PANCE - Bacterial Endocarditis

Here are key facts for PANCE Examination from the Bacterial Endocarditis tutorial, as well as points of interest at the end of this document that are not directly addressed in this tutorial but should help you prepare for the boards.

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1. Staphylococcus aureus is the leading cause of infective endocarditis; associated with a high mortality rate due to its aggressive nature and antibiotic resistance. 2. S. aureus exists in the normal human flora, commonly found in the nares (nostrils), which can be a source of bacteremia. 3. Highest risk patients include those with compromised immune systems and/or prosthetic cardiac devices. 1. Infective endocarditis presents with inflammation affecting valves with vegetation blocking blood flow. 2. Endocarditis can affect the atrioventricular valve or walls of the heart (mural endocarditis). 3. Vegetations are composed of fibronectin, fibrinogen, platelets, and bacteria forming thrombotic masses. 1. Treatment requires prolonged intravenous administration of antibiotics; S. aureus is resistant to penicillin. 2. For methicillin-resistant strains (MRSA), vancomycin or daptomycin, sometimes in combination with other antibiotics, are administered intravenously. 3. Methicillin-resistant strains (MRSA) display changes in penicillin-binding proteins to increase tolerance. 1. Vegetations can break free and cause an embolism, even stroke, requiring vigilant monitoring. 2. S. aureus releases toxins and acts as a superantigen to provoke immune responses that ultimately destroy host cells. 3. The aggressive nature of S. aureus enables invasion of endocardial cells and promotes highly destructive inflammatory processes.

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1. S. aureus adheres to endothelial cells and extracellular proteins via surface adhesion protein. 2. Invasion of endocardial cells allows bacteria to release toxins protected from immune responses. 3. Evasion of host defenses occurs through creation of a protective biofilm (slime layer) comprising polysaccharides and proteins. 4. S. aureus can "hide" from the host immune system and antibiotic treatments via phenotype switching to small colony variants. 1. Fibronectin acts as a "bridge" between endothelial cells and bacteria, adhering to endothelial cells via alpha-5 beta-1 integrins. 2. Fibrinogen forms a bridge by adhering to S. aureus via Clumping factor A, and to endocardial cells via alpha-5 beta-1 integrin. 3. Platelets adhere to fibrinogen via integrin GPIIb/IIIa, forming connections that create a thrombus. 4. Platelet activation induces release of pro-inflammatory molecules, binding of leukocytes, and release of pro-coagulation molecules. 1. S. aureus is resistant to penicillin, limiting first-line treatment options. 2. MRSA is increasingly common in both hospital and community settings, requiring broader antibiotic coverage. 3. The S. aureus-fibronectin connection enables endocytosis into endocardial cells, where bacteria are protected. 4. Small colony variants allow bacteria to lie dormant within host tissues, only to reemerge as an infective pathogen when conditions are favorable. 1. The protective biofilm inhibits thrombus destruction, allowing S. aureus to proliferate and destroy underlying tissues. 2. Endocarditis with vegetations can lead to valvular dysfunction and heart failure. 3. Treatment must continue long enough to eradicate dormant bacteria that may reemerge. 4. Methicillin (meticillin), a synthetic derivative of penicillin, has been used to treat S. aureus infections since the 1960s but resistance is common.

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Below is information not explicitly contained within the tutorial but important for PANCE preparation. 1. Modified Duke criteria are essential for diagnosis, including major criteria (positive blood cultures, echocardiographic evidence) and minor criteria (predisposition, fever, vascular phenomena). 2. Physical examination may reveal new cardiac murmurs, Janeway lesions, Osler nodes, Roth spots, and splinter hemorrhages. 3. Serial blood cultures from different sites before antibiotic administration are crucial for confirming diagnosis. 1. Echocardiography is the primary imaging modality, with TEE having higher sensitivity than TTE for vegetation detection. 2. Laboratory studies typically show elevated inflammatory markers (ESR, CRP) and may reveal anemia of chronic disease. 3. ECG may demonstrate conduction abnormalities if abscess formation affects the cardiac conduction system. 1. Empiric therapy should be initiated promptly, with definitive therapy guided by culture and sensitivity results. 2. Surgical consultation is indicated for heart failure, persistent bacteremia, perivalvular abscess, or large mobile vegetations. 3. Antibiotic prophylaxis for high-risk cardiac conditions before dental procedures follows specific guidelines that PAs must know.