1. A 44-year-old man with a 2-month history of weight loss, fatigue, cough, and night sweats Joe Kovaz, M.D. December 8, 2004

2. No financial disclosures

3. 9/2/04 n 44 yo man with the following problems: –Ischemic Heart Disease (stenting of right coronary artery 10/01) –Ventricular Septal Defect and Atrial Septal Defect –Tobacco Addiction (2 packs daily for many years) –Type II Diabetes Mellitus –Obstructive Sleep Apnea –Hyperlipidemia –Hypertension –Chronic cellulitis/erysipelas of left leg

4. 9/2/04 n Discontinued all of his medications one week prior to his visit because: “They were killing me.” –Simvastatin 80 mg –Niaspan 2000 mg –Losartan/hydrochlorothiazide 100/25 –Aspirin 325 mg –Atenolol 100 mg –Spironolactone 25 mg twice a day –Metformin 500 mg twice a day –Flonase

5. n Had multiple dental extractions done in early June while taking dicloxacillin 1 gram twice a day and benzathine penicillin 1.2 million units every four weeks. Had been on this regimen since 9/03. n Felt somewhat better after stopping his medications, but still had a cough and night sweats.

6. Past Medical History n Chronic cellulitis/erysipelas began in 10/02 after he was hit in the left leg with a sledge hammer by one son and a week later with a brick by another son. n Admitted for incision and drainage of an abscess of the left leg. n …had six additional episodes of cellulitis from 10/02 to 8/03 which responded to oral antibiotics, except for one episode requiring admission.

7. Past Medical History, continued 8/21/03 n First seen by Dr. Vogelman, who initiated treatment with dicloxacillin for recurrent cellulitis and terbinafine for tenia pedis. 9/4/03 n Benzathine penicillin 1.2 million units intramuscularly every four weeks was added for strep coverage.

8. Past Medical History, continued n Last seen by Dr. Vogelman on 8/26/04 who stopped antibiotics due to complete clearing of cellulitis/erysipelas. n Noted anemia (Hct 33) as well as a 2 month history of weight loss, fatigue, myalgias, and night sweats.

9. Physical Exam n Pulse: 112 bpmBP: 148/80 mmHg n Temperature: 99°FChest: Clear n Heart: Harsh IV/VI systolic murmur along the left sternal margin, apex and base. n Well healed scar, left leg

10. Initial Lab and X-Rays n Sed Rate: 115 n Normal PA and Lateral Chest Film/Sinus Series

11. Additional Lab and Imaging Studies n Initial blood culture grew Strep viridans (within 18 hours) followed by two subsequent sets which also grew Strep viridans (6 of 6 bottles) n Transthoracic echocardiogram—no vegetations. VSD and ASD noted. n Transesophageal echocardiogram—sub-pulmonic pedunculated mass in the RV outflow tract. Located where flow across the VSD hits the outflow track. Pulmonic regurgitation.

12. Hospital Course n Admitted and started on intravenous penicillin. Gentamycin was added later. n Infectious disease consult—Strep viridans probably due to dental work. n MIC Ceftriaxone.064 s Penicillin.064-.125 s n Discharged on Ceftriaxone 2 grams IV daily. n “I never knew I could feel this good.”

13. Learning Objectives  Recognize the protean signs and symptoms associated with bacterial endocarditis  Become familiar with the common microorganisms which cause acute and subacute bacterial endocarditis  Become familiar with the Modified Duke Criteria for the diagnosis of infective endocarditis  Review the current recommendations for the treatment of, and prophylaxis for infective endocarditis

14. Definition n Microbial infection of a cardiac valve or mural endocardium n Mortality –Almost 100% in preantibiotic era –10% streptococcal endocarditis –35% staphylococcal endocarditis –25-50% with prosthetic valve endocarditis n 20,000-30,000 new cases/year primarily among newborn and elderly

16. Causes of Prosthetic Valve Endocarditis

17. Pathogenesis n Blood is driven from a high pressure area through a cardiac defect into a low pressure sink. n A platelet-fibrin aggregate forms in the low pressure sink. n During bacteremia, avirulent/virulent organisms adhere to the platelet-fibrin aggregate forming a vegetation.

18. Clinical presentations n Subacute bacterial endocarditis –Duration of more than six weeks n Symptoms may begin insidiously and last for months n Fever, sweats, weakness, myalgias, arthralgias, malaise, anorexia, and fatigability are common

19. Subacute bacterial endocarditis, continued n May be caused by avirulent bacteria, such as streptococci which are part of the indigenous flora n Cutaneous manifestations –Petechiae-conjunctivae, oropharynx, skin –Osler’s nodes—tender, purplish subcutaneous nodules in the pulp of the fingers –Janeway lesions-nodular, nonpainful erythematous or hemorrhagic areas on the palms or soles.

23. Subacute bacterial endocarditis, continued n Musculoskeletal features—myalgias, arthralgias, arthritis40-50% n Ocular findings—Roth spots—oval white areas surrounded by a zone of hemorrhage 3-5% n Splenomegaly—15-30% with infarcts in 40% and abscesses in 5% of patients with SBE

24. Subacute bacterial endocarditis, continued n Renal manifestations –Hematuria in 50% –Embolic renal infarction—flank pain –Membranoproliferative glomerulonephritis n Embolic phenomenon (cerebral or systemic) 25-50% n Mycotic aneurysms 2-10%

25. Subacute bacterial endocarditis, continued n Neurological complications30-40% due either to emboli or mycotic aneurysms n Cardiac findings –Murmur present in 90% of patients –Heart failure-usually due to involvement of aortic or mitral valves –New conduction abnormalities due to involvement of the membranous septum in the area of the AV node

26. Acute bacterial endocarditis n Organisms are more invasive (s. aureus, s pneumoniae, gram negative bacilli) n Onset is abrupt, with rigors and temperatures over 102° F (duration less than six weeks) n Cutaneous manifestations, petechiae may be prominent, especially when caused by s. aureus n Emboli are common n Metastatic infections-cause organ-specific symptoms

29. Echocardiography n 60% of vegetations can be detected using transthoracic echocardiography n 87-94% of vegetations can be detected with transesophageal echocardiography n Transesophageal echocardiography is indicated as the initial method for difficult to image patients, possible prosthetic valve infections, in patients with intermediate to high clinical suspicion or in patients for a high risk of complications