Acute Bacterial Endocarditis - Erler Zimmer
Clinical History
A 15-year-old adolescent with a persistent cough and sputum experienced an abrupt onset of high fever and chest discomfort several days before being hospitalized in an unconscious state. Upon examination, an early diastolic murmur was detected at the aortic region, radiating down the left sternal edge. Despite undergoing antibiotic treatment, his condition rapidly worsened, ultimately resulting in fatality. Blood cultures indicated the presence of Staphylococcus aureus.
Pathology
This diminutive heart specimen reveals the left ventricle and associated valves. The non-coronary cusp of the aortic valve exhibited ulceration and perforation, with fragile vegetations attached. Immediately below this cusp, a perforation extended into the right atrium, just above the tricuspid valve (refer to the back of the specimen). The other aortic cusp also displayed thickening. These findings are indicative of acute bacterial endocarditis involving aortic cusp and atrioventricular perforations.
Further Information
Acute bacterial endocarditis, a variant of infective endocarditis, may also result from fungal infections, although the latter are uncommon.
Under ordinary circumstances, the endothelial lining of the heart and valves exhibits relative resistance to infection by most bacteria or fungi. The occurrence of infective endocarditis necessitates initial damage or injury to the endocardial tissue, often leading to the aggregation of platelets and fibrin, which subsequently become infected, giving rise to vegetation—a nidus for infection. Staphylococcus aureus, owing to its high virulence, can occasionally infect normal heart valves.
Following the initial platelet-fibrin aggregation, there is further activation of the coagulation system via the extrinsic clotting pathway and initiation of the inflammatory response via monocytes. This leads to the continued growth of the vegetation/thrombus. Microbial growth typically takes place within the fibrin matrix, posing a challenge for the immune system to eliminate the infection. Moreover, these infected thrombi can embolize, causing infections in distant sites through smaller capillaries (e.g., in the kidney).
Risk factors for developing infective endocarditis include valvular heart disease, such as prior rheumatic heart disease, congenital heart disease (e.g., ventricular septal defect or bicuspid aortic valve), prosthetic heart valves, or any previous invasive cardiac procedures. Individuals at risk may require administration of antithrombotic medications like heparin or aspirin. Diagnosis involves clinical examination, pathology (blood cultures), and diagnostic imaging, with transthoracic echocardiogram often being the initial choice followed by transesophageal echocardiogram. Treatment encompasses antimicrobial therapy, anticoagulants, and, in some complex cases, surgical intervention such as valve surgery.
