1

Infective endocarditis

Lívia Jánoskuti

2

Definition

• Bacterial or fungal

– (chlamydial, rickettsial also occur)

• Infection

• Within the heart

3

Classification • Infective organism

– (Gram pos., Gram neg, fungal, hemoculture negative IE)

• Native valve , prosthetic valve

– (early:within 12 month after operation, > 12 month after operation)

• Population

– (iv drug abusers, children, old patients)

• Nosocomial

– IE developing > 48 h prior to the onset of signs and symptoms consistent with IE

• Active at operation

– (fever, positive hemoculture)

• Recidive: 1 year after recovery

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Epidemiology

• 60/1 million inhabitants/year

• Hungary:24/ 1 M / year

Predisposing lesions:

• Prostetic valve and mitral valve prolapse sclerosis,degenerative valve increasing incidence

• Rheumatic valve disease decreasing incidence in association with IE

• Iv drug abusers have an unique propensity to develope IE of the tricuspid valve

Mortality: 16-33%, early prosthetic valve IE 80%

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Pathogenesis

• Bacteria enters the blood stream

– (oral or other source)

• Lodge in the heart valves, that already may

bear platelet-fibrin thrombi

• Bacteria proliferate freely-vegetation

develops

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Complications of the disease

• Emboli: brain, spleen, kidney,right sided-pulmonary

• Valve destruction: regurgitation, obstruction

• Extension: septum-AV block, fistulas-pericardium (sinus Valsalva aneurysm rupture into the pericardium)

• IC vasculitis: arthritis, glom. nephritis, Osler nodes, Roth spots, Latex positivity

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Peripheral manifestations of IE

Physical finding Pathogenesis Most common

organism

Petechiae(20-40%)red,

nonblanching lesions in crops on

conjuctivae, buccal mucosa, palate,

extremities

Vasculitis or

emboli

Streptococcus

Staphylococcus

Splinter hemorrhages(15%) linear

red streaks proximal in nailbed

Vasculitis or

emboli

Staphylococcus

Streptococcus

Osler s nodes(10-25%) 2-5mm

painful nodules on pads of fingers

or toes

Vasculitis Streptococcus

Janeway lesions (<10%) macular

red or hemorrhagic painless patches

on palm or soles)

Emboli Staphylococcus

Roth s spots (<5%) oval pale retinal

lesions surrounded by hemorrhage

Vasculitis Streptococcus

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Janeway lesion

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Osler nodul and Janeway lesion

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Splinter hemorrhage

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Clinical features

Symptoms of IE starts within 2 weeks of

precipitating bacteremia

• Malaise, night sweats, weight loss with

organism of low pathogenicity (viridans

streptococci)

• Explosive onset with organims of high

pathogenicity ( Staphylococcus aureus)

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Symptoms Fever In almost all patients

Heart murmurs (new) Up 99%

Splenomegaly 30 %

Petechiae, (Osler nodes, Janeway

etc.)

20-40%

Musculoskeletal complaints Arthralgias, arthitis

Pulmonary emboli In tricuspid valve IE

Clubbing Duration longer than 6 weeks

Neurological( headache) Brain abscesses,meningitis,arteritis

Congestive heart failure

Renal disease Nephritis 80%,infarction-50%,absc.

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Diagnostic criteria (Duke)

• Certain:

– pathological criteria: surgical or autopsy findings,

– clinical criteria: 2 major, 1 major+3 minor, 5 minor criteria

• Possible: hemoculture positivity+ new heart murmur, or known valve disease+vasculitis

• Not possible: recovery in 4 days, negative surgical, or autopsy findings

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Diagnostic criteria (Duke)

Major:

1. positive hemoculture ( typical agent and 2 tests positivity)

2. positive echocardiography (vegetation, abscess)

3. new regurgitation murmur

Minor:

1. predisposing heart disease

2. fever

3. vascular symptoms

4. immune phenomenons

5. echocardiographically possible, but not certain

6. microbiologically possible, but not certain

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Differential diagnosis

Missleading clinical presentations:

• Young adult with stroke

• Adult with confusion( but fever, murmur)

Blood cultures are negative:

Acute rheumatic fever

Multiple pulm. embolism

Atrial myxoma

SLE-Libman Sacks endocarditis

malignancy

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Indications of TEE in IE

• 1.Suspected prosthetic valve IE

• 2.Suspected native valve IE, but TTE is

uncertain, or certain, but patient has high

risk (large vegetation)

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Syndromes suggesting specific

bacteria causing IE

• Indolent course: – viridans streptococci, streptococcus bovis (colon cc),

Streptococcus faecalis

• Aggressive course: – staphylococcus aureus, str. pneumoniae, str.pyogenes,

neisseria gonorrhoea

• Drug users: – staphylo.aureus, pseudomonas, candida

• Frequent major emboli: – haemophilus sp., bacterioides sp, Candida sp.

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Native valve endocarditis

Most people (60-80%) have an identifiable predisposing cardiac lesion

• Rheumatic heart disease

• Congenital heart disease (bicuspic aortic valve, M valve prolapse with regurg., HOCM, Marfane with AI)

• Aortic sclerosis, calcified mitral anulus, ventricular aneurysms

• Diabetes mell-accel.artscler+infections

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Native valve endocarditis/

Microbiology

• Streptococci (50-70%) cure rate 90%

• Enterococci (10%) cure rate 75-90%

• Staphylococci (25%) cure rate 60-70%

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Native valve endocarditis/mortality

30%

Poorer prognosis

• Old or very young

• Aortic, versus mitral valve

• Left sided versus right sided

• Large vegetations (more than 10mm)

• Delay of diagnosis

• Staphylococcus

• Enterococci (10%) cure rate 75-90%

• Staphylococci (25%) cure rate 60-70%

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Prostetic valve endocarditis/5-15%

of all IE cases

Cardiac valve

replacement

Early-<12month Late->12month

Bacteria Staph.epiderm.

Staph.aureus

diphteroids

Strept.viridans

Mortality 75% 40%

Therapy Vancomycin+

gentamycin(Ripha

mpicin)

Surgical treatment

Penicillin+

gentamycin

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Endocarditis in iv drug abusers

• Male/female ratio 3:1

• Right sided predilection

• Staphylococcal 60%, polymicroorganism 5%

• Migratory pneumonia

– (multiple septic pulm. emboli)

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IE in children

• Rare 34/1 million inhab./year

• Rheumatic heart disease, congenital heart

disease

• Str viridans

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Therapy

• Early antibiotic treatment with bactericid

AB

• Duration of iv treatment 4-6 weeks

• No anticoagulation (but in prosthetic valve

cases it is necessary)

• No steroid

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Empiric therapy

Native valve endocarditis

• 4x3gr Ampicillin/sulbactam or

A/clavulanate

with 3mg/kg/die Gentamycin

Ampicillin intolerance:

• 30mg/kg/die Vancomycin+ Gentamycin +

Ciprofloxacine (800mg/die iv)

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Empiric therapy

Early prostetic valve IE (< 12 month)

• Vancomycin 6 weeks+Gentamycin (2

weeks) iv+ Rifampícin 1200mg/die pos(2

weeks)

Late prostetic valve IE (>12 month)

• As in native IE

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Treatment

• Streptococcus viridans-10-20 ME penicillin or

Ceftriaxon 2 gr/day

• Enterococcal-Ampicillin 4x3gr/die +Gentamycin

1,5mg/kg/die

• Staphylococcal-Oxacillin 12g/die+Gentamycin

Methicillin resistant species or at penicillin allergie

2x1gr Vancomycin+ Gentamycin/die

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Surgery

Absolute indications:

• Refractory heart failure

• Myocardial, paravalvular abscess

• Ineffective therapy

• Repeated relapses

Relative indications:multiple embolic

episodes

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Endocarditis profilaxis

recommended

• Prosthetic cardiac valves

• Previous IE

• Congenital malformations

A. Cyanotic CHD without surgical correction, or

with residual defects, or palliative shunts

B.For 6 month after complete surgical repaire

C.After surgical correction with residual defects

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IE profilaxis is not recommended

• Isolated sec. atrial septal defect

• Surgical repair without residua beyond 6 month of ASD-II,VSD, or patent duct.art.

• ACBG

• Mitral valve prolapse without regurg.

• Previous rheumatic fever without valvular dysfunction

• Cardiac pacemakers and impl. defibrillators

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IE profilaxis for patients undergoing dental or

upper resp. procedures

• 1 hour before the procedure 2 gr Amoxicillin

orally

• Penicillin allergic patients: Clindamycin

600mg, or 500mg Claritromycin, or

Azitromycin orally

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B.A. 34 year old man

Case report 1.

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Past history

• Patient 6 years old - tonsillectomie

• Patient 8 years old - rheumatic fever ( migratory ankle and knee arthritis, AST ) – Penicillin therapy for years

• Patient 34 years old, when recurrent dentological interventions were done

• Two month after this intervention, 3 weeks before admission, he got

– weekness,

– afternoons fever,

– arthralgias,

– recurrent transient visual loss.

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Physical examination

• Pale, maculopapular rash on the chest

• No lymph node enlargement

• No pulmonary abnormalities

• Diastolic murmur in the II.III. right intercostal

space

• Pulse 96/min ,RR 130/60

• Negative abdomen

• Fever: 38,5

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Lab values

• Urin sediment: 40-50 rbc, 4-5wbc

• Sediment rate 90mm/h Ht 0,34 HB 9,5 wbc

10000 Se 83% Se protein 73 ELFO

gammaglob 21% IC, RF negative

• ECG: Sinus tachycardia QRS left deviation.

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Imagine methods

• Chest X-ray:neg

• Abd. US: cystae renis.l.u.

• Fundus: neg.

• Cardiac US: bicusp. aortic valve with

vegetation, AI-III.

• TEE: large, moblie vegetation, with cusp

fenestration

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TTE

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Therapy

• Hemocultures (nutritionally varinat Streptococcus, sensitive to Penicillin, gentamycin)

• Penicillin 4x5M unit/day + Tobramycin 160mg/day

• Constant fever.

• Cardiac surgery: arteficial aortic valve implantation.

• After 12 years patient has no complaines, he is a dancer, can work without problems.

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D.T-59 year old man

Case report 2.

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Past history • Tonsillectomie in his childhood.

• In 1994, in his age 59, in March 3 days fever without any concomittant symptoms

• In April: transient dizziness and double-vision. Neurological, ophtalmological and rheumatological examinations were performed. Dg. Spondylosos cerv.

• In May: sudden left leg spasm-pain

Phys. examination:out of soft aortic systolic murmur, normal.

Lab values: normal sed. rate, urin, blood smear

Imagine methods: chest Xray, arterial and venous Doppler, carotis Doppler negative

Dg.Myalgia cruris

He travelled to the USA, where he got fever and cough

• In June: admission to our hospital because of 3 weeks fever and weakness

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Results and history

• Physical: pale, pulmonary rales, loud diastolic murmur above the aorta.

2cm liver enlargement. Temp: 37,1

• Lab: Sed.rate 60mm/h Ht 0,36 wbc 9,9 IC positive

• Chest X ray: pulmonary congestion

• TTE: vegetation on the aortic valve, AI-II-III

• TEE: bicuspid aotic valve, 9mm large veg on it.

• Hemoculture (was negative)

• Therapy 20Me penicillin-160mg Tobramycine

• After 2 weeks of therapy recurrent fever-TTE control: vegetation

became larger

• Surgery: artefic. valve implanation.

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J.L. 82 year old man

Case report 3.

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History

• Treated because of NHL in Central Institute

of Oncology.

• For 4 weeks he has had fever. No

explanation of it was found. Weekness,

dyspnoe at 20 m walk.

• TTE was requested.

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TTE

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Results and history

• Physical: pale, no lymph nodes, Loud systolic murmur at the apex, radiated to the axillary line. Palpable spleen.

• Lab: CRP 58 Ht 0,28 wbc 2,8 Se 78% Urin sed. Neg.

• Hemoculture neg

• Augmentin, later Imipenem therapy for 5 weeks- no fever, no dyspnoe.

• TEE controll: no vegetation on mitral valve.

MI-III. Good left ventricular function.

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P.A. 44 year old woman

Case report 4.

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History

• No previous illness

• In 2008.Aug. she got fever and chills.

• Because of cough and dyspnoe she was admitted

to the Institute of Pulmonolgy.

• Physical examination : systolic murmur at the

apex, diastolic murmur above the aorta was heard

• Chest X ray showed pneumonia

• TTE: showed aortic and mitral valve vegetations

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TEE

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Results and history

• Hemoculture was positive

– (staphylococcus aureus)

• Vancomycin therapy started

• Because hemodinamic insufficiency aortic

and mitral arteficial valve was implanted.

• 5 weeks post op. antibiotic therapy.

• CRP normal, patient is well.

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SZ-M 65 year old man

Case report 5.

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Past history

• 5 years ago working in Cyprus has had a severe pneumonia. Since he has been weak, and has had dyspnoe at exertion.He has been treated with bronchodilatators on Pulmonology, with the diagnosis of COPD.

• In Dec. 2006. CLL and AIHA was diagnosed. Medrol and Cytoxan therapy have induced complet remission.

• Present therapy: Symbicort, Spiriva, Berodual, Verospiron, Lokren, Medrol, Cytoxan

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Complaines

• On 15. January 2007. he got chest pain,

radiating to the right shoulder, the pain

increased with breathing. He got fever 40 C,

with cough and dyspnoe.

• Physical examination showed diffuse

pulmonary wheezels. Diminished heart

sounds. Blood pressure 150/70 , pulse rate

100/min. Palpable spleen.

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Examinations

• Labor: Ht 0,31 wbc 13,950 thrcyta 80 000 Ly 78% DDimer 2,2 SGOT 76 GPT 90 LDH 340 SAP 58 CRP 135

• pO2 68 pCO2 27 O2 sat 96% with oxygen

• Pulmonary scintigraphy: Multiple segmental, bilateral perfusion defects.

• Chest X ray: negative

• TTE: for the detection of acute right heart enlargement and pulmonary hypertension

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Echocardiography/ the surprise

• TTE:10mm vegetation on the noncoron

cusp of the aortic valve. A vegetation on the

septal cusp of the mitral valve. AI-I. MI-II.

Pulm systolic pressure 36HGmm

• TEE: Aortic, and mitral valve vegetation.

Normal pulmonary and tricuspid valves.

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History

• Hemoculture: Enterococcus sp.

• Therapy:4x3gr Ampicillin 3x80mg

gentamycin.

• No fever after 2 weeks , CRP 25,9

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V.Cs. 27 year old women

Case report 6.

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Anamnesis.

• Marfan sy, 2 years ago luxatio lentis( Her

mother had Marfan sy)

• On the 18.07.2006. Mitral valve and aortic

valve and aorta asc. conduit,biological was

performed.

• Since 2 days, chills and fever 38-40 C. No

cough, no dyspnoe, no dysuria.

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Physical examination:

• Tall stature, arachnodactyly, joint

hyperflexibility, ectopia lentis. 1/6 systolic

murmur p.max at the aortic region. Blood

pressure100/70 P 88/min

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Labor

• We: 14 CRP 37 -26-28 Ht 0,33 thrcyta 96 wbc

4004 SGOT 103 GPT 121 Urine sediment:15-20

wbc

• Next day: CRP 43 SGOT 94 GPT 137

• Hemoculture

• Chest Xray: neg.

• Abdominal US: negative

• TTE: aortic non coron cusp is thicker. Small AI.

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History

• Every day chills and fever

• TEE no vegetation was found.

• One week later procalcitonin 20,3

• wbc 11 000 CRP 132

• TEE :vegetation on the aortic valve and on

the septal cusp of the mitral valve, the

suspition of a paravalvular abscess.

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V.Cs. 29 years old female

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History

• Early prosthetic valve endocarditis?

• Therapy: Vancomycin-Gentamycin

• wbc 8,7 procalcitonin 10,3 CRP 63, but fever on every day

• Hemoculture:haemophilus parainfluenzae

• Therapy: 2 gr Ceftriaxone

• Fever on every day: 2x2 gr Ceftriaxone/day

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History

• 01.20-26 . Continous fever during this

therapy.

• Abdominal US: abscess?- negative

• TTE. The mitral vegetation disappeared, but

the aortic valve vegetation is the same.

• Consultation with surgeon-operation is

possible only, if there is no inflammation.

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Present situation

• From 26.01 no fever.

• CRP 11 fvs 7,6

• We are waiting for complete

remission(calcification of the vegetation)

(Operation has a very high risk)

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A patient with migratory

pneumonia

Lívia Jánoskuti

3rd Dept. of Medicine Semmelweis

University

Budapest, Hungary

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History 1 65 year old woman,

with hypertension and diabetes mellitus type 2.

Recurrent urinary tract infections for 3 years

• In February 2005

she got acute renal failure during acute pyelonephritis, hemodialysis was performed

• At the end of March 2005

hemodialysis was stopped because patient’s renal function has normalized

• In summer 2005

recurrent short fevers, due to urinary tract infections, which were treated by antibiotics

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History 2 • In September 2005

fever, right sided pneumonia, hydrothorax (bacteriology negative)

• In November 2005 fever, left sided pneumonia, hydrothorax, later spleen abscess

blood culture positive: Enterococcus faecalis

After splenectomy, and 4 weeks Clindamycin-amoxicillin therapy; patient’s condition stabilized, became free of fever

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Question

• What is the pathomechanism of the

migratory pneumonias and the splenic

abscess?

1. Urosepsis

2. Right sided endocarditis and sepsis

3. Left sided endocarditis and sepsis

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TEE on 22. December 2005. • Aortic , mitral and pulmonary valves are normal

• Tricuspid valve endocarditis was detected

– On the lateral cusp

echodens 1,5 cm large mobile vegetation

– On the septal cusp

echodens 0,5 cm large mobile vegetation

• No PFO

• TI III. Pulmonary systolic pressure 35Hgmm

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TEE dec.22.

72

TEE dec.22.

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History 3

After 8 weeks of AB therapy in January 2006

• No change on TEE control

• Calcified vegetations on the tricuspid valves

• No embolic phenomenons

• No inflammatory labor signs

• Consultant heart surgeon suggested observation

Control on April 2006

• No fever

• Because of TI III-IV, diuretic therapy was intensified

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New risk factors of IE

• IV. Drug abusers

• Intensive care settings

• Hemodialysis

• Elderly age

• Degenerative valve diseases

• Cirrhosis hepatis, diabetes mellitus

• Skin infections

• Gastrointestinal tumors

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Endocarditis of tricuspid valve

• Clinical characteristics: migratory pneumonias

• Frequent among iv drug abusers. Incidence 2-5% per year ( tricuspid valve is the most frequently affected (60-70%),followed by the mitral and aortic valves( 20-30%)

• The most common etiological agent is Staphylococcus aureus, being usually sensitive to methicillin

• The prognosis of right side IE is generally good,

Overall mortality is <5%, and with surgery <2%

• Mortality of HIVinfected iv drug abusers is higher

one year survival 65%, 5 year survival 35%.

» Miro J.M. Cardiology Clinics 21 (2) 164-84 2003.

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Infectious tricuspid valve endocarditis in a

chronic hemodialysis patient

• 67-year old male with chr. Renal failure, complained of

fever up to 38 degrees C after hemodialysis.

• Blood culture negative, CRP high

• TEE:13x25 mm large vegetation on the tricuspid valve

• He got a bioprosthetic valve

• Extensive vegetation was found in each cusps of the

tricuspid valve.

• 9 month after surgery; no signs of reccurence were

obsereved

Yoshida Japanese Journal of Thoracic Surgery 59(3):235-7 2006.

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Message

Think of right sided endocarditis in the case of

migratory pneumonia.

By effective and ongoing therapy, further

complications may be prevented and the

illness may be cured.