Article Text

Download PDFPDF
Immune responses in endocarditis
  1. Division of Infectious Diseases,
  2. St George’s Hospital Medical School,
  3. Cranmer Terrace, London SW17 0RE, UK

Statistics from

Request Permissions

If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.

In 1885 William Osler delivered the Gulstonian lectures describing the broad clinical manifestations of bacterial endocarditis.1 The past 30 years have seen concerted attempts to explain the pathogenetic mechanisms behind the syndrome: heart failure out of proportion to the valve insufficiency; the presence of renal lesions in the majority of cases; arthritis, vasculitis, and splenomegaly as well as the classic cutaneous signs. What is clear is that an encounter between a circulating bacterium and an abnormal valve, with subsequent embolisation, can explain neither the initial establishment of the vegetation nor the myriad of extracardiac sequelae. Moreover, in most cases the microorganisms implicated are of low virulence, but when sequestered in a vegetation they are capable of inducing uncharacteristically severe disease.

The understanding of endocarditis as an immune complex mediated syndrome and the identification of factors necessary for the genesis of the vegetation have clarified some of these contradictions. Recent appreciation of the specific roles for cytokines in inflammation and control of sepsis enable further understanding of the diverse pathophysiological findings in infective endocarditis.

Pathogenesis of the cardiac vegetation

The animal model of endocarditis, in which a polyethylene catheter is passed across the aortic valve of a rabbit, producing initially a non-bacterial thrombotic vegetation and subsequently bacterial colonisation, has been a useful pathophysiological tool.2 ,3 Bacterial factors such as dextran, slime, fibronectin binding, and teichoic acid have been implicated in bacterial adherence to the platelet–fibrin matrices on the damaged valve. Other studies, investigating the role of the host immune response in protection against endocarditis, employed whole cell vaccines with varied results. In some cases, active (but not passive) immunisation prevented endocarditis without accelerating the rate of bacterial clearance from the circulation, suggesting a mechanism related to interference with bacterial adherence to …

View Full Text