. For prescription antibiotics with time dependent impacts (β lactams), the period between infusions should be adjusted to take the elimination half life into account. For prescription antibiotics with concentration dependent impacts (aminoglycosides), two times or thrice daily administration is recommended. There are scientific and experimental data in favour of oncedaily administration of gentamicin or netilmicin in IE caused by penicillin sensitive streptococci (50,51,52). Both the efficacy and the tolerance of the treatment need to be carefully kept an eye on. In terms of effectiveness, apart from the lack of relapse at the end of the treatment, there is no completely trustworthy scientific or biological criterion. This emphasises the significance of biological and scientific security (disappearance of fever, sterilisation of blood cultures, and normalisation of inflammation markers) throughout treatment and in the subsequent four weeks (duration of optimum risk of regression of IE). The decision of blood concentrations of prescription antibiotics, particularly aminoglycosides, is useful to confirm both that the peak concentrations are high enough (effectiveness objective) and that the trough concentrations are not exceedingly high (tolerance goal). The most current recommendations for the antibiotic treatment of IE were provided by the European Society of Cardiology (53) and the American Heart Association (54). are summed up in (Table 1 and 2). Table 1: Antibiotic treatment for infective endocarditis caused by penicillin susceptible (MIC <0.1 mg/l) or penicillin relatively resistant (0.1< MIC 0.5 mg/l) streptococcal endocarditis (53,54) No allergy to penicillin Allergy to penicillin Drug Dosage Drug Dosage Penicillin susceptible streptococci (MIC <0.1 mg/l) Non complicated native valve IE Complicated and/or prosthetic valve IE *Other choice: netilmicin (5 6 mg/kg/d); for both drugs, once daily administration. Including tolerant streptococci (MBC/MIC >32) for which amoxicillin is to be preferred to penicillin. IE, infective endocarditis; MBC, minimal bactericidal concentration; MIC, minimal inhibitory concentration. Duration Penicillin G U/kg/d Vancomycin 30 mg/kg/d 2 weeks or amoxicillin 100 mg/kg/d or teicoplanin 6 10 mg/kg/d combination or ceftriaxone 2 g/d ± gentamicin* 3 mg/kg/d or 4 weeks β lactam ± gentamicin* 3 mg/kg/d Penicillin G U/kg/d Vancomycin 30 mg/kg/d 2 weeks combination or amoxicillin 100 mg/kg/d or teicoplanin 6 10 mg/kg/d weeks β lactam + gentamicin* 3 mg/kg/d ± gentamicin* 3 mg/kg/d Penicillin relatively resistant streptococci G (0.1< MIC 0.5 mg/l) Non complicated native valve IE Complicated and/or prosthetic valve IE Penicillin G U/kg/d Vancomycin 30 mg/kg/d 2 weeks combination or amoxicillin 200 mg/kg/d or teicoplanin 6 10 mg/kg/d + 2 weeks β lactam + gentamicin* 3 mg/kg/d + gentamicin* 3 mg/kg/d Penicillin G U/kg/d Vancomycin 30 mg/kg/d 2 weeks combination or amoxicillin 200 mg/kg/d or teicoplanin 6 10 mg/kg/d weeks β lactam + gentamicin* 3 mg/kg/d + gentamicin* 3 mg/kg/d Page 864

5 Table 2: Antibiotic treatment for enterococcal, nutritionally variant and penicillin resistant (MIC >0.5 mg/l) streptococcal endocarditis (54,55) No allergy to penicillin Allergy to penicillin Condition Enterococcal strain susceptible to penicillin, aminoglycosides, and vancomycin Enterococcal strain susceptible to penicillin, streptomycin, vancomycin, and resistant to gentamicin Enterococcal strain resistant to penicillin (intrinsic resistance), susceptible to gentamicin and vancomycin Enterococcal strain resistant to penicillin (β lactam producing), susceptible to gentamicin and vancomycin Streptococcal and enterococcal strains with high level resistance to all aminoglycosides E faecalis resistant to penicillin, aminoglycosides and vancomycin E faecium resistant to penicillin, aminoglycosides and vancomycin Drug Dosage Drug Dosage Duration Amoxicillin or 200 mg/kg/d Vancomycin 30 mg/kg/d 4 6 penicillin G U/kg/d or teicoplanin 6 10 mg/kg/d weeks + gentamicin* 3 mg/kg/d + gentamicin* 3 mg/kg/d Amoxicillin or 200 mg/kg/d Vancomycin 30 mg/kg/d 4 6 penicillin G U/kg/d or teicoplanin 6 10 mg/kg/d weeks + streptomycin 15 mg/kg/d + streptomycin 15 mg/kg/d Vancomycin 30 mg/kg/d Vancomycin 30 mg/kg/d 6 weeks or teicoplanin 6 10 mg/kg/d or teicoplanin 6 10 mg/kg/d + gentamicin* 3 mg/kg/d + gentamicin* 3 mg/kg/d Co amoxyclav 175 mg/kg/d amoxicillin Vancomycin 30 mg/kg/d 6 weeks + gentamicin* 3 mg/kg/d or teicoplanin 6 10 mg/kg/d + gentamicin* 3 mg/kg/d Amoxicillin >200 mg/kg/d Vancomycin 30 mg/kg/d 8 weeks Amoxicillin 200 mg/kg/d 8 + ceftriaxone or 2 g/d weeks imipenem 2 g/d Linezolid, or 1200 mg/d Linezolid, or 1200 mg/d 8 quinupristindalfopristin 22.5 mg/kg/d quinupristindalfopristin 22.5 mg/kg/d weeks *Two or three daily doses. Duration of aminoglycoside administration could be shortened to 2 3 weeks; the total duration of treatment should be 6 weeks when vancomycin or teicoplanin are used. Two daily doses. 4. CONCLUSION Optimal antibiotic recommending for enterococcal IE requires that MICs of penicillin, amoxicillin, aminoglycosides, and glycopeptides be determined. When the strain shows only low level resistance to aminoglycoside, advised therapy is a combination of high dose β lactam ( million units/day penicillin or 200 mg/kg/day amoxicillin) plus gentamicin for 4-6 weeks. The aminoglycoside element ought to be administered in two or three equally divided doses; this suggestion is based on outcomes of speculative studies. When it comes to high level resistance to gentamicin, crossresistance may be expected with all other aminoglycosides, other than often streptomycin. If the stress reveals low level resistance to streptomycin, the latter can be utilized in mix with high doses of a cell wall active representative, either a glycopeptide or a β lactam. The best treatment choice is monotherapy with amoxicillin or a glycopeptide provided at high Page 865

6 dosage for at least 8 weeks if the pressure shows high level resistance to streptomycin as well. Even with such extended treatment, antibiotic therapy often stops working, and surgical treatment is most likely to be needed. REFERENCES [1] Hoen B, Duval X.. Infective endocarditis. N Engl J Med. 2013;369 (8):785. [2] Hoen B, Duval X.. Clinical practice. Infective endocarditis. N Engl J Med. 2013;368 (15): [3] Sy RW, Kritharides L.. Health care exposure and age in infective endocarditis: results of a contemporary populationbased profile of 1536 patients in Australia. Eur Heart J. 2010;31 (15): [4] Keynan Y, Rubinstein E.. Pathophysiology of infective endocarditis. Curr Infect Dis Rep. 2013;15 (4): [5] Chan KL, Dumesnil JG, Cujec B, et al.. A randomized trial of aspirin on the risk of embolic events in patients with infective endocarditis. J Am Coll Cardiol. 2003;42 (5): [6] Chan KL, Tam J, Dumesnil JG, et al.. Effect of long-term aspirin use on embolic events in infective endocarditis. Clin Infect Dis. 2008;46 (1):37 4. [7] Fowler VG, Scheld WM, Bayer AS. Endocarditis and intravascular infections. In: Mandell GL, Bennett JE, Dolin R, editors. Mandell, Douglas and Bennett s Principles and Practice of Infectious Diseases. 6. Philadelphia: Churchill Livingstone; pp [8] Cabell CH, Fowler VG, Jr, Engemann JJ, et al. Endocarditis in the elderly: Incidence, surgery, and survival in 16,921 patients over 12 years. Circulation. 2002;106(19):547. [9] Thayer WS. Studies on bacterial (infective) endocarditis. Johns Hopkins Hosp Rep. 1926;22:1 8. [10] Miro JM, Anguera I, Cabell CH, et al. Staphylococcus aureus native valve infective endocarditis: Report of 566 episodes from the International Collaboration on Endocarditis Merged Database. Clin Infect Dis. 2005;41: [11] Selton-Suty C, Hoen B, Grentzinger A, et al. Clinical and bacteriological characteristics of infective endocarditis in the elderly. Heart. 1997;77(3): [12] McDonald JR, Olaison L, Anderson DJ, et al. Enterococcal native valve endocarditis: Report of 107 episodes from the International Collaboration on Endocarditis Merged Database. Am J Med. 2005;11: [13] Griffin MR, Wilson WR, Edwards WD, et al. Infective endocarditis. Olmsted County, Minnesota, 1950 through JAMA. 1985;254: [14] Michel PL, Acar J. Native cardiac disease predisposing to infective endocarditis. Eur Heart J. 1995;16(SupplB):2 9. [15] Weinberger I, Rotenberg Z, Zacharovitch D, et al. Native valve infective endocarditis in the 1970s versus 1980s: underlying cardiac lesions and infecting organisms. Clin Cardiol. 1990;13:94 8. [16] Clemens JD, Horwitz RI, Jaffe CC, et al. A controlled evaluation of the risk of bacterial endocarditis in persons with mitral-valve prolapse. N Engl J Med. 1982;307: [17] Moreillon P, Que Y A. Infective endocarditis. Lancet [18] Hoen B, Alla F, Béguinot I. et al Changing profile of infective endocarditis results of a one year survey in France in JAMA [19] Hogevik H, Olaison L, Andersson R. et al Epidemiologic aspects of infective endocarditis in an urban population. A 5 year prospective study. Medicine (Baltimore) [20] Berlin J A, Abrutyn E, Strom B L. et al Incidence of infective endocarditis in the Delaware Valley, Am J Cardiol [21] Delahaye F, Goulet V, Lacassin F. et al Characteristics of infective endocarditis in France in A 1 year survey. Eur Heart J Page 866

7 [22] Morris NA, Matiello M, Lyons JL, Samuels MA. Neurologic Complications in Infective Endocarditis: Identification, Management, and Impact on Cardiac Surgery. Lyons J, ed. The Neurohospitalist. 2014;4(4): doi: / [23] Snygg-Martin U, Gustafsson L, Rosengren L, et al.. Cerebrovascular complications in patients with left-sided infective endocarditis are common: a prospective study using magnetic resonance imaging and neurochemical brain damage markers. Clin Infect Dis. 2008;47 (1):23 30 [24] Sonneville R, Mirabel M, Hajage D, et al.. Neurologic complications and outcomes of infective endocarditis in critically ill patients: the ENDOcardite en REAnimation prospective multicenter study. Crit Care Med. 2011;39 (6): [25] Novy E, Sonneville R, Mazighi M, et al.. Neurological complications of infective endocarditis: New breakthroughs in diagnosis and management. Med Mal Infect. 2013;43 (11-12): [26] Hess A, Klein I, Iung B, et al.. Brain MRI findings in neurologically asymptomatic patients with infective endocarditis. AJNR Am J Neuroradiol. 2013;34 (8): [27] Derex L, Bonnefoy E, Delahaye F.. Impact of stroke on therapeutic decision making in infective endocarditis. J Neurol. 2010;257 (3): [28] Walker KA, Sampson JB, Skalabrin EJ, Majersik JJ.. Clinical characteristics and thrombolytic outcomes of infective endocarditis-associated stroke. Neurohospitalist. 2012;2 (3):87 91 [29] Klein I, Iung B, Labreuche J, et al.. Cerebral microbleeds are frequent in infective endocarditis: a case-control study. Stroke. 2009;40 (11): [30] Okazaki S, Sakaguchi M, Hyun B, et al.. Cerebral microbleeds predict impending intracranial hemorrhage in infective endocarditis. Cerebrovasc Dis. 2011;32 (5): [31] Klein I, Iung B, Wolff M, et al.. Silent T2* cerebral microbleeds: a potential new imaging clue in infective endocarditis. Neurology. 2007;68 (23):2043. [32] Gopalakrishnan PP, Shukla SK, Tak T. Infective Endocarditis: Rationale for revised guidelines for antibiotic prophylaxsis. Clin Med Res. 2009;7(3): [33] Wilson W, Taubert KA, Gewitz M, Lockhart PB, Baddour LM, Levison M, et al. Prevention of infective endocarditis. Guidelines from the American Heart Association Circulation Oct 9. Circulation. 2007: [34] Cowper T. Pharmacologic mamagement of the patient with disorders of the cardiovascular system: Infective endocarditis. Dent Clinic North Am. 1996;40: [35] Vander Meer JT, Thompson J, Valkenburg HA, Michael MF. Epidemology of bacterial endocarditis in the Netherlands II antecedent procedures and uses of prophylaxis. Arch Intern Med. 1992;152: [36] Storm BL, Abruptyn E, Berlin JA, Finman JL, Feldman RS, Stolley PD, et al. Dental and cardiac risk factors for infective endocarditis. A population based case-control study. Arch Intern Med. 1998;129: [37] Guntheroth WG. How important are dental procedures as a cause of infective endoarditis. Am J Cardiol. 1984;54: [38] Lockhart PB. An analysis of bacteremias during dental extraction. A double-blind placebo-controlled study of chlorhexidine. Arch Intern Med. 1996;156: [39] Otten JE, Pelz K, Christmann G. Anaerobic bacteremia following tooth extraction and removal of osteosynthesis plates. J Oral Maxillofac Surg. 1987;45: [40] Gauser MP, Bernard JP, Moreillon P, Francioli P. Succesful single dose amoxicillin prophylaxis against experimental streptococcal endocarditis: evidence for two mechanisms of protection. J Infect Dis. 1983;147: [41] Vera JRM, Gomez-Lus Centelles ML. Antimicrobial prophylaxis in oral surgery and dental procedures. Med Oral Patol Circ Buccal. 2007;12: Page 867

8 [42] Dajani AS, Taubert KA, Wilson W, Bolger AF, Bayer A, Ferrieri P, Gewitz MH, et al. Prevention of bacterial endocarditis: Recommendations by the American heart association. Clinic Infect Dis. 1979;25: [43] Dajani A, Bawden RE, Berry MC. Oral amoxicillin as a prophylaxis for endocarditis: What is the optimal dose. Clin Infect Dis. 1994;18: [44] Durack DT. Prophylaxis of infective endocarditis. In: Mandell GL, Bennett JE, Dolin R, editors. Mandell, Douglas and Bennett principles and practice of infectious diseases. 6th ed. Philadelphia: Elsevier Churchill Livingstone; pp [45] Gilmore WC, Jacobus NV, Gorbach SL, Doku HC. A prospective double-blind evaluation of penicillin versus clindamycin in the treatment of odontofenic infections. J Oral Maxillofac Surg. 1988;46: [46] Pogrel MA, Welsby PD. The dentist and prevention of infective endocardititis. Br Dent J. 1975;139: [47] Cunha BA, D'Ella AA, Pawar N, Scoch D. Viridans streptococcal (Streptococcus intermedius) mitral valve sub acute bacterial endocarditis( SBE) in a patient with mitral valve prolapsed after a dental procedure: the importance of antibiotic prophylaxis. Heart Lung. 2010;39(1): [48] Thornhill MH, Dayer MJ, Forde JM, Corey GR, Hock G, Chu VH, et al. Impact of the NICE guideline recommending cessation of antibiotic prophylaxis for prevention of infective endocarditis: before and after study. BMJ. 2011;342:d2392. [49] French Health Products Safety Agency Prescribing antibiotics in odontology and stomatology. Recommendations by the French Health Products Safety Agency. Fundament Clin Pharmacol. 2003;17: [50] Blatter M, Fluckiger U, Entenza J. et al Simulated human serum profiles of one daily dose of ceftriaxone plus netilmicin in treatment of experimental streptococcal endocarditis. Antimicrob Agents Chemother [51] Francioli P, Ruch W, Stamboulian D. Treatment of streptococcal endocarditis with a single daily dose of ceftriaxone and netilmicin for 14 days: a prospective multicenter study. Clin Infect Dis [52] Sexton D J, Tenenbaum M J, Wilson W R. et al Ceftriaxone once daily for four weeks compared with ceftriaxone plus gentamicin once daily for two weeks for treatment of endocarditis due to penicillin susceptible streptococci. Clin Infect Dis [53] Horstkotte D, Follath F, Gutschik E. et al Guidelines on prevention, diagnosis and treatment of infective endocarditis executive summary; the task force on infective endocarditis of the European Society of Cardiology. Eur Heart J [54] Baddour L M, Wilson W R, Bayer A S. et al Infective endocarditis: diagnosis, antimicrobial therapy, and management of complications: a statement for healthcare professionals from the Committee on Rheumatic Fever, Endocarditis, and Kawasaki Disease, Council on Cardiovascular Disease in the Young, and the Councils on Clinical Cardiology, Stroke, and Cardiovascular Surgery and Anesthesia, American Heart Association: endorsed by the Infectious Diseases Society of America. Circulation e394 e434.e434o Page 868