Infective Endocarditis in Childhood: 2015 Update
2015; Lippincott Williams & Wilkins; Volume: 132; Issue: 15 Linguagem: Inglês
10.1161/cir.0000000000000298
ISSN1524-4539
AutoresRobert S. Baltimore, Michael H. Gewitz, Larry M. Baddour, Lee B. Beerman, Mary Anne Jackson, Peter B. Lockhart, Elfriede Pahl, Gordon E. Schutze, Stanford T. Shulman, Rodney E. Willoughby,
Tópico(s)Streptococcal Infections and Treatments
ResumoHomeCirculationVol. 132, No. 15Infective Endocarditis in Childhood: 2015 Update Free AccessResearch ArticlePDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessResearch ArticlePDF/EPUBInfective Endocarditis in Childhood: 2015 UpdateA Scientific Statement From the American Heart Association Robert S. Baltimore, MD, Michael Gewitz, MD, FAHA, Larry M. Baddour, MD, FAHA, Lee B. Beerman, MD, Mary Anne Jackson, MD, Peter B. Lockhart, DDS, Elfriede Pahl, MD, FAHA, Gordon E. Schutze, MD, Stanford T. Shulman, MD and Rodney WilloughbyJr, MDon behalf of the American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee of the Council on Cardiovascular Disease in the Young and the Council on Cardiovascular and Stroke Nursing Robert S. BaltimoreRobert S. Baltimore , Michael GewitzMichael Gewitz , Larry M. BaddourLarry M. Baddour , Lee B. BeermanLee B. Beerman , Mary Anne JacksonMary Anne Jackson , Peter B. LockhartPeter B. Lockhart , Elfriede PahlElfriede Pahl , Gordon E. SchutzeGordon E. Schutze , Stanford T. ShulmanStanford T. Shulman and Rodney WilloughbyJrRodney WilloughbyJr and on behalf of the American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee of the Council on Cardiovascular Disease in the Young and the Council on Cardiovascular and Stroke Nursing Originally published15 Sep 2015https://doi.org/10.1161/CIR.0000000000000298Circulation. 2015;132:1487–1515Other version(s) of this articleYou are viewing the most recent version of this article. Previous versions: January 1, 2015: Previous Version 1 In 2002, the American Heart Association (AHA) published "Unique Features of Infective Endocarditis in Childhood,"1 which reviewed epidemiology, pathogenesis, diagnosis, clinical and laboratory findings, treatment, and prevention of infective endocarditis (IE) with particular attention to children. Since that time, other AHA reports have focused on new recommendations for treatment of IE in adults (in 20052) and on major changes regarding prevention of IE (in 20073). This document updates these issues and other concerns regarding IE, with specific attention to the disease as it affects infants and children. In particular, the impact of increased survival for children with congenital heart disease (CHD) on the epidemiology of IE is updated, and newer tools useful for diagnosis and treatment in the pediatric population are reviewed. This review emphasizes changing management perspectives and discussion of new agents that have utility for treatment of resistant organisms. In addition, proper use of the diagnostic microbiology laboratory remains critical to the diagnosis and management of children with IE, and newer diagnostic guidelines that have improved sensitivity and specificity for confirming the diagnosis of IE will be reviewed. Because of improved infrastructure available for home intravenous therapy, an update on outpatient management, an increasingly accepted approach for stable patients who are at low risk for complications, will also be discussed. Finally, since the publication of the last AHA document on pediatric IE, recommendations for prevention of IE have been modified substantially, and the most current recommendations are incorporated from the perspective of pediatric cardiovascular concerns.Classification of RecommendationsIn pediatrics, there are not likely to be any randomized controlled trials for treatment of IE, which posed a challenge for the writing group in compiling recommendations. Therefore, many of the indications are based on consensus. In cases of strong consensus that an intervention be considered as standard-of-care practice with scientific evidence, interventions were designated as Class I indications. Where the wording of treatments indicates a recommendation, the standard classification is used. Strength of the recommendation is according to the ACC/AHA classification system for recommendations (Table 1).Table 1. Applying Classification of Recommendations and Level of EvidenceTable 1. Applying Classification of Recommendations and Level of EvidenceEpidemiology and Clinical Findings of IE in ChildrenIn a previous report, IE occurred less often in children than in adults and accounted for approximately 1 in 1280 (0.78 per 1000) pediatric admissions per year from 1972 to 1982 at a referral insitution.4 In a recent multicenter report,5 the annual incidence rate in the United States was between approximately 0.05 and 0.12 cases per 1000 pediatric admissions from 2003 to 2010, without a significant trend. Although the reported hospitalization rates for IE vary considerably among published series, both the overall frequency of endocarditis among children and a shift toward those with previous cardiac surgery appear to have increased in recent years in some reports.5–8 This may be related to improved survival among children who are at risk for endocarditis, such as those with CHD (with or without surgery) and hospitalized newborn infants.Before the 1970s, 30% to 50% of US children with IE had underlying rheumatic heart disease.9 Because the prevalence of rheumatic heart disease has declined in developed countries, including the United States, it has now become relatively unusual for patients with IE from the developed world to have underlying rheumatic heart disease. In the past 2 decades, CHD has become the predominant underlying condition for IE in children from the developed world >2 years of age. In fact, there has been an increase in cases of IE associated with CHD because most patients with CHD survive much longer than they did several decades ago. Early surgical correction of lesions that were major risk factors for IE in the past has also changed the substrate for this disease. Although congenital heart defects, such as aortic valve abnormalities, ventricular septal defect, and tetralogy of Fallot, are still common underlying conditions, an increasing proportion of children with IE have had previous corrective or palliative surgery for complex cyanotic CHD, with or without implanted vascular grafts, patches, or prosthetic cardiac valves.10–14 Postoperative IE is a long-term risk after correction of complex CHD, especially in those with residual defects or in cases in which a surgical shunt is constructed or other prosthetic material is left in place.Increasingly, IE develops in the absence of CHD. This circumstance is often associated with central indwelling venous catheters (central lines). The complexities of patient management in neonatal and pediatric intensive care units have increased the risk of IE in children with structurally normal hearts. Currently, in approximately 8% to 10% of pediatric cases,13 IE develops without structural heart disease or any other readily identifiable risk factors. In these situations, the infection usually involves the aortic or mitral valve secondary to Staphylococcus aureus bacteremia.6,10–12 Recent initiatives developed to reduce central line bloodstream infections will likely improve the prognosis for all critically ill children, including those with cardiac conditions, and may impact IE development further in the diverse group of vulnerable patients with central lines. Interestingly, children with congenital or acquired immunodeficiencies but without identifiable risk factors for IE do not appear to be at increased risk for endocarditis compared with the general population. Furthermore, factors often associated with IE in adults, such as intravenous drug abuse and degenerative heart disease, are not common predisposing factors in children.7–11IE in Children With Previous Cardiac Surgery or After Placement of Transcatheter DevicesCorrective surgery with no residual defect eliminates the attributable risk for endocarditis in children with ventricular and atrial septal defects or patent ductus arteriosus 6 months after surgery. However, surgery itself, including such elements as central vascular catheters, intravenous alimentation, and days the patient resides in the intensive care unit, may be important risk factors for the development of IE. Approximately 50% of children with IE complicating CHD have had previous cardiac surgery, particularly palliative shunt procedures or complex intracardiac repairs. Morris et al12 reviewed cumulative incidences of endocarditis for a number of congenital cardiac lesions in a follow-up series of Oregon residents. The highest annualized risk for IE was found in children who had had repair or palliation of cyanotic CHD. The greatest risk among those patients was for those who had either undergone surgery for obstruction to pulmonary blood flow or had prosthetic aortic valve replacement. In a follow-up of the series of Oregon residents, the highest incidence of IE in postoperative patients has been in the cohort with aortic valve stenosis, and this has increased over time, with a cumulative incidence of 13.3% at 25 years.12 Endocarditis may manifest as a late complication, with presentation years after congenital heart surgical repair, and may be associated with a fulminant course or antibiotic failure.14,15The incidence of IE in the first postoperative month is low for most defects and increases with time after surgery. An exception to this trend is that when prosthetic valves or conduits are used in surgical repairs and hemodynamic problems persist, the risk of IE is high even in the immediate postoperative period (first 2 weeks after surgery).12 Two recently published studies showed a 25% incidence of previous cardiac surgery in patients with congenital heart disease who required surgery during active IE.16,17Russell et al18 reported 34 patients who met indications for surgical management of IE (of whom 37% had prior cardiac surgery) from a 21-year single-center review through 2011 at Children's Memorial Hospital, Chicago, IL. Five had operative mortality, and all deaths occurred in infants, with a mean age of 2.5 months. The infective organisms were identified in 86% of cases, with the most common being S aureus (n=8) and viridans streptococci (n=6). The Ross operation was performed successfully in 5 children with severe aortic valve disease. Ten of the 34 patients required reoperations at a later time.The increasing prevalence of transcatheter placement of devices such as septal or vascular occluders and coils provides another potential risk factor for IE, particularly in the early postdeployment period before endothelialization has occurred.3 Although a long-term study of transcatheter closure of atrial septal defects19 showed no cases of IE, several case reports of endocarditis related to transcatheter device treatment of atrial and ventricular septal defects and patent ductus arteriosus do suggest that residual defects after device placement may be a factor in the risk for IE.20–23IE in Newborn InfantsIn a recent multicenter review, 7.3% of cases of pediatric IE (108 of 1480) were diagnosed in the first month of life.24 Improved and widely available imaging technology, particularly echocardiography, and increased clinical awareness have greatly facilitated the diagnosis of IE in this patient group. The incidence of neonatal IE has increased in the past 2 decades in large measure because of the increasing use of invasive techniques to manage neonates with multiple complex medical problems, even those with structurally normal hearts. Central venous catheters designed to be in place for prolonged periods of time, such as peripherally inserted central catheters and tunneled central venous catheters, provide a portal of entry for surface bacterial despite the most meticulous management. As a result of the indwelling lines, infections frequently involve right-sided heart structures. It has been estimated that fewer than one-third of cases of neonatal endocarditis occur in the presence of congenital cardiac disease.24–26 A recent review showed that 31% of infants who died of IE were premature.24 The most common infecting organisms were S aureus, coagulase-negative staphylococcus strains, Gram-negative bacterial species, and Candida species.The clinical manifestations of IE in the neonate are variable and nonspecific and may be indistinguishable from septicemia or from congestive heart failure associated with other causes.27–29 In infants, septic emboli from IE are common, resulting in foci of infection outside the heart (eg, osteomyelitis, meningitis, or pneumonia). Neonates with IE often have feeding difficulties, respiratory distress, tachycardia, and hypotension. As with older children, neonates also may have a new or changing heart murmur. Many neonates with IE also have neurological signs and symptoms (eg, seizures, hemiparesis, or apnea). However, although arthritis and arthralgia are common findings in older children with IE, arthritis is rarely described in neonates. Osler nodes, Roth's spots, Janeway lesions, and splinter hemorrhages are also not mentioned in published cases of IE in neonates.PathogenesisEarly histopathologic studies in humans and decades-long investigations that have included an animal model of experimental endocarditis have confirmed 2 critical histopathologic findings: (1) Damaged or denuded endothelium is necessary for initial pathogen colonization of a cardiac nidus; and (2) Gram-positive cocci, the predominant pathogens in both native and prosthetic value infections, express multiple adhesins that serve as virulence factors through their ability to enhance host cell/substrate attachments that are important in both the initiation and propagation of endocardial infection. (Adhesins are discussed further in a separate section.)Denuded cardiac endothelium can occur when there is turbulence caused by abnormal cardiac structures, in particular stenotic or regurgitant valves, that results in high-velocity jets of blood. Once the endothelium is damaged, the host response includes platelet and fibrin deposition, leading to so-called nonbacterial thrombotic endocarditis (NBTE), at the wound site. NBTE serves as an excellent nidus for subsequent bacterial or fungal colonization in a patient with bacteremia or fungemia. The prevailing notion is that activities of daily living, such as chewing food, toothbrushing, and flossing, account for most bloodstream seeding of an NBTE site.There are additional mechanisms involved in endocarditis pathogenesis. Right-sided endocarditis can occur when there are intravenous catheters, illicit intravenous drug use, or cardiovascular implantable electronic device leads that dwell in the right side of the heart. Damage to the endothelium occurs by 2 mechanisms. One involves direct damage produced by the foreign body "rubbing" directly against the endothelial surface. The other is via an indirect effect, such as when a foreign device interferes with normal tricuspid valve function and causes regurgitant jets of blood. Bacteremia may be caused by entry of organisms at the skin site of percutaneous catheters or leads, via the catheter lumen, or in contaminated infusate. Microorganisms carried by the bloodstream enter the right side of the heart, potentially causing IE on preexisting NBTE.IE can also occur as a result of direct infection of an indwelling device. This occurs at the time of device placement into a cardiac locus (eg, valves, leads, other types of devices) and is an example of surgical site infection. These infections can occur despite the administration of antibiotic prophylaxis at the time of placement of cardiovascular devices such as heart valves, pacemaker leads, or left ventricular devices.AdhesinsVirulence factors that are involved in bacterial adherence, so-called adhesins, have received the bulk of recent investigative attention. Advances in molecular biological techniques have been crucial in characterizing these cell surface structures, with attention specifically to staphylococcal, streptococcal, and enterococcal species, which account for the large majority of IE cases. These adhesins attach to either host cell structures or extracellular molecules that bind to host cells or to extracellular matrix.The availability of an experimental animal model of endocarditis has been a pivotal aspect of these pathogenesis investigations. It has served as the ultimate evaluation of in vitro molecular techniques to obtain mutant and recombinant isolates that are developed to examine the effects of a single purported virulence factor expressed by a wild-type strain. Considering the fact that Gram-positive cocci typically express multiple adhesins, the ability to demonstrate the role of a single adhesin in infection pathogenesis is remarkable. For example, this approach demonstrated pilus involvement in attachment to collagen by Streptococcus gallolyticus. This was the first time that a virulence factor was demonstrated in an animal model of endocarditis.30 Interestingly, strains that expressed pil1 did not adhere to either fibronectin or fibrinogen but did form biofilm in vitro. A nonpathological Lactococcus lactis strain that by recombinant techniques expressed Pil1 in vitro was examined with its parent strain that did not express Pil1 in a rat model of experimental endocarditis. The results suggested that Pil1 was important in vivo as a virulence factor; 82% of rats challenged with the Pil1+ strain developed experimental endocarditis, in contrast to the animals that received the Pil1− strain (36%, P=0.03).30The "big 3" pathogens (viridans group streptococci [VGS], S aureus, and Enterococcus species) that account for the large majority of endocarditis cases have been the primary focus of pathogenesis studies.31 Adhesins of S aureus, which have been referred to as MSCRAMMs (microbial surface components recognizing adhesive matrix molecules), are surface molecules involved in staphylococcal attachment to collagen, thrombospondin, laminin, fibrinogen, and fibronectin.32 These interactions with host proteins not only may be important in the initial adherence of bacteria to a site of endothelial damage but also may be operative in bacterial persistence and engulfment by the host cell (endothelial cells, platelets). Similarly, there have been several bacterial surface structures identified in strains of VGS and Enterococcus species that appear critical in endocarditis pathogenesis.Study of pathogenic mechanisms in IE is pivotal as we consider potential advances in infection treatment and prevention in the future. This knowledge serves as a foundation for the development of novel clinical tools that include therapeutics and vaccines. Indeed, identification of a virulence factor resulted in development of a vaccine that reduced the risk of endocarditis development in an animal model.33Pathogenesis of IE on Prosthetic MaterialBecause perivalvular infection that involves the sewing ring is commonplace among patients with prosthetic valve endocarditis, particularly mechanical valves, the pathogenic mechanisms reviewed previously in this section apply to prosthetic valve endocarditis. In addition, biofilm formation can be operative in infection of prosthetic valves, similar to infection of a broad array of indwelling cardiovascular and noncardiovascular devices.34A mature biofilm represents a unique and complex environment for organisms to attach to and thrive on a device surface. Both antimicrobial agents and immune cells have difficulty in penetrating biofilm, and because of metabolic changes of infecting organisms in biofilm, the ability of antimicrobial agents to kill biofilm-associated organisms is greatly reduced. Because of this, infection relapse at a prosthetic valve site is thought to be increased.Oral/Dental ConsiderationsThe oral mucosa and tooth surfaces of children who are beyond infancy are populated by a variety of pathogenic and nonpathogenic bacteria, which are representative of hundreds of strains of aerobic and anaerobic species.35,36 This oral flora, in both health and disease, is different from adults and less diverse, but it becomes more like that of adults as the child ages, including increases in the percentage of VGS (α-hemolytic streptococci), Prevotella, and Actinomyces species.35–38 In health, the child's oral flora has a variety of VGS, Neisseria species, Haemophilus species, and Staphylococcus species. In older children, species responsible for periodontal diseases (eg, Capnocytophaga) can be found along with others known to cause IE (eg, Aggregatibacter actinomycetemcomitans).39 This is particularly relevant with regard to the formation of plaque on the teeth of children at risk for IE.Dental plaque biofilm formation begins soon after a tooth surface is cleaned, and in the absence of oral hygiene, this biofilm thickens and evolves to include a more pathogenic bacterial flora largely isolated from the immune system. In contrast to plaque in adults, plaque bacteria on the visible surfaces of the teeth (supragingival) in children are similar to those in the gingival crevice (subgingival space), where there are more Gram-negative and anaerobic species than other sites in the oral cavity.35 The host response to plaque is gingival inflammation and enlargement (gingivitis). Gingivitis can result in an increased depth to this shallow gingival crevice between the tooth surface and the gingival crevicular mucosa that is more difficult to clean with a toothbrush and floss. In the absence of disease, the crevicular mucosa serves as a barrier to bacterial invasion. As in adults, however, the child's gingival crevice is most likely the source of virtually all transient bacteremia that occur from the mouth, whether from office-based dental procedures or routine activities of daily living such as toothbrushing. Gingival inflammation, however, may lead to thinning and ulceration, allowing dense colonies of bacteria and bacterial byproducts ready access to the increased gingival capillary circulation. Bacteremia may then result from minimal gingival manipulation. Children have a much lower prevalence and severity of gingivitis and periodontitis than adults, and data from bacteremia studies in adults may not be representative of children.Bacteremia From Dental ProceduresDental procedures are a frequent source of bacteremia, particularly from VGS.40–48 Multiple clinical studies of children over the past 40 years focused on the impact of ≥1 of the following risks for development of bacteremia: class of prophylactic antibiotic drug49; nature and invasiveness of dental procedures42,44–47,49–53; indices of oral hygiene and disease41,45,48,49,51,54,55; timing of blood culture draws before, during, and after the dental procedure45,48,56; various methods of microbial analysis and identification44,57; and the impact of these variables on surrogate measures of risk for IE, such as the incidence, duration, nature, and magnitude of bacteremia.44–48 Clearly, these surrogate measures are also influenced by multiple host factors.These variable risks are associated with a wide range (0%–97%) in the incidence of bacteremia in children after various dental procedures and other manipulations of the gingiva, for example, tooth extractions (0%–96%)41,44,45,48–50,53,57–60; teeth cleaning and electric toothbrushing (0%–78%)42,45,47,55,61–63; restorations (16%–66%)45,46,50; dental injections (16%–97%)52,64; and other manipulations (13%–44%).42,44,46,51–53 Of the more than 100 oral bacterial species recovered from blood cultures in children after dental procedures, the number and variety of species reflect the spectrum of oral flora in health and disease (Table 2). They also reflect the varied microbiological methodologies used in these studies (eg, culture-based rather than molecular), with the recognition that many bacterial species clearly enter the bloodstream but are not cultivable and therefore not recorded.44,49,57 Of greatest importance is the subset of bacterial species reported in blood cultures after dental procedures that are known to cause IE.66 Finally, the varied methodologies and results make it impossible to differentiate among procedures with regard to their risk for causing bacteremia. The collective published data from adult and pediatric studies suggest that the vast majority of dental office visits result in some degree of risk for bacteremia, and the emphasis has therefore changed from a focus on specific dental procedures to a focus on gingival manipulation of any kind.3Table 2. Bacteria Recovered From Blood After Dental Procedures* in ChildrenAbiotrophia43Aggregatibacter actinomycetemcomitans43Actinomyces45,47,49,52,56,64; A georgiae46; A gerensceriae46; A israelii45,47; A iwolffii56; A lingnae46; A meyeri56; A meyeri/odontolyticus45; A naeslundii46,56; A neuii47; A odontolyticus45,46,48; A viscosus45,46,56; A urinae57; A viridans46Arthrobacter sp47,56Bacillus42; B licheniformis57; B megaterium57; B pumilus57Bacteroides41,44,49,51,64,65; B capillosus40; B distasonis48; B fragilis48Bifidobacterium45,48Brachybacterium spp46Brevibacterium50Capnocytophaga49Cardiobacterium hominis45Cellulomonas spp47Corynebacterium40–43,44–47,49,50,52,57,61,64; C hofmanii45,51Eikenella45Enterobacter aerogenes48Enterococcus faecalis57Enterococcus gallinarum48Eubacterium45,61; E aerofaciens45,48; E lentum45; E ventriosum40Fusobacterium49,61; F fusiforme45; F nucleatum45,48; F varium48Gemella44,45,48,56,64Haemophilus45,49; H parainfluenza40,42,44–46,48,50Lactobacillus45,49,52,64; L acidophilus48; L brevis47; L casei56; L paracasei56Lactococcus cremoris42,44Leuconostoc53Listeria42; L greyi47Micrococcus spp40,42,45,50,52,56,57,64Micrococcus luteus46Moraxella42,44,45; M nonliquefaciens45Neisseria41,42,44,45,51,52,57,64,65; N catarrhalis45; N cinerea47,48; N flava46; N lactamica48; N pharynges46; N polysaccharea53; N sicca/subflava48Pantoea agglomerans46Pediococcus50Peptostreptococcus41,45,53,61; P asaccharolyticus45; P micros45,48,56; P prevotii45Prevotella45; P acnes46; P corporis48; P melaninogenica45,50,61Propionibacterium42,43,50,62; P acnes43,54; P jensenii38Rothia; R dentocariosa44,54; R mucilaginosus44Saprophytic neisseria43Staphylococcus; S aureus42,44,52,53,57; S auricularis48; S capitis46–48,56,57; S cohnii46; S epidermidis40–42,44–48,51,53,56,57,61,64; S haemolyticus46–48; S hominis46,47,53,56; S pasteuri56; S saccharolyticus48; S saprophyticus46; S schleiferi46,48; S simulans47; S warneri46,47,56Stenotrophomonas maltophilia56Streptococcus acidominimus42,44,64Streptococcus capitis51Streptococcus faecalis40,57Streptococcus gordoni56Streptococcus morbillorum44,64Streptococcus peroris46,56Streptococcus porcinus57Streptococcus australis46Viridans streptococci40,41,51,60,61,65 S anginosus group42,43,45,49,53,64; S anginosus48,56; S constellatus45,46; S intermedius45,47,56,57 S bovis group; S bovis42,48,64; S gordonii46,52,57 S mutans group; S mutans42,44–46,48,51,53,54,56,57; S sobrinus47,56,64 S mitis group; S infantis44; S mitis42,44–48,51–53,56,57,64; S pneumoniae46,53; S oralis (S mitior, S sanguis II)40,44–47,49,52,57,64 S sanguinis group; S parasanguinis46,56; S sanguinis40,42,44–47,49,50,53,56,57,64 S salivarius group57; S salivarius45–48,52,53,56,57,64; S vestibularis47,52Veillonella41,44,45,49,51,56,57,65; V alcalescens61; V dispar56; V parvula40,44,48*Dental procedures include dental extractions, restorations, dental hygiene (cleaning) procedures, toothbrushing, and other procedures.The role of duration of bacteremia as a risk factor for IE is uncertain. Older guidelines and some pediatric bacteremia studies reported positive blood cultures for only short periods (10–15 minutes) after tooth extraction(s),56,67 but the vast majority of studies did not include blood draws beyond that time frame. A study of teenagers and adults demonstrated that blood cultures can remain positive for upwards of an hour after a dental procedure,48 and a pediatric study reported that blood cultures can remain positive for >45 minutes.46 The incidence of positive blood cultures drops sharply after the procedure such that the period of risk rarely exceeds 30 minutes.A few studies report the magnitude of bacteremia in children after dental procedures,43,44,47,49,56,57 often using cell lysis filtration or centrifugation rather than conventional broth-based methods. Cell lysis methods can be problematic, being time consuming, expensive, less sensitive for some oral bacterial species, and slower in detection, and having an increased risk of contamination. Results from different studies reflect the difficulty of determining magnitude, but the collective results suggest that the magnitude from dental procedures is low. Data from a large study of adults that used broth-based methods and molecular methodology for identification suggest that the magnitude of bacteremia resulting from toothbrushing and a dental extraction, opposite ends of the spectrum of gingival invasiveness, are both relatively low at <104 colony-forming units per milliliter of blood.68The degree to which systemic antibiotic drugs reduce the incidence, duration, nature, or magnitude of bacteremia associated with dental procedures is controversial. Large, well-designed studies suggest that amoxicillin has a highly statistically significant impact on reducing the incidence and duration of bacteremia and changes the species identified after dental procedures in children.45 It is not clear whether this antibiotic elimination of bacteria takes place in the gingival crevice or the bloodstream or whether it reduces the risk for IE.Given the variability in outcomes from bacteremia studies and the mounting evidence that dental office procedures are at most a rare cause of IE, there has been a steady shift in the direction away from an emphasis on antibiotic prophylaxis and toward a focus on oral hygiene and diseases as far more impo
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