Acute Bacterial Endocarditis - Erler Zimmer 3D anatomy Series MP2041

This dissection model highlighting acute bacterial Endocarditis is part of the exclusive Monash 3D anatomy series, a comprehensive series of human dissections reproduced with ultra-high resolution color 3D printing.

Clinical History.

A 15-year-old boy with a cough and sputum developed a frantic (spicy) fever and chest pain a few days before being admitted in a comatose condition. Examination revealed an early diastolic murmur in the aortic area, radiating along the left sternal border. He deteriorated very rapidly and died despite antibiotic chemotherapy. Blood cultures developed Staphylococcus aureus.

Pathology

This small heart shows the left ventricle and associated valves. The non-coronary cusp of the aortic valve is ulcerated and perforated and has friable vegetations attached. Immediately below this cusp a perforation extends into the right atrium just above the tricuspid valve (see back of specimen. The other aortic cusp is also thickened. This is an acute bacterial endocarditis with aortic cusp and atrioventricular perforations.

Additional Information.

Acute bacterial endocarditis is a form of infective endocarditis.
Under normal circumstances, the endothelial lining of the heart and valves is relatively resistant to infection by most bacteria or fungi. Therefore, for infective endocarditis to occur, there must be initial damage or injury to the endocardial tissue. This often results in the aggregation of platelets and fibrin, which then become infected, leading to the formation of vegetation (i.e., an infectious nidus). Staphylococcus aureus, however, is highly virulent and can sometimes infect normal heart valves.

After initial platelet-fibrin aggregation, there is further activation of the coagulation system through the extrinsic coagulation pathway and initiation of the inflammatory response by monocytes, resulting in further growth of vegetation/thrombus. Microbial growth tends to occur within the fibrin matrix, which makes it difficult for immune responses to eradicate the infection. An additional problem is that these infected tombi can also embolize causing distant sites of infection in smaller capillaries (e.g., in the kidney).
Risk factors for the development of infective endocarditis include valvular heart disease, such as previous rheumatic heart disease, congenital heart disease (e.g., ventricular septal defect or bicuspid aortic valve), prosthetic heart valves, or any previous invasive cardiac procedure. It may be necessary to administer antithrombotic drugs, e.g., heparin or aspirin, to patients at risk. Diagnosis is initially made by clinical examination followed by pathology (blood cultures) and imaging. Transthoracic echocardiogram is often first line, followed by transesophageal echocardiogram. Treatment includes antimicrobial therapy, anticoagulants, and, in some complicated cases, surgery such as valve surgery.

What advantages does the Monash University anatomical dissection collection offer over plastic models or plastinated human specimens?

• Each body replica has been carefully created from selected patient X-ray data or human cadaver specimens selected by a highly trained team of anatomists at the Monash University Center for Human Anatomy Education to illustrate a range of clinically important areas of anatomy with a quality and fidelity that cannot be achieved with conventional anatomical models-this is real anatomy, not stylized anatomy.
• Each body replica has been rigorously checked by a team of highly trained anatomists at the Center for Human Anatomy Education, Monash University, to ensure the anatomical accuracy of the final product.
• The body replicas are not real human tissue and therefore not subject to any barriers of transportation, import, or use in educational facilities that do not hold an anatomy license. The Monash 3D Anatomy dissection series avoids these and other ethical issues that are raised when dealing with plastinated human remains.