AssessmentsEndocarditis: Pathology review
USMLE® Step 1 style questions USMLE
A 67-year-old man presents to the primary care physician with a several week history of worsening fatigue, blurry vision, and rectal bleeding. Medical history is notable for ulcerative colitis, hypertension, and hyperlipidemia. The patient’s last colonoscopy was at age 50. Temperature is 37.6°C (99.7°F), pulse is 96/min, respirations are 18/min, and blood pressure is 122/63 mmHg. BMI is 34 kg/m2. Physical examination demonstrates an obese habitus. The patient’s skin appears pale with noted conjunctival pallor. Cardiopulmonary examination demonstrates a 3/6 holosystolic murmur best at the cardiac apex which was not present at the previous office visit 3 months ago. Retinal examination demonstrates round white spots on the retina surrounded by hemorrhage. Rectal examination is positive for scant blood in the rectal vault. Laboratory values are demonstrated below:
|Complete Blood Count, Serum|
|Leukocyte count||14,100 /mm3|
Two people came into the cardiology ward.
One of them was 25 year old Darren, who came in with a fever, chills and fatigue.
On the clinical examination, his fingernails had splinter hemorrhages and the palm of his hands had some erythematous flat lesions.
There were also some track marks on his forearm.
The other one is 75 year old Anna, who also had a fever and the same splinter hemorrhages and erythematous flat lesions that we previously saw.
On auscultation, a heart murmur was heard.
On her history, she said she was at the dentist 2 weeks ago.
Okay, so both people likely have endocarditis, or inflammation of the inner layer of the heart.
Remember that the heart’s wall is made up of three layers, the epicardium being the outermost layer, then the myocardium, and the endocardium, which is the layer that gets inflamed.
The inflammation can affect the heart valves, the mural endocardium or even prosthetic valves!
For non-infective endocarditis, the first step is usually damage to the endocardium.
Damage exposes the underlying collagen and tissue factor, which causes platelets and fibrin to adhere, which forms tiny blood clots.
This is called Nonbacterial Thrombotic Endocarditis or NBTE.
Tiny clots and fibrin can develop into vegetation, especially on the heart valves which damages them and makes it harder for them to open or close.
This can happen with hypercoagulable states, like when there’s a malignancy, especially pancreatic adenocarcinoma.
Another situation where NBTE can happen is with systemic lupus erythematosus,
This is an autoimmune disease involving antigen-antibody complexes, and in this case they settle in the endocardium and cause inflammation, leading to a particular type of endocarditis, called Libman-Sacks endocarditis.
Remember that it’s associated with large vegetations, sometimes described as verrucous vegetations since they look like warts.
Now, infective endocarditis occurs when pathogens find their way to the endocardium, typically from the heart valves.
Every day, there are opportunities for pathogens like bacteria and fungi to get into the bloodstream, but this is not a problem because they are usually few in number and can easily be cleared by our immune system.
However, sometimes a larger quantity of microbes can get into the bloodstream, like if a person has an obvious open wound or an abscess, during a dental or surgical procedure, or use of infected needles.
These microbes can float around in the blood for long enough to reach the heart.
A particular site that’s prone to infections is the heart valve which is supplied by tiny blood vessels.
Now, most often the valves on the left side are affected, the most common being the mitral valve and than the aortic valve.
This is sometimes due to predisposing conditions, with the most common one in high- and middle-income countries being mitral valve prolapse and, less often, bicuspid aortic valves.
So on these valves bacterial colonies, clots and fibrin, can also form vegetations.
They usually present on the mitral or aortic valve, but what’s special here is that they can present on either surface of the valve, though most commonly, on the undersurface.
They have low virulence, are found in the mouth, and they typically only affect valves that have had some previous damage, so think older patients or those with a history of heart valve disease after a dental procedure.
That’s because S. sanguinis uses special molecules on its surface, called dextrans, that bind to fibrin-platelet aggregates on damaged heart valves.
This usually results in small vegetations which don’t destroy the valve.
Staphylococcus aureus, on the other hand, is a highly virulent bacteria that can be found on the skin, and it can infect damaged valves.
They are often introduced via surgical procedures, wounds, or intravenous drug use, and often affects the tricuspid valve.
S aureus causes large vegetations that can destroy the valves.
Next we have Staphylococcus epidermidis.
A high yield fact is that this bacteria loves foreign prosthetic material, like prosthetic heart valves and this could be your best clue on a test.
This bacteria is usually introduced into the body at the time of heart valve surgery and it literally creates an extracellular matrix around itself called biofilm which allows it to stick around on the valve.
Another common point of entry into the body is through an infected intravenous catheter.
Enterococcus is a part of the normal urogenital flora.
Another bacterial species is Streptococcus gallolyticus, previously known as Streptococcus bovis which is normally found in the gut flora.
- "Robbins Basic Pathology" Elsevier (2017)
- "Harrison's Principles of Internal Medicine, Twentieth Edition (Vol.1 & Vol.2)" McGraw-Hill Education / Medical (2018)
- "Management Considerations in Infective Endocarditis" JAMA (2018)
- "Infective Endocarditis in Adults: Diagnosis, Antimicrobial Therapy, and Management of Complications" Circulation (2015)
- "2015 ESC Guidelines for the management of infective endocarditis" European Heart Journal (2015)
- "Poor oral hygiene as a risk factor for infective endocarditis–related bacteremia" The Journal of the American Dental Association (2009)
- "Clinical Presentation, Etiology, and Outcome of Infective Endocarditis in the 21st Century" Archives of Internal Medicine (2009)
- "2017 AHA/ACC Focused Update of the 2014 AHA/ACC Guideline for the Management of Patients With Valvular Heart Disease" Journal of the American College of Cardiology (2017)
- "Antibiotic prophylaxis for infective endocarditis: a systematic review and meta-analysis" Heart (2017)