Bacterial endocarditis – morphology and complications

Infective endocarditis is a microbial infection of the heart valves or mural endocardium that leads to the formation of vegetations composed of thrombotic debris and organisms, often associated with destruction of the underlying cardiac tissue

Morphology

Classic hall mark of Infective endocarditis is vegetations on heart valves
Common sites – valves of left heart (Valves of right heart are involved in intravenous drug abusers)
Most frequently on the mitral followed by aortic, simultaneous involvement of both mitral and aortic and rarely on the valves of right heart
In SABE, vegetations are found on diseased valves and in ABE, vegetations are found on previously normal valves
Location – on the atrial surface of atrioventricular valve and ventricular surface of semilunar valves
Vegetations can be single or multiple and may involve more than one valve
Occasionally they can erode into underlying myocardium and produce an abscess (ring abscess)
Gross
- Size – from few mm to several centimeters
- Appearance – Flat, filiform, fungating or polypoidal
- Grey-tawny to greenish, irregular, single or multiple and typically friable present along the closure of cusps
- Vegetations in ABE are bulkier and globular than those of SABE.
- Vegetations in ABE may cause ulceration or perforation of the underlying valve leaflet or may produce myocardial abscess
Microscopy
- Vegetations consists of 3 zones
  - Outer layer or cap – consists of eosinophilic material composed of fibrin and platelets
  - Underneath this layer is basophilic zone containing colonies of bacteria
  - Deeper zone – consists of non-specific inflammatory reaction. In SABE there may be granulation tissue (evidence of repair)
  - In Acute BE – inflammatory infiltrate consists mainly of neutrophils and is accompanied by tissue necrosis and abscess in the valve ring
  - In Subacute BE – healing by granulation tissue with mononuclear infiltrate and proliferating fibroblast are present
Complications of Infective endocarditis
- Complications begin in first few weeks of onset and are divided into cardiac and extra cardiac
- Cardiac complications
  - Valvular stenosis or insufficiency
  - Perforation, rupture and aneurysm of valve leaflets
  - Abscess in the valve ring
  - Myocardial abscesses
  - Suppurative pericarditis
  - Cardiac failure from one or more of the foregoing complications
- Extra cardiac complications
  - Extra cardiac manifestations are due to friable vagetations which get dislodged into the blood stream forming emboli
  - Emboli from left side of the heart – Enters the systemic circulation and affect organs like spleen, brain, kidneys producing infarcts, abscesses and mycotic aneurysms
  - Kidneys – petechial hemorrhages (Flea bitten). Focal glomerulonephritis and infarction may develop
  - Spleen – Splenic enlargement and infarction with pain
  - Brain – infarction with neurological dysfunction
  - Emboli from right side of the heart – enters the pulmonary circulation and produces pulmonary abscesses
  - Petechiae may be seen in skin and conjunctiva due to emboli or toxic damage to capillaries
  - In SABE, Oslers nodes, Roth spots and in ABE , Janeway lesions may appear due to toxic or allergic inflammation of the vessel wall
    - Oslers nodes – Painful small swelling (1cm) appearing at the tip of fingers or toes caused by deposition of immune complex and hypersensitivity vasculitis
    - Janeway lesions –
      - Small erythematous or hemorrhagic, macular non-tender lesions on palms and soles
      - These are microabscess of the dermis with marked necrosis and inflammatory infiltrate not involving the epidermis
      - They are caused by septic emboli which deposit bacteria, forming microabscesses
    - Roth spots –
      - Caused by immune complex mediated vasculitis
      - Retinal hemorrhages with pale center composed of coagulated fibrin
  - Focal necrotizing glomerulonephritis due to circulating immune complexes

Reference

Vinay kumar, Abul K.Abbas, Nelson Fausto, Jon C. Aster. Robbins and Cotran Pathologic basis of disease. 8th edition

Bacterial endocarditis – morphology and complications

Infective endocarditis is a microbial infection of the heart valves or mural endocardium that leads to the formation of vegetations composed of thrombotic debris and organisms, often associated with destruction of the underlying cardiac tissue

Morphology

Classic hall mark of Infective endocarditis is vegetations on heart valves

Common sites – valves of left heart (Valves of right heart are involved in intravenous drug abusers)

Most frequently on the mitral followed by aortic, simultaneous involvement of both mitral and aortic and rarely on the valves of right heart

In SABE, vegetations are found on diseased valves and in ABE, vegetations are found on previously normal valves

Location – on the atrial surface of atrioventricular valve and ventricular surface of semilunar valves

Vegetations can be single or multiple and may involve more than one valve

Occasionally they can erode into underlying myocardium and produce an abscess (ring abscess)

Gross

Size – from few mm to several centimeters

Appearance – Flat, filiform, fungating or polypoidal

Grey-tawny to greenish, irregular, single or multiple and typically friable present along the closure of cusps

Vegetations in ABE are bulkier and globular than those of SABE.

Vegetations in ABE may cause ulceration or perforation of the underlying valve leaflet or may produce myocardial abscess

Microscopy

Vegetations consists of 3 zones

Outer layer or cap – consists of eosinophilic material composed of fibrin and platelets

Underneath this layer is basophilic zone containing colonies of bacteria

Deeper zone – consists of non-specific inflammatory reaction. In SABE there may be granulation tissue (evidence of repair)

In Acute BE – inflammatory infiltrate consists mainly of neutrophils and is accompanied by tissue necrosis and abscess in the valve ring

In Subacute BE – healing by granulation tissue with mononuclear infiltrate and proliferating fibroblast are present

Complications of Infective endocarditis

Complications begin in first few weeks of onset and are divided into cardiac and extra cardiac

Cardiac complications

Valvular stenosis or insufficiency

Perforation, rupture and aneurysm of valve leaflets

Abscess in the valve ring

Myocardial abscesses

Suppurative pericarditis

Cardiac failure from one or more of the foregoing complications

Extra cardiac complications

Extra cardiac manifestations are due to friable vagetations which get dislodged into the blood stream forming emboli

Emboli from left side of the heart – Enters the systemic circulation and affect organs like spleen, brain, kidneys producing infarcts, abscesses and mycotic aneurysms

Kidneys – petechial hemorrhages (Flea bitten). Focal glomerulonephritis and infarction may develop

Spleen – Splenic enlargement and infarction with pain

Brain – infarction with neurological dysfunction

Emboli from right side of the heart – enters the pulmonary circulation and produces pulmonary abscesses

Petechiae may be seen in skin and conjunctiva due to emboli or toxic damage to capillaries

In SABE, Oslers nodes, Roth spots and in ABE , Janeway lesions may appear due to toxic or allergic inflammation of the vessel wall

Oslers nodes – Painful small swelling (1cm) appearing at the tip of fingers or toes caused by deposition of immune complex and hypersensitivity vasculitis

Janeway lesions –

Small erythematous or hemorrhagic, macular non-tender lesions on palms and soles

These are microabscess of the dermis with marked necrosis and inflammatory infiltrate not involving the epidermis

They are caused by septic emboli which deposit bacteria, forming microabscesses

Roth spots –

Caused by immune complex mediated vasculitis

Retinal hemorrhages with pale center composed of coagulated fibrin

Focal necrotizing glomerulonephritis due to circulating immune complexes

Reference

Vinay kumar, Abul K.Abbas, Nelson Fausto, Jon C. Aster. Robbins and Cotran Pathologic basis of disease. 8th edition