Book contents
- Frontmatter
- Contents
- Preface
- Contributors
- Part I Clinical Syndromes – General
- Part II Clinical Syndromes – Head and Neck
- Part III Clinical Syndromes – Eye
- Part IV Clinical Syndromes – Skin and Lymph Nodes
- Part V Clinical Syndromes – Respiratory Tract
- Part VI Clinical Syndromes – Heart and Blood Vessels
- 36 Endocarditis of Natural and Prosthetic Valves: Treatment and Prophylaxis
- 37 Acute Pericarditis
- 38 Myocarditis
- 39 Mediastinitis
- 40 Vascular Infection
- 41 Pacemaker, Defibrillator, and VAD Infections
- Part VII Clinical Syndromes – Gastrointestinal Tract, Liver, and Abdomen
- Part VIII Clinical Syndromes – Genitourinary Tract
- Part IX Clinical Syndromes – Musculoskeletal System
- Part X Clinical Syndromes – Neurologic System
- Part XI The Susceptible Host
- Part XII HIV
- Part XIII Nosocomial Infection
- Part XIV Infections Related to Surgery and Trauma
- Part XV Prevention of Infection
- Part XVI Travel and Recreation
- Part XVII Bioterrorism
- Part XVIII Specific Organisms – Bacteria
- Part XIX Specific Organisms – Spirochetes
- Part XX Specific Organisms – Mycoplasma and Chlamydia
- Part XXI Specific Organisms – Rickettsia, Ehrlichia, and Anaplasma
- Part XXII Specific Organisms – Fungi
- Part XXIII Specific Organisms – Viruses
- Part XXIV Specific Organisms – Parasites
- Part XXV Antimicrobial Therapy – General Considerations
- Index
36 - Endocarditis of Natural and Prosthetic Valves: Treatment and Prophylaxis
from Part VI - Clinical Syndromes – Heart and Blood Vessels
Published online by Cambridge University Press: 05 March 2013
- Frontmatter
- Contents
- Preface
- Contributors
- Part I Clinical Syndromes – General
- Part II Clinical Syndromes – Head and Neck
- Part III Clinical Syndromes – Eye
- Part IV Clinical Syndromes – Skin and Lymph Nodes
- Part V Clinical Syndromes – Respiratory Tract
- Part VI Clinical Syndromes – Heart and Blood Vessels
- 36 Endocarditis of Natural and Prosthetic Valves: Treatment and Prophylaxis
- 37 Acute Pericarditis
- 38 Myocarditis
- 39 Mediastinitis
- 40 Vascular Infection
- 41 Pacemaker, Defibrillator, and VAD Infections
- Part VII Clinical Syndromes – Gastrointestinal Tract, Liver, and Abdomen
- Part VIII Clinical Syndromes – Genitourinary Tract
- Part IX Clinical Syndromes – Musculoskeletal System
- Part X Clinical Syndromes – Neurologic System
- Part XI The Susceptible Host
- Part XII HIV
- Part XIII Nosocomial Infection
- Part XIV Infections Related to Surgery and Trauma
- Part XV Prevention of Infection
- Part XVI Travel and Recreation
- Part XVII Bioterrorism
- Part XVIII Specific Organisms – Bacteria
- Part XIX Specific Organisms – Spirochetes
- Part XX Specific Organisms – Mycoplasma and Chlamydia
- Part XXI Specific Organisms – Rickettsia, Ehrlichia, and Anaplasma
- Part XXII Specific Organisms – Fungi
- Part XXIII Specific Organisms – Viruses
- Part XXIV Specific Organisms – Parasites
- Part XXV Antimicrobial Therapy – General Considerations
- Index
Summary
DEFINITION AND PATHOGENESIS
The term infective endocarditis (IE) denotes an infection of the endothelial surface of the heart. This is usually a valvular surface, but nonvalvular extracardiac endothelium can also be infected.
In the past, IE was classified as acute or subacute, depending on the severity of clinical presentation. Since the advent of antibiotics, classification and therefore therapeutic decisions are based on the bacteriology and the valvular tissue involved, that is, native valve versus prosthetic valve.
The animal model of endocarditis has improved the understanding of the in vivo aspect of the pathogenesis of this disease. Any structural abnormalities that cause turbulent blood flow across a high to low pressure gradient denude epithelium from surfaces impacted on by the turbulence. Such damaged areas (most commonly valvular surfaces) are predisposed to platelet and fibrin deposition and eventually to the formation of sterile vegetation, also known as nonbacterial thrombotic endocarditis (NBTE).
When transient bacteremia occurs after injury to mucosal surfaces in the oropharynx, genitourinary tract, or gastrointestinal tract, organisms are deposited onto the NBTE, where they adhere firmly, multiply, and stimulate further deposition of platelets and fibrin. The infected site is sustained by inaccessibility of the organisms to host defenses. Enlargement of the lesion into a mature vegetation may result in destruction of valves and may cause complications through local bacterial spread or through embolization of fragments of the vegetation.
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- Chapter
- Information
- Clinical Infectious Disease , pp. 253 - 264Publisher: Cambridge University PressPrint publication year: 2008