Infective Endocarditis

• This is inflammatory disease of the heart valves or mural endocardium due to direct infection, usually bacterial (in which case it’s termed “bacterial endocarditis”).
   

A. Etiology and pathogenesis

     1. Risk factors

·      Pre-existing cardiac valve abnormality (like the stuff we just talked about)

·      Prosthetic valve

·      Source of infection (i.e., bacteremia), especially Streptococci

·      Presence of thrombi (remember, they’re bacteria magnets)

     2. What happens?

            a)  Endocardial abnormality predisposes to the development of platelet-fibrin thrombi.

            b)  Bacteria in the blood grow on the thrombi and then invade the valve.

            c)  This results in acute inflammation. The thrombosis and inflammation are referred to
                 together as “vegetation.” They’re large, irregular, and mushroom-like.

            d)  The friable vegetations (easily broken apart) can dislodge and travel to cause septic
                  embolism elsewhere in the body.

B. Classification

• Before the advent of antibiotics, acute vs. subacute IE was distinguished based on the infecting organism and disease morphology, severity, and course. Modern treatments for IE make it difficult to track disease severity so this classification isn’t as useful.

Many patients with acute IE will die despite intervention due to highly virulent organisms.

D. Morphological features

1. Can affect single or multiple valves (usually the mitral and/or aortic).
2. Vegetations may be single or multiple. They vary in size (small vs. large/bulky). This depends on the organism and previous antibiotic treatment.
3. Remember, vegetations = fibrin (thrombus) + masses of bacteria and inflammatory cells.
   Subacute vegetations have granulation tissue at the base; acute vegetations do not. Vegetations will stain pink (due to compacted fibrin) and may Gram stain (due to bacteria).

E.  Complications

*These relate to the virulence of the organism and severity and spread of infection.

1. Valvular insufficiency or stenosis, leading to heart failure
2. Rupture of infected valve cusp due to vegetation
3. Abscess due to spread of infection to the myocardium from the endocardium. These areas would appear pale due to liquefactive necrosis. The abscess can rupture, perforating the valve.
4. Bacterial or septic thromboembolism:
   a)  Osler’s nodes: swollen, erythematous, tender areas of the fingers and toes
   b)  Janeway’s lesions: hemorrhagic, nontender, pustular lesions on the soles and palms.
   c)  Splinter hemorrhages: linear hemorrhages below the nailbeds of the fingers and toes.
   d)  Roth spots: rupture and hemorrhage of retinal blood vessels
   e)  Septic infarction of other organs. The example was of a kidney, which had a wedge-
        shaped pale area (it was filled with pus from liquefactive necrosis due to spread of
        infection from the IE).
5. Entrapment of circulating Ab-Ag complexes in other organs. This results in immune-mediated diseases such as glomerulonephritis.

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