View source for Endocarditis

{{Infobox_Disease |
  Name           = {{PAGENAME}} |
  Image          = 1698.jpg |
  Caption        = Mitral valve vegetations in a patient with bacterial endocarditis. |
  DiseasesDB     = 4224 |
  ICD10          = {{ICD10|I|33||i|30}} |
  ICD9           = {{ICD9|421}} |
  ICDO           = |
  OMIM           = |
  MedlinePlus    = 001098 |
  eMedicineSubj  = emerg |
  eMedicineTopic = 164 |
  eMedicine_mult = {{eMedicine2|med|671}} {{eMedicine2|ped|2511}} |
  MeshID         = D004696 |
}}

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'''''Related Key Words and Synonyms:'''''  Infective endocarditis, IE, subacute bacterial endocarditis, acute bacterial endocarditis, fungal endocarditis, nosocomial infective endocarditis, NIE, intravenous drug abuse endocarditis, intravenous drug abuse infective endocarditis, IVDA endocarditis, IVDA IE, prosthetic valve endocarditis, PVE, pacemaker endocarditis, PM infective endocarditis, PM IE, endocardial infection, native valve endocarditis, NVE, HACEK infection, bloodstream infection, marantic endocarditis

== Overview ==

'''Endocarditis''' is an [[inflammation]] of the inner layer of the [[heart]], the [[endocardium]]. The most common structures involved are the [[heart valve]]s.

[[Endocarditis]] can be classified by etiology as either ''non-infective'' or ''infective'', depending on whether a [[microorganism]] is the source of the problem.  

Traditionally, infective endocarditis has been clinically divided into ''acute'' and ''subacute'' (because the patients tend to live longer in subacute as opposed to acute) endocarditis.  This classifies both the rate of progression and severity of disease. Thus subacute bacterial endocarditis (SBE) is often due to [[streptococci]] of low virulence and mild to moderate illness which progresses slowly over weeks and months, while acute bacterial endocarditis (ABE) is a fulminant illness over days to weeks, and is more likely due to ''[[Staphylococcus aureus]]'' which has much greater virulence, or disease-producing capacity.

This terminology is now discouraged.  The terms ''short incubation'' (meaning less than about six weeks), and ''long incubation'' (greater than about six weeks) are preferred. 

Infective endocarditis may also be classified as ''culture-positive'' or ''culture-negative''. Culture-negative endocarditis is due to micro-organisms that require a longer period of time to be identified in the laboratory. Such organisms are said to be '[[Growth medium|fastidious]]' because they have demanding growth requirements. Some pathogens responsible for culture-negative endocarditis include ''[[Aspergillus]] species'', ''[[Brucella]] species'', ''[[Coxiella burnetii]]'', ''[[Chlamydia]] species'', and [[HACEK organism|HACEK bacteria]].

Finally, the distinction between ''native-valve endocarditis'' and ''prosthetic-valve endocarditis'' is clinically important. Prosthetic-valve endocarditis constitutes 10-20% of cases of endocarditis. The greatest risk is during the first 6 months after valve surgery. [[Staphylococcus epidermidis]] is the most common cause. The infection often extends into the anulus and cardiac tissues.

Patients who inject [[narcotics]] intravenously may introduce infection which will travel to the right side of the heart. In other patients without a history of intravenous exposure, [[endocarditis]] is more frequently left-sided.

=== Non-infective endocarditis ===
Non-infective or marantic endocarditis is [[rare disease|rare]]. A form of sterile [[endocarditis]] is termed [[Libman-Sacks endocarditis]]; this form occurs more often in patients with [[lupus erythematosus]] and the [[antiphospholipid syndrome]]. Non-infective endocarditis may also occur in patients with [[cancer]], particularly mucinous [[adenocarcinoma]].

=== Infective endocarditis ===
Given the poor vascular supply of the heart valves, entrance of infection fighting components of the bloodstream (such as [[white blood cell]]s) are reduced. So if an organism (such as [[bacterium|bacteria]]) establishes a foothold in the valves, the bodies ability to fight the infection inside the valve structures is reduced.

Normally, blood flows smoothly through these valves. If they have been damaged (for instance in [[rheumatic fever]]) the trauma of non-laminar flow can increase the risk of infection.

==Historical Background of Endocarditis==

*1554: Earliest report of endocarditis in medical books
*1669: Accurately described [[tricuspid valve]] [[endocarditis]]
*1646: Described unusual "outgrowths" from autopsy of patient with endocarditis; detected murmurs by placing hand on patient's chest
*1708: Described unusual structures in entrance of aorta
*1715: Described abnormality in [[aortic|aortic valve]] and [[mitral valve]]
*1749: Described valvular lesions
*1769: Linked infectious disease and [[endocarditis]]; observed association with the spleen
*1784: Accurately drew intracardiac abnormalities
*1797: Showed relationship between rheumatism and heart disease
*1799: Described inflammatory process associated with [[endocarditis]]
*1806: Described unusual structures in heart as "vegetations," syphilitic virus as causative agent of [[endocarditis]], and theory of antiviral treatment of [[endocarditis]]
*1809: Indicated vegetations were not "outgrowths" or "buds" but particles adhering to heart wall
*1815: Elucidated inflammatory processes associated with [[endocarditis]]
*1816: Invented cylindrical stethoscope to listen to heart murmurs; dismissed link between venereal disease and [[endocarditis]]
*1832: Confirmed Laennec's observations
*1835-40: Named [[endocardium]] and [[endocarditis]]; described symptoms; prescribed herbal tea and bloodletting as treatment regimen; described link between acute [[rheumatoid arthritis]] and [[endocarditis]]
*1852: Described consequences of embolization of vegetations throughout body. Described cutaneous nodules (named "[[Osler's nodes]]" by Libman)
*1858-71: Examined fibrin vegetation associated with [[endocarditis]] by microscope; coined term "embolism;" discussed role of bacteria, vibrios, and micrococci in [[endocarditis]] 
*1861: Confirmed Virchow's theory on emboli
*1862: Described granulations or foreign elements in blood and valves, which were motile and resistant to alkalis
*1868-70: Described infected arterial blood as originating from heart; proposed scarlet fever as cause of [[endocarditis]]
*1869: Established "parasites" on skin transported to heart and attached to [[endocardium]]; named "mycosis endocardii"
*1872: Detected microorganisms in vegetations of [[endocarditis]]
*1878: All cases of [[endocarditis]] were infectious in origin
*1878: Combined experimental physiology and infection to produce animal model of [[endocarditis]] in rabbit; noted valve had to be damaged before bacteria grafted onto valve
*1878: Micrococci enter vessels that valves were fitted into; valves exposed to abnormal mechanical attacks over long period created favorable niche for bacterial colonization
*1879: Virchow's student; employed early animal model of [[endocarditis]]  
*1879: Proposed etiology of [[endocarditis]] was based on infectious model and treatment should focus on eliminating "parasitic infection"
*1880: Working with Pasteur, proposed use of routine blood cultures
*1881-86: Believed [[endocarditis]] could appear during various infections; noted translocation of respiratory pathogen from pulmonary lesion to valve through blood
*1883: Believed microorganisms were result, not cause, of endocarditis
*1884: Named disease "[[infective endocarditis]]"
*1886: Demonstrated various bacteria introduced to bloodstream could cause [[endocarditis]] on valve that had previous lesion
*1885: Synthesized work of others relating to [[endocarditis]]
*1899: Described streptococcal, staphylococcal, pneumococcal, and gonococcal endocarditis
*1903: First described "endocarditis lenta"
*1909: Credited by Osler as first to observe cutaneous nodes (named "Osler's nodes" by Libman) in patients with [[endocarditis]]
*1909: Analyzed 150 cases of [[endocarditis]] and published diagnostic criteria relating to signs and symptoms
*1910: Described initial classification scheme to include "subacute endocarditis," with clinical signs/symptoms; absolute diagnosis required blood cultures
*1981: Described Beth Israel criteria based on strict case definitions
*1994: New criteria utilizing specific echocardiographic findings
*1995: Antibiotic treatment of adults with [[infective endocarditis]] caused by streptococci, enterococci, staphylococci, and           HACEK (a) microorganisms
*1996: Modified [http://www.medcalc.com/endocarditis.html Duke Criteria] to allow serologic diagnosis of [[Coxiella burnetii]]
*1997: Guidelines for preventing bacterial [[endocarditis]]
*1997: Suggested modifications to Duke criteria for clinical diagnosis of native valve and prosthetic valve endocarditis:            analysis of 118 pathologically proven cases
*1998: Guidelines for antibiotic treatment of streptococcal, enterococcal, and staphylococcal endocarditis 
*1998: Antibiotic treatment of infective endocarditis due to viridans streptococci, enterococci, and other streptococci; recommendations for surgical treatment of endocarditis
*2000: Updated and modified [http://www.medcalc.com/endocarditis.html Duke Criteria] 
*2002: [http://www.medcalc.com/endocarditis.html Duke Criteria] to include a molecular diagnosis of causal agents
*2001-3: Described etiology of Bartonella spp., [[Tropheryma whipplei]], and [[Coxiella burnetii]] in [[endocarditis]]

== Epidemiology and Demographics ==

The incidence of IE is approximately 2-4 cases per 100,000 persons per year worldwide. This rate has not changed in the past 5-6 decades. 

IE may occur in a person of any age. The frequency is increasing in elderly individuals, with 25-50% of cases occurring in those older than 60 years of age. The occurrence of IE is 3 times more common in males than in females.

== Risk Factors ==

'''Adults and children with underlying cardiac conditions placing them at ''highest risk'' for adverse outcomes of infective endocarditis (IE) including those with:'''
*Prosthetic cardiac valve or prosthetic cardiac valve repair
*Previous infective endocarditis
*Congenital heart disease (CHD) associated with
**Unrepaired cyanotic CHD, including palliative shunts and conduits
**Completely repaired congenital heart defect with prosthetic material or device, whether placed by surgery or by catheter intervention, during the first 6 months after the procedure
**Repaired CHD with residual defects at the site or adjacent to the site of a prosthetic patch or prosthetic device (which inhibit endothelialization)
*Cardiac transplantation patients who develop cardiac valvulopathy

== Screening ==

Among those patients at high risk, careful monitoring should be undertaken to detect the early development of complications such as:

#Valvular dysfunction, usually insufficiency of the mitral or aortic valves; 
#Myocardial or septal [[abscess]]es
#[[Congestive heart failure]]
#Metastatic infection
#Embolic phenomenon

== Pathophysiology & Etiology==

As previously mentioned, altered blood flow around the valves is a risk factor for the development of endocarditis. The valves may be damaged congenitally, from [[surgery]], by [[auto-immune]] mechanisms, or simply as a consequence of old age. The damaged part of a heart valve becomes covered with a blood clot, a condition known as non-bacterial thrombotic endocarditis (NBTE).

In a healthy individual, a [[bacteremia]] (where bacteria get into the blood stream through a minor cut or wound) would normally be cleared quickly with no adverse consequences. If a heart valve is damaged and covered with [[thrombus]], these structures can provide a nidus for bacteria to attach themselves and an infection can be established.

The bacteremia is often caused by [[dentistry|dental]] procedures, such as a cleaning or [[Extraction (dental)|extraction]] of a [[tooth]]. It is important that a [[dentist]] or a [[dental hygienist]] therefore be  told of any heart problems before beginning the procedure. Prophylactic [[antibiotics]] are administered to patients with certain heart conditions as a precaution.

Another cause of [[infective endocarditis]] is a scenario in which an excess number of bacteria enter the bloodstream. [[Colorectal cancer]], serious [[urinary tract infection]]s, and [[IV drug]] use can all introduce large numbers of such bacteria. When a large burden of bacteria are introduced, a normal heart valve may be infected. A more virulent organism (such as ''[[Staphylococcus aureus]]'', but see [[#Micro-organisms_responsible|below]] for others) is often responsible for infecting a normal valve.

Infections of the [[tricuspid valve]] and less frequently the [[pulmonic valve]] tend to occur in intravenous drug users given the high pathogen burden from their introduction in the [[vein]]. The diseased valve is most commonly affected when there is a pre-existing disease. In rheumatic heart disease this is the [[aortic valve]] and the [[mitral valve]]s, on the left side of the heart.

Complications of endocarditis can occur as a result of the locally destructive effects of the infection. These complications include perforation of valve leaflets, perforation of fistula between blood vessels or cardiac chambers, abscesses and disruption of conduction system.

== Natural History and Complications==

Complications of infective endocarditis include the following:

*'''Cardiac''' 
#[[Murmur]] 
#New aortic diastolic murmur suggests dilatation of the aortic annulus or eversion, rupture, or fenestration of an aortic leaflet
#Sudden onset of loud mitral pansystolic murmur suggests rupture of chorda tendineae or fenestration of a [[mitral valve]] leaflet
#[[Congestive heart failure]] 
#[[Arrhythmias|Cardiac rhythm disturbances]] 
#Occasionally, [[pericarditis]] 

*'''Cutaneous''' 
#[[Petechiae]] of the [[conjunctiva]], [[oropharynx]], [[skin]], and legs
#Linear subungual [[splinter haemorrhage]]s of the lower or middle nail bed
#[[Oslers nodes]]
#[[Janeway lesion]]s

*'''Musculoskeletal''' 
#[[Myalgias]]
#[[Arthralgias]]
#[[Arthritis]]
#[[Low back pain]]
#[[Rheumatoid factor]] in up to 50% of patients with [[endocarditis]] for > 6 wk
#[[Clubbing|Clubbing of fingers]] in < 15% of patients

*'''Ocular'''
#[[hemorrhages|Petechial hemorrhages]], 
#[[hemorrhages|Flame-shaped hemorrhages]], 
#[[Roth's spot]]s, 
#[[exudate|Cotton-wool exudates]] in the retina

*'''Embolic'''
#Significant [[emboli|arterial emboli]] occur in 30%–50% of patients, causing the following: 
#:[[Stroke]] 
#:[[blindness|Monocular blindness]] 
#:[[abdominal pain|Acute abdominal pain]], [[ileus]], and [[melena]] 
#:[[Pain]] and [[gangrene]] in the extremities
#[[emboli|CNS emboli]] are common 
#[[emboli|Coronary emboli]], often asymptomatic, can cause [[myocardial infarction]] 
#[[Pulmonary emboli]] common in right-sided [[endocarditis]], causing pulmonary infarcts or focal [[pneumonitis]]

*'''Splenic''' 
#[[Splenomegaly]] in 15%–30% of patients 
#[[Splenic |Splenic infarcts]] in up to 40% of patients 
#[[Splenic |Splenic abscess]]es in ~ 5% of patients

*'''Renal''' 
#[[hematuria|Microscopic hematuria]] in ~ 50% of patients 
#Embolic renal infarction 
#[[membranoproliferative glomerulonephritis|Diffuse membranoproliferative glomerulonephritis]] 

*'''Mycotic aneurysms''' 
Occur in any artery in 2%–8% of patients, causing the following: 
#[[Pain]] or [[headache]] 
#Pulsatile mass 
#[[Fever]] 
#[[hematoma|Sudden expanding hematoma]] 
#Signs of major blood loss

*'''Neurologic''' 
#Neurologic complications occur in 25%–40% of cases 
#[[Stroke]]s caused by cerebral embolisms in ~ 15% of cases, causing the following: 
#:[[consciousness|Altered level of consciousness]] 
#:[[Seizures]] 
#:Fluctuating focal neurologic signs
#Cerebral aneurysms occur in 1%–5% of cases, causing the following: 
#:[[Headache]] 
#:Focal signs 
#:Acute [[intracerebral hemorrhage|intracerebral]] or [[subarachnoid hemorrhage]] caused by rupture 
#:Mild meningeal irritation resulting from slow leakage 
#[[Brain abscess]]es may occur in acute [[endocarditis]] caused by [[Staphylococcus aureus]]
#[[Seizure]]s

== Diagnosis == 

In general, a patient should fulfill the [http://www.medcalc.com/endocarditis.html Duke Criteria]<ref name=Durack>{{cite journal | author = Durack D, Lukes A, Bright D | title = New criteria for diagnosis of infective endocarditis: utilization of specific echocardiographic findings. Duke Endocarditis Service. | journal = Am J Med | volume = 96 | issue = 3 | pages = 200-9 | year = 1994 | id = PMID 8154507}}</ref> in order to establish the diagnosis of [[endocarditis]].

As the [http://www.medcalc.com/endocarditis.html Duke Criteria] relies heavily on the results of [[echocardiography]], research has addressed when to order an [[echocardiogram]] by using signs and symptoms to predict occult endocarditis among patients with intravenous drug abuse<ref name=Weisse>{{cite journal | author = Weisse A, Heller D, Schimenti R, Montgomery R, Kapila R | title = The febrile parenteral drug user: a prospective study in 121 patients. | journal = Am J Med | volume = 94 | issue = 3 | pages = 274-80 | year = 1993 | id = PMID 8452151}}</ref><ref name=Samet>{{cite journal | author = Samet J, Shevitz A, Fowle J, Singer D | title = Hospitalization decision in febrile intravenous drug users. | journal = Am J Med | volume = 89 | issue = 1 | pages = 53-7 | year = 1990 | id = PMID 2368794}}</ref><ref name=Marantz>{{cite journal | author = Marantz P, Linzer M, Feiner C, Feinstein S, Kozin A, Friedland G | title = Inability to predict diagnosis in febrile intravenous drug abusers. | journal = Ann Intern Med | volume = 106 | issue = 6 | pages = 823-8 | year = 1987 | id = PMID 3579068}}</ref> and among non drug abusing patients <ref name=Leibovici>{{cite journal | author = Leibovici L, Cohen O, Wysenbeek A | title = Occult bacterial infection in adults with unexplained fever. Validation of a diagnostic index. | journal = Arch Intern Med | volume = 150 | issue = 6 | pages = 1270-2 | year = 1990 | id = PMID 2353860}}</ref><ref name=Mellors>{{cite journal | author = Mellors J, Horwitz R, Harvey M, Horwitz S | title = A simple index to identify occult bacterial infection in adults with acute unexplained fever. | journal = Arch Intern Med | volume = 147 | issue = 4 | pages = 666-71 | year = 1987 | id = PMID 3827454}}</ref>. ''Unfortunately, this research is over 20 years old and it is possible that changes in the epidemiology of [[endocarditis]] and bacteria such as [[staphylococcus]] make the following estimates incorrectly low.''

'''Among patients who do not use illicit drugs and have a [[fever]] in the emergency room''', there is a less than 5% chance of occult endocarditis. Mellors <ref name=Mellors>.</ref> in 1987 found no cases of endocarditis nor of [[staphylococcal]] bacteremia among 135 febrile patients ''in the emergency room''. The upper [http://medinformatics.uthscsa.edu/calculator/calc.shtml confidence interval] for 0% of 135 is 5%, so for statistical reasons alone, there is up to a 5% chance of endocarditis among these patients. In contrast, Leibovici <ref name=Leibovici>.</ref> found that among 113 non-selected adults ''admitted to the hospital'' because of fever there were two cases (1.8% with 95%CI: 0% to 7%) of [[endocarditis]].

'''Among patients who do use illicit drugs and have a fever in the emergency room''', there is about a 10% to 15% prevalence of [[endocarditis]]. This estimate is not substantially changed by whether the doctor believes the patient has a trivial explanation for their fever<ref name=Marantz>.</ref>. Weisse<ref name=Weisse>.</ref> found that 13% of 121 patients had endocarditis. Marantz <ref name=Marantz>.</ref> also found a prevalence of endocarditis of 13% among such patients in the emergency room with fever. Samet <ref name=Samet>.</ref> found a 6% incidence among 283 such patients, but after excluding patients with initially apparent major illness to explain the fever (including 11 cases of manifest endocarditis), there was a 7% prevalence of endocarditis.

'''Among patients with staphylococcal bacteremia (SAB)''', one study found a 29% prevalence of [[endocarditis]] in community-acquired SAB versus 5% in nosocomial SAB<ref name=Kaech>{{cite journal | author = Kaech C, Elzi L, Sendi P, Frei R, Laifer G, Bassetti S, Fluckiger U | title = Course and outcome of Staphylococcus aureus bacteraemia: a retrospective analysis of 308 episodes in a Swiss tertiary-care centre. | journal = Clin Microbiol Infect | volume = 12 | issue = 4 | pages = 345-52 | year = 2006 | id = PMID 16524411 | doi=10.1111/j.1469-0691.2005.01359.x}}</ref>. However, only 2% of strains were resistant to [[methicillin]] and so these numbers may be low in areas of higher resistance.

===Common Causes===

Many types of organism can cause infective endocarditis. These are generally isolated by [[blood culture]], where the patient's blood is removed, and any growth is noted and identified.

Alpha-haemolytic [[Streptococcus|streptococci]], that are present in the mouth will often be the organism isolated if a dental procedure caused the bacteraemia.

If the bacteraemia was introduced through the skin, such as contamination in surgery, during catheterisation, or in an IV drug user, ''Staphylococcus aureus'' is common.

A third important cause of endocarditis is ''[[Enterococcus|Enterococci]]''. These bacteria enter the bloodstream as a consequence of abnormalities in the gastrointestinal or urinary tracts. ''[[Enterococcus|Enterococci]]'' are increasingly recognized as causes of nosocomial or hospital-acquired endocarditis. This contrasts with alpha-haemolytic streptococci and ''[[Staphylococcus aureus]]'' which are causes of community-acquired endocarditis.

Some organisms, when isolated, give valuable clues to the cause, as they tend to be specific.
*''[[Candida albicans]]'', a [[yeast]], is associated with IV drug users and the [[immunocompromised]]. Fungal endocarditis accounts for 5% of cases of native endocarditis and 10% of cases of prosthetic valve endocarditis. A diagnosis of fungal endocarditis is difficult, because many patients are afebrile with a normal white blood cell count (WBC). The fungus is often difficult to culture, and blood cultures typically negative. Fungal infections often result in large vegetations, systemic embolization, myocardial invasion, and are extremely resistant to medical therapy. Early surgical intervention is warranted because medical mortality approaches 100% Anti-fungal therapy for life is required.
*''[[Pseudomonas]]'' species, which are very resilient organisms that thrive in water, may contaminate street drugs that have been contaminated with drinking water.  [[Pseudomonas aeruginosa|P. aeruginosa]] can infect a child through foot punctures, and can cause both endocarditis and [[septic arthritis]].<ref>http://wordnet.com.au/Products/topics_in_infectious_diseases_Aug01.htm Topics in Infectious Diseases Newsletter, August 2001, Pseudomonas aeruginosa.</ref>
*''[[Streptococcus bovis]]'' and ''Clostridium septicum'', which are part of the natural flora of the bowel, are associated with [[colon cancer|colonic malignancies]]. When they present as the causative agent in endocarditis, it usually call for a concomitant [[colonoscopy]] due to worries regarding hematogenous spread of bacteria from the colon due to the neoplasm breaking down the barrier between the gut lumen and the blood vessels which drain the bowel.<ref>{{cite web|url=http://www.blackwell-synergy.com/doi/abs/10.1046/j.1445-1433.2001.02231.x?cookieSet=1&journalCode=ans|title=Clostridium septicum and malignancy |author=Simon S. B. Chew, David Z. Lubowski|date=2001|source=ANZ Journal of Surgery 71 (11), 647–649}}</ref>
*''[[HACEK organisms]]'' are a group of bacteria that live on the dental gums, and can be seen with IV drug abusers who contaminate their needles with saliva. Patients may also have a history of poor dental hygiene, or pre-existing valvular disease.<ref>{{cite web|url=http://www.emedicine.com/med/topic935.htm|title=HACEK Group Infections|author=Mirabelle Kelly, MD|date= June 7, 2005}}</ref>

==Differential Diagnosis of Risk Factors for or Causes of {{PAGENAME}}==

{|style="width:90%; height:100px" border="1"
|style="height:100px"; style="width:25%" border="1" bgcolor="LightSteelBlue" | '''Cardiovascular'''
|style="height:100px"; style="width:75%" border="1" bgcolor="Beige" | • [[Asymmetric septal hypertrophy]] • [[aortic stenosis | Calcific aortic stenosis]] • [[Cardiac catheterization]] • [[Cardiac surgery]] • [[Congenital Heart Disease]] • [[Mitral valve prolapse]] • [[Prosthetic heart valve]] • [[atrial septal defect|Septal defects]] • [[valvular heart disease|Valve disease]] • [[bacterial endocarditis|Previous bacterial endocarditis]] • [[Rheumatic Heart Disease]] • [[Sclerotherapy]] • [[Myxoma|Cardiac myxoma]]
|-
|-bgcolor="LightSteelBlue"
| '''Chemical / poisoning'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Dental'''
|bgcolor="Beige"| • [[Dental extractions]] • [[Dental implants]] • [[Root canals]] • 
|-
|-bgcolor="LightSteelBlue"
| '''Dermatologic'''
|bgcolor="Beige"| • [[Skin infection]] • 
|-
|-bgcolor="LightSteelBlue"
| '''Drug Side Effect'''
|bgcolor="Beige"| • [[IV drug|IV drug use]] • 
|-
|-bgcolor="LightSteelBlue"
| '''Ear Nose Throat'''
|bgcolor="Beige"| • [[Adenoidectomy]] • 
|- 
|-bgcolor="LightSteelBlue"
| '''Endocrine'''
|bgcolor="Beige"| No underlying causes
|- 
|-bgcolor="LightSteelBlue"
| '''Environmental'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Gastroenterologic & Genito-Uriner'''
|bgcolor="Beige"| • [[Biliary tract|Biliary tract surgery]] • [[Cystoscopy]] • [[Endoscopic retrograde cholangiopancreatography]] • Urethral dilation • [[Prostatic|Prostatic surgery]] • 
|-
|-bgcolor="LightSteelBlue"
| '''Genetic'''
|bgcolor="Beige"| • [[Marfan's syndrome|Marfan's Syndrome]] • 
|-
|-bgcolor="LightSteelBlue"
| '''Hematologic'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Iatrogenic'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Infectious Disease'''
|bgcolor="Beige"| • [[Diphtheria]] • [[Staphylococcus epidermidis]] • [[Staphylococcus aureus]] • [[Streptococcus bovis]] • [[Viridans streptococci]] • [[Group A streptococcus]] • [[Gram negative|Gram negative rods]] • [[Enterococuss]] • [[Candida]] • [[Tuberculosis]] • [[Salmonellosis]] 
|-
|-bgcolor="LightSteelBlue"
| '''Musculoskeletal / Ortho'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Neurologic'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Nutritional / Metabolic'''
|bgcolor="Beige"| No underlying causes 
|-
|-bgcolor="LightSteelBlue"
| '''Obstetrics & Gynecology'''
|bgcolor="Beige"| • [[Childbirth]] • 
|-
|-bgcolor="LightSteelBlue"
| '''Oncologic'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Opthalmologic'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Overdose / Toxicity'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Psychiatric'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Pulmonary'''
|bgcolor="Beige"| • [[Respiratory infection]] • Respiratory tract procedures • 
|-
|-bgcolor="LightSteelBlue"
| '''Renal / Electrolyte'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Rheum / Immune / Allergy'''
|bgcolor="Beige"| • [[Juvenile rheumatoid arthritis]] • [[Polymyalgia rheumatica]] • [[Acute rheumatic fever]] • [[Polyarteritis nodosa]] • [[Systemic lupus erythematosus]] • [[Antiphospholipid antibody syndrome]] • 
|-
|-bgcolor="LightSteelBlue"
| '''Trauma'''
|bgcolor="Beige"| No underlying causes
|-
|-bgcolor="LightSteelBlue"
| '''Miscellaneous'''
|bgcolor="Beige"| • Surgical systemic-pulmonary shunts and conduits • 
|-
|}

=== History and Symptoms ===

====A. Subacute Bacterial Endocarditis (SBE)==== 
*Insidious onset
*[[Fever]]
*[[Sweat]]s
*[[Weakness]]
*[[Myalgia]]s
*[[Arthralgia]]s
*[[Malaise]]
*[[Anorexia]]
*[[Fatigue]]
*[[Splenomegaly]], [[clubbing]], and [[Oslers nodes]] in long-standing SBE

====B. Acute Bacterial Endocarditis====

*Abrupt onset 
*[[Rigors]]
*[[Fever]]s as high as 102.9° to 105.1° F (39.4° to 40.6° C), often remittent

====C. Endocarditis Associated with Parenteral Drug Use==== 
#[[fever|High fever]]s, [[chills]], [[rigors]], [[malaise]], [[cough]], and [[chest pain|pleuritic chest pain]]
#[[pulmonary emboli|Septic pulmonary emboli]] causing [[sputum]] production, [[hemoptysis]], and signs suggesting [[pneumonia]]
#[[murmur|Cardiac murmurs]]
#[[Tricuspid insufficiency]]
#Metastatic infections
#Neurologic manifestations
#Peripheral emboli

====D. Prosthetic Valve Endocarditis====
#Occurs in 1%–2% of cases at 1 yr and in 4%–5% of cases at 4 yr after implantation
#Infection of perivalvular tissues
#Valvular dysfunction
#[[abscess|Myocardial abscesses]]
#[[Fever]]
#[[Petechiae]], [[Roth's spot]]s, [[Osler's nodes]], [[Janeway lesion]]s
#[[Emboli]]

=== Physical Examination ===

====Vital Signs====

A [[fever]] will likely be present. Rigors may be present.

====Skin====

*[[Petechiae]] 10 - 40%
*[[Splinter haemorrhage]] 5 - 15%
*[[Oslers nodes]] 7 - 10% (tender subcutaneous nodules in pulp of digits)
*[[Janeway lesion]] 6 - 10% (erythematous, nontender lesions on palm or sole)

==== Eyes ====
[[Image:Roth-spot (white-centered hemorrhage - endocarditis).jpg|left|150px|[[Roth's spot]]s (white centered hemorrhage)|thumb]]
*[[Conjunctival hemorrhage]]
*[[Roth's spot]]s in the [[retina]]
<br clear="left"/>

==== Ear Nose and Throat ====

In patients in whom there is new acute onset of [[aortic regurgitation]], bobbing of the [[uvula]] may be present.

==== Heart ====
*[[Murmur|Heart Murmur]]s: 80 - 85%

==== Lungs ====

Signs of [[heart failure]] may present

==== Abdomen ====

*[[Abdominal pain]] may be present due to mesenteric embolization or [[ileus]]
*[[Splenomegaly]] may be found in 15-30% patients. Left upper quadrant (LUQ) pain may be present as a result of a splenic infarct from embolization
*[[Flank pain]] may be present as a result of an embolus to the kidney

==== Extremities ====
[[Image:Osler's Lesions (Endocarditis).jpg|Osler's nodes|left|thumb]]
*[[Janeway lesion]]s (painless hemorrhagic cutaneous lesions on the palms and soles)
*[[Gangrene]] of fingers may occur
*The fingers may show [[splinter haemorrhage]]s
*[[Osler's node]]s ([[lesions|painful subcutaneous lesions in the distal fingers]])
<br clear="left"/>

==== Neurologic ====

[[Septic emboli]] may result in [[stroke]] and focal neurologic findings

[[Intracranial hemorrhage]] may occur

==== Symptoms Frequency ====

*[[Fever]] 80 - 85%, often spiking
*[[Chills]] 42 - 75%
*[[Anorexia]] 25 - 55%
*[[Malaise]] 25 - 40%
*[[Weight loss]] 25 - 35%
*[[Back pain]]
*[[Stroke]] may be present in 10 - 15% of patients as a result of cerebral embolization
*[[Chest pain]] may be present as a result of embolzation in the coronary artery. The infarcts are usually not transmural. Pulmonary emboli, often septic, occur in 75% of patients with tricuspid endocarditis
* [[Abdominal pain]] may be present due to mesenteric embolization or [[ileus]]
* [[Blindness]] may be present due to retinal embolization in 3% of patients

=== Laboratory Findings === 

An elevated [[erythrocyte sedimentation rate]] is present

A marked [[leukocytosis]] is present

A positive serum [[rheumatoid factor]] may be present (in approximately 50% of patients with subacute disease). It becomes negative after successful treatment.

The serum [[BUN]] and [[Cr]] may be elevated if [[glomerulonephritis]] is present

====Urinalysis====
[[Glomerulonephritis]] may be present

==== Electrocardiogram ====

There is no spesific [[EKG]] changes for diagnosis of [[Infective Endocarditis]]. [[EKG]] may help to detect the 10% of patients who develop a conduction delay during [[Infective Endocarditis]] by documenting an increased [[PR interval]].

==== Chest X Ray ====

There are no specific [[chest x-ray]] findings specific for the diagnosis of endocarditis. Non specific findings would include findings of [[congestive heart failure]].

==== MRI and CT ====

*A CT scan of the head should be obtained in patients who exhibit CNS symptoms or findings consistent with a mass effect (eg, macroabscess of the brain).

=== Echocardiography===
[[Image:Vegetation on aortic valve in endocarditis.jpg|left|190px|thumb]]
Echocardiography is useful for risk stratification. Although the data are inconsistent, evidence suggests that vegetation size can predict embolic complications. 

In general, transthoracic echocardiography (TTE) is adequate for diagnosis of infective endocarditis in cases where cardiac structures-of-interest are well visualized.

Specific situations where transesophageal echocardiography (TEE) is preferred over TTE include the presence of a prosthetic valvular device, suspected periannular complications, children with complex congenital cardiac lesions, patients with S. Aureus caused bacteremia and pre-existing valvular abnormalities that make TTE interpretation more difficult (e.g. calcific aortic stenosis).

The transthoracic echocardiogram has a sensitivity and specificity of approximately 65% and 95% if the echocardiographer believes there is 'probabable' or 'almost certain' evidence of endocarditis<ref name=Shively>{{cite journal | author = Shively B, Gurule F, Roldan C, Leggett J, Schiller N | title = Diagnostic value of transesophageal compared with transthoracic echocardiography in infective endocarditis. | journal = J Am Coll Cardiol | volume = 18 | issue = 2 | pages = 391-7 | year = 1991 | id = PMID 1856406}}</ref><ref name=Erbel>{{cite journal | author = Erbel R, Rohmann S, Drexler M, Mohr-Kahaly S, Gerharz C, Iversen S, Oelert H, Meyer J | title = Improved diagnostic value of echocardiography in patients with infective endocarditis by transoesophageal approach. A prospective study. | journal = Eur Heart J | volume = 9 | issue = 1 | pages = 43-53 | year = 1988 | id = PMID 3345769}}</ref>.

=== Aims of echocardiography ===
# Determine the presence, location and size of vegetations
# Assess the damage to the valve apparatus and determine the haemodynamic effects.
# The dimensions and function of the ventricles.
# Identify  any abscess formation
# Need for surgical intervention. 

=== Echocardiographic features ===
* Irregular [[echogenic mass]] attached to valve leaflet
* attachment of the vegetation is on the upstream side of the valve leaflet
* independent movement of the mass (chaotic) 
* minimum size of the vegetation identifiable on trans thoracic echocardiography is 3mm and by transoesophageal route is 2mm. 
* With treatment and time, the vegetation shrinks and can get fibrosed or calcified - may not disappear completely.
* Large vegetations occur with fungal endocarditis or staph. aureus endocarditis. 
* the haemodynamical effect is mostly due to regurgitation as a result of valve destruction.

=== Local complications ===
* Abscess
* Fistula
* Perforation
* Prosthetic dehiscence

=== When to do trans esophageal echocardiogram?  ===
* Prosthetic valve endocarditis
* Poor trans thoracic views
* continuing sepsis in spite of adequate antibiotic therapy
* new PR prolongation
* No signs of endocarditis on trans thoracic echocardiography, but high clinical suspicion.

*Video 1: 2 D Echo shows Mitral Valve Vegetation, 
<youtube v=5LogTcWG_u4/> 
*Video 2: 2 D Echo shows Aortic and Mitral Valve Vegetations
<youtube v=fyrI9RR5DZY/>
*Video 3: 2D Echo Tricuspid Valve Vegetation  
<googlevideo>-5198562295572873918&hl=en</googlevideo>
*Fungal Endocarditis 1
<googlevideo>7982129228294522803&hl=en</googlevideo>
*Fungal Endocarditis 2
<googlevideo>365208208714072490&hl=en</googlevideo>
*Fungal Endocarditis 3
<googlevideo>-4564538766847216719&hl=en</googlevideo>
*Fungal Endocarditis 4
<googlevideo>-6464177311760516420&hl=en</googlevideo>
*Fungal Endocarditis 5
<googlevideo>-6146773792630914635&hl=en</googlevideo>

==== Other Imaging Findings ====
*Various radionuclide scans using, for example, gallium Ga 67–tagged white cells and indium In 111–tagged white cells, have proven to be of little use in diagnosing IE. 

Radionuclide scans of the spleen are useful to help rule out a splenic abscess, which is a cause of bacteremia that is refractory to antibiotic therapy.

===Pathology===

====In acute phase====

* Aneurysms
* Infected thrombi or vegetations
* Valve ulcers or erosions
* Rupture of chordaes
* Endocardial jet lesions
* Flail leaflets or cusps
* Abcess formation (annular and ring) 

====In chronic phase====

* Perforations
* Nodular calcifications
* Tissue defects of valves
* Fibrosis of valves 

====Gross Pathology====
Images shown in this section are courtesy of Professor Peter G. Anderson D.V.M. PhD, and published with permission.

[http://peir.net © PEIR, University of Alabama at Birmingham, Department of Pathology]

<div align="left">
<gallery heights="175" widths="175">
Image:765.jpg|Thrombotic Nonbacterial Endocarditis: (Gross) An excellent example of thrombi on [[aortic valve]].
Image:767.jpg|Thrombotic Nonbacterial Endocarditis: (Gross) [[Mitral valve]] lesion appears that have been present for at least several days.
</gallery>
</div>


<div align="left">
<gallery heights="175" widths="175">
Image:776.jpg|Bacterial Endocarditis: (Gross) Perforated [[aortic valve]] cusp is shown.
Image:869.jpg|Thrombotic Nonbacterial Endocarditis: (Gross) [[Aortic valve]] with two small vegetations.
</gallery>
</div>


<div align="left">
<gallery heights="175" widths="175">
Image:872.jpg|Thrombotic Nonbacterial Endocarditis: (Gross) [[Mitral valve]] thrombi in chorda.
Image:1423.jpg|(Gross) A very good example of focal necrotizing lesions in distal portion of digit associated with bacterial endocarditis
</gallery>
</div>


<div align="left">
<gallery heights="175" widths="175">
Image:1438.jpg|Bacterial Endocarditis: (Gross) A lesion on non-coronary cusp of [[aortic valve]].
Image:1648.jpg|Bacterial Endocarditis: (Gross) An excellent view of [[mitral valve|mitral]] scarring due to [[rheumatic fever]] healing infectious lesion.
</gallery>
</div>


<div align="left">
<gallery heights="175" widths="175">
Image:1662.jpg|Bacterial Endocarditis: (Gross) [[Aortic valve]] prosthesis ring infection extending into left atrium.
Image:1698.jpg|Bacterial Endocarditis: (Gross) An excellent close-up view of [[mitral valve]] vegetations
</gallery>
</div>


<div align="left">
<gallery heights="175" widths="175">
Image:1701.jpg|Bacterial Endocarditis: (Gross) vegetations on [[mitral valve]] and left atrial endocardium due to [[actinomycosis]]
Image:1702.jpg|Bacterial Endocarditis: (Gross) An excellent image of vegetation on [[aortic valve]]
</gallery>
</div>


<div align="left">
<gallery heights="175" widths="175">
Image:1706.jpg|Bacterial Endocarditis: (Gross) An excellent image of vegetations on [[mitral valve]] evidence of rheumatic scarring
Image:1845.jpg|Thrombotic Nonbacterial Endocarditis: (Gross) [[Mitral valve]], an excellent example
</gallery>
</div>


<div align="left">
<gallery heights="175" widths="175">
Image:1911.jpg|Thrombotic Nonbacterial Endocarditis: (Gross) [[Mitral valve]]: an excellent image, identical to acute rheumatic lesion
Image:2030.jpg|Verrucous Nonbacterial Endocarditis: (Gross) An excellent example of an infant heart 
</gallery>
</div>


<div align="left">
<gallery heights="175" widths="175">
Image:2225.jpg|Purpura of cerebrum, cerebellum and brain stem in 36 years old female with [[Cushing syndrome]] and bacterial endocarditis caused by [[Staphylococcus aureus]]
Image:3181.jpg|Spleen infarct: (Gross) A typical small infarct with necrotic central portion (originated from infected marantic endocarditis on [[aortic valve|aortic]] and [[mitral valve]]s)
</gallery>
</div>


<div align="left">
<gallery heights="175" widths="175">
Image:3183.jpg|Kidney infarct: (Gross) A natural color close-up and excellent image of yellow infarct marantic endocarditis on [[aortic valve|aortic]] and [[mitral valve]]s
Image:3802.jpg|Thrombotic Nonbacterial Endocarditis Infected: (Gross) Natural color of [[pulmonary valve]]. An excellent example of patient with [[multiple myeloma]]
</gallery>
</div>


<div align="left">
<gallery heights="175" widths="175">
Image:9960.jpg|Thrombotic Non Bacterial Endocarditis: (Gross) Natural color of [[pulmonary valve]].
Image:9961.jpg|Thrombotic Non Bacterial Endocarditis: (Gross) Natural color and good example of [[tricuspid valve]] lesions
</gallery>
</div>


<div align="left">
<gallery heights="175" widths="175">
Image:203196.jpg|[[Disseminated intravascular coagulation]] in endocarditis; [[tricuspid valve]] showing NBTE in [[DIC]]
Image:249017.jpg|Eye: Bacterial Endocarditis complicated as [[petechiae]]. Septic emboli to [[conjunctiva]]
</gallery>
</div>

<br>

===Bacterial Endocarditis===

<youtube v=fH5DggA3q1w/>

==Differential Diagnosis==

* [[Antiphospholipid syndrome]]
* [[Reactive arthritis]]
* [[Atrial myxoma]]
* [[Systemic lupus erythematosus]]
* [[Primary cardiac neoplasms]]
* [[Lyme disease]]
* [[Polymyalgia rheumatica]]
* [[Thrombotic nonbacterial endocarditis]]
* [[Vasculitis]]
* [[Temporal arteritis]]

== Treatment ==

High dose [[antibiotic]]s are administered by the intravenous route to maximize diffusion of antibiotic molecules into vegetation(s) from the blood filling the chambers of the heart. This is necessary because neither the heart valves nor the vegetations adherent to them are supplied by blood vessels. Antibiotics are continued for a long time, typically two to six weeks. Specific drug regimens differ depending on the classification of the endocarditis as acute or subacute (acute necessitating treating for [[Staphylococcus aureus]] with [[oxacillin]] or [[vancomycin]] in addition to [[gram-negative]] coverage). [[Fungal]] [[endocarditis]] requires specific anti-fungal treatment, such as [[amphotericin B]].<ref name= Baddour>{{cite journal | author = Baddour Larry M., Wilson Walter R., Bayer Arnold S., Fowler Vance G. Jr, Bolger Ann F.,  Levison Matthew E.,  Ferrieri Patricia, Gerber Michael A., Tani Lloyd Y., Gewitz Michael H., Tong David C., Steckelberg James M., Baltimore Robert S., Shulman Stanford T., Burns Jane C., Falace Donald A., Newburger Jane W., Pallasch Thomas J., Takahashi Masato,  Taubert Kathryn A.| title = 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-Executive Summary: Endorsed by the Infectious Diseases Society of America. | journal = Circulation | volume = 111 | issue = 23 | pages = 3167-84 | year = 2005 | id = PMID 15956145 }}</ref>

Surgical removal of the valve is necessary in patients who fail to clear micro-organisms from their blood in response to antibiotic therapy, or in patients who develop cardiac failure resulting from destruction of a valve by infection. A removed valve is usually replaced with an artificial valve which may either be mechanical (metallic) or obtained from an animal such as a pig; the latter are termed bioprosthetic valves.<ref name= Baddour>{{cite journal | author = Baddour Larry M., Wilson Walter R., Bayer Arnold S., Fowler Vance G. Jr, Bolger Ann F.,  Levison Matthew E.,  Ferrieri Patricia, Gerber Michael A., Tani Lloyd Y., Gewitz Michael H., Tong David C., Steckelberg James M., Baltimore Robert S., Shulman Stanford T., Burns Jane C., Falace Donald A., Newburger Jane W., Pallasch Thomas J., Takahashi Masato,  Taubert Kathryn A.| title = 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-Executive Summary: Endorsed by the Infectious Diseases Society of America. | journal = Circulation | volume = 111 | issue = 23 | pages = 3167-84 | year = 2005 | id = PMID 15956145 }}</ref>

[[Infective endocarditis]] is associated with a 10-25% mortality.

=== Pharmacotherapy ===

Effective treatment requires identification of the etiologic agent and determination of its antimicrobial susceptibility.

Antibiotic therapy for subacute or indolent disease can be delayed until results of blood cultures are known; in fulminant infection or valvular dysfunction requiring urgent surgical intervention, begin empirical antibiotic therapy promptly after blood cultures have been obtained.

For prosthetic valve [[endocarditis]], treatment should be continued for 6–8 weeks.

==== Acute Pharmacotherapies ====

=====Penicillin-Susceptible Viridans and Other Nonenterococcal Streptococci<ref name= Baddour>{{cite journal | author = Baddour Larry M., Wilson Walter R., Bayer Arnold S., Fowler Vance G. Jr, Bolger Ann F.,  Levison Matthew E.,  Ferrieri Patricia, Gerber Michael A., Tani Lloyd Y., Gewitz Michael H., Tong David C., Steckelberg James M., Baltimore Robert S., Shulman Stanford T., Burns Jane C., Falace Donald A., Newburger Jane W., Pallasch Thomas J., Takahashi Masato,  Taubert Kathryn A.| title = 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-Executive Summary: Endorsed by the Infectious Diseases Society of America. | journal = Circulation | volume = 111 | issue = 23 | pages = 3167-84 | year = 2005 | id = PMID 15956145 }}</ref>===== 

The minimum inhibitory concentration [MIC] <0.2 µg/ml

*[[Penicillin]] G: preferred regimen 

'''Dose''': 12–18 million units I.V. daily in divided doses q. 4 hour for 4 weeks

*[[Penicillin]] G + [[gentamicin]] or [[ceftriaxone]]: preferred regimen 

'''Dose''': [[penicillin]] G, 12–18 million units I.V. daily in divided doses q. 4 hour for 4 weeks; [[gentamicin]], 3 mg/kg I.M. or I.V. daily in divided doses q. 8 hour for 2 weeks (peak serum concentration should be ~ 3 µg/ml and trough concentrations < 1 µg/ml); [[ceftriaxone]], 2 g I.V. daily as a single dose for 2 weeks

*[[Vancomycin]]: for patients with history of [[penicillin]] [[hypersensitivity]] 

'''Dose''': 30 mg/kg I.V. daily in divided doses q. 12 hour for 4 weeks

=====Relatively Penicillin-Resistant Streptococci<ref name= Baddour>{{cite journal | author = Baddour Larry M., Wilson Walter R., Bayer Arnold S., Fowler Vance G. Jr, Bolger Ann F.,  Levison Matthew E.,  Ferrieri Patricia, Gerber Michael A., Tani Lloyd Y., Gewitz Michael H., Tong David C., Steckelberg James M., Baltimore Robert S., Shulman Stanford T., Burns Jane C., Falace Donald A., Newburger Jane W., Pallasch Thomas J., Takahashi Masato,  Taubert Kathryn A.| title = 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-Executive Summary: Endorsed by the Infectious Diseases Society of America. | journal = Circulation | volume = 111 | issue = 23 | pages = 3167-84 | year = 2005 | id = PMID 15956145 }}</ref>=====

A- MIC 0.2–0.5 µg/ml 

*[[Penicillin]] G + gentamicin: preferred regimen 

'''Dose''': [[penicillin]] G, 20–30 million units I.V. daily in divided doses q. 4 hour for 4 weeks; [[gentamicin]], 3 mg/kg I.M. or I.V. daily in divided doses q. 8 hr for 2 wk (peak serum concentration should be ~ 3 µg/ml and trough concentrations < 1 µg/ml)

B- MIC > 0.5 µg/ml 

*[[Penicillin]] G + [[gentamicin]]: preferred regimen 

'''Dose''': [[penicillin]] G, 20–30 million units I.V. daily in divided doses q. 4 hour for 4 week; [[gentamicin]], 3 mg/kg I.M. or I.V. daily in divided doses q. 8 hour for 4 week (peak serum concentration should be ~ 3 µg/ml and trough concentrations < 1 µg/ml) 

*[[Vancomycin]]: regimen for patients with history of [[penicillin]] [[hypersensitivity]] 

'''Dose''': 30 mg/kg I.V. daily in divided doses q. 12 hour for 4 weeks 

=====Enterococci<ref name= Baddour>{{cite journal | author = Baddour Larry M., Wilson Walter R., Bayer Arnold S., Fowler Vance G. Jr, Bolger Ann F.,  Levison Matthew E.,  Ferrieri Patricia, Gerber Michael A., Tani Lloyd Y., Gewitz Michael H., Tong David C., Steckelberg James M., Baltimore Robert S., Shulman Stanford T., Burns Jane C., Falace Donald A., Newburger Jane W., Pallasch Thomas J., Takahashi Masato,  Taubert Kathryn A.| title = 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-Executive Summary: Endorsed by the Infectious Diseases Society of America. | journal = Circulation | volume = 111 | issue = 23 | pages = 3167-84 | year = 2005 | id = PMID 15956145 }}</ref>=====

*[[Penicillin]] G + [[gentamicin]]: preferred regimen 

'''Dose''': [[penicillin]] G, 20–30 million units I.V. daily in divided doses q. 4 hr for 4–6 weeks; [[gentamicin]], 3 mg/kg I.M. or I.V. daily in divided doses q. 8 hour for 4–6 weeks (peak serum concentration should be ~ 3 µg/ml and trough concentrations < 1 µg/ml) 

*[[Ampicillin]] + [[gentamicin]] 

'''Dose''': ampicillin, 12 g I.V. daily in divided doses q. 4 hour for 4–6 weeks; [[gentamicin]], dose as above

*[[Vancomycin]] + [[gentamicin]]: regimen for patients with history of [[penicillin]] [[hypersensitivity]] 

'''Dose''': [[vancomycin]], 30 mg/kg I.V. daily in divided doses q. 12 hour for 4–6 weeks; [[gentamicin]], dose as above

=====Staphylococci (Methicillin Susceptible) in the Absence of Prosthetic Material<ref name= Baddour>{{cite journal | author = Baddour Larry M., Wilson Walter R., Bayer Arnold S., Fowler Vance G. Jr, Bolger Ann F.,  Levison Matthew E.,  Ferrieri Patricia, Gerber Michael A., Tani Lloyd Y., Gewitz Michael H., Tong David C., Steckelberg James M., Baltimore Robert S., Shulman Stanford T., Burns Jane C., Falace Donald A., Newburger Jane W., Pallasch Thomas J., Takahashi Masato,  Taubert Kathryn A.| title = 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-Executive Summary: Endorsed by the Infectious Diseases Society of America. | journal = Circulation | volume = 111 | issue = 23 | pages = 3167-84 | year = 2005 | id = PMID 15956145 }}</ref>=====

*[[Nafcillin]] or [[oxacillin]] + [[gentamicin]] (optional): preferred regimen 

'''Dose''': [[nafcillin]] or [[oxacillin]], 12 g I.V. daily in divided doses q. 4 hour for 4–6 weeks; [[gentamicin]], 3 mg/kg I.M. or I.V. daily in divided doses q. 8 hr for 3–5 days (peak serum concentration should be ~ 3 µg/ml and trough concentrations <1 µg/ml) 

*[[Cefazolin]] + [[gentamicin]] (optional): alternative regimen for patients with history of [[penicillin]] [[hypersensitivity]] 

'''Dose''': [[cefazolin]], 12 g I.V. daily in divided doses q. 4 hour for 4–6 weeks; [[gentamicin]], dose as above 

*[[Vancomycin]]: alternative regimen for patients with history of [[penicillin]] [[hypersensitivity]] 

'''Dose''': 30 mg/kg I.V. daily in divided doses q. 12 hr for 4–6 weeks

=====Staphylococci (Methicillin Resistant) in the Absence of Prosthetic Material<ref name= Baddour>{{cite journal | author = Baddour Larry M., Wilson Walter R., Bayer Arnold S., Fowler Vance G. Jr, Bolger Ann F.,  Levison Matthew E.,  Ferrieri Patricia, Gerber Michael A., Tani Lloyd Y., Gewitz Michael H., Tong David C., Steckelberg James M., Baltimore Robert S., Shulman Stanford T., Burns Jane C., Falace Donald A., Newburger Jane W., Pallasch Thomas J., Takahashi Masato,  Taubert Kathryn A.| title = 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-Executive Summary: Endorsed by the Infectious Diseases Society of America. | journal = Circulation | volume = 111 | issue = 23 | pages = 3167-84 | year = 2005 | id = PMID 15956145 }}</ref>=====

*[[Vancomycin]]

'''Dose''': 30 mg/kg I.V. daily in divided doses q. 12 hour for 4–6 weeks

=====Staphylococci (Methicillin Susceptible) in the Presence of Prosthetic Material<ref name= Baddour>{{cite journal | author = Baddour Larry M., Wilson Walter R., Bayer Arnold S., Fowler Vance G. Jr, Bolger Ann F.,  Levison Matthew E.,  Ferrieri Patricia, Gerber Michael A., Tani Lloyd Y., Gewitz Michael H., Tong David C., Steckelberg James M., Baltimore Robert S., Shulman Stanford T., Burns Jane C., Falace Donald A., Newburger Jane W., Pallasch Thomas J., Takahashi Masato,  Taubert Kathryn A.| title = 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-Executive Summary: Endorsed by the Infectious Diseases Society of America. | journal = Circulation | volume = 111 | issue = 23 | pages = 3167-84 | year = 2005 | id = PMID 15956145 }}</ref>=====

*[[Nafcillin]] or [[oxacillin]] + [[rifampin]] + [[gentamicin]]
 
'''Dose''': [[nafcillin]] or [[oxacillin]], 12 g I.V. daily in divided doses q. 4 hour for 6–8 weeks; rifampin, 300 mg p.o., q. 8 hour for 6–8 weeks; [[gentamicin]] (administer during the initial 2 weeks), 3 mg/kg I.M. or I.V. daily in divided doses q. 8 hour for 2 weeks

=====Staphylococci (Methicillin Resistant) in the Presence of Prosthetic Material<ref name= Baddour>{{cite journal | author = Baddour Larry M., Wilson Walter R., Bayer Arnold S., Fowler Vance G. Jr, Bolger Ann F.,  Levison Matthew E.,  Ferrieri Patricia, Gerber Michael A., Tani Lloyd Y., Gewitz Michael H., Tong David C., Steckelberg James M., Baltimore Robert S., Shulman Stanford T., Burns Jane C., Falace Donald A., Newburger Jane W., Pallasch Thomas J., Takahashi Masato,  Taubert Kathryn A.| title = 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-Executive Summary: Endorsed by the Infectious Diseases Society of America. | journal = Circulation | volume = 111 | issue = 23 | pages = 3167-84 | year = 2005 | id = PMID 15956145 }}</ref>=====

*[[Vancomycin]] + [[rifampin]] + [[gentamicin]] 

'''Dose''': [[vancomycin]], 30 mg/kg I.V. daily in divided doses q. 12 hour for 6–8 weeks; [[rifampin]], 300 mg p.o., q. 8 hour for 6–8 weeks; [[gentamicin]] (administer during the initial 2 weeks), 3 mg/kg I.M. or I.V. daily in divided doses q. 8 hour for 2 weeks

=====[[HACEK organism|HACEK Organisms]]<ref name= Baddour>{{cite journal | author = Baddour Larry M., Wilson Walter R., Bayer Arnold S., Fowler Vance G. Jr, Bolger Ann F.,  Levison Matthew E.,  Ferrieri Patricia, Gerber Michael A., Tani Lloyd Y., Gewitz Michael H., Tong David C., Steckelberg James M., Baltimore Robert S., Shulman Stanford T., Burns Jane C., Falace Donald A., Newburger Jane W., Pallasch Thomas J., Takahashi Masato,  Taubert Kathryn A.| title = 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-Executive Summary: Endorsed by the Infectious Diseases Society of America. | journal = Circulation | volume = 111 | issue = 23 | pages = 3167-84 | year = 2005 | id = PMID 15956145 }}</ref>=====

*[[Ceftriaxone]] or another [[cephalosporin|third-generation cephalosporin]] 

'''Dose''': 2 g I.V. daily as a single dose for 4 weeks

==== Antithrombotic Therapy<ref name= Baddour>{{cite journal | author = Baddour Larry M., Wilson Walter R., Bayer Arnold S., Fowler Vance G. Jr, Bolger Ann F.,  Levison Matthew E.,  Ferrieri Patricia, Gerber Michael A., Tani Lloyd Y., Gewitz Michael H., Tong David C., Steckelberg James M., Baltimore Robert S., Shulman Stanford T., Burns Jane C., Falace Donald A., Newburger Jane W., Pallasch Thomas J., Takahashi Masato,  Taubert Kathryn A.| title = 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-Executive Summary: Endorsed by the Infectious Diseases Society of America. | journal = Circulation | volume = 111 | issue = 23 | pages = 3167-84 | year = 2005 | id = PMID 15956145 }}</ref>====

* [[Anticoagulant]]s can cause or worsen hemorrhage in patients with [[endocarditis]] but may be carefully administered when needed
* [[Prothrombin time]] should be carefully maintained at INR of 2.0–3.0
* Anticoagulation should be reversed immediately in the event of CNS complications and interrupted for 1–2 wk after acute embolic stroke
* Avoid [[heparin]] administration during active [[endocarditis]] if possible

==== Chronic Pharmacotherapies <ref name= Baddour>{{cite journal | author = Baddour Larry M., Wilson Walter R., Bayer Arnold S., Fowler Vance G. Jr, Bolger Ann F.,  Levison Matthew E.,  Ferrieri Patricia, Gerber Michael A., Tani Lloyd Y., Gewitz Michael H., Tong David C., Steckelberg James M., Baltimore Robert S., Shulman Stanford T., Burns Jane C., Falace Donald A., Newburger Jane W., Pallasch Thomas J., Takahashi Masato,  Taubert Kathryn A.| title = 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-Executive Summary: Endorsed by the Infectious Diseases Society of America. | journal = Circulation | volume = 111 | issue = 23 | pages = 3167-84 | year = 2005 | id = PMID 15956145 }}</ref>====

=== Surgery and Device Based Therapy === 

==== Indications for Surgery ====

Indications for surgical debridement of vegetations and infected perivalvular tissue, with valve replacement or repair as needed are listed below:<ref name= Baddour>{{cite journal | author = Baddour Larry M., Wilson Walter R., Bayer Arnold S., Fowler Vance G. Jr, Bolger Ann F.,  Levison Matthew E.,  Ferrieri Patricia, Gerber Michael A., Tani Lloyd Y., Gewitz Michael H., Tong David C., Steckelberg James M., Baltimore Robert S., Shulman Stanford T., Burns Jane C., Falace Donald A., Newburger Jane W., Pallasch Thomas J., Takahashi Masato,  Taubert Kathryn A.| title = 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-Executive Summary: Endorsed by the Infectious Diseases Society of America. | journal = Circulation | volume = 111 | issue = 23 | pages = 3167-84 | year = 2005 | id = PMID 15956145 }}</ref>

#Moderate to severe [[congestive heart failure]] due to valve dysfunction
#Unstable valve prosthesis
#Uncontrolled infection for > 1–3 week despite maximal antimicrobial therapy
#Persistent bacteremia
#[[endocarditis|Fungal endocarditis]]
#Relapse after optimal therapy (prosthesis)
#Vegetation in Situ
#Prosthetic valve [[endocarditis]] with perivalvular invasion
#[[Endocarditis]] caused by [[Pseudomonas aeruginosa]] or other gram-negative bacilli that has not responded after 7–10 days of maximal antimicrobial therapy
#Perivalvular extension of infection and abscess formation
#Staphylococcal infection of prosthesis
#Persistent fever (culture negative)
#Large vegetation (>10 mm = increased embolism)
#Relapse after optimal therapy (native valve)
#Vegetations that obstruct the valve orifice

====Principles of Surgical Management====
#Excise all infected valve tissue
#Drain and debride abscess cavities
#Repair or replace damaged valves
#Repair associated pathology such as septal defect, fistulas <ref name= Baddour>{{cite journal | author = Baddour Larry M., Wilson Walter R., Bayer Arnold S., Fowler Vance G. Jr, Bolger Ann F.,  Levison Matthew E.,  Ferrieri Patricia, Gerber Michael A., Tani Lloyd Y., Gewitz Michael H., Tong David C., Steckelberg James M., Baltimore Robert S., Shulman Stanford T., Burns Jane C., Falace Donald A., Newburger Jane W., Pallasch Thomas J., Takahashi Masato,  Taubert Kathryn A.| title = 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-Executive Summary: Endorsed by the Infectious Diseases Society of America. | journal = Circulation | volume = 111 | issue = 23 | pages = 3167-84 | year = 2005 | id = PMID 15956145 }}</ref>

=====Aortic Valve - Surgical Options=====
If the infection limited is limited to the leaflets, then replace the aortic valve.

If the infection extends to anulus or beyond, then debride the infected tissues, drain any abscesses to the pericardial sac and replace the aortic root.

=====Atrioventricular Valve - Surgical Options=====
If the infection is limited to the leaflets, then perform a vegectomy, repair perforations, and perform a reduction annuloplasty

If the infection extends to the anulus or beyond, then perform valve replacement, debride and abliterate abscesses. In some cases the tricuspid valve may be excised, but 20-30% of patients will develop [[congestive heart failure]].

====Surgical Outcomes====
Operative mortality is 15 - 20%. The development of an infection of a prosthetic valve during operation for [[endocarditis|native valve endocarditis]] is 4%, it is higher (12 - 16%) if active [[endocarditis]] is present at the time of the surgery. Late survival at 5 years for [[endocarditis|native valve endocarditis]] is 70 - 80% and for [[endocarditis|prosthetic valve endocarditis]] is 50 - 80%.<ref name= Baddour>{{cite journal | author = Baddour Larry M., Wilson Walter R., Bayer Arnold S., Fowler Vance G. Jr, Bolger Ann F.,  Levison Matthew E.,  Ferrieri Patricia, Gerber Michael A., Tani Lloyd Y., Gewitz Michael H., Tong David C., Steckelberg James M., Baltimore Robert S., Shulman Stanford T., Burns Jane C., Falace Donald A., Newburger Jane W., Pallasch Thomas J., Takahashi Masato,  Taubert Kathryn A.| title = 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-Executive Summary: Endorsed by the Infectious Diseases Society of America. | journal = Circulation | volume = 111 | issue = 23 | pages = 3167-84 | year = 2005 | id = PMID 15956145 }}</ref>

===Antibiotic Prophylaxis with Dental Procedures===
{{MWT}}

====Background====
*Endodontic procedures have been associated with a high incidence of bacteremia since the 1920s. Therefore, dental procedures were implicated as an independent risk factor for the development of bacterial endocarditis.
** However, only 4%-7.5% of all bacterial endocarditis cases are related to endodontic associated bacteremia.<ref>Gendron R, Grenier D, Maheu-Robert L. The oral cavity as a reservoir of bacterial pathogens for focal infections. Microbes Infect. 2000;2:897-906.  </ref>
;'''AHA Guidelines'''
In 1955, the American Heart Association (AHA) published the first of ten subsequent IE prevention guidelines. 
Most recent, 2007 guidelines underwent changes intended to clarify patient eligibility criteria for receiving IE prophylaxis.
*Major changes include, the consideration that frequent exposures to bacteremias associated with daily activities are considered more likely to induce IE then are endodontic-procedural induced bacteremias. 
#Optimal oral hygiene is emphasized as an important practice for IE prevention. 
#A patient’s lifetime acquisition risk of IE is no longer a consideration for initiating prophylactic antibiotic therapy. 
#The AHA now recommends the administration of single-dose prophylactic antibiotics prior to endodontic procedure only to patients with cardiac conditions associated with the highest risk of adverse outcomes following the acquisition of bacterial endocarditis.
<blockquote>'''2007 AHA Guideline Recommendation for Which patients require Antiobiotic Prophylaxis Prior to Dental Procedure are those with documented'''</blockquote>
#Prosthetic cardiac valve.
#Previous IE
#Cardiac transplantation recipients who develop cardiac valvulopathy.
#Congential heart disease:
#*Unrepaired cyanotic CHD: shunts and conduits
#*Completely repaired congential heart defect during 1st 6months following procedure.
#*Repaired CHD with residual defects at site of prostetic patch or device.

====Endodontic Procedures and Endocarditis risk====
*Following dental intervention, the absolute risk for developing IE is estimated at 1 case per 14 million dental procedures.<ref>Pallasch TJ. Antibiotic prophylaxis: problems in paradise. Dent Clin
North Am. 2003;47:665-679.
</ref>
*IE acquisition risk estimates following an endodontic induced bacteremia in patients with congenital heart disease are 1 per 475,000; rheumatic heart disease, 1 per 142,000; prosthetic heart valve, 1 per 114,000; and previous IE, 1 per 95,000 dental procedures.<ref>Pallasch TJ, Wahl MJ. Focal infection: new age or ancient history?
Endodontic Topics. 2003;4:32-45.
</ref>
*Inocula of 1 x 108 (100 million) colony forming units [cfu]/mL or greater are required to consistently induce experimental endocarditis.
**Recent human quantitative blood culture data support the implication that endodontic associated bacteremia inocula are of insufficient magnitude to induce endocarditis. Bacteremia intensities immediately following invasive human dental procedures are 1.5 cfu/ml-5.9 cfu/ml 10 fold less then necessary to induce IE in the animal model.<ref>Roberts GJ. Dentists are innocent! Everyday" bacteremia is the real culprit: A review and assessment of the evidence that dental surgical procedures are a principal cause of bacterial endocarditis in children. Pediatric Cardiology. 1999;20:317.</ref>

*The most recent case-control study of 104 patients with known, high-risk structural heart disease discovered that patients who developed IE were actually less likely to have experienced an endodontic procedure within the 180 days prior to diagnosis than did control patients who did not develop IE (OR 0.2 [95% CI 0.04-0.7]).<ref>Strom BL, Abrutyn E, Berlin JA, Kinman JL, Feldman RS, Stolley PD, et al. Dental and cardiac risk factors for infective endocarditis: A population-based, case-control study. Ann Int Med. 1998;129:761-769.</ref>

*Among high-risk patients with underlying structural heart disease, kidney disease (OR 16.9 [95% CI 1.5-193.0]), diabetes (OR 2.7 [95% CI 1.4-5.2]) and skin flora infection (OR 3.5 [95% CI 0.7-17.0]) were associated with a greater risk for the development of bacterial endocarditis.<ref>Strom BL, Abrutyn E, Berlin JA, Kinman JL, Feldman RS, Stolley PD, et al. Risk factors for infective endocarditis: oral hygiene and nondental exposures. Circulation. 2000;102:2842.</ref>
*Daily activities such as chewing and oral hygiene practices result in bacteremias more frequently, of longer duration and of greater magnitude in comparison to high-risk endodontic procedures.
'''These findings have led the AHA to conclude that the cumulative background bacteremia associated with chewing, daily dental hygiene practices, kidney disease, diabetes, and skin colonization present a greater risk of significant bacteremia than any single invasive dental procedure.'''

====Prophylactic Antibiotic Efficacy====
*The efficacy of antibiotic regimens for IE prophylaxis has never been assessed under the scrutiny of a randomized controlled trial. 
*Evidence supporting pre-endodontic chemoprophylaxis efficacy is extrapolated from data demonstrating reductions in bacteremia magnitudes immediately following the administration of antibiotics.

'''Antibiotic prophylaxis is reasonable for patients with the conditions who undergo any dental procedure that involves the gingival tissues or periapical region of a tooth and for those procedures that perforate the oral mucosa. Although Infective Endocarditis prophylaxis is reasonable for these patients, its effectiveness is unknown.'''

=====Efficacy Assesment=====
The '''Cochran Collaboration''' assessed whether prophylactic administration of penicillin to moderate- to high-risk patients prior to endodontic intervention conferred a mortality, serious illness or endocarditis incidence benefit.<ref>Oliver R, Roberts GJ, Hooper L. Penicillins for the prophylaxis of bacterial endocarditis in dentistry. Cochrane Database of Systematic Reviews 2004, Issue 2.</ref>
*The pooled, adjusted Odds Ratio across all studies for the development of IE among patients receiving prophylaxis was non-significant (0.56 [95% CI (0.15-2.15)]). 
'''The Cochrane Collaboration concluded; it is unclear whether antibiotic prophylaxis is effective and there is a lack of evidence to support published guidelines using penicillin as chemoprophylaxis for IE.'''

'''' To date, only 4 case-control studies has assessed antibiotic efficacy for IE prevention.''''
#Strom et al discovered the administration pre-endodontic procedural antibiotics did not provide a protective benefit against the development of IE (OR 0.5 [CI .01-9.6]).
#Van Der Meer et al,<ref>Van der Meer JT, Thompson J, Valkenburg HA, Michel MF. Epidemiology of bacterial endocarditis in The Netherlands II. Antecedent procedures and use of prophylaxis. Arch Intern Med. 1992;152:1869-1873.</ref>8/48 case pts (16%) received antibiotics.26/200 control pts (13%) received antibiotics.Stratified Odds Ratio: 0.51 (0.11-2.29).Protective Efficacy 49%.
#Lacassin et al<ref>Lacassin F, Hoen B, Leport C, Selton-Suty C, Delahaye F, Goulet V, et al. Procedures associated with infective endocarditis in adults - A case control study. Eur Heart J. 1995;16:1968-1974.</ref>6/37 case pts (23%) received antibiotics.6/33 control pts (27%) received antibiotics.Matched and Adjusted Odds Ratio: 0.2 (0-0.8) Protective Efficacy 20%.
#Imperiale et al<ref>Imperiale TF, Horwitz RI. Does prophylaxis prevent post-dental infective endocarditis? A controlled evaluation of protective efficacy. Am J Med. 1990;88:131-136.</ref>
1/8 case pts (13%) received antibiotics.15/24 control pts (63%) received antibiotics.
Matched Odds Ratio: .09 (CI upper limit of 0.93) (p=.025)Protective Efficacy 91%.


====Safety Concerns with Antibiotic Prophylaxis====
''Adverse reactions associated with the administration of beta-lactam antibiotics are common.''
*Ranging in severity from purititus to fatal anaphylactic shock, the frequency of all adverse reactions from the administration of penicillin to the general population is 0.7% to 10%.<ref>Idsoe O, Guthe T, Willcox RR, De Weck A. Nature and extent of penicillin side-reactions, with particular reference to fatalities from anaphylactic shock. Bull World Health Organ. 1968;38:159-188.</ref> 
*Fatal anaphylaxis among patients receiving single-dose penicillin, ampillicin or amoxicillin therapy is approximately 20 cases per 1 million patients treated.<ref>The International Collaborative Study of Severe Anaphylaxis. Risk of anaphylaxis in a hospital population in relation to the use of various drugs: an international study. Pharmacoepidemiology and drug safety. 2003;12:195-202.</ref> 
*Single-dose, cephalosporin-associated fatal anaphylaxis risk is estimated at 0.5-5.7 cases per 10 million patients treated.<ref>Kelkar P,James T. Current concepts: cephalosporin allergy. N Engl J Med. 2001;345:804-9.</ref> 
*Macrolide and clindamycin single-dose fatal anaphylaxis risk is estimated at 0-5 cases per 1 million patients treated.<ref>Mazur N, Greenberger P, Regalado J. Clindamycin hypersensitivity
appears to be rare. Ann Allergy Asthma Immunol. 1999;82:443–5.
</ref>
'''With the highest associated mortality rate of all the recommended antibiotic regimens, the risk of anaphylaxis with the initiation of beta-lactam IE prophylactic therapy must be considered.'''

#The risk of mortality associated with the single-dose administration of beta-lactam antibiotics for IE prophylaxis is estimated at 1-3 anaphylactic deaths per 1 million patients treated.
#According to the AHA, single dose administration of a beta-lactam antibiotic for IE prophylactic therapy is a safe practice as it has never resulted in a reportable case of fatal anaphylaxis.

====Cost Effectiveness of Oral Antibiotic Prophylaxis====
''To date, one report has addressed the cost-effectiveness of providing chemoprophylaxis to patients of moderate- and high-risk of IE acquisition prior to endodontic procedure.''<ref>Agha Z, Lofgren RP, VanRuiswyk JV. Is antibiotic prophylaxis for bacterial endocarditis cost-effective? Med Decis Making. 2005;25:308-320.</ref> 
#The risk of drug-induced anaphylaxis and associated loss of QALYs with prophylactic oral amoxicillin or ampicillin to moderate-risk patients rendered this practice ineffective and therefore the authors did not complete a cost-effectiveness analysis. 
#The estimated cost-effectiveness ratio for the prophylaxis of 10 million moderate-risk patients with clarithromycin, clindamycin or cephalexin, was $88,007, $101,142 and $99,373 per QALY saved, respectively.
#Cost-effectiveness ratio for the use of clarithromycin in patients with the prior diagnosis of endocarditis was $40,334, and in patients with prosthetic valves, $16,818 per QALY saved. 
#Cost-effectiveness ratio of treating 10 million high-risk patients administered single dose clindamycin was $46,678 (prior endocarditis) and $19,936 (prosthetic valve) per QALY saved. #Cephalexin was associated with a cost-effectiveness of $37,916 per QALY saved in patients with a history of IE and $14,060 per QALY saved, in patients with a prosthetic valves. 
'''''The cost-effective analyses suggest that the 2007 AHA IE prevention guidelines advocating chemoprophylaxis to patients with a high-risk of adverse outcomes upon acquisition of IE is a reasonable, cost-effective practice.'''''

The term of prophylaxis required procedure '''include''' biopsies, suture removal, and placement of orthodontic bands, but it '''does not include''' routine anesthetic injections through non-infected tissue, the taking of dental radiographs, placement of removable prosthodontic or orthodontic appliances, placement of orthodontic brackets, or adjustment of orthodontic appliances. 

===SUMMARY for antibiotic prophlaxis prior to endodontic procedure===
*The presumed correlation of endodontic induced bacteremia, and new onset IE made pre-procedural antibiotic prophylaxis a reasonable practice for the preceding 60 years. However, there is a paucity of evidence in support of providing chemoprophylaxis for effective IE prevention.
*Chewing, dental hygiene practices, kidney disease, diabetes, and skin colonization present a greater risk of significant bacteremia and greater cumulative IE acquisition risk than any single invasive dental procedure.
*The AHA recommends reducing the incidence of bacteremia with the optimization of oral hygiene in at-risk patients and does not recommend indiscriminant pre-procedural chemoprophylaxis as a safe, IE prevention practice. 

*Case-control studies have reported conflicting results on the protective efficacy conferred from providing pre-procedural antibiotic prophylaxis to at-risk patients.
The AHA acknowledges that even if chemoprophylaxis conferred 100% efficacy, few cases of IE would be prevented as the incidence of endodontic induced IE is so low. 
<blockquote>The AHA now recommends the administration of pre-endodontic procedural prophylactic antibiotics to patients with the highest risk of adverse outcomes subsequent to the development of IE.</blockquote> 

*Acknowledging an estimated 10-20 fold greater risk of single-dose fatal anaphylaxis with amoxicillin compared to single dose cephalosporin, macrolide and clindamycin regimens, the AHA believes prophylaxis with amoxicillin is a safe practice as there have been no reports of fatal anaphylaxis from a single-dose of pre-dental IE prophylaxis oral amoxicillin.
*'''The 2007, AHA guidelines appropriately advocate against providing chemoprophylaxis to moderate-risk patients and appropriately advocate for chemoprophylaxis to high-risk patients prior to endodontic procedure as this is a cost-effective practice for IE prevention.''' 


Finally, there are other events that are not dental procedures and for which prophylaxis is not recommended, such as shedding of deciduous teeth and trauma to the lips and oral mucosa.

In this limited patient population, prophylactic antimicrobial therapy should be directed against [[Streptococcus viridans]].

As a summary; individuals at the highest risk group who need procedures listed below require proper antibiotic prophylaxis;<ref name=Wilson>{{cite journal | author = Wilson W, Taubert KA, Gewitz M, Lockhart PB, Baddour LM, Levison M, Bolger A, Cabell CH, Takahashi M, Baltimore RS, Newburger JW, Strom BL, Tani LY, Gerber M, Bonow RO, Pallasch T, Shulman ST, Rowley AH, Burns JC, Ferrieri P, Gardner T, Goff D, Durack DT| title = American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee; American Heart Association Council on Cardiovascular Disease in the Young; American Heart Association Council on Clinical Cardiology; American Heart Association Council on Cardiovascular Surgery and Anesthesia; Quality of Care and Outcomes Research Interdisciplinary Working Group. Prevention of infective endocarditis: guidelines from the American Heart Association: a guideline from the American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee, Council on Cardiovascular Disease in the Young, and the Council on Clinical Cardiology, Council on Cardiovascular Surgery and Anesthesia, and the Quality of Care and Outcomes Research Interdisciplinary Working Group| journal = Circulation | volume = 116 | issue = 15 | pages = 1736-54 | year = 2007 | id = PMID 17446442}}</ref>

*Any type of dental extractions 
*Any type of periodontal procedures and gingival surgery 
**Placement of dental implants and avulsed teeth replantation 
**Dental canal or root surgery 
**Antibiotic fibres or strips placement at subgingival area
**Initial placement of orthodontic brackets 
**Intraligamentous injection of local anesthetic drugs  
**Bleeding during prophylactic cleaning of teeth or implants


====Antibiotic prophylaxis with Procedures on Infected Skin, Skin Structure, or Musculoskeletal Tissue====

These infections are often polymicrobial, but only staphylococci and beta hemolytic [[streptococci|beta-hemolytic streptococci]] are likely to cause Infective Endocarditis. 

For patients with high risk conditions who undergo a surgical procedure that involves infected skin, skin structure, or musculoskeletal tissue, it may be reasonable that the therapeutic regimen administered for treatment of the infection contain an agent active against [[staphylococci]] and [[streptococci|beta-hemolytic streptococci]], such as an antistaphylococcal [[penicillin]] or a [[cephalosporin]].

[[Vancomycin]] or [[clindamycin]] may be administered to patients unable to tolerate a [[beta-lactam]] or who are known or suspected to have an infection caused by a [[methicillin-resistant staphylococcus aureus]].<ref name=Wilson>{{cite journal | author = Wilson W, Taubert KA, Gewitz M, Lockhart PB, Baddour LM, Levison M, Bolger A, Cabell CH, Takahashi M, Baltimore RS, Newburger JW, Strom BL, Tani LY, Gerber M, Bonow RO, Pallasch T, Shulman ST, Rowley AH, Burns JC, Ferrieri P, Gardner T, Goff D, Durack DT| title = American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee; American Heart Association Council on Cardiovascular Disease in the Young; American Heart Association Council on Clinical Cardiology; American Heart Association Council on Cardiovascular Surgery and Anesthesia; Quality of Care and Outcomes Research Interdisciplinary Working Group. Prevention of infective endocarditis: guidelines from the American Heart Association: a guideline from the American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee, Council on Cardiovascular Disease in the Young, and the Council on Clinical Cardiology, Council on Cardiovascular Surgery and Anesthesia, and the Quality of Care and Outcomes Research Interdisciplinary Working Group| journal = Circulation | volume = 116 | issue = 15 | pages = 1736-54 | year = 2007 | id = PMID 17446442}}</ref>

===Primary Prevention in Specific Situations and Circumstances===

====Patients Already Receiving Antibiotics====

If a patient is already receiving long-term antibiotic therapy with an antibiotic that is also recommended for Infective Endocarditis prophylaxis for a dental procedure, it is prudent to select an antibiotic from a different class rather than to increase the dosage of the current antibiotic. For example, antibiotic regimens used to prevent the recurrence of acute [[rheumatic fever]] are administered in dosages lower than those recommended for the prevention of [[Infective Endocarditis]]. 

Individuals who take an oral penicillin for secondary prevention of rheumatic fever or for other purposes are likely to have
viridans group streptococci in their oral cavity that are relatively resistant to [[penicillin]] or [[amoxicillin]]. In such cases, the provider should select either [[clindamycin]], [[azithromycin]], or [[clarithromycin]] for IE prophylaxis for a dental procedure, but only for patients shown in the table above. Because of possible cross-resistance of viridans group streptococci with [[cephalosporin]]s, this class of antibiotics should be avoided. 

If possible, it would be preferable to delay a dental procedure until '''at least 10 days after completion of the antibiotic therapy'''. This may allow time for the usual oral flora to be reestablished. <ref name= Baddour>{{cite journal | author = Baddour Larry M., Wilson Walter R., Bayer Arnold S., Fowler Vance G. Jr, Bolger Ann F.,  Levison Matthew E.,  Ferrieri Patricia, Gerber Michael A., Tani Lloyd Y., Gewitz Michael H., Tong David C., Steckelberg James M., Baltimore Robert S., Shulman Stanford T., Burns Jane C., Falace Donald A., Newburger Jane W., Pallasch Thomas J., Takahashi Masato,  Taubert Kathryn A.| title = 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-Executive Summary: Endorsed by the Infectious Diseases Society of America. | journal = Circulation | volume = 111 | issue = 23 | pages = 3167-84 | year = 2005 | id = PMID 15956145 }}</ref> <ref name=Wilson>{{cite journal | author = Wilson W, Taubert KA, Gewitz M, Lockhart PB, Baddour LM, Levison M, Bolger A, Cabell CH, Takahashi M, Baltimore RS, Newburger JW, Strom BL, Tani LY, Gerber M, Bonow RO, Pallasch T, Shulman ST, Rowley AH, Burns JC, Ferrieri P, Gardner T, Goff D, Durack DT| title = American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee; American Heart Association Council on Cardiovascular Disease in the Young; American Heart Association Council on Clinical Cardiology; American Heart Association Council on Cardiovascular Surgery and Anesthesia; Quality of Care and Outcomes Research Interdisciplinary Working Group. Prevention of infective endocarditis: guidelines from the American Heart Association: a guideline from the American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee, Council on Cardiovascular Disease in the Young, and the Council on Clinical Cardiology, Council on Cardiovascular Surgery and Anesthesia, and the Quality of Care and Outcomes Research Interdisciplinary Working Group| journal = Circulation | volume = 116 | issue = 15 | pages = 1736-54 | year = 2007 | id = PMID 17446442}}</ref>

====Patients Who Receive Anticoagulants====

Intramuscular injections for [[Infective Endocarditis]] prophylaxis should be avoided in patients who are receiving [[anticoagulant]] therapy. In these circumstances, orally administered regimens should be given whenever possible. Intravenously administered antibiotics should be used for patients who are unable to tolerate or absorb oral medications. <ref name= Baddour>{{cite journal | author = Baddour Larry M., Wilson Walter R., Bayer Arnold S., Fowler Vance G. Jr, Bolger Ann F.,  Levison Matthew E.,  Ferrieri Patricia, Gerber Michael A., Tani Lloyd Y., Gewitz Michael H., Tong David C., Steckelberg James M., Baltimore Robert S., Shulman Stanford T., Burns Jane C., Falace Donald A., Newburger Jane W., Pallasch Thomas J., Takahashi Masato,  Taubert Kathryn A.| title = 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-Executive Summary: Endorsed by the Infectious Diseases Society of America. | journal = Circulation | volume = 111 | issue = 23 | pages = 3167-84 | year = 2005 | id = PMID 15956145 }}</ref> <ref name=Wilson>{{cite journal | author = Wilson W, Taubert KA, Gewitz M, Lockhart PB, Baddour LM, Levison M, Bolger A, Cabell CH, Takahashi M, Baltimore RS, Newburger JW, Strom BL, Tani LY, Gerber M, Bonow RO, Pallasch T, Shulman ST, Rowley AH, Burns JC, Ferrieri P, Gardner T, Goff D, Durack DT| title = American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee; American Heart Association Council on Cardiovascular Disease in the Young; American Heart Association Council on Clinical Cardiology; American Heart Association Council on Cardiovascular Surgery and Anesthesia; Quality of Care and Outcomes Research Interdisciplinary Working Group. Prevention of infective endocarditis: guidelines from the American Heart Association: a guideline from the American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee, Council on Cardiovascular Disease in the Young, and the Council on Clinical Cardiology, Council on Cardiovascular Surgery and Anesthesia, and the Quality of Care and Outcomes Research Interdisciplinary Working Group| journal = Circulation | volume = 116 | issue = 15 | pages = 1736-54 | year = 2007 | id = PMID 17446442}}</ref>

====Patients Who Undergo Cardiac Surgery====

Patients who undergo surgery for placement of prosthetic heart valves or prosthetic intravascular or intracardiac materials are at risk for the development of infection. Because the morbidity and mortality of infection in these patients are high, perioperative prophylactic antibiotics are recommended. 

Early-onset prosthetic valve [[endocarditis]] is most often caused by [[S. aureus]], coagulase-negative staphylococci, or diphtheroids. No single antibiotic regimen is effective against all these microorganisms. Prophylaxis at the time of cardiac surgery should be directed primarily against staphylococci and should be of short duration. A first-generation [[cephalosporin]] is most often used, but the choice of an antibiotic should be influenced by the antibiotic  susceptibility patterns at each hospital. For example, a high prevalence of infection by [[methicillin-resistant Staphylococcus aureus]] (MRSA) should prompt the consideration of the use of [[vancomycin]] for perioperative prophylaxis. 

The majority of nosocomial coagulase-negative staphylococci are methicillin-resistant. Nonetheless, surgical prophylaxis with a first-generation cephalosporin may be recommended for these patients. In hospitals with a high prevalence of methicillin-resistant strains of [[S. epidermidis]], surgical prophylaxis with [[vancomycin]] may be reasonable but has not been shown to be superior to prophylaxis with a [[cephalosporin]]. 

Prophylaxis should be initiated immediately before the operative procedure, repeated during prolonged procedures to maintain serum concentrations intraoperatively, and continued for no more than 48 hours postoperatively to minimize emergence of resistant microorganisms. The effects of cardiopulmonary bypass and compromised renal function on antibiotic concentrations in serum should be considered and dosages adjusted as necessary before and during the procedure. <ref name= Baddour>{{cite journal | author = Baddour Larry M., Wilson Walter R., Bayer Arnold S., Fowler Vance G. Jr, Bolger Ann F.,  Levison Matthew E.,  Ferrieri Patricia, Gerber Michael A., Tani Lloyd Y., Gewitz Michael H., Tong David C., Steckelberg James M., Baltimore Robert S., Shulman Stanford T., Burns Jane C., Falace Donald A., Newburger Jane W., Pallasch Thomas J., Takahashi Masato,  Taubert Kathryn A.| title = 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-Executive Summary: Endorsed by the Infectious Diseases Society of America. | journal = Circulation | volume = 111 | issue = 23 | pages = 3167-84 | year = 2005 | id = PMID 15956145 }}</ref> <ref name=Wilson>{{cite journal | author = Wilson W, Taubert KA, Gewitz M, Lockhart PB, Baddour LM, Levison M, Bolger A, Cabell CH, Takahashi M, Baltimore RS, Newburger JW, Strom BL, Tani LY, Gerber M, Bonow RO, Pallasch T, Shulman ST, Rowley AH, Burns JC, Ferrieri P, Gardner T, Goff D, Durack DT| title = American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee; American Heart Association Council on Cardiovascular Disease in the Young; American Heart Association Council on Clinical Cardiology; American Heart Association Council on Cardiovascular Surgery and Anesthesia; Quality of Care and Outcomes Research Interdisciplinary Working Group. Prevention of infective endocarditis: guidelines from the American Heart Association: a guideline from the American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee, Council on Cardiovascular Disease in the Young, and the Council on Clinical Cardiology, Council on Cardiovascular Surgery and Anesthesia, and the Quality of Care and Outcomes Research Interdisciplinary Working Group| journal = Circulation | volume = 116 | issue = 15 | pages = 1736-54 | year = 2007 | id = PMID 17446442}}</ref>

=== Secondary Prevention and Follow-Up===

====Short-Term Follow-Up====

The majority of patients with IE are cured with appropriate medical and, if necessary, surgical treatment. Before completing antimicrobial therapy, the patient should receive TTE (Class IIb, Level of Evidence: C) to establish a new baseline for subsequent comparison. 

A referral to a program to assist in cessation of drug use should be made for IDU patients. Patients should be educated about the signs of [[endocarditis]] and urged to seek immediate medical attention should they occur. A thorough dental evaluation should be obtained and all active sources of oral infection should be eradicated. 

All catheters used to infuse antimicrobial treatment should be promptly removed at the end of therapy. In the short-term follow-up, patients should be monitored for development of several complications. A relapse of endocardial infection is a primary concern. Patients should be aware that relapses can occur and that new onset of fever, chills, or other evidence of systemic toxicity mandates immediate evaluation, including obtaining ≥3 sets of blood  cultures from different phlebotomy sites after a thorough
history and physical examination.<ref name= Baddour>{{cite journal | author = Baddour Larry M., Wilson Walter R., Bayer Arnold S., Fowler Vance G. Jr, Bolger Ann F.,  Levison Matthew E.,  Ferrieri Patricia, Gerber Michael A., Tani Lloyd Y., Gewitz Michael H., Tong David C., Steckelberg James M., Baltimore Robert S., Shulman Stanford T., Burns Jane C., Falace Donald A., Newburger Jane W., Pallasch Thomas J., Takahashi Masato,  Taubert Kathryn A.| title = 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-Executive Summary: Endorsed by the Infectious Diseases Society of America. | journal = Circulation | volume = 111 | issue = 23 | pages = 3167-84 | year = 2005 | id = PMID 15956145 }}</ref> <ref name=Wilson>{{cite journal | author = Wilson W, Taubert KA, Gewitz M, Lockhart PB, Baddour LM, Levison M, Bolger A, Cabell CH, Takahashi M, Baltimore RS, Newburger JW, Strom BL, Tani LY, Gerber M, Bonow RO, Pallasch T, Shulman ST, Rowley AH, Burns JC, Ferrieri P, Gardner T, Goff D, Durack DT| title = American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee; American Heart Association Council on Cardiovascular Disease in the Young; American Heart Association Council on Clinical Cardiology; American Heart Association Council on Cardiovascular Surgery and Anesthesia; Quality of Care and Outcomes Research Interdisciplinary Working Group. Prevention of infective endocarditis: guidelines from the American Heart Association: a guideline from the American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee, Council on Cardiovascular Disease in the Young, and the Council on Clinical Cardiology, Council on Cardiovascular Surgery and Anesthesia, and the Quality of Care and Outcomes Research Interdisciplinary Working Group| journal = Circulation | volume = 116 | issue = 15 | pages = 1736-54 | year = 2007 | id = PMID 17446442}}</ref>

====Long-Term Follow-Up====

Months to years after completion of medical therapy for IE, patients need ongoing observation and education regarding recurrent infection and delayed onset of worsening valvular dysfunction. Ongoing daily dental hygiene should be stressed, with serial evaluations by a dentist who is familiar with this patient population. 

Patients should be questioned about the symptoms of decreased cardiac output and CHF. A thorough cardiac examination will be needed. Additional evaluations with TTE will be necessary in selected patients with positive findings from history and physical examination. Patients must be reminded to seek immediate medical evaluation for fever. This is necessary because IE can mimic a panoply of febrile illnesses. 

Antibiotic therapy should not be initiated for treatment of undefined febrile illnesses without obtaining previous blood cultures. Antibiotics prescribed for nonspecific or unproved febrile syndromes are the major cause of (blood) culture negative endocarditis and should be strongly discouraged. <ref name= Baddour>{{cite journal | author = Baddour Larry M., Wilson Walter R., Bayer Arnold S., Fowler Vance G. Jr, Bolger Ann F.,  Levison Matthew E.,  Ferrieri Patricia, Gerber Michael A., Tani Lloyd Y., Gewitz Michael H., Tong David C., Steckelberg James M., Baltimore Robert S., Shulman Stanford T., Burns Jane C., Falace Donald A., Newburger Jane W., Pallasch Thomas J., Takahashi Masato,  Taubert Kathryn A.| title = 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-Executive Summary: Endorsed by the Infectious Diseases Society of America. | journal = Circulation | volume = 111 | issue = 23 | pages = 3167-84 | year = 2005 | id = PMID 15956145 }}</ref> <ref name=Wilson>{{cite journal | author = Wilson W, Taubert KA, Gewitz M, Lockhart PB, Baddour LM, Levison M, Bolger A, Cabell CH, Takahashi M, Baltimore RS, Newburger JW, Strom BL, Tani LY, Gerber M, Bonow RO, Pallasch T, Shulman ST, Rowley AH, Burns JC, Ferrieri P, Gardner T, Goff D, Durack DT| title = American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee; American Heart Association Council on Cardiovascular Disease in the Young; American Heart Association Council on Clinical Cardiology; American Heart Association Council on Cardiovascular Surgery and Anesthesia; Quality of Care and Outcomes Research Interdisciplinary Working Group. Prevention of infective endocarditis: guidelines from the American Heart Association: a guideline from the American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee, Council on Cardiovascular Disease in the Young, and the Council on Clinical Cardiology, Council on Cardiovascular Surgery and Anesthesia, and the Quality of Care and Outcomes Research Interdisciplinary Working Group| journal = Circulation | volume = 116 | issue = 15 | pages = 1736-54 | year = 2007 | id = PMID 17446442}}</ref>

== Cost-Effectiveness of Therapy ==
Although cost-effectiveness calculations suggest that [[TEE]] should be the first examination in adults with suspected [[IE]], particularly in the setting of staphylococcal bacteriemia, many patients are not candidates for immediate [[TEE]] because of oral intake during the preceding 6 hours or because the patients are in institutions that cannot provide 24-hour [[TEE]] services. When [[TEE]] is not clinically possible or must be delayed, early [[TTE]] should be performed without delay.<ref name= Baddour>{{cite journal | author = Baddour Larry M., Wilson Walter R., Bayer Arnold S., Fowler Vance G. Jr, Bolger Ann F.,  Levison Matthew E.,  Ferrieri Patricia, Gerber Michael A., Tani Lloyd Y., Gewitz Michael H., Tong David C., Steckelberg James M., Baltimore Robert S., Shulman Stanford T., Burns Jane C., Falace Donald A., Newburger Jane W., Pallasch Thomas J., Takahashi Masato,  Taubert Kathryn A.| title = 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-Executive Summary: Endorsed by the Infectious Diseases Society of America. | journal = Circulation | volume = 111 | issue = 23 | pages = 3167-84 | year = 2005 | id = PMID 15956145 }}</ref> <ref name=Wilson>{{cite journal | author = Wilson W, Taubert KA, Gewitz M, Lockhart PB, Baddour LM, Levison M, Bolger A, Cabell CH, Takahashi M, Baltimore RS, Newburger JW, Strom BL, Tani LY, Gerber M, Bonow RO, Pallasch T, Shulman ST, Rowley AH, Burns JC, Ferrieri P, Gardner T, Goff D, Durack DT| title = American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee; American Heart Association Council on Cardiovascular Disease in the Young; American Heart Association Council on Clinical Cardiology; American Heart Association Council on Cardiovascular Surgery and Anesthesia; Quality of Care and Outcomes Research Interdisciplinary Working Group. Prevention of infective endocarditis: guidelines from the American Heart Association: a guideline from the American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee, Council on Cardiovascular Disease in the Young, and the Council on Clinical Cardiology, Council on Cardiovascular Surgery and Anesthesia, and the Quality of Care and Outcomes Research Interdisciplinary Working Group| journal = Circulation | volume = 116 | issue = 15 | pages = 1736-54 | year = 2007 | id = PMID 17446442}}</ref>

== Future or Investigational Therapies ==

Considering [[infective endocarditis]] to be an "emerging" problem in the 21st century may seem unusual, given that the illness has been well documented over the last 450 years. However, such emergence can be attributed to several factors: 

#The emergence of antimicrobial resistance in classic [[infective endocarditis]] microflora, namely, the gram-positive cocci; 
#The existence of antimicrobial resistance in complex ecologic biofilms; 
#The changing pattern of causal agents now regarded as important pathogens of [[infective endocarditis]], e.g., Bartonella spp., T. whipplei, and fungi;
#Changing epidemiologic trends of persons who acquire [[infective endocarditis]], including '''injection drug users''', '''persons with HIV/AIDS''', '''children with congenital heart defects''', and persons undergoing '''body piercing'''. 

Furthermore, the way we provide inpatient medical care has also been associated with the emergence of nosocomial [[infective endocarditis]], which can result from invasive '''procedures such as catheterization''', although no cardiac surgery has been performed. 

The forthcoming years will likely witness the emergence of even more changing trends of [[infective endocarditis]], which as yet have not been well recognized. <ref>Millar BC, Moore JE. Emerging issues in infective endocarditis. Emerg Infect Dis 2004 Jun [Access date: 03-03-2008]. Available from: http://www.cdc.gov/ncidod/EID/vol10no6/03-0848.htm</ref> <ref name=Wilson>{{cite journal | author = Wilson W, Taubert KA, Gewitz M, Lockhart PB, Baddour LM, Levison M, Bolger A, Cabell CH, Takahashi M, Baltimore RS, Newburger JW, Strom BL, Tani LY, Gerber M, Bonow RO, Pallasch T, Shulman ST, Rowley AH, Burns JC, Ferrieri P, Gardner T, Goff D, Durack DT| title = American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee; American Heart Association Council on Cardiovascular Disease in the Young; American Heart Association Council on Clinical Cardiology; American Heart Association Council on Cardiovascular Surgery and Anesthesia; Quality of Care and Outcomes Research Interdisciplinary Working Group. Prevention of infective endocarditis: guidelines from the American Heart Association: a guideline from the American Heart Association Rheumatic Fever, Endocarditis, and Kawasaki Disease Committee, Council on Cardiovascular Disease in the Young, and the Council on Clinical Cardiology, Council on Cardiovascular Surgery and Anesthesia, and the Quality of Care and Outcomes Research Interdisciplinary Working Group| journal = Circulation | volume = 116 | issue = 15 | pages = 1736-54 | year = 2007 | id = PMID 17446442}}</ref>

=="The Way I Like To Do It ..." Tips and Tricks From Clinicians Around The World==

===Suggested Revisions to the Current Guidelines===

==References==
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<references/>
</div>

==External Links and Patient Resources==

*[http://www.annals.org/cgi/reprint/146/8/574.pdf Brief Communication: Treatment of Enterococcus faecalis Endocarditis with Ampicillin plus Ceftriaxone]
*[http://www.utmem.edu/cardiology/articles/InfectiveEndocarditisreview01.pdf Infective Endocarditis in Adults]
*[http://jama.ama-assn.org/cgi/reprint/293/24/3022 Temporal Trends in Infective Endocarditis]

===For Patients:===
*[http://www.americanheart.org/presenter.jhtml?identifier=4436 A.H.A. Patient Information for Infective Endocarditis]

== Acknowledgements ==
The content on this page was first contributed by: [[C. Michael Gibson, M.S., M.D.]]

==Contributors==

{{Electrocardiography}}
{{Circulatory system pathology}}
{{SIB}}

[[tr:İnfektif endokardit]]

[[Category:Emergency medicine]]
[[Category:Cardiology]]


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