Profilaxia endocarditei infectioase, reevaluare critica

Gabriel-Adrian Popescu(1), Alina Tone(2)

1. Institutul National de Boli Infectioase "Prof. dr. M. Bals"

2. Hopital G. Dron, Service Maladies Infectieuses et Tropicales, Tourcoing, France
Abstract
For a long period of time, the adherence to infective endocarditis (IE) prophylaxis represented a criteria for
a healthcare system. Recently, several trials indicated that only a few IE cases are related to dental
procedures; for this reason, antimicrobial prophylaxis remain an option only for high risk group of patients
with underlying cardiac condition or with a greater risk for severity if IE developed

Rezumat
Pentru o lunga perioada de timp, gradul de aderenta la profilaxia antibiotica a endocarditei infectioase a
reprezentat un criteriu de evaluare a competitivitatii unui sistem sanitar. Studii recente au aratat insa ca
doar putine cazuri de endocardita pot fi corelate cu manopere stomatologice, acestea determinand doar un
procent redus dintre bacteriemiile cu germeni din cavitatea bucala; de aceea, atitudinea actuala se bazeaza
pe o profilaxie selectiva, doar la pacientii cu risc ridicat de a dezvolta endocardita infectioasa si/sau la care
aceasta afectiune ar putea evolua sever.

In ultimii ani au fost publicate in Europa si in SUA recomandari privind profilaxia endocarditei infectioase (EI)
care au starnit controverse aprinse datorita distantarii semnificative fata de protocoalele anterioare ale
acelorasi societati medicale(1-3), cat si fata de practica medicala curenta. Principala problema dezbatuta
este cea a situatiilor si a pacientilor la care manopere parenterale ar trebuie precedate de administrarea de
antibiotice pentru a diminua riscul aparitiei EI.
Problema
a. Timp de decenii - eforturi vadite pentru a introduce profilaxia EI
Streptococcus viridans a fost pentru aproape un secol si ramane in cele mai multe zone principala etiologie a
endocarditei bacteriene; fiind un germene endogen, ce apartine florei cavitatii bucale, s-a considerat ca o
profilaxie antibiotica adecvata inaintea interventiilor stomatologice ar putea diminua semnificativ incidenta
endocarditei bacteriene. De aceea, recomandarile de conduita privind profilaxia endocarditei infectioase au
inclus administrarea de antibiotice inaintea manoperelor stomatologice, inca din 1951 - la mai putin de un
deceniu de la introducerea in clinica a penicilinei( 4-6). Intrucat numeroase studii au evidentiat gradul redus
de complianta a practicienilor fata de asemenea recomandari (15-35%)(7), s-au depus eforturi si s-a insistat
asupra necesitatii de a se conforma la acestea - atat din punct de vedere al indicatiilor, cat mai ales al
antibioticelor utilizate, al dozelor administrate si al duratei de administrare( 8-12).
b. Date recente - la ce bun?
Eforturile anterioare pentru educarea clinicienilor in directia efectuarii profilaxiei antibiotice a endocarditei
bacteriene inaintea interventiilor stomatologice au fost puse sub semnul intrebarii privind utilitatea lor, in
momentul in care studii epidemiologice nu au regasit o corelatie intre asemenea manopere si aparitia
endocarditei, principalul fundament al unor recomandari extensive ramanand traditia medicala. De aceea,
recomandarile societatilor medicale de profil publicate in ultimii ani restrang semnificativ sfera indicatiilor
acestei antibioticoprofilaxii.
Analiza problemei
Este problema reala si de interes? EI reprezinta o problema pentru sistemul medical prin letalitatea care o
insoteste (depasind 15-20% chiar si in sistemele medicale performante) si din cauza costurilor economice
legate de ingrijirea acestor pacienti (spitalizare prelungita, necesitatea protezarii valvulare la aproximativ
25-30% dintre pacienti). Totusi, deoarece incidenta ei este redusa, in pofida frecventei ridicate a premiselor
de aparitie (pacienti cu leziuni cardiace, respectiv manopere cu risc de bacteriemie), se considera utila
definirea situatiilor cu risc crescut pentru aparitia EI, astfel incat masurile de profilaxie sa realizeze
dezideratul de eficientizare a costurilor.

Cresterea si descresterea interesului pentru profilaxia EI

a. Anii PRO
Un consens al opiniilor privind utilitatea profilaxiei antibiotice a reprezentat fundamentul recomandarilor in
cazul EI; chiar in absenta unor date furnizate de studii clinice riguroase, s-a decis recursul la aceasta.
Argumentul teoretic era reprezentat de silogismul:

bacteriemia este premisa indispensabila pentru producerea EI;

manoperele dentare pot declansa bacteriemii cu germeni ai florei orale (in special Streptococcus
viridans);
de aceea, administrarea de antibiotice inaintea manoperelor stomatologice, reducand riscul
bacteriemiilor, ar diminua implicit si incidenta EI.
Datele clinice care sustin o asemenea abordare sunt:
- cresterea riscului EI dupa diverse manopere invazive, nu numai stomatologice; datele existente provin din
prezentari de cazuri si nu din studii controlate( 13-16);
- reducerea riscului de EI prin recursul la antibioticoprofilaxie; rezultatele unor studii sustin acest beneficiu
in cazul interventiilor stomatologice: o rata a protectivitatii de 91% derivata dintr-un studiu analizand
evolutia a 32 de pacienti cu risc ridicat de EI care au suportat asemenea manopere(17).

b. Contraargumentele
Trei tipuri de argumente au sustinut atitudinea contrara - limitarea recursului la antibiotice ca profilaxie a EI:

economic: orice extindere a utilizarii antibioticelor creste riscul selectarii rezistentei bacteriene fata

de acestea; tinand cont si de aceste considerente pentru termen mediu, daca indicatia de a le folosi este
incerta, raportul cost/ eficienta devine cert nefavorabil antibioticoprofilaxiei. De asemenea, riscul efectelor
adverse severe (in special a socului anafilactic) nu poate fi neglijat intr-o asemenea evaluare pentru cele
mai utilizate antibiotice in profilaxia EI - penicilinele. aa raportul cost-eficienta evaluat pentru profilaxia EI
este unul nefavorabil(18): din 10 milioane de persoane cu risc mediu sau inalt la care se administreaza o
penicilina ca profilaxie a EI, 181 decedeaza prin soc anafilactic si doar la 19 se previne aparitia EI.
patogenic: de fapt, majoritatea bacteriemiilor cu germeni ai florei orale survin dupa acte cotidiane

ale existentei umane: periaj dentar, masticatie (19- 20); doar 10-20% dintre pacientii cu EI au in
antecedentele recente (sub 6 luni) o interventie stomatologica(21). Chiar in conditiile unei eficiente
maxime, profilaxia antibiotica a EI legata de manopere invazive determina o reducere minima a incidentei
acestei afectiuni.
epidemiologic: exista studii ale caror rezultate dovedesc ca de fapt nu exista un beneficiu
semnificativ al profilaxiei asupra incidentei EI: Strom BL si colaboratorii regasesc o frecventa mai ridicata
a procedurilor stomatologice la pacientii din grupul martor (care nu au EI) fata de cei cu EI, p = 0,03(22);
un studiu francez recent publicat estimeaza la 1/46.000 rata prevenirii EI la protezati valvular si
1/150.000 la persoane cu valve native in cazul profilaxiei pentru interventii stomatologice( 23). O prima
consecinta a fost reducerea numarului de doze administrate pentru a diminua presiunea de selectie a unor
tulpini rezistente din cadrul florei endogene; daca recomandarile Asociatiei Americane de Cardiologie
(AHA) din 1957 considerau ca sunt necesare 6-8 doze, in 197 numarul dozelor s-a redus la doua - pre- si
post-interventie, iar la revizuirea recomandarilor AHA din 1984 s-a renuntat si la administrarea
postinterventie( 1).

Tabelul 1. Situatii care

implica un risc ridicat de
evolutie nefavorabila a EI
(recomandarile AHA)
protezai valvular
EI n antecedente
unele maladii congenitale de

cord:
- maladii cianogene
necorectate
chirurgical;
- maladii corectate
chirurgical utiliznd material
protetic (primele 6 luni postintervenie, timp necesar
endotelizrii protezelor
utilizate).
pacieni cu transplant
cardiac la care s-a dezvoltat
o valvulopatie
c. Concilierea
Abordarea care poate concilia cele doua tendinte recunoaste importanta profilaxiei EI pentru anumite
grupuri de pacienti; raman de definit cat mai precis aceste categorii de pacienti, pentru a evita in acelasi
timp utilizarile excesive, dar si subutilizarea antibioticelor. Pacientii carora li se recomanda in prezent
profilaxie antibiotica a EI sunt prezentati in tabelele 1 si 2 (1, 2).
In plus, este necesara constientizarea riscului reprezentat de alte manopere invazive, mai putin evocate in
discutiile asupra acestei teme, in special cele asupra tegumentului infectat (risc de EI stafilococica) sau
asupra tractului urinar (risc de EI enterococice).
d. Situatii particulare
Recomandarile generale privind schemele de profilaxie se adapteaza in cazul in care pacientul primeste
antibiotice din clasele utilizate la profilaxia EI: se prefera incheierea terapiei antibiotice in curs si respectarea
unui interval de 10 zile pana la interventia programata, pentru a permite suselor susceptibile din flora
endogena sa redevina dominante; in situatii care nu permit temporizarea, se prefera profilaxie cu antibiotic
dintr-o alta clasa (de exemplu, clindamicina in cazul in care pacientul primeste peniciline).

Tabelul 2. Situatii in
care se recomanda
profilaxie inainte de
interventii
stomatologice
EI in antecedente
Protezare valvular (cu
valve mecanice sau
biologice)
unturi sistemice sau
pulmonare n condiiile
n care urmeaz o
procedur
stomatologic cu
afectare
gingival

Perspective

Evolutiile din aceste decenii de utilizare a profilaxiei antibiotice a EI contureaza doua tendinte: reducerea
numarului de doze administrate si selectivitate sporita a pacientilor care necesita profilaxie; singurul mod
stiintific de a creste si mai mult mult gradul de adecvare a recomandarilor de profilaxie la necesitatile reale
este de a recurge la studii comparative versus placebo sau intre diverse scheme antibiotice si la grupe de
pacienti cu factori de risc diferiti; considerente de etica limiteaza insa o asemenea abordare. Proliferarea
recomandarilor de profilaxie mai selective in ultimii ani pune insa clinicianul (stomatolog de regula) in fata
dilemei:

antibioticoprofilaxie in pofida recomandarilor - cum justific aparitia unui efect advers intr-o

asemenea situatie (de exemplu, anafilaxie);

conformare la recomandari, cu neadministrare de profilaxie in situatii de risc mediu/scazut - cum
justific aparitia unei EI la un asemenea pacient.
Concluzii
Dincolo de negarea completa sau de aplicarea fara rezerve, profilaxia antibiotica a EI in cazul interventiilor
stomatologice are indicatii selective, legate de:
a) gradul de risc al pacientului pentru a dezvolta EI care sa evolueze sever (legat de afectarea endocardica
preexistenta): proteza valvulara, antecedente de endocardita infectioasa, transplant cardiac cu valvulopatie,
boala cardiaca congenitala cianogena;
b) intensitatea potentiala a bacteriemiei dupa respectiva interventie stomatologica: interventii asupra
tesutului gingival sau periapical, manopere cu lezarea mucoasei bucale.
In cazurile in care se considera utila o asemenea profilaxie, se recomanda a fi folosite: aminopeniciline sau
clindamicina, pentru o singura administrare, cu 30-60 de minute inainte de interventia respectiva.
Prevenirea si tratamentul precoce ale afectiunilor stomatologice poate fi o alternativa mult mai eficienta
pentru reducerea incidentei EI cu germeni ai florei orale.

Bibliografie
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American Heart Association. Circulation. 2007; 116: 1.736-54.
2. Gould F.K., Elliott T.S., Foweraker J. et al. Guidelines for the prevention of endocarditis: report of the
Working Party of the British Society for Antimicrobial Chemotherapy. J Antimicrob Chemother. 2006; 57:
1.035-42.
3. Socite de pathologie infectieuse de langue franaise (Spilf). Revision of the March 1992 consensus
conference recommendations for the prophylaxis of infectious endocarditis Ann Fr Anesth Reanim. 2003;
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4. Ernstene A.C., McGarvey C.J., Ecker J.A. The prophylaxis of subacute bacterial endocarditis. Cleve Clin Q.
1951; 18: 1-5.
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1952; 8: 138-57.
6. Jones T.D., Baumgartner L., Bellows M.T. et al. Prevention of rheumatic fever, and bacterial endocarditis
through control of streptococcal infection. Circulation 1955; 21:317-20.
7. R.A. Seymour, R. Lowry, J.M. Whitworth and M.V. Martin Infective endocarditis, dentistry and antibiotic
prophylaxis; time for a rethink? Br Dent J. 2000 Dec 9; 189(11):610-6.
8. Scully C.M., Levers B.G., Griffiths M.J., Shirlaw P.J. Antimicrobial prophylaxis of infective endocarditis:
effect of BSAC recommendations on compliance in general practice. J Antimicrob Chemother. 1987; 19:
521-6.
9. Nelson C.L., Van Blaricum C.S. Physician and dentist compliance with American Heart Association
guidelines for prevention of bacterial endocarditis. J Am Dent Assoc. 1989; 118: 169-73.
10. Bennis A., Soulami S., Khadir R., Chraibi N. Survey on the practice of antibiotic prophylaxis of infective
endocarditis by dentists Arch Mal Coeur Vaiss. 1996; 89: 713-8.
11. Panos G., Giamarellou H., Papazachos G., Birbilis T., Toutouzas P. Greek physicians and dentists
compliance with the British society for antimicrobial chemotherapy (BSAC) guidelines for preventing
bacterial endocarditis. J Chemother. 1996; 8: 270-7.
12. Epstein J.B., Chong S., Le N.D. A survey of antibiotic use in dentistry. J Am Dent Assoc. 2000; 131:
1600-9.

13. Okell C.C., Elliott S.D. Bacteraemia and oral sepsis: with special reference to the aetiology of subacute
endocarditis. Lancet 1935; 2: 869-72.
14. Baltch A.L., Schaffer C., Hammer M.C. et al. Bacteraemia following dental cleaning in patients with and
without penicillin prophylaxis. Am Heart J 1982; 104: 1.335-9.
15. Park S., Montoya A., Moreno N. et al. Infective aortic endocarditis after percutaneous balloon aortic
valvuloplasty. Ann Thorac Surg 1993; 56: 1.161-2.
16. Ochsenfahrt C., Friedl R., Hannekum A. et al. Endocarditis after nipple piercing in a patient with a
bicuspid aortic valve. Ann Thorac Surg 2001; 71: 1.365-6.
17. Imperiale T.F. Does prophylaxis prevent postdental infective endocarditis? A controlled evaluation of
protective efficacy. Am J Med, 1990; 88: 131-6.
18. Agha Z., Lofgren R.P., VanRuiswyk J.V. Is antibiotic prophylaxis for bacterial endocarditis cost-effective?
Med Decis Making 2005; 25: 308-20.
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of the evidence dental surgical procedures are a principle cause of endocarditis in children. Paediatr Cardiol
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20. Seymour R.A. Dentistry and the medically compromised patient. Surgeon 2003; 1: 207-14.
21. van der Meer J.T., Thompson J., Valkenburg H.A., Michel M.F. Epidemiology of bacterial endocarditis in
The Netherlands, part II: antecedent procedures and use of prophylaxis. Arch Intern Med 1992; 152: 1.86973.
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population-based, case-control study. Ann Intern Med 1998; 129: 761-9.
23. Duval X., Alla F., Hoen B. et al. Estimated risk of endocarditis in adults with predisposing cardiac
conditions undergoing dental procedures with or without antibiotic prophylaxis. Clin Infect Dis. 2006; 42:
e102-7.

Infective Endocarditis (previously referred to as bacterial endocarditis)

What is infective endocarditis?

Infective endocarditis is an infection of the heart's inner lining (endocardium) or the heart valves. This can damage or even
destroy your heart valves.
How does it occur?
Infective endocarditis occurs when bacteria in the bloodstream (bacteremia) lodge on abnormal heart valves or other
damaged heart tissue. Certain bacteria normally live on parts of your body, such as the mouth and upper respiratory system,
the intestinal and urinary tracts, and the skin. Some surgical and dental procedures cause a brief bacteremia. Bacteremia is
common after many invasive procedures, but only certain bacteria commonly cause endocarditis.
Who is at risk?
Endocarditis rarely occurs in people with normal hearts. However, if you have certain preexisting heart conditions, you're at
increased risk for endocarditis.* Some of these conditions include having...

an artificial (prosthetic) heart valve

a history of previous endocarditis
heart valves damaged (scarred) by conditions such as rheumatic fever
various kinds of congenital heart defects
hypertrophic cardiomyopathy (hi"per-TRO'fik kar"de-o-mi-OP'ah-the)
people who have had a heart transplant who develop a heart valve abnormality

* Only some of these patients will need antibiotic prophylaxis before dental procedures (see next section).
Some congenital heart defects, including a ventricular septal defect, an atrial septal defect, or a patent ductus arteriosus,
can be successfully repaired surgically. After this you'll no longer be at increased risk for endocarditis.

Although endocarditis is a very serious disease, and many people may be at increased risk for developing it, most of these
people do not contract it. According to the American Heart Association, there are about 29,000 cases of endocarditis
diagnosed a year.
Can endocarditis be prevented?
Endocarditis is much more likely to result from frequent exposure to random bacteremias associated with daily activities
than from bacteremia caused by a dental, gastrointestinal (GI) tract, or genitourinary (GU) tract procedure. Prophylaxis may
prevent an exceedingly small number of cases of endocarditis, if any, in individuals who undergo a dental, GI tract, or GU
tract procedure.
The risk of antibiotic-associated adverse events exceeds the benefit, if any, from prophylactic antibiotic therapy.
Maintenance of optimal oral health and hygiene may reduce the incidence of bacteremia from daily activities and is more
important than prophylactic antibiotics for a dental procedure to reduce the risk of endocarditis.
Not all cases of endocarditis can be prevented, because we don't always know when a bacteremia occurs. In past years, the
American Heart Association has recommended that patients at increased risk for endocarditis take prophylactic antibiotics
before certain dental, GI and GU procedures. Recently, the American Heart Associations Endocarditis Committee, together
with national and international experts on endocarditis, extensively reviewed published studies in order to determine whether
dental, GI or GU tract procedures are possible causes of endocarditis. These experts concluded that there is no conclusive
evidence linking dental, GI or GU tract procedures with the development of endocarditis. They also concluded that
endocarditis is much more likely to result from frequent exposure to random bacteremias associated with daily activities than
from bacteremia caused by a dental, GI or GU tract procedure.
Therefore, the current practice of giving patients antibiotics prior to a dental procedure is no longer recommended EXCEPT
for patients with the highest risk of adverse outcome resulting from endocarditis. Those people at highest risk include those
with:

Prosthetic cardiac valve or prosthetic material used for cardiac valve repair
Previous endocarditis
Congenital heart disease for these conditions:
Unrepaired cyanotic congenital heart disease, 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 six months after the procedure
Repaired congenital heart disease with residual defects (persisting leaks or abnormal flow) at the site or
adjacent to the site of a prosthetic patch or prosthetic device (which inhibit endothelialization)
Cardiac transplantation recipients who develop cardiac valve abnormalities

The American Heart Association has concluded that an exceedingly small number of cases, if any, of endocarditis may be
prevented by giving antibiotics prior to a dental procedure. If such benefit from prophylaxis exists, it should be reserved
ONLY for those patients at highest risk (listed above) who would have the worst outcomes if they contract endocarditis.
The American Heart Association recognizes the importance of good oral and dental health including regular brushing and
flossing and regular visits to the dentist for patients at risk of endocarditis.
The American Heart Association no longer recommends administering antibiotics solely to prevent endocarditis in patients
who undergo a GI or GU tract procedure.
What can you do?
Changes in these guidelines do not change the fact that your cardiac condition puts you at increased risk for developing
endocarditis. If you develop signs or symptoms of endocarditis such as unexplained fever see your doctor right away. If
blood cultures are necessary (to determine if endocarditis is present), it is important for your doctor to obtain these cultures
and other relevant tests BEFORE antibiotics to treat endocarditis are started.
If you've been told you have any of the cardiac conditions listed above, be sure to tell your dentist and other physicians who
may be treating you.

Prophylaxis is recommended because endothelialization of prosthetic material occurs within six months after the procedur

The Council on Scientific Affairs of the American Dental Association has approved the American Heart Association's
statement as it relates to dentistry.

Infective Endocarditis and Dentistry: Outcome-based Research

Joel B. Epstein, DMD, MSD, FRCD(C)

ABSTRACT
Antibiotic prophylaxis for prevention of infective endocarditis has long been recommended for
patients receiving dental care. Two studies of patients with endocarditis found limited risk associated
with dental treatment. It is imperative that guidelines for therapy be based on outcome studies and on
evidence of safety, efficacy and cost effectiveness.
MeSH Key Words:antibiotic prophylaxis; dental care; endocarditis infective/prevention and control..
J Can Dent Assoc 1999; 65:95-6

[Introduction| References]
Introduction
For years, guidelines for the prevention of infective endocarditis have recommended antibiotic
prophylaxis for certain patients receiving dental care. The guidelines are revised from time to time,
with the most recent revision completed in 1997. These guidelines have been based on animal studies
and reports of individual patients where infective endocarditis has developed. Over the years, case
reports and potential legal implications have motivated health care providers, including physicians and
dentists, to recommend and institute antibiotic prophylaxis before dental procedures for individuals
with specific heart conditions, particularly those with valvular disease, valve replacement or valvular
regurgitation.
The most recent guidelines for the prevention of infective endocarditis and their implications for
dental practice were recently reviewed in a paper published in the Journal.1 That paper highlighted that
infective endocarditis is an extremely rare condition and that the attendance for dental management is
common in Western society. Correlation between dental visits and subsequent endocarditis does not
prove cause and effect, especially in light of the fact that dental treatment is a possible cause of very
few cases of infective endocarditis.
Two important outcome studies have recently been published.2, 3 These two outcome-based studies
have similar findings and indicate that the current guidelines, which are not based on population-based
outcome studies, require further review.
A Dutch study2 assessed 427 patients with endocarditis and found that 64% of these patients would
have been eligible for antibiotic prophylaxis based on previously known cardiac conditions. Twentythree per cent had undergone a procedure that would have indicated prophylaxis within one-half year
of onset of endocarditis, and 11% had undergone a procedure within 30 days of onset. It was thought
that prophylaxis may have prevented 17% of cases within 180 days of onset, a period of time that
extends beyond what many believe to be the appropriate incubation period, and 11% of cases within
30 days, representing only 5.3% of cases. Therefore, even if antibiotic prophylaxis was 100% effective
and was provided for all at-risk patients receiving dental treatment, only a small fraction of cases of
endocarditis (5.3%) would be potentially prevented.
A more recent study assessed patients in 54 hospitals in the Philadelphia area.3 A total of 287 cases of
endocarditis were identified; excluded from analysis were patients with endocarditis associated with
intravenous drug use. It was found that in the three months preceding the diagnosis of endocarditis,
dental treatment was no more frequent in these patients than in non-infected age- and sex-matched
control patients. Of the 273 patients with endocarditis, 38% knew of cardiac conditions; of the control
patients, only 6% were aware of cardiac conditions. Patients with endocarditis had a history of mitral

valve prolapse, congenital heart disease, valve surgery, rheumatic fever or heart murmur more
frequently than did control patients. In the at-risk patients with known cardiac lesions, dental therapy
was significantly less common than among the control patients. In this study, dental treatment was not
seen to represent a risk for infective endocarditis, even in patients with cardiac valve abnormalities.
However, the presence of cardiac valvular abnormalities did represent a risk factor. No dental
procedures other than tooth extraction in the two months prior to hospital admission were identified as
risk factors; however, dental extractions were uncommon. Of the patients with endocarditis who had a
known cardiac valvular abnormality and dental treatment (10.6%) in the previous three months, those
who had dental therapy one month prior to diagnosis of endocarditis (4.4%) were found to be at no
significantly increased risk from dental treatment, although the number of at-risk patients was small.
The statistical risk for endocarditis did not change regardless of whether antibiotics were used in
dental treatment. Very few cases of infective endocarditis would be prevented even if antibiotic
prophylaxis was provided for dental procedures and was 100% effective.
It is important to recognize that failures of prophylactic antibiotic regimens have been recorded and
indeed have been used to assist in modifying guidelines for prophylaxis coverage. Additional concerns
about antibiotic prophylaxis include cost effectiveness and the increased risk of resistant bacteria in
society.1, 4
It is imperative that guidelines for therapy be based on outcome studies (when available) and on
evidence of safety, efficacy and, increasingly, cost effectiveness. The new data available about
infective endocarditis, including the limited risk associated with dental treatment, the time of
incubation and the increasingly available outcome-based evidence, require continual review of the
current historically and empirically based recommendations. Current recommendations are essentially
based on animal models and limited human studies. As these guidelines adapt to current information, it
becomes increasingly important that the medical, dental and legal professions and the public be
informed and up-to-date about knowledge and guidelines.
[ Top ]

Dr. Epstein is head of dentistry at the Vancouver Hospital and Health Sciences Centre; on the
medical-dental staff of the B.C. Cancer Agency; professor and head of hospital dentistry at the
University of British Columbia; and research associate professor at the University of Washington.
Reprint requests to: Dr. J.B. Epstein, Vancouver General Hospital, Department of Dentistry, 855 West
12th Ave., Vancouver, BC V5Z 1M9.

References
1. Epstein JB. Infective endocarditis: dental implications and new guidelines for antibiotic
prophylaxis. J Can Dent Assoc 1998; 64:281-92.
2. Vandermeer JTM, Thompson J, Valkenburg HA, and others. Epidemiology of infective endocarditis
in the Netherlands. Arch Intern Med 1992; 152:1863-73.
3. Strom BL, Abrutyn E, Berlin JA, and others. Dental and cardiac risk factors for infective
endocarditis, a population based case control study. Ann Intern Med 1998; 129:761-9.
4. Haas DA, Epstein JB, Eggert FM. Antimicrobial resistance: dentistry's role. J Can Dent Assoc 1998;
64:496-502.
Penicillins for the prophylaxis of bacterial endocarditis in dentistry

Oliver R, Roberts GJ, Hooper L

Summary
There is no evidence about whether penicillin prophylaxis is effective or ineffective against
bacterial endocarditis in people at risk who are about to undergo an invasive dental procedure.
There is a lack of evidence to support published guidelines in this area. It is not clear whether
the potential harms and costs of penicillin administration outweigh any beneficial effect.
Ethically practitioners need to discuss the potential benefits and harms of antibiotic prophylaxis
with their patients before a decision is made about administration.
This is a Cochrane review abstract and plain language summary, prepared and maintained by
The Cochrane Collaboration, currently published in The Cochrane Database of Systematic
Reviews 2008 Issue 1, Copyright 2008 The Cochrane Collaboration. Published by John Wiley
and Sons, Ltd.. The full text of the review is available in The Cochrane Library (ISSN 1464780X).
This record should be cited as: Oliver R, Roberts GJ, Hooper L. Penicillins for the prophylaxis
of bacterial endocarditis in dentistry. Cochrane Database of Systematic Reviews 2004, Issue 2.
Art. No.: CD003813. DOI: 10.1002/14651858.CD003813.pub2
This version first published online: April 19. 2004
Date of last subtantive update: February 23. 2004
Abstract
Background
Many dental procedures cause bacteraemia and it is believed that this may lead to bacterial
endocarditis (BE) in a few people. Guidelines in many countries recommend that prior to
invasive dental procedures antibiotics are administered to people at high risk of endocarditis.
However, it is unclear whether the potential risks of this prophylaxis outweigh the potential
benefits.
Objectives
To determine whether prophylactic penicillin administration compared to no such
administration or placebo before invasive dental procedures in people at increased risk of BE
influences mortality, serious illness or endocarditis incidence.
Search strategy
The search strategy was developed on MEDLINE and adapted for use on the Cochrane Oral
Health, Heart and Infectious Diseases Groups' Trials Registers (to October 2003), as well as the
following databases: Cochrane Central Register of Controlled Trials (CENTRAL) (The
Cochrane Library, Issue 2, 2002), OLDMEDLINE (1966 to June 2002); EMBASE (1980 to June
2002); SIGLE (to June 2002); and the Meta-register of current controlled trials.
Selection criteria
Due to the low incidence of BE it was anticipated that few if any trials would be located. For this
reason, cohort and case controlled studies were included where suitably matched control or
comparison groups had been studied. The intervention was the administration of penicillin
compared to no such administration before a dental procedure in people with an increased risk
of BE. Cohort studies would need to follow those at increased risk and assess outcomes following
any invasive dental procedures, grouping by whether prophylaxis was received. Included case
control studies would need to match people who had developed endocarditis (and who were
known to be at increased risk before undergoing an invasive dental procedure preceding the
onset of endocarditis) with those at similar risk but who had not developed endocarditis.
Outcomes of interest were: mortality or serious adverse event requiring hospital admission;
development of endocarditis following any dental procedure in a defined time period;
development of endocarditis due to other non-dental causes; any recorded adverse events to the
antibiotics; and cost implications of the antibiotic provision for the care of those patients who
develop endocarditis.
Data collection and analysis
Two reviewers independently selected studies for inclusion, then assessed quality and extracted
data from the included study.
Main results
No RCTs, CCTs or cohort studies were included. One case-control study met the inclusion
criteria. It collected all the cases of endocarditis in the Netherlands over 2 years, finding a total

of 24 people who developed endocarditis within 180 days of an invasive dental procedure,
definitely requiring prophylaxis according to current guidelines and who were at increased risk
of endocarditis due to a pre-existing cardiac problem. This study included participants who died
because of the endocarditis (using proxys). Controls attended local cardiology outpatient clinics
for similar cardiac problems, had undergone an invasive dental procedure within the past 180
days and were matched by age with the cases. No significant effect of penicillin prophylaxis on
the incidence of endocarditis could be seen. No data were found on other outcomes.
Authors' conclusions
There is no evidence about whether penicillin prophylaxis is effective or ineffective against
bacterial endocarditis in people at risk who are about to undergo an invasive dental procedure.
There is a lack of evidence to support published guidelines in this area. It is not clear whether
the potential harms and costs of penicillin administration outweigh any beneficial effect.
Ethically practitioners need to discuss the potential benefits and harms of antibiotic prophylaxis
with their patients before a decision is made about administration.
Aetiology and risk factors of infective endocarditis
Abstract number: 903_r1910
Slavcovici A.
"

Objective:
The purpose of our study is to investigate the aetiology and risk factors of infective endocarditis (IE) in
our geographic area.

Methods:
In a retrospective chart review all 125 patients who fulfilled the Duke criteria for IE between January
1998 and December 2003 were included in the study. For reasons of accuracy for the aetiological
diagnosis we have used the automatic method for bacterial detection (BacT/Alert system). The strains
were identified by API system.

Results:
The persistent bacteraemia was demonstrated in 63.2% cases. The majority of endocarditis were caused
by gram-positive cocci (78.5%): Streptococcus viridans (25.3%), Streptococcus bovis (5%),
Enterococcus spp. (6.3%), Staphylococcus aureus 34% (MSSA24%, MRSA 10%). Gram-negative
bacilli were detected in 19% cases. Viridans streptococcal endocarditis were associated with dental
procedures (P = 0.000) and staphylococcal endocarditis were associated with prosthetic valve or
intravascular devices. Frequency of Gram-negative endocarditis was correlated with urinary and
gastrointestinal diseases or procedures.

Conclusions:
A large variety of microorganisms was implicated in IE, but staphylococci and streptococci remained
the most common etiologic agents. The streptococcus aetiology is associated with stomatological
invasive procedures or periodontal infections. The prosthetic valve represents an important risk of
staphylococcus endocarditis. The endocarditis prophylaxis is not adequate at such time, especially in
situations of stomatological or genitourinary invasive procedures.
"
Session Details

Date:
Time:
Session name:
Subject:
Location:

01/08/2007
00:00-00:00
XXIst ISTH Congress
Oxford, UK

Endocarditis:
A Surgical Conservative Treatment With Favorable Outcome
of an Infective Endocarditis Due to Staphylococcus
Lugdunensis
M EL FEGHALY
Division of Cardiovascular Surgery
Rangueil Hospital
C. DAMBRIN
Division of Cardiovascular Surgery
Rangueil Hospital
A. ELGHAOUI
Division of Gynecology and Obstetrics
La Grave Hospital
J.A. TRILLES
>Division of pneumology
Rangueil Hospital
P. NAKHL
Division of Gynecology and Obstetrics
La Grave Hospital
A. CERENE
Division of Cardiovascular Surgery
Rangueil Hospital

Citation:
M EL FEGHALY, C. DAMBRIN, A. ELGHAOUI, J.A. TRILLES, P. NAKHL, A. CERENE:
Endocarditis: A Surgical Conservative Treatment With Favorable Outcome of an Infective
Endocarditis Due to Staphylococcus Lugdunensis. The Internet Journal of Thoracic and
Cardiovascular Surgery. 1997. Volume 1 Number 1.

Keywords: surgery, medicine, cardiac, heart, vascular, chest, heart-lung machine, cardio-pulmonary,
bypass surgery, aneurysm, aorta, vessel, cardiothoracic, thoracic, cardiopulmonary bypass, valve,
carotid

Introduction
Staphylococcus lugdunensis, a coagulase negative species, has been recently recognized (1988) and
described as a rare cause of endocarditis.
Endocarditis due to this organism has been reported to have a high mortality rate in most published
cases, and involves native valves more frequently than other coagulase negative staphylococci , . In
contrast to the few embolic phenomena associated with other coagulase negative staphylococcal
endocarditis, S. Lugdun is reported to have a higher incidence of embolic phenomena . There are few
data concerning the epidemiology and ecology of S. Lug, but we believe as many others do, that this
organism is similar to other coag. neg. species in that it is ubiquitary, found on the skin andmucous
membranes. However, in most reported cases, the portal of entry has not been identified.
1

In this paper we report a case of a young patient who underwent a conservative surgical treatment with
favorable outcome for an infective endocarditis due to Staphylococcus Lugdunensis.

Case
A 20-year-old white male patient, with no significant past medical history, was admitted to our
hospital in March 1997 with a history of exertion dyspnea, extreme fatigue, fever, night sweats,
abdominal pain and vomiting. There was no history of dental extraction or upper respiratory tract
infection before the onset of present illness. Laboratory tests were performed and showed a severe
hypoxia: PO2 61 mmHg: PCO2 30 mmHg, and the other following values: WBC 12800/mm3, ESR
30, Hb 13.8, Na 132, K 3.24, Cl 92, creat 113.
Chest X- Ray showed a diffuse bilateral interstitial infiltrative process predominating mostly on the
right lung. On physical exam, the patient was pale and extremely tired, the heart rate was 90 per
minute. Diminished breath sounds were noted at both bases of the lungs with crepitations of the right
lung. A loud pansystolic cardiac murmur of grade 2/6 was heard at the apex without irradiation, this
was considered to be partially attributable to high fever. However we decided at that time to postpone
any exploration of this murmur after total recovery of the patient.
The initial interpretation of these data was suggestive of an interstitial acute lung infection, and the
patient was started on a 4 week course of empirical antibiotherapy initially including Erythromycin
and Ceftriaxone with adequate doses of methylprednisolone succinate. (Solumedrol). Shortly after,
Erythromycin was replaced by Ofloxacine because we have detected biologic signs of hepatic
cytolysis. After the patient was discharged home with resolution of pain and temperature, blood
cultures were proved to be positive for coagulase negative staphylococcus that was subsequently
identified as Staphylococcus Lugdunensis.
Five days after the last dose of antibiotics, the patient has presented again to the emergency room for
recurrence of fever with obvious change in his previously noted systolic ejection murmur on physical
exam, there was no evidence of hepatosplenomegaly or other peripheral manifestations of
endocarditis.
An intensive work up was carried out including laboratory tests (WBC 9000, ESR 26), a bone scan
which revealed a homogeneous fixation without any infectious bony localization, a two dimensional
echocardiography identified a mild mitral valve regurgitation, and demonstrated the existence of large
vegetations at the anterior and posterior leaflets of the mitral valve, which was confirmed by transoesophageal echography. A specialized stomatology consultation was significant for severe dental
caries.

On the basis of susceptibility testing results, cefazolin (6 g daily) and netilmicin (300 mg daily) and
rifampin (1.2 g daily) were started. Despite its susceptibility, penicillin was excluded from the regimen
because allergic problem. Dose adaptation was made according to serum bactericidal activity.
Hyperoxemia has been induced to increase aminoglycosides activity in poorly oxygenated vegetation
tissue. A clear improvement of the clinical and biologic status was noted, with CRP falling into normal
range. Valvular vegetations were shown to be stable on echocardiography follow-up. After few days of
apyrexia, recurring low-grade fever was attributed to a deep venous thrombosis localized at the left
peroneal vein. We did not anticoagulate, but followed-up the patient closely with duplex scan. After
reviewing numerous reports by many authors highlighting the aggressive nature and virulence of S.
Lugdunensis, and once the patient has been stable on medical treatment, he was taken to surgery and
underwent a mitral valvuloplasty. Before the Cardio- Pulmonary Bypass was established we identified
an important mitral regurgitation in contrast to what was demonstrated on preoperative
echocardiography. We did a transseptal approach and found huge vegetation localized at the anterior
leaflet of the mitral valve, the posterior leaflet was almost non-existent. Finally, in order to reduce the
risk of infection, we abstained from introducing any synthetic material. We simply resected the
pathologic area of the anterior leaflet and performed an annuloplasty by placing stitches at the anteroexternal commissure thus minimizing the mitral regurgitation without creating any iatrogenic stenosis.
The competence of the valve was then interrogated and a minimal residual regurgitation was detected.
The postoperative recovery was satisfying with no misfortunate events noted. An intraoperative Gram
stain of the mitral vegetations was negative for bacteria; as were blood cultures. Repeated
transoesophageal echocardiography showed a non-significant mitral incompetence with no evidence of
residual vegetations. Postoperatively the patient was maintained on intravenous antibiotics for 10 days
and discharged home on a 3-week course of oral antibiotics (Pefloxacine, Fucidine and Rifadine). A 6month follow-up postoperatively has been gratifying.

Discussion
Trying to explain the increasing incidence of native valve endocarditis caused by coag. neg.
staphylococci, the increased use of indwelling intravascular catheters and the increased recognition of
the coag neg staphylococci as pathogens are the most accepted reason. 3 to 5% of cases of native valve
endocarditis are due to these pathogens , Staph epidermidis being the most common species involved
in native valve endocarditisThe predilection of Staph. Lug for native valves was evident in the
literature where 67% of reported cases involved native valves (the mitral valve in 67% and the aortic
valve in 33% of cases. We didnt find in our patient any previous history of valvular disease and no
obvious portal of entry for bacteremia, except for the dental caries. The same pathogen is a rare cause
of endocarditis and is characterized by its highly pathogenic potential . This aggressive natural
history is due to the acute hemodynamic compromise frequently encountered with this particular
pathogen and can be explained by the ability of this organism to destroy the native valve. This
particular pathogen behaves like S. aureus, which is a coagulase positive organism. According to
Lambe et al. , it seems that S.lug is able to bind vitronectin and fibrinogen to extracellular matrix
protein similar to S. aureus. In his review of the literature, Koh concluded that the use of commercial
identification systems can lead to misidentification of S. lug with other staphylococci and
consequently delay appropriate treatment. 1,2, . Isolates of coag neg should undergo detailed
identification, and the detection of coagulase fibrinogen affinity factor and ornithine decarboxylase are
substantial in the diagnosis of S. lug. 1.
4

Based on our own experience and supported by the world wide literature, we believe that embolic
complications are rarely seen in cases of infective endocarditis caused by coagulase negative
staphylococci compared to other organisms. Such recognition isnt the rule in the case of S. Lugdun
which, to the contrary, is more frequently emboligenic 3. With our particular patient we suspected an
embolic infarction of the spleen on an abdominal ultrasound basis, but serial abdominal echography
failed to demonstrate any detectable lesion.

Conclusion
In this paper we presented a case of a staphylococcus lugdunensis endocarditis affecting the native
mitral valve, upon which we performed a mitral valvuloplasty, thus avoiding valve replacement with
all its complications as a foreign body. In conclusion, one should always be aware that this particular
form of endocarditis is different from other coagulase negative staphylococci endocarditis, since it
involves predominately native valves, and it has a destructive and aggressive course with a high
mortality rate in contrary to other coag neg species. However we are convinced that medical treatment
should seek use of synergic antibiotics carefully monitored on detailed in vitro data for each patient,
and early diagnosis and tailored surgery are crucial for a better outcome.

References
1. Shuttleworth R, Colby WD: Staphylococcus lugdunensis endocarditis. J Clin Microbiol
1992; 30: 1948-52.
2. Etienne J, Pangon B, Leport C et al: Staphylococcus lugdunensis endocarditis. LANCET
1989; 1: 390.
3. Fleurette J, Bes M, Brun Y et al. Clinical isolates of staphylococcal lugdunensis and S.
Schleiferi: bacteriological characteristics and susceptibility to antimicrobial agents. Res
Microbiol 1989; 140: 107-118.
4. Vandenesh F, Etienne J, Reverdy ME, Eykin SJ: Endocarditis due to staphylococcus
lugdunensis: report of 11 cases and review. Clin Infect Dis 1993; 17: 871-6.
5. Paulsson M, Peterson AC, Ljungh A. Serum and tissue protein binding and cell surface
properties of staphylococcus lugdunensis. J Med Microbiol 1993; 38: 96-102.

Febra prelungita secundara unei interventii stomatologice

la pacient cu endocardita bacteriana in antecedente: prezentare de caz

Rezumat
Prezentam cazul unei paciente cu endocardita infectioasa (EI) in antecedente, la care, in pofida profilaxiei
antibiotice adecvate, o interventie stomatologica s-a soldat cu osteita de creasta alveolara. Tratamentul
antimicrobian nu a controlat procesul infectios, fiind necesara asanarea chirurgicala a procesului septic.
Abstract
We report the case of a patient with prolonged fever of unknown origin with previous infective endocarditis.
The final diagnosis was alveolar osteitis. The outcome was favourable with a combined therapy: surgical and
antimicrobial.
INTRODUCERE
Endocarditele sunt intlnite mai ales la persoanele in vrsta. Aproximativ 50% din cazuri sunt diagnosticate
la pacienti cu vrsta de peste 50 de ani. Aceasta afectiune este de doua ori mai frecventa la barbati, iar la
cei in vrsta, de 8 ori mai frecventa comparativ cu femeile vrstnice. La copiii si la adultii tineri, cele mai
multe cazuri de endocardite (75%) apar in conditiile unor afectiuni cardiace congenitale.
Factori de risc
Cele mai multe dintre endocardite sunt determinate de infectii bacteriene. Pacientii care au afectiuni

cardiace congenitale sau dobndite au un risc crescut, in lipsa lor boala intlnindu-se rar. Dintre factorii de
risc, cel mai frecvent intlniti amintim: defect septal atrial, defect septal ventricular, sunt chirurgical intre
aorta si artera pulmonara, afectiuni valvulare. Mecanismele de aparitie a endocarditelor sunt numeroase,
bacteriile putnd ajunge in circulatia sangvina pe mai multe cai. Sunt insa anumite proceduri medicale care
au un risc crescut precum: adenoidectomiile, amigdalectomiile, extractiile dentare si examinarile
endoscopice sau chirurgicale ale cailor respiratorii, tractului gastrointestinal sau urinar. La pacientii
spitalizati, abordul intravenos, cateterele sau administrarea intravenoasa a unor produse contaminate
reprezinta de asemenea factori de risc. Varietatea simptomatologiei la debut (febra, frison, fatigabilitate,
transpiratii, dureri musculare si articulare, scaderea apetitului si scaderea in greutate), precum si lipsa unei
simptomatologii specifice initiale, face ca diag-nosticul acestei afectiuni sa fie dificil si adesea intrziat.
Ulterior, apar manifestari cardiace precum regurgitari vasculare insotite uneori de aritmii (tahicardie,
fibrilatie atriala), noduli Osler, leziuni Janeway, petesii conjunctivale sau insuficienta renala cronica. Prezenta
anemiei, a bacteriemiei persistente, prezenta vegetatiilor valvulare decelate prin ecografie cardiaca
transtoracica sau transesofagiana, orienteaza spre diagnosticul de endocardita.
PREZENTARE DE CAZ
Prezentam cazul unei paciente in vrsta de 63 de ani, din Constanta, aflata in supravegherea Clinicii de Boli
Infectioase pentru prevenirea recaderilor in urma unei endocardite infectioase cu punct de plecare dentar,
pentru care pacienta a fost investigata si tratata in urma cu 2 ani. In acest interval, pacienta a avut mai
multe lucrari dentare care s-au realizat sub protectie de antimicrobiene, la recomandarea noastra. In urma
unei asemenea interventii, desi aceasta a fost realizata sub protectie de antimicrobiene cu spectru larg,
bolnava a dezvoltat un sindrom febril insotit de dureri toracice posterioare, transpiratii nocturne si astenie
fizica marcata. Simptomatologia actuala a debutat in urma cu 10 zile anterior internarii. Din antecedentele
patologice personale ale pacientei mentionam:

Sepsis cu Enterobacter (ESBL) cu punct de plecare focare infectioase dentare;

Endocardita infectioasa subacuta;
Pericardita exudativa.
La examenul obiectiv s-a constatat: TA = 95/60mmHg, suflu sistolic in focarul mitralei si suflu sistolic
tricuspidian, frecatura pericardica. Analizele de laborator au evidentiat leucocitoza cu neutrofilie (72%),
prezenta sindromului inflamator: VSH = 85/1h, fibrinogen = 440mg/dl, PCR = pozitiv. Hemoculturile pe
medii aerobe si anaerobe au fost negative.

S-a efectuat ecografia cardiaca cu urmatorul rezultat:

defect septal interventricular (flux turbulent la baza marilor vase, in sectiune transversala), cu mic
sunt stngadreapta;
insuficienta mitrala gradul I, insuficienta tricuspidiana gradul II;
fina lama de lichid in cavitatea pericardica (aproximativ 4 mm), lateral de VS si anterior de VD;
Nu s-au decelat vegetatii la nivelul valvelor.

S-a instituit terapie antimicrobiana pe criterii de probabilitate cu ceftriaxona si amikacina initial, apoi cu
meropenem. Curba febrila nu a fost influentata semnificativ, ca de altfel si stare clinica generala a bolnavei,
timp de 20 de zile. Consulturile stomatologice repetate au infirmat initial posibilitatea cauzei dentare a
sindromului febril. In urma consultului OMF-oromaxilofacial s-a decis efectuarea unei radiografii panoramice
a maxilarului inferior, unde se aflau cei patru dinti la care se efectuasera interventii. S-a constatat ca
lucrarea dentara recent efectuata s-a finalizat cu introducerea in canalele alveolare a unor fire de srma de
nichel, la doi dintre acesti dinti firele depasind dimensiunea canalului, ceea ce a determinat aparitia de
focare distale inflamatorii granulomatoase. S-a reevaluat cazul si s-a diagnosticat osteita de creasta

alveolara dinti 33, 34 pentru care s-a practicat extractia dentara si remodelarea crestei alveolare. In urma
celei de-a doua extractii, bolnava a devenit afebrila si dupa efectuarea curei antimicrobiene complete, s-a
externat vindecata.
DISCUTII
Cazul prezentat readuce in actualitate utilitatea urmaririi riguroase a pacientilor cu predispozitii la infectii
sistemice cu punct de plecare dentar, la necesitatea unei mai bune colaborari cu medicii dentisti pentru
cunoasterea in amanunt a tehnicilor si metodelor terapeutice pe care acestia le abordeaza la pacienti, in
vederea evaluarii riscurilor potentiale de diseminare a unor infectii locale. Cazul in sine a fost un succes
terapeutic si datorita pacientei, care in conditiile in care clinicianul a infirmat orice alta cauza a sindromului
infectios, iar dentistul a negat implicarea focarului dentar, a consimtit la investigatii suplimentare de inalta
performanta, inaccesibile uzual, singurele care au permis precizarea diagnosticului. S-a reconfirmat ca
infectiile de focar cu diseminare sistemica nu pot fi rezolvate numai cu tratament antimicrobian adecvat,
decisiva fiind rezolvarea focarului ce a initiat infectia.
BIBLIOGRAFIE

1. Bayer AS, Bolger AF, Taubert KA, Wilson W - Diagnosis and Management of Infective Endocarditis

and Its Complications - Circulation. 1998;98:2936- 2948

2. Fowler VG Jr, Li J, Corey GR et al. Role of echocardiography in evaluation of patients with

Staphylococcus aureus bacteremia: experience in 103 patients. J Am Coll Cardiol. 1997;30:10721078.

3. Gagliardi JP, Nettles RE, McCarthy DE, Sanders LL, Corey GR, Sexton DJ. Native valve infective

endocarditis in elderly and younger adult patients. Clin Infect Dis. 1998;26:11651168
4. Keith A. M. - Endocarditis - Updated: September 5, 2006 5. Popescu C., Popescu G.A. Sepsis
Actualitati si controverse Editura Agerpress Typo 200

The teeth and infective endocarditis.

J Clin Microbiol. 2005 Mar ;43 (3):1405-7 15750118 (P,S,E,B)
Infective endocarditis caused by Granulicatella elegans originating in the oral cavity.
Yuko Ohara-Nemoto, Kayo Kishi, Mamoru Satho, Shihoko Tajika, Minoru Sasaki, Akiko
Namioka, Shigenobu Kimura
Department of Oral Microbiology, Iwate Medical University School of Dentistry, 1-3-27
Chuodori, Morioka 020-8505, Japan. ynemoto@iwate-med.ac.jp
We studied the pheno- and genotypes of an oral Granulicatella elegans strain in comparison with
those of a blood-derived isolate which caused infective endocarditis. The two isolates exhibited
identical biochemical characteristics and had the same drug MICs. Their genotypes were
indistinguishable, indicating that these were from the same clone. The transmission of G. elegans
from the oral cavity thus should be noted as a possible cause of infective endocarditis.
Mesh-terms: Endocarditis, Bacterial :: etiology; Female; Genotype; Gram-Positive Bacterial
Infections :: etiology; Humans; Middle Aged; Mouth :: microbiology; Polymerase Chain
Reaction; RNA, Ribosomal, 16S :: genetics; Research Support, Non-U.S. Gov't;
Streptococcaceae :: classification; Streptococcaceae :: genetics; Streptococcaceae :: isolation &
purification;
J Bacteriol. 2003 Oct ;185 (20):5967-75 14526007 (P,S,E,B) Cited:3
The sloABCR operon of Streptococcus mutans encodes an Mn and Fe transport system required
for endocarditis virulence and its Mn-dependent repressor.
Sehmi Paik, Arunsri Brown, Cindy L Munro, Cynthia Nau Cornelissen, Todd Kitten
The Philips Institute of Oral and Craniofacial Molecular Biology, Virginia Commonwealth
University, Richmond, Virginia 23298, USA.
Streptococcus mutans belongs to the viridans group of oral streptococci, which is the leading
cause of endocarditis in humans. The LraI family of lipoproteins in viridans group streptococci
and other bacteria have been shown to function as virulence factors, adhesins, or ABC-type
metal transporters. We previously reported the identification of the S. mutans LraI operon,

sloABCR, which encodes components of a putative metal uptake system composed of SloA, an
ATP-binding protein, SloB, an integral membrane protein, and SloC, a solute-binding
lipoprotein, as well as a metal-dependent regulator, SloR. We report here the functional analysis
of this operon. By Western blotting, addition of Mn to the growth medium repressed SloC
expression in a wild-type strain but not in a sloR mutant. Other metals tested had little effect.
Cells were also tested for aerobic growth in media stripped of metals then reconstituted with Mg
and either Mn or Fe. Fe at 10 micro M supported growth of the wild-type strain but not of a sloA
or sloC mutant. Mn at 0.1 micro M supported growth of the wild-type strain and sloR mutant
but not of sloA or sloC mutants. The combined results suggest that the SloABC proteins
transport both metals, although the SloR protein represses this system only in response to Mn.
These conclusions are supported by (55)Fe uptake studies with Mn as a competitor. Finally, a
sloA mutant demonstrated loss of virulence in a rat model of endocarditis, suggesting that metal
transport is required for endocarditis pathogenesis.
Mesh-terms: ATP-Binding Cassette Transporters :: genetics; ATP-Binding Cassette
Transporters :: metabolism; Animals; Bacterial Proteins :: genetics; Bacterial Proteins ::
metabolism; Culture Media; Endocarditis, Bacterial :: microbiology; Ferric Compounds ::
metabolism; Gene Expression Regulation, Bacterial; Humans; Manganese :: metabolism;
Mutation; Operon; Rats; Repressor Proteins :: genetics; Repressor Proteins :: metabolism;
Research Support, U.S. Gov't, P.H.S.; Streptococcal Infections :: microbiology; Streptococcus
mutans :: genetics; Streptococcus mutans :: growth & development; Streptococcus mutans ::
pathogenicity; Virulence;
Infect Immun. 2002 Jan ;70 (1):422-5 11748213 (P,S,E,B) Cited:2
Vaccination with FimA from Streptococcus parasanguis protects rats from endocarditis caused
by other viridans streptococci.
Todd Kitten, Cindy L Munro, Aijuan Wang, Francis L Macrina
The Philips Institute of Oral and Craniofacial Molecular Biology, Department of Adult Health
Nursing, Virginia Commonwealth University, Richmond, Virginia 23298, USA. tkitten@vcu.edu
The FimA protein of Streptococcus parasanguis is a virulence factor in the rat model of
endocarditis, and immunization with FimA protects rats against homologous bacterial challenge.
Because FimA-like proteins are widespread among the oral streptococci, the leading cause of
native valve endocarditis, we evaluated the ability of this vaccinogen to protect rats when
challenged by other streptococcal species. Here we report that FimA vaccination produced
antibodies that cross-reacted with and protected against challenge by the oral streptococci S.
mitis, S. mutans, and S. salivarius. FimA thus has promise as a vaccinogen to control infective
endocarditis caused by oral streptococci.
Mesh-terms: Animals; Antibodies, Bacterial :: blood; Antibodies, Bacterial :: immunology;
Bacterial Proteins :: immunology; Cross Reactions; Disease Models, Animal; Endocarditis,
Bacterial :: prevention & control; Fimbriae Proteins; Humans; Male; Rats; Rats, SpragueDawley; Recombinant Fusion Proteins :: immunology; Research Support, Non-U.S. Gov't;
Research Support, U.S. Gov't, P.H.S.; Streptococcal Vaccines :: immunology; Streptococcus ::
immunology; Streptococcus mutans :: immunology; Vaccination; Vaccines, Synthetic ::
immunology;
Heart. 1997 Mar ;77 (3):
191...
(P,S,E,B)
Infective endocarditis: some popular tenets debunked?
S J Eykyn
Division of Infection, UMDS St Thomas' Hospital, London.
Mesh-terms: Endocarditis, Bacterial :: diagnosis; Endocarditis, Bacterial :: drug therapy;
Endocarditis, Bacterial :: microbiology; Endocarditis, Bacterial :: prevention & control;
Gingivitis :: complications; Human; Oral Hygiene; Penicillins :: therapeutic use; ProsthesisRelated Infections :: drug therapy; Prosthesis-Related Infections :: etiology; Streptococcal
Infections :: diagnosis; Streptococcal Infections :: drug therapy;
Br J Ophthalmol. 1996 Dec ;80 (12):1112-3 9059284 (P,S,E,B)
An unusual corneal injury.
R S Newsom, S L Oberstein, M G Falcon

Mesh-terms: Accidents, Occupational; Burns, Chemical :: etiology; Calcium Hydroxide ::

adverse effects; Corneal Opacity :: etiology; Explosions; Eye Burns :: classification; Human;
Industry; Keratoplasty, Penetrating; Male;
Br J Ophthalmol. 1996 Dec ;80 (12):1111-2 9059283 (P,S,E,B)
Recurrent septic retinal emboli following dental surgery.
D J Kilmartin, P Barry
Mesh-terms: Adult; Embolism :: diagnosis; Embolism :: etiology; Endophthalmitis :: etiology;
Fluorescein Angiography; Human; Male; Periapical Abscess :: complications; Postoperative
Complications; Retinal Artery :: pathology; Retinal Diseases :: etiology;
J Bacteriol. 1992 Jun ;174:3577-86 1534326 (P,S,E,B) Cited:17
Identification of a gene, rgg, which regulates expression of glucosyltransferase and influences the
Spp phenotype of Streptococcus gordonii Challis.
M C Sulavik, G Tardif, D B Clewell
Department of Microbiology and Immunology, School of Medicine, University of Michigan, Ann
Arbor 48109-0402.
Streptococcus gordonii Challis was previously shown to give rise to phase variants expressing
high (Spp+) or low (Spp-) levels of extracellular glucosyltransferase (GTF) activity. Here,
shotgun cloning of an S. gordonii Spp+ chromosomal digest resulted in a chimeric plasmid
(pAM5010) able to complement the Spp- phenotype. In addition, introduction of pAM5010 into
an Spp+ strain resulted in a 10-fold increase in GTF expression. Deletion analysis of pAM5010
identified a 1.2-kb DNA segment which exhibited the same functional properties as pAM5010.
Nucleotide sequence analysis of this region revealed a gene approximately 1 kb in size. The gene
was designated rgg. Disruption of the chromosomal rgg gene open reading frame in an Spp+
strain resulted in strain DS512, which displayed an Spp(-)-like phenotype and had 3% of wildtype GTF activity. A plasmid containing the rgg gene was able to complement the DS512
phenotype and significantly increase GTF expression above wild-type levels. Sequence analysis
and other data showed that the S. gordonii GTF determinant, designated gtfG, is located 66 bp
downstream of the rgg gene. The sequence also revealed interesting inverted repeats which may
play a role in the regulation of gtfG. We conclude that rgg positively regulates the expression of
GTF and influences expression of the Spp phenotype.
Mesh-terms: Amino Acid Sequence; Bacterial Proteins :: genetics; Base Sequence; Cloning,
Molecular; DNA-Binding Proteins; Gene Expression Regulation, Bacterial; Genes, Regulator ::
genetics; Genetic Complementation Test; Glucosyltransferases :: biosynthesis;
Glucosyltransferases :: genetics; Molecular Sequence Data; Mutagenesis; Nucleic Acid
Conformation; Phenotype; Regulatory Sequences, Nucleic Acid; Streptococcus :: genetics;
Streptococcus sanguis :: genetics; Support, U.S. Gov't, P.H.S.; Trans-Activators;

Endocarditis, Bacterial :: etiology

Latest Paper:
Schweiz Rundsch Med Prax. 2007 Oct 10;96 (41):1577-8 17987927 (P,S,E,B)

[Endocarditis of Mr. C]
S Bopp, K Bouzerda, C Haeberli
Mesh-terms:

Abscess

::

etiology;

Aged;

Blood

::

microbiology;

Diagnosis,

Differential;

Echocardiography;

Electrocardiography; Endocarditis, Bacterial :: diagnosis; Endocarditis, Bacterial :: drug therapy; Endocarditis, Bacterial ::
etiology; Endocarditis, Bacterial :: ultrasonography; Humans; Intervertebral Disk Displacement :: surgery; Lumbar
Vertebrae; Male; Postoperative Complications; Spinal Diseases :: etiology; Staphylococcal Infections :: diagnosis;
Staphylococcal Infections :: drug therapy; Staphylococcal Infections :: etiology; Staphylococcal Infections ::
ultrasonography; Staphylococcus aureus :: isolation & purification;

Most cited papers:

Microbiol Rev. 1980 Jun ;44 (2):331-84 6446023 (P,S,E,B) Cited:202

Biology, immunology, and cariogenicity of Streptococcus mutans.

S Hamada, H D Slade
Mesh-terms: Animals; Antigens, Bacterial :: analysis; Bacteriocins :: biosynthesis; Cell Adhesion; Cell Wall ::
ultrastructure; Dental Caries :: etiology; Dental Caries :: prevention & control; Endocarditis, Bacterial :: etiology;
Glucose :: metabolism; Glucosidases :: metabolism; Glucosyltransferases :: metabolism; Human; Immune Sera ::
immunology; Lectins :: pharmacology; Lysogeny; Mouth :: microbiology; Plasmids; Polysaccharides, Bacterial ::
biosynthesis; Serotyping; Streptococcus mutans :: classification; Streptococcus mutans :: genetics; Streptococcus
mutans :: immunology; Streptococcus mutans :: metabolism; Streptococcus mutans :: physiology; Sucrase ::
metabolism; Sucrose :: adverse effects; Sucrose :: metabolism; Teichoic Acids :: metabolism; Transformation, Bacterial;
Vaccination;
J Clin Microbiol. 1985 Dec ;22 (6):996-1006 3905855 (P,S,E,B) Cited:73

Adherence of coagulase-negative staphylococci to plastic tissue culture plates: a quantitative model for
the adherence of staphylococci to medical devices.
G D Christensen, W A Simpson, J J Younger, L M Baddour, F F Barrett, D M Melton, E H Beachey
The adherence of coagulase-negative staphylococci to smooth surfaces was assayed by measuring the optical densities
of stained bacterial films adherent to the floors of plastic tissue culture plates. The optical densities correlated with the
weight of the adherent bacterial film (r = 0.906; P less than 0.01). The measurements also agreed with visual assessments
of bacterial adherence to culture tubes, microtiter plates, and tissue culture plates. Selected clinical strains were passed
through a mouse model for foreign body infections and a rat model for catheter-induced endocarditis. The adherence
measurements of animal passed strains remained the same as those of the laboratory-maintained parent strain.
Spectrophotometric classification of coagulase-negative staphylococci into nonadherent and adherent categories
according to these measurements had a sensitivity, specificity, and accuracy of 90.6, 80.8, and 88.4%, respectively. We
examined a previously described collection of 127 strains of coagulase-negative staphylococci isolated from an outbreak
of intravascular catheter-associated sepsis; strains associated with sepsis were more adherent than blood culture
contaminants and cutaneous strains (P less than 0.001). We also examined a collection of 84 strains isolated from
pediatric patients with cerebrospinal fluid (CSF) shunts; once again, pathogenic strains were more adherent than were
CSF contaminants (P less than 0.01). Finally, we measured the adherence of seven endocarditis strains. As opposed to
strains associated with intravascular catheters and CSF shunts, endocarditis strains were less adherent than were
saprophytic strains of coagulase-negative staphylococci. The optical densities of bacterial films adherent to plastic tissue
culture plates serve as a quantitative model for the study of the adherence of coagulase-negative staphylococci to
medical devices, a process which may be important in the pathogenesis of foreign body infections.
Mesh-terms: Animals; Bacteriological Techniques; Catheterization :: adverse effects; Coagulase :: metabolism;
Endocarditis, Bacterial :: etiology; Endocarditis, Bacterial :: microbiology; Evaluation Studies; Humans; Models,
Biological; Plastics; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.; Spectrophotometry;
Staphylococcal Infections :: etiology; Staphylococcal Infections :: microbiology; Staphylococcus :: cytology;
Staphylococcus :: isolation & purification; Staphylococcus :: pathogenicity;
Yale J Biol Med. 1971 Oct ;44 (2):206-13 5123055 (P,S,E,B) Cited:67

Experimental endocarditis. II. Staphylococcal infection of the aortic valve following placement of a
polyethylene catheter in the left side of the heart.
B B Perlman, L R Freedman

Mesh-terms: Animals; Aortic Valve; Disease Models, Animal; Endocarditis :: etiology; Endocarditis :: pathology;
Endocarditis, Bacterial :: etiology; Endocarditis, Bacterial :: pathology; Heart Catheterization; Myocardium :: pathology;
Polyethylenes; Rabbits; Staphylococcal Infections :: etiology; Staphylococcal Infections :: pathology;
Yale J Biol Med. 1970 Jun ;42 (6):394-410 5431862 (P,S,E,B) Cited:46

Experimental endocarditis I. Staphylococcal endocarditis in rabbits resulting from placement of a

polyethylene catheter in the right side of the heart.
P K Garrison, L R Freedman
Mesh-terms: Animals; Disease Models, Animal; Endocarditis, Bacterial :: etiology; Endocarditis, Bacterial :: microbiology;
Endocarditis, Bacterial :: pathology; Heart Catheterization :: adverse effects; Kidney :: pathology; Liver :: pathology; Lung
:: pathology; Methods; Myocardium :: pathology; Rabbits; Spleen :: pathology; Staphylococcal Infections :: etiology;
Staphylococcal Infections :: microbiology; Staphylococcal Infections :: pathology; Staphylococcus :: classification;
Staphylococcus :: isolation & purification;
Ann Intern Med. 1983 Apr ;98 (4):447-55 6838067 (P,S,E,B) Cited:44

Staphylococcus epidermidis causing prosthetic valve endocarditis: microbiologic and clinical observations
as guides to therapy.
A W Karchmer, G L Archer, W E Dismukes
Seventy-five episodes of prosthetic valve endocarditis from Staphylococcus epidermidis were studied retrospectively.
Methicillin-resistant isolates caused 53 (87%) of 61 infections occurring within 1 year of surgery but only two of the nine
after 1 year (p less than 0.001). Resistance to methicillin was heterogeneic and extended to the cephalosporins. Of 55
isolates, 43 (78%) were susceptible to gentamicin and all to vancomycin and rifampin. In 55 patients, prosthetic valve
endocarditis was complicated by tissue invasion or valve dysfunction. Among these 55 patients, 30 of the 32 who were
cured needed surgery. Prosthetic valve endocarditis from methicillin-resistant S. epidermidis was cured in 21 of 26
patients treated with vancomycin and 10 of 20 treated with beta-lactam antibiotic therapy (p = 0.055). Cure rates of patients
treated with vancomycin but not beta-lactam antibiotics were increased by the addition of rifampin or gentamicin to
therapy. Prosthetic valve endocarditis from methicillin-resistant S. epidermidis should be treated with vancomycin plus
rifampin, or an aminoglycoside. Surgical intervention is important in treating complications of prosthetic valve
endocarditis.
Mesh-terms: Adolescent; Adult; Aged; Anti-Bacterial Agents :: pharmacology; Anti-Bacterial Agents :: therapeutic use;
Endocarditis, Bacterial :: drug therapy; Endocarditis, Bacterial :: etiology; Endocarditis, Bacterial :: microbiology;
Endocarditis, Bacterial :: surgery; Female; Heart Valve Prosthesis :: adverse effects; Human; Lactams; Male; Microbial
Sensitivity Tests; Middle Aged; Penicillin Resistance; Staphylococcal Infections :: drug therapy; Staphylococcal Infections
:: therapy; Support, Non-U.S. Gov't; Support, U.S. Gov't, P.H.S.;
Rev Infect Dis. ;1 (6):955-66 551516 (P,S,E,B) Cited:43

Viridans streptococcal endocarditis: the role of various species, including pyridoxal-dependent

streptococci.
R B Roberts, A G Krieger, N L Schiller, K C Gross
The viridans streptococci are a heterogeneous group of organisms frequently associated with microbial endocarditis.
Isolates from consecutive patients with endocarditis due to viridans streptococci who were seen at The New York Hospital
from 1944 to 1955 and from 1970 to 1978 were speciated, and the relative frequencies and patterns of sus ceptibility to
penicillin were determined. Vitamin B6-dependent streptococci, classified as Streptococcus mitior, accounted for 5%-6%
of microbial endocarditis in both time periods. Since these nutritional variants require the active forms of vitamin B6 for
growth in routein media, they can be responsible for culture-negative endocarditis. Media must be supplemented with
either pyridoxal hydrochloride or pyridoxamine dihydrochloride (the active forms of vitamin B6) for isolation,

identification, and subsequent testing of susceptibility to antimirobial agents. Pyridoxine hydrochloride does not support
the growth of these organisms in vitro.
Mesh-terms: Endocarditis, Bacterial :: drug therapy; Endocarditis, Bacterial :: etiology; Human; Penicillins :: therapeutic
use; Pyridoxine :: pharmacology; Streptococcal Infections; Streptococcus :: classification; Streptococcus :: isolation &
purification;
Br J Exp Pathol. 1973 Apr ;54 (2):142-51 4700697 (P,S,E,B) Cited:40

Experimental bacterial endocarditis. 3. Production and progress of the disease in rabbits.

D T Durack, P B Beeson, R G Petersdorf
Mesh-terms: Animals; Candida; Candidiasis; Disease Models, Animal; Endocarditis; Endocarditis, Bacterial :: etiology;
Endocarditis, Bacterial :: mortality; Heart Catheterization; Polyethylenes; Proteus Infections; Rabbits; Staphylococcal
Infections; Streptococcal Infections :: mortality; Thrombosis;
Arch Intern Med. 1970 Feb ;125 (2):258-64 5460884 (P,S,E,B) Cited:35

Enterococcal endocarditis. An analysis of 38 patients observed at the New York Hospital-Cornell Medical
Center.
G L Mandell, D Kaye, M E Levison, E W Hook
Mesh-terms: Adult; Ampicillin :: therapeutic use; Endocarditis, Bacterial :: diagnosis; Endocarditis, Bacterial :: drug
therapy; Endocarditis, Bacterial :: epidemiology; Endocarditis, Bacterial :: etiology; Endocarditis, Bacterial ::
microbiology; Female; Human; Male; Middle Aged; Penicillins :: adverse effects; Penicillins :: therapeutic use; Pregnancy;
Pregnancy Complications, Infectious; Streptococcal Infections :: drug therapy; Streptococcal Infections :: epidemiology;
Streptococcal Infections :: etiology; Streptomycin :: therapeutic use; Urinary Tract Infections :: complications;
Vancomycin :: therapeutic use;
Infect Immun. 1985 Sep ;49 (3):775-9 4030104 (P,S,E,B) Cited:34

Correlation of plasmid type and disease caused by Coxiella burnetii.

J E Samuel, M E Frazier, L P Mallavia
The obligate intracellular bacterium Coxiella burnetii is the etiological agent of acute Q-fever and chronic endocarditis in
humans and of several zoonotic infections. The DNA from a variety of these disease isolates was compared for homology
to the plasmid QpH1, found in the Nine Mile strain. Three patterns of homology were found in these isolates, i.e., one
pattern identical to that of QpH1, one common to several endocarditis isolates and goat abortion isolates, and one
common to the remaining group of endocarditis isolates. Plasmid DNA from the endocarditis-abortion isolate group,
designated QpRS, was mapped by restriction enzyme analysis and compared with QpH1. These data show that QpRS was
2 to 3 kilobase pairs larger, contained DNA not found in QpH1, but was not generated from QpH1 by a single insertional
event. Isolation of plasmid DNA from the second endocarditis group of isolates was not successful and may indicate that
the plasmid has integrated into the chromosome. This analysis provides the first clear evidence that differences exist
between C. burnetii isolates which cause various diseases, indicating that different C. burnetii strains may have unique
virulence characteristics.
Mesh-terms: Animals; Base Sequence; Cattle; Chick Embryo; Coxiella :: genetics; Coxiella :: pathogenicity; DNA,
Bacterial :: analysis; Endocarditis, Bacterial :: etiology; Human; Humans; Plasmids; Q Fever :: etiology; Research
Support, U.S. Gov't, P.H.S.; Support, U.S. Gov't, P.H.S.; Virulence;
J Infect Dis. 1975 Apr ;131 (4):367-75 1117194 (P,S,E,B) Cited:32

Antimicrobial therapy of experimental endocarditis caused by Staphylococcus aureus.

M A Sande, M L Johnson
The rate at which various antimicrobial agents eradicated Staphylococcus aureus from cardiac vegetations in a rabbit
model of endocarditis was studied. The rate at which various drugs and combinations killed high titers of bacteria in broth

correlated with the relative effectiveness of the agents in vivo. Gentamicin plus penicillin proved to be synergistic in vitro
and more effective in eradicating bacteria from cardiac vegetations in vivo than was penicillin alone. Vancomycin killed
bacteria at a rate similar to that for the combination of penicillin and gentamicin, and the rate for cefazolin was similar to
that for penicillin alone. Clindamycin was less effective in vivo and in vitro than penicillin. Therapy with rifampin led to the
emergence of resistant organisms, and, when penicillin, this drug was less effective in vitro and in vivo than was penicillin
alone. This model appears to offer an effective method for evaluation of antimicrobial treatment of staphylococcal
endocarditis.
Mesh-terms: Animals; Anti-Bacterial Agents :: therapeutic use; Cephalothin :: therapeutic use; Clindamycin :: therapeutic
use; Disease Models, Animal; Drug Therapy, Combination; Endocarditis, Bacterial :: drug therapy; Endocarditis,
Bacterial :: etiology; Endocarditis, Bacterial :: pathology; Gentamicins :: therapeutic use; Penicillins :: therapeutic use;
Rabbits; Rifampin :: therapeutic use; Staphylococcal Infections :: complications; Staphylococcal Infections :: drug
therapy; Time Factors; Vancomycin :: therapeutic use;

Diagnosis of Heart Infections: Bacterial Endocarditis

What is bacterial endocarditis?
Bacterial endocarditis is a serious infection of the heart caused by germs called bacteria that get into the blood and stay in
the heart. It is also called subacute bacterial endocarditis (SBE).
A child with an existing heart problem might get bacterial endocarditis while having an operation or dental treatment that
causes bleeding. Usually, a childs body can kill the bacteria, and he does not get sick. But if blood does not flow through
your childs heart or valves smoothly because of heart problems, your child is more likely to get bacterial endocarditis. It is
more likely to occur in children with complex cyanotic defects, shunts, and artificial heart valves.
While the chance of getting this infection is low, knowing how to prevent it is important, since it can be very serious, possibly
resulting in damage to the heart or death, if untreated.

What causes bacterial endocarditis?

Bacteria get into the bloodstream and lodge inside the heart. The bacteria can sometimes get into the blood after an
operation or dental cleaning that causes bleeding.

What are the signs of bacterial endocarditis?

a slight fever of 37.5C to 38.5C that you cannot explain and that lasts for 5 to 7 days
sweating
loss of appetite
pain in the muscles and joints, such as the knees, shoulders, or knuckles
loss of weight
a skin rash
headaches
a general feeling of weakness
The signs of bacterial endocarditis are like the signs of the flu. You may find it hard sometimes to know if your child has
bacterial endocarditis. If your child has some of these signs and they do not go away, have your paediatrician or family
doctor check your child.

How does bacterial endocarditis affect the heart and body?

The bacteria that get into the heart will grow and cause large pieces of vegetation to form. This can damage the part of the
heart where the bacteria are growing. Also, these chunks of vegetation can break away from the heart's surface and move
into other parts of the body, like the lungs, potentially causing blockage, which can be damaging.

How is bacterial endocarditis diagnosed?

There are tests that can help the doctors find out if your child has bacterial endocarditis:

blood tests to check for bacteria (your child may need to have several blood samples taken at different times)
a urine test, which tests your childs urine for the blood and inflammation that can accompany endocarditis
an echocardiogram, which is a recording of the positions and movement of the walls of the heart or the parts inside
the heart, such as the valves

How is bacterial endocarditis treated?

If your child has bacterial endocarditis, the doctor will give him antibiotics through an IV. Your child may need antibiotics for
as long as 6 weeks or more. He may need to stay in the hospital or be treated at home by nurses from a home care service
for part of the 6 weeks. For more serious cases, surgery may be needed.

What are the long-term outcomes of bacterial

endocarditis?
With early diagnosis and aggressive intervention, outcomes for
children who develop bacterial endocarditis are generally positive.
Left untreated, this infection can be fatal. Preventing it from occurring
is the main goal.

How can bacterial endocarditis be prevented?

You can prevent your child getting bacterial endocarditis by taking
these simple steps.
Take good care of your childs teeth. These instructions will help you
keep your childs teeth healthy and avoid infection in the mouth.

Start early. Get your baby used to having a clean mouth. Wipe his gums gently with a damp face cloth after every
feeding. This will help your baby get used to having his gums touched, and they will become less sensitive. You should
start wiping his teeth as soon as your baby gets them. This starts when your baby is about 6 months old. Usually, you can
use a toothbrush to clean your babys teeth when he is 1 year old.
Do not let your baby or child sleep with a bottle of milk or juice. A bottle of water is okay because it does not have
sugar that can cause cavities. Breastfeeding or bottle-feeding on demand, which means when your baby wants it, can
also cause cavities. You should clean your babys teeth after you breastfeed or bottle-feed your baby.
If your baby usually falls asleep right after the last breastfeeding or bottle-feeding, make sure you clean his teeth
just before you give him this last feeding.
Do not use toothpaste to clean your childs teeth until your child is 2 years old. Too much fluoride may harm your
childs teeth. Your young child needs only a little fluoride. Use infant toothpaste with very little fluoride. While your child is
between 2 and 6 years old, he should use toothpaste only in very small amounts, or use a toothpaste with little fluoride.
(Fluoride is a mineral in toothpaste that helps keep the teeth healthy.)
Make sure your child brushes his teeth after every meal and snack. Your child should also brush his teeth after
taking liquid medicine. Liquid medicine may have a lot of sugar that needs to be cleaned away.
Get your child to start flossing his teeth when his back teeth touch each other. Your child will need help flossing
until he gets used to doing it. Make sure your child flosses the teeth that touch each other. A toothbrush cannot clean
between these teeth. During a visit to the dentists office, ask the dentist to show your child how to floss properly.
Take your child to the dentist for regular check-ups and make sure you tell the dentist about your child's heart
condition.
Make sure your child takes antibiotics before any treatment that may cause him to get bacterial endocarditis.
Before a potentially infective procedure, your doctor will tell you whether your child needs antibiotics. Situations that could
potentially put your child at risk include:
Some operations, such as having the tonsils or the adenoids taken out (Tonsils are round pieces of tissue at the
back of the mouth beside the tongue. Adenoids are like tonsils, but they are out of sight up behind the nose.). Taking
antibiotics also applies if your child will be having a G-tube put in or having a bladder test.
Some deep cuts, particularly if they need stitches or look infected.
Some work on the teeth (for example, having a tooth taken out, cleaning the teeth in the dentists office, fillings
near the gums, or when braces are put on for the first time).
Some body piercing. Check with your childs cardiologist.
Some children with heart problems may need to take antibiotics for the rest of their lives to prevent bacterial
endocarditis. If you are not sure if your child needs antibiotics, ask your childs doctor.
Get your child a Medic Alert bracelet, if he needs one. Your child may need a medic alert bracelet, which is a
special bracelet that says what your childs condition is. This bracelet helps a doctor know what special treatment your
child may need when there is no one to speak for him. Ask your cardiologist if your child needs a medic alert bracelet. It is
much better to prevent bacterial endocarditis than to treat it.