Transcript LEVAQUIN® (levofloxacin IV/tablets)

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
No financial disclosures
9/2/04

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
9/2/04

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

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.

Felt somewhat better after stopping his
medications, but still had a cough and night
sweats.
Past Medical History

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.

Admitted for incision and drainage of an abscess of
the left leg.

…had six additional episodes of cellulitis from 10/02
to 8/03 which responded to oral antibiotics, except
for one episode requiring admission.
Past Medical History, continued
8/21/03

First seen by Dr. Vogelman, who initiated
treatment with dicloxacillin for recurrent
cellulitis and terbinafine for tenia pedis.
9/4/03

Benzathine penicillin 1.2 million units
intramuscularly every four weeks was added
for strep coverage.
Past Medical History, continued

Last seen by Dr. Vogelman on 8/26/04 who
stopped antibiotics due to complete clearing
of cellulitis/erysipelas.

Noted anemia (Hct 33) as well as a 2 month
history of weight loss, fatigue, myalgias, and
night sweats.
Physical Exam

Pulse: 112 bpm
BP: 148/80 mmHg

Temperature: 99°F
Chest: Clear

Heart: Harsh IV/VI systolic murmur along
the left sternal margin, apex and base.

Well healed scar, left leg
Initial Lab and X-Rays

Sed Rate: 115

Normal PA and Lateral Chest Film/Sinus
Series
Additional Lab and Imaging Studies

Initial blood culture grew Strep viridans (within 18
hours) followed by two subsequent sets which also
grew Strep viridans (6 of 6 bottles)

Transthoracic echocardiogram—no vegetations. VSD
and ASD noted.

Transesophageal echocardiogram—sub-pulmonic
pedunculated mass in the RV outflow tract. Located
where flow across the VSD hits the outflow track.
Pulmonic regurgitation.
Hospital Course

Admitted and started on intravenous penicillin.
Gentamycin was added later.

Infectious disease consult—Strep viridans probably
due to dental work.

MIC Ceftriaxone .064 s Penicillin .064-.125 s

Discharged on Ceftriaxone 2 grams IV daily.

“I never knew I could feel this good.”
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
Definition
 Microbial infection of a cardiac valve or mural
endocardium

Mortality
–
–
–
–
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Almost 100% in preantibiotic era
10% streptococcal endocarditis
35% staphylococcal endocarditis
25-50% with prosthetic valve endocarditis
20,000-30,000 new cases/year primarily
among newborn and elderly
Causes of Prosthetic Valve Endocarditis
Pathogenesis

Blood is driven from a high pressure area
through a cardiac defect into a low pressure
sink.

A platelet-fibrin aggregate forms in the low
pressure sink.

During bacteremia, avirulent/virulent
organisms adhere to the platelet-fibrin
aggregate forming a vegetation.
Clinical presentations
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Subacute bacterial endocarditis
– Duration of more than six weeks
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Symptoms may begin insidiously and last for
months
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Fever, sweats, weakness, myalgias,
arthralgias, malaise, anorexia, and
fatigability are common
Subacute bacterial endocarditis, continued

May be caused by avirulent bacteria, such as
streptococci which are part of the indigenous
flora
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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.
Subacute bacterial endocarditis, continued
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Musculoskeletal features—myalgias,
arthralgias, arthritis
40-50%
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Ocular findings—Roth spots—oval
white areas surrounded by a zone of
hemorrhage
3-5%
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Splenomegaly—15-30% with infarcts in 40%
and abscesses in 5% of patients with SBE
Subacute bacterial endocarditis, continued
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Renal manifestations
– Hematuria in 50%
– Embolic renal infarction—flank pain
– Membranoproliferative glomerulonephritis
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Embolic phenomenon (cerebral or systemic)
25-50%
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Mycotic aneurysms
2-10%
Subacute bacterial endocarditis, continued
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Neurological complications
30-40% due
either to emboli or mycotic aneurysms
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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
Acute bacterial endocarditis
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Organisms are more invasive (s. aureus,
s pneumoniae, gram negative bacilli)
Onset is abrupt, with rigors and temperatures
over 102° F (duration less than six weeks)
Cutaneous manifestations, petechiae may be
prominent, especially when caused by
s. aureus
Emboli are common
Metastatic infections-cause organ-specific
symptoms
Echocardiography
 60% of vegetations can be detected using
transthoracic echocardiography

87-94% of vegetations can be detected with
transesophageal echocardiography

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