Infective Endocarditis

Infective endocarditis (IE) is a rare but potentially severe, life-threatening infection of the inner lining of the heart and the surface of valves known as the endocardium. If IE is left untreated, local tissue destruction occurs and heart valves become damaged due to pathogen invasion resulting in severe regurgitation of blood.
Consequently, the heart becomes less proficient at pumping blood around the body which can lead to congestive heart failure that is the main cause of death from IE1. IE is a rare affecting around 1 in 30,000 individuals each year in England but is important as despite antimicrobial therapy, severe complications including stroke, heart failure or even death2.
Delayed clinical diagnosis of IE is common as the initial symptoms such as fever and fatigue are varied and non-specific. Early diagnosis is crucial to enable faster treatment of IE critical for reducing morbidity and mortality. This review will discuss the aetiology and pathophysiology of IE alongside the standard procedures used for diagnosis.

Aetiology of IE:IE is mostly caused by gram-positive cocci with Streptococci, Staphylococci and Enterococci which usually originate from oral, skin and gastrointestinal tract flora respectively, accounting for 85% of cases3,4. IE can also be caused by fungal infections such as Candida or Aspergillus colonising the endocardium5.
Individuals at risk of include those that inject drugs or have a central venous catheter inserted as medical instruments can be infected by opportunistic pathogens, so manipulation of the skin disrupts the physical barrier allowing transient bacteria to enter the bloodstream6. Despite medical advancements, rates of IE are increasing due to a rise in surgery for valve replacement2.Pathophysiology: Understanding the pathophysiology of IE provides an insight into disease progression and aids in diagnosis7.
The endocardium has an outer endothelium with an underlying basal lamina and an inner sub-endothelial layer made of loose connective tissue, fibroblasts and collagen fibrils8. Despite the presence of transient bacteraemia in the bloodstream, IE is rare due to the resistance provided by the intact endothelium lining the heart valves, heart chamber and great vessels9.
If endothelial erosion occurs by altered haemodynamics, valvular heart disease, or mechanical lesions from artificial heart valves, blood would be exposed to the sub-endothelial layer and to stromal cells, thromboplastin and collagen present3. Exposure results in activation of the coagulation cascade resulting in fibrin deposition and platelet aggregation7.
Consequently, small masses known as sterile thrombotic vegetations mainly made of platelets, fibrin, red and white blood cells4 form on the damaged endothelium on cardiac valve leaflets resulting in non-bacterial thrombotic endocarditis [Figure 1]. Vegetations are frequently found in low-pressure areas on cardiac valves due to the Venturi effect where blood flows to a lower-pressure area. Greater mechanical stresses are imposed on the left cardiac valves as blood is pumped under higher pressure.
Thus, vegetations are usually identified by echocardiography on the atrial surface of the mitral valve and the ventricular surface of the aortic valve10. Knowing the common vegetation sites enables faster diagnosis of IE. Colonisation of an initially sterile vegetation may occur by adhesion of transient bacteria in the bloodstream [Figure 2].
Adhesion of gram-positive bacteria occurs as adhesins present on the surface of gram-positive bacteria recognise the exposed fibronectin, fibrinogen and platelets3. Bacterial colonisation and growth results in leukocyte infiltration into the vegetation further activating the host coagulation cascade.
Vegetation enlargement occurs as bacteria grow and produce a biofilm made of polysaccharides and proteins which aids bacterial persistence11. Pathogen binding initiates neutrophil chemotaxis and infiltration occurs concentrating proteases and oxidative activities12 which can cause valvular damage and cusp perforation [Figure 2].
Thrombotic vegetations can disseminate and become septic emboli possibly resulting in the blockage of small vessels, organ failure or stroke if a cerebral artery is occluded13. Clinical presentation:Delayed diagnosis of IE is common as IE has varied presentations; therefore, blood cultures and echocardiography are predominantly used in diagnosis and clinical presentations are used to help guide diagnosis.
IE is traditionally classified as either acute where a sudden development of IE occurs within days, or as subacute if a gradual development of IE occurs over weeks to a few months14. Patients usually present with persistent or recurrent fever, chills, or with non-specific and highly variable symptoms such as malaise, night sweats, myalgia, arthralgia or anorexia16.
If the onset of the disease process is slow, classic examination findings such as Osler nodes (red nodular lesions found on fingers and toes), Roth spots (a white-centred haemorrhage in the retina) and Janeway lesions (non-tender, haemorrhagic plaques usually on palms and soles)15 may present [Table 1].
Auscultation of the heart is important as regurgitant murmurs are identified in nearly half of patients16. Identifying regurgitant murmurs is critical as murmurs are a result of valvular insufficiency which commonly develops as a result of IE. As clinical presentations are non-specific and highly variable, a low threshold criterion for further investigation is needed to avoid delay in identifying individuals with IE16.
Diagnosis:Rapid diagnosis of IE is essential to initiate antibiotic therapy and avoid progressive, irreversible valve damage7. In comparison to the original Von Reyn criteria for the diagnosis of IE which only consisted of clinical and microbiological investigations, the modified Duke criteria is used in secondary care as the latter is more effective in diagnosis by incorporating echocardiographic findings18 to provide a greater insight into any endocardial pathogenesis [Table 1].
Two major, one major with three minor, or five minor criteria are required for a definitive diagnosis. For example, an echocardiogram showing endocardial involvement alongside a positive blood culture result is sufficient for a definitive diagnosis of IE [Table 1]. Possible diagnosis of IE requires at least one major and one minor criterion or three minor criteria.
In clinical practice, the Duke criteria is used but does not replace clinical judgement otherwise misdiagnosis or delayed would result due to the varied clinical presenations19. Microbiological Tests: Identifying underlying microbial aetiology is essential for optimal individual patient treatment.
Microbiological tests are performed to identify positive blood cultures. Prior to initiating antibiotic treatment, two sets of blood cultures are taken20. Incubation of a standard blood culture lasts for five days to recover nearly all cultivatable causes of IE21. However, negative tests in around 10% of patients22 may result from antibiotics being given prior to blood cultures or alternative diagnoses such as non-bacterial endocarditis.
Around two-thirds of initially culture negative patients are identified as positive with further testing such as serological testing for Bartonella and Coxiella22; therefore, the incorporation of serological testing in the modified Duke criteria is critical to avoid delayed diagnosis.
Echocardiography: Echocardiography is crucial in the diagnosis of IE and in predicting the embolic risk. Performing echocardiography as early as possible is essential to diagnose IE and thus initiate treatment23. Transthoracic echocardiography (TTE) and transoesophageal echocardiography (TOE) can be involved in diagnosis [Figure 3].
In TTE the transducer is placed on the chest wall and sends out ultrasound waves which pass through the chest wall into the heart. As TTE is non-invasive, it is initially used to identify evidence of endocardial involvement that is stated in the modified Duke Criteria such as vegetations or valvular perforation24, [Table 1].
TTE has a lower sensitivity of 60-75% in comparison to TOE which is more than 90% sensitive; therefore, most patients also have the TOE test where the transducer is attached to a tube, is guided down the pharynx and larynx into the oesophagus to achieve a more detailed image of the heart23, [Figure 3].
Conclusion:Rapid diagnosis is critical as IE has high mortality with over a third of patients dying a year after diagnosis despite advancements in the sensitivity of the diagnostic criteria1.
Delayed diagnosis contributes to mortality as vegetation enlargement and subsequent cusp perforation continues resulting in blood flow disruption, deterioration of cardiac function or systemic effects from emboli.

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