Bartonella henselae bacilli in cardiac valve of a patient with blood culture-negative endocarditis. The bacilli appear as black granulations.
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Bacterial endocarditis

Endocarditis is an inflammation of the inner layer of the heart, the endocardium. The most common structures involved are the heart valves. more...

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Endocarditis can be classified by etiology as either infective or non-infective, depending on whether a foreign micro-organism is causing the problem.

Infective endocarditis

As the valves of the heart do not actually receive any blood supply of their own, which may be surprising given their location, defense mechanisms (such as white blood cells) cannot enter. So if an organism (such as bacteria) establish hold on the valves, the body cannot get rid of them.

Normally, blood flows pretty smoothly through these valves. If they have been damaged (for instance in rheumatic fever) bacteria have a chance to take hold.

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Preventing bacterial endocarditis: American Heart Association guidelines
From American Family Physician, 2/1/98 by Kathryn A. Taubert

Bacterial endocarditis is a relatively

uncommon, life-threatening

infection of the

endothelial surface of the

heart, including the heart

valves. Despite advances in antimicrobial

therapy and the diagnosis and treatment

of complications, bacterial endocarditis

continues to be responsible for substantial

morbidity and mortality.

While anyone can contract endocarditis,

the infection usually develops in individuals

with underlying structural cardiac

defects. It can occur whenever these persons

develop bacteremia with the organisms

likely to cause endocarditis. Bacteremia

may occur spontaneously (i.e.,

caused by organisms introduced through

food chewing or tooth brushing), or it

may develop as a complication of a focal

infection, such as a periodontal or periapical

infection, a urinary tract infection,

pneumonia or cellulitis. Selected surgical

and dental procedures and instrumentations,

especially those involving mucosal

surfaces or contaminated tissue, can cause

a transient bacteremia that rarely persists

for more than a few minutes.

For endocarditis to develop, two independent

events are normally required: an

area of endothelium must be damaged, and

a bacteremia caused by adherent organisms

must occur. If endothelium is damaged but

a bacteremia does not occur, bacterial

endocarditis will not develop. Conversely, if

a bacteremia occurs, normal undamaged

heart endothelium is not conducive to bacterial

colonization. In congenital or

acquired cardiac lesions, endothelium can

be damaged by an abnormally high-velocity

jet-stream--like flow that results in turbulent,

rather than laminar, blood flow.

A model was developed to delineate the

hemodynamic mechanisms for the development

of endocarditis.[1] This model

showed that endothelial damage and bacterial

deposition occur in the low-pressure

area immediately distal to an obstruction,

such as coarctation of the aorta, a regurgitant

mitral or aortic valve, or a ventricular

septal defect. Thus, endothelium on the

ventricular side of a regurgitant aortic

valve would be damaged, and the right

ventricular wall (or right heart valves)

would be damaged from the jet-stream--like

blood flow created by a ventricular

septal defect. Endothelium can also be damaged

by direct trauma caused by a device (e.g.,

an indwelling cardiac catheter) or by intracardiac

surgery.

Trauma to the endothelium of a cardiac

valve or to the endocardium can induce thrombogenesis

(deposition of fibrin and platelets),

which leads to a nonbacterial, thrombotic

endocardial lesion. This lesion is more susceptible

to bacterial colonization than is normal,

undamaged endothelium.

Although bacteremia is a frequent problem

after many invasive procedures, only certain bacteria

commonly cause endocarditis. Vegetation

can develop following a bacteremia with one of

these organisms. This vegetation is composed of

fibrin, platelets, red blood cells, a few white blood

cells and the infecting microorganisms.

The incidence of endocarditis following

most procedures is low in patients with underlying

cardiac disease. According to the

American Heart Association (AHA),[2] a reasonable

approach to endocarditis prophylaxis

should consider the following points:

1. The degree to which the patient's underlying

condition creates a risk of endocarditis.

2. The apparent risk of bacteremia with the

procedure.

3. The potential adverse effects of the prophylactic

antimicrobial agent to be used.

4. The cost-benefit aspects of the recommended

prophylactic regimen.

It is not always possible to predict which

patients will develop bacterial endocarditis and

which procedure will be responsible. In fact,

most cases of endocarditis are not attributable

to a specific invasive procedure. Nonetheless,

certain bacteria are known to be associated

with endocarditis in at-risk patients. Consequently,

recommendations for the prevention

of endocarditis have been issued by various

organizations throughout the world. The AHA

developed the recommendations that are most

widely followed in the United States. These

recently revised guidelines serve as a point of

reference for the discussion in this article.[2]

The AHA recommendations are designed to

assist in the rational use of prophylaxis for the

prevention of bacterial endocarditis. The

guidelines take into account both the patient's

underlying cardiac condition and the risk of an

endocarditis-producing bacteremia during a

surgical or dental procedure. The recommendations

are not intended to be the standard of

care for all patients or to serve as a substitute

for clinical judgment. Physicians and dentists

must use their own judgment in selecting an

antibiotic and determining the number of

doses that are to be administered in individual

patients or in special circumstances.

Even with appropriate antibiotic prophylaxis,

endocarditis may occur. Consequently,

physicians and dentists should maintain a high

index of suspicion regarding any unusual clinical

events that occur following procedures in

which antibiotic prophylaxis was administered.

Particular attention should be given to unexplained

fever, night chills, weakness, myalgia,

arthralgia, lethargy or malaise in a patient who

has had a dental or surgical procedure.

Cardiac Conditions and Endocarditis Prophylaxis

Endocarditis is associated with some cardiac

conditions more often than with others.[3]

Furthermore, when enclocarditis develops in

patients with underlying cardiac conditions,

disease severity and ensuing morbidity can be

variable. Thus, endocarditis prophylaxis is recommended

for use in patients who are at

higher risk for endocarditis than persons in

the general population. Prophylaxis is particularly

important for patients in whom endocardial

infection would be most likely to cause

severe morbidity or even mortality.

Cardiac conditions for which prophylaxis is

or is not recommended are listed in Table 1.[2]

These conditions are stratified into high-,

moderate- and negligible-risk categories

based primarily on the potential outcome if

enclocarditis occurs. The negligible-risk category

includes cardiac conditions in which

endocarditis develops no more often than in

the general population.

Consequently, they are listed in the moderate-risk

category. On the other hand, patients in

whom regurgitation has not been documented

are at no higher risk for endocarditis than persons

in the general population and therefore

do not need prophylaxis.

A detailed discussion of the pathophysiology

of mitral valve prolapse is found in the AHA

guidelines.[2] A clinical approach to determining

the need for endocarditis prophylaxis in the

patient with suspected mitral valve prolapse is

presented in Figure 1.[2] Details about the role of

echocardiography in the diagnosis of mitral

valve prolapse are provided elsewhere.[13]

[Figure 1 ILLUSTRATION OMITTED]

Although endocarditis can occur in anyone,

including persons with no underlying cardiac

defects, the negligible-risk category includes

cardiac conditions in which the risk of endocarditis

is no higher than in the general population.

Patients with these cardiac conditions

do not require endocarditis prophylaxis.

Procedures That Can Cause Bacteremia

Bacteremias commonly occur during activities

of daily living, such as routine tooth

brushing or food chewing. With respect to

endocarditis prophylaxis, significant bacteremias

are caused only by the organisms

commonly associated with endocarditis and

attributable to identifiable procedures.

Prophylaxis is recommended for procedures

that are known to induce significant bacteremias

with the organisms commonly associated

with endocarditis and attributable to

identifiable procedures. Invasive procedures

performed through surgically scrubbed skin

are not likely to produce such bacteremias.

Dental and Oral Procedures

Both the incidence and the magnitude of

bacteremias of oral origin are proportional to

the degree of oral inflammation and infection.[14,15]

Therefore, it is important that patients

at risk for endocarditis maintain good

oral health to reduce potential sources of bacterial

seeding. Oral maintenance includes regular

brushing (with manual or powered

toothbrushes) and flossing at home, as well as

regular visits to the dentist. Some authorities

recommend the use of an antiseptic mouth

rinse, such as chlorhexidine (Peridex) or povidone-iodine

(Betadine), immediately before

dental procedures to help reduce the incidence

and magnitude of bacteremia.[2,14]

Dental and oral procedures for which anti-microbial

prophylaxis is or is not recommended

are listed in Table 2.[2] In general, prophylaxis

is recommended for procedures

associated with significant bleeding from hard

or soft tissues, including periodontal surgery,

scaling and professional teeth cleaning. Prophylaxis

is also recommended for tonsillectomy

or adenoidectomy. Antimicrobial prophylaxis

is not recommended for procedures in which

significant bleeding is not anticipated.

or removal of an intrauterine device, and

prophylaxis may be warranted.

Recommended Prophylactic Regimens

Prophylactic regimens are directed at the

organisms most likely to result in bacteremia

during a procedure. Enclocarditis prophylaxis

is most effective when an antibiotic is given

perioperatively in a dose sufficient to ensure

an adequate serum concentration of the drug

during and after the procedure. To reduce the

likelihood of microbial resistance, prophylactic

antibiotic therapy should be used only during

the perioperative period.

The antimicrobial regimens listed in Table 4[2]

are designed to be initiated shortly (hours to

days) before a procedure. A follow-up dose is

recommended in only a few situations.

Table 4

Endocarditis Prophylactic Regiments for Dental, Oral,

Respiratory Tract and Esophageal Procedure

Taubert KA, Wilson W, Bolger AF, Bayer A, Ferrieri P,

et al. Prevention of bacterial endocarditis.

Recommendations by the American Heart Association.

JAMA 1997;277:1794-801.

The Council on Scientific Affairs of the American

Dental Association has approved the American

Heart Association guidelines as they relate to

dentistry. The American Society for Gastrointestinal

Endoscopy has approved the guidelines as they

relate to gastroenterology.

REFERENCES

[1.] Rodbard S. Blood velocity and endocarditis.

Circulation 1963;27:18.

[2.] Dajani AS, Taulbert KA, Wilson W, Bolger AF, Bayer

A, Ferrieri F, et al. Prevention of bacterial endocarditis.

Recommendations by the American Heart Association. JAMA

1997;277:1794-801.

[3.] Steckellberg JIM, Wilson WR. Risk factors for

infective endocarditis. Infect Dis Clin North Am 1993;

7:9-19.

[4.] Saiman L, Prince A, Gersony WM. Pediatric infective

endocarditis in the modern era. J Pediatr 1993;

122:847-53.

[5.] Gersony WM, Hayes CJ, Driscoll DJ, Keane JF, Kidd

L, O'Fallon WM, et al. Bacterial endocarditis in

patients with aortic stenosis, pulmonary stenosis,

or ventricular septal defect. Circulation 1993;87

(Suppl 1):1121-6.

[6.] Prabhu SD, O'Rourke RA. Mitral valve prolapse. In:

Rahimtoola SH, ed. Atlas of heart diseases. Valvular

heart disease. Vol 11. St. Louis: Mosby, 1997.

[7.] Boudoulas H, Wooley CF. Mitral valve prolapse. In:

Emmanouilides GC, et al., eds. Moss and Adams

Heart disease in infants, children, and adolescents:

including the fetus and young adult. 5th ed. Baltimore:

Williams & Wilkins, 1995:1063-86.

[8.] Carabello BA. Mitral valve disease. Curr Probl

Cardiol 1993;18(7):423-78.

[9.] Devereux RB, Hawkins I, Kramer-Fox R, Lutas EM,

Hammond IW, Spitzer MC, et al. Complications of

mitral valve prolapse: disproportionate occurrence in

men and older patients. Am J Med 1986;81:751-8.

[10.] Danchin N, Voiriot P, Briancon S, Bairati I, Mathieu

F, Deschamps JP, et al. Mitral valve prolapse as a

risk factor for infective endocarditis. Lancet

1989;1(8641):743-5.

[11.] MacMahon SW, Roberts JK, Kramer-Fox R, Zucker

DM, Roberts RB, Devereux RB. Mitral valve prolapse

and infective enclocarditis. Am Heart J

1987;113:1291-8.

[12.] Marks AR, Choong CY, Sanfilippo AJ, Ferre M,

Weyman AE. Identification of high-risk and low-risk

subgroups of patients with mitral-valve prolapse.

N Engl J Med 1989;320:1031-6.

[13.] Cheitlin MID, Alpert JS, Armstrong WF, Aurigemma

GP, Beller GA, Bierman FZ, et al. ACC/AHA guidelines

for the clinical application of echocardiography.

A report of the American College of Cardiology/

American Heart Association Task Force on Practice

Guidelines (Committee on Clinical Application of

Echocardiography). Circulation 1997;95:1686-744.

[14.] Pallasch TJ, Slots J. Antibiotic prophylaxis and the

medically compromised patient. Periodontol 2000

1996;10:107-38.

[15.] Bender 113, Naidorf IJ, Garvey GJ. Bacterial

endocarditis: a consideration for physician and dentist. J

Am Dent Assoc 1984;109:415-20.

[16.] DaJani AS, Bisno AL, Chung KJ, Durack DT, Freed

M, Gerber MA, et al. Prevention of bacterial endocarditis.

JAMA 1990;264:2919-22.

[17.] Botoman VA, Surawicz CM. Bacteremia with

gastrointestinal endoscopic procedures. Gastrointest

Endosc 1986;32:342-6.

[18.] Byrne W, Euler AR, Campbell M, Eisenach KD.

Bacteremia in children following upper gastrointestinal

endoscopy or colonoscopy. J Pediatr Gastroenterol

Nutr 1982;1:551-3.

[19.] Shull HJ, Greene BM, Allen SID, Dunn GD, Schenker

S. Bacteremia with upper gastrointestinal endoscopy

Ann Intern Med 1975;83:212-4.

[20.] Low DE, Shoenut JF, Kennedy JK, Sharma GF,

Harding GK, Den Boer B, et al. Prospective assessment

of risk of bacteremia with colonoscopy and

polypectomy. Dig Dis Sci 1987;32:1239-43.

[21.] Vosti KL. Special problems in prophylaxis of

endocarditis following genitourinary tract and

obstetrical and gynecological procedures. In: Proceedings

of a seminar on infective endocarditis. American

Heart Association monograph no. 52. Dallas:

American Heart Association Symposium, 1976:75-9.

[22.] Durack DT Prevention of infective endocarditis. N

Engl J Med 1995;332:38-44.

[23.] Sullivan NM, Sutter VL, Mims MM, Marsh VH,

Finegold SM. Clinical aspects of bacteremia after

manipulation of the genitourinary tract. J Infect Dis

1973;127:49-55.

[24.] Sugrue D, Blake S, Troy P, MacDonald D. Antibiotic

prophylaxis against infective endocarditis after normal

delivery-is it necessary? Br Heart J 1980;

44:499-502.

[25.] Dajani AS, Bawdon RE, Berry MC. Oral amoxicillin

as prophylaxis for endocarditis: what is the optimal

dose? Clin Infect Dis 1994;18:157-60.

[26.] Fluckiger U, Francioli P, Blaser J, Glauser MP,

Moreillon P. Role of amoxicillin serum levels for

successful prophylaxis of experimental endocarditis

due to tolerant streptococci. J Infect Dis 1994;169:

1397-400.

[27.] Berney P, Francioli P. Successful prophylaxis of

experimental streptococcal endocarditis with

single-dose amoxicillin administered after bacterial

challenge. J Infect Dis 1990;161:281-5.

[28.] Durack DT, Kaplan EL, Bisno AL. Apparent failures

of enclocarditis prophylaxis. Analysis of 52 cases

submitted to a national registry. JAMA 1983;250:

2318-22.

[29.] American Dental Association and American

Academy of Orthopaedic Surgeons. Advisory statement:

antibiotic prophylaxis for dental patients with total

joint replacements. J Am Dent Assoc 1997;128:

1004-8.

KATHRYN A. TAUBERT, PH.D., is senior scientist in the Department of Science

and Medicine at the American Heart Association, Dallas, as well as adjunct

associate professor of physiology at the University of Texas Southwestern

Medical School, also in Dallas. Dr. Taulbert received her doctorate in medical

physiology from the University of Texas Southwestern Medical School and

completed a postdoctoral fellowship in the Department of Cardiology at Dallas

Veterans Affairs Hospital.

ADNAN S. DAJANI, M.D., is professor of pediatrics at Wayne State University

School of Medicine, Detroit, where he is also director of infectious disease

at Children's Hospital of Michigan. Dr. Dajani received his medical degree

from the American University of Beirut, Lebanon. He completed a residency in

pediatrics at Case Western Reserve University, Cleveland, and a fellowship in

pediatric infectious diseases at the University of North Carolina, Chapel Hill.

Address correspondence to Kathryn A. Taubert, Ph.D., Department of Science

and Medicine, American Heart Association, 7272 Greenville Ave., Dallas, TX

75231. Reprints are not available from the authors.

COPYRIGHT 1998 American Academy of Family Physicians
COPYRIGHT 2000 Gale Group

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