Professional Documents
Culture Documents
2008/05/09
劉志強
Case I 97/03/12 0468013
• 70 y/o male P’t
• Complain of intermittent spiking fever
(39C) for the past 1 month.
• Presented to ER with fever 38C and mild
SOB and chest tightness was also noted
• Denied any other systemic disease
PE and Lab Data
• Chronic ill looking p’t
• Grade 4/6 systolic murmur over LSB
• WBC: 10100/cumm N/L: 87/5
• AST:27 Cr: 1.1
• U/A : Negative
• CXR
Further Studies
• Blood Culture : Streptococcus Gr.Viridians X IV
• Cardiac Echo :
• Normal LV contractility with severe LVOT
obstruction with LVOT PG~ 80-120 mmHg.
• Dilated LA and Aortic sclerosis
• MV vegetation with severe eccentric MR, mild
TR.
• Diagnosis :Infective endocarditis ( IE ):definite,
HOCM
Case II 97/04/13 0248419
• 46 y/o male P’t
• Sent to ER the chief complaint of fever,
headache and R’t side weakness
• Denied any other systemic disease
PE and Lab Data
• Acute ill looking p’t
• GCS : E3V2M5
• WBC: 17500/cumm N/L: 85/9
• AST:24 Cr: 0.9
• CXR and Brain CT
Further Studies
• Blood Culture : Streptococcus Gr.Viridians X III
• Cardiac Echo:
• 1.A vegetation at the anterior leaflet of mitral
valve(about 1.3*0.8cm) with severe MR
• **Diagnosis:infective endocarditis : definite
• Abd Sono:
• Spleen:one irregular shaped hypoechoic mass with
small hyperechoic nodules in the margin 5.8X3.7cm at
lower pole of spleen
• R/O intrasplenic hematoma, abscess, or post-infaction
• related intrasplenic hemorrhage
Infective
Endocarditis
What is Infective Endocarditis (IE)?
• IE is a microbial infection of the inner lining of the heart, the
endocardium.
• While incidence has remained steady over the past five decades, the
disease has evolved drastically.
• The heart has four valves. In counterclockwise order, they are: the aortic valve, the
tricuspid valve, the pulmonary valve, and the mitral valve.
• The arrows indicate blood flow. Red arrows indicate the flow of oxygen-rich blood
and blue oxygen-poor.
• Unable to facilitate the one-way flow of blood, damaged heart valves hinder the
pumping of blood efficiently throughout the body, leading to congestive heart
failure. This is one reason the mortality rate of IE remains high even today.
Pathogenesis
• At a previously-damaged cardiac valve, a jet stream of blood with an abnormally
high velocity damages the endothelium
• This damaged surface becomes a starting point for the deposition of platelets and
the formation of a platelet-fibrin clot, causing nonbacterial thrombotic endocarditis
(NBTE).
• IE develops after bacteria enter the bloodstream and colonize the clot.
• Platelets and fibrin accumulate over the bacteria, increasing the size of the
vegetation.
Leukocytes are unable to penetrate the vegetation as additional layers of fibrin are
added. Treatment with antibiotics can also be problematic because the bacteria
within the vegetation often become less metabolically active, and many antibiotics
require active bacterial growth to be effective.
Not every incidence of bacteremia leads to IE. Not only must the blood-borne pathogen be
present in significant enough numbers to establish infection, it must possess the capacity
(determinants of virulence) necessary to adhere to and colonize the damaged endothelium.
Infective Endocarditis requires bacteremia and quite often requires
an underlying heart defect to be exploited by the blood-borne
pathogens.
• Other bacteria
– The HACEK Group
• Haemophilus species, Actinobacillus actinomycetemcomitans, Cardiobacterium
hominis, Eikenella corrodens, and Kingella species
– Usual bacterial causes
• Bacillus cereus, Clostridium perfringens, Mycobacterium tuberculosis, Nocardia
asteroides, Coxiella burnetii, etc.
• Fungi
– Candida and Aspergillis species
The figure to the right shows one portion (called a leaflet) of the mitral valve.