Infective endocarditis Medical Assignment Help

Infective endocarditis is an infection of the endocardium or vascular endothelium. The disease may occasionally occur as a fulminating or acute infection, but more commonly runs an insidious course and is known as subacute  (bacterial) endocarditis (SBE). The incidence is 6-7 per 100000 per year in the UK, but is much more common in developing countries. Endocarditis occurs most commonly on rheumatic or congenitally abnormal valves as well as in mitral valve prolapse and calcified aortic valve disease. It also occurs in association with congenital lesions such as ventricular septal defect or persistent  ductus arteriosus. A very similar disease may occur from infection of arteriovenous fistulas. Prosthetic valves or prosthetic vascular material may be similarly infected and this is one of the reasons for the increasing incidence of endocarditis in developed countries. The organisms are often non-virulent. Virulent organisms may infect normal valves, especially when the victim is generally debilitated or immunologically incompetent.
The term ‘infective endocarditis’ is preferred because not all the infecting organisms are bacteria.


Many organisms cause infective endocarditis. At the present time the three most common organisms are:
1 Streptococcus viridans (e.g. Strep. viridans mitis and Strep. viridans sanguis) (50% of cases). These organisms are part of the bacterial flora of the pharynx and upper respiratory tract, and the infection may follow dental extraction or cleaning, tonsillectomy or bronchoscopy.
2 Enterococcus faecalis (found in perineal and faecal bacterial flora). Infections with this organism are more usual in older men with prostatic disease, in womenwith genitourinary infections, or following pelvic surgery.
3 Staphylococcus aureus. This organism may cause subacute endocarditis and is responsible for 50% of the acute forms. Patients with central venous catheters used for parenteral feeding, temporary pacemaker electrode catheters or pulmonary artery (Swan-Ganz) catheters are prone to this infection. Cellulitis or skin abscesses are often the origin of the infection, particularly in drug addicts who ‘mainline’. Infective endocarditis can also be caused by:
1 Staphylococcus epidermidis, Histoplasma, Brucella, Candida and Aspergillus. Infections with these organisms are particularly common in intravenous drug addicts, alcoholics and patients with prosthetic heart valves.
2 Coxiella burnetii (the causative organism of Q fever. This may cause a subacute infection. Although Gram-negative bacteraemia/septicaemia frequently occur, endocarditis with these organisms is unusual.


Infection occurs along the edges of the heart valves. It is more common on the left side, with mitral and aortic regurgitation being the commonest valve lesions complicated by endocarditis. In drug addicts the valves in the right heart are usually affected. The endocardium on the low-pressure side of a shunt such as ventricular septal defect is infected and it is the pulmonary artery that is infected when a persistent ductus arteriosus is present; in both instances the lesions are ‘jet lesions’ produced on the wall opposite the shunt.

Hypertrophic cardiomyopathy, syphilitic aortic regurgitation, prolapsing mitral valve and arteriosclerotic valve lesions may also be rarely complicated by endocarditis. The lesion of infective endocarditis is a mass of fibrin,  platelets and infecting organisms known as a vegetation. The chance of an organism sticking to a vegettion is increased because of the clumping together of bacteria caused by agglutinating antibodies. These can develop because of repeated infection with the bacterium over a period of years. In acute endocarditis, vegetations may be very large and may embolize. Virulent microorganisms may rapidly destroy the valve cusp, producing ulceration and regurgitation.
The extracardiac manifestations result either from embolization or from the deposition of immune complexes. The latter is thought to be responsible for arthralgia, Roth spots and Janeway lesions, focal glomerulonephritis and acute vasculitis .
Splenic and renal infarcts are produced by emboli. Myocardial infarction can result from coronary emboli, and pulmonary infarction may occur if right-sided lesions embolize.


Subacute endocarditis

The patient presents with fever, night sweats, weight loss, weakness and symptoms due to cardiac failure or embolism. Another important presentation is the combination of renal failure and a heart murmur. It is not usually possible to date the onset of the illness.

Jet lesions produced in infective endocarditis.

Jet lesions produced in infective endocarditis.

Acute endocarditis

In intravenous drug abusers or following an acute suppurative illness such as pneumonia or meningitis, the development of acute endocarditis is suggested by the persistence of fever and the development of heart murmurs, vasculitis (with petechial haemorrhage) and emboli, including metastatic abscesses. The onset of severe heart failure may indicate chordal rupture or acute valvular destruction.

Prosthetic endocarditis

There are two varieties: the first develops soon after surgery and is due to infection of the prosthesis at surgery, and the second occurs late and follows a bacteraemia. In both cases it is the valve ring that is infected. This produces myocardial abscesses and damage, for example to the conduction system. Vegetations in the valve may prevent it from opening and closing properly. Emboli are common.


The patients are often elderly. They appear pale (often anaemic) and ill. They are intermittently pyrexial and may complain of myalgia and arthralgia. Some of the following signs and symptoms may be present but endocarditis must always be suspected in a patient with a heartmurmur and a fever.

Clinical features of infective endocarditis.

Clinical features of infective endocarditis.

Vascular lesions

Small petechial or mucosal haemorrhages occur because of vasculitis. They are usually small and red, usually with a pale centre. They frequently appear on the mucosa of the pharynx and conjunctivae. Sometimes they are seen on the retinae (Roth spots). Small, flat, erythematous, non-tender macules are seen mainly on the thenar and hypothenar eminences (Janeway lesions); these blanch with pressure. Splinter haemorrhages may develop . Embolic lesions such as hard, painful, tender, subcutaneous swellings occur in the fingers, toes, palms and soles (Osler’s nodes).

Clubbing of the fingers

Mild clubbing of the fingers and toes appears late in the disease, and thus it only occurs in subacute endocarditis. It is rare nowadays because of relatively rapid diagnosis and treatment of the endocarditis.


Slight splenomegaly is common. If a splenic infarct has occurred, the spleen may be painful and tender and a friction rub may be heard over it.

Renal lesions

Haematuria is common, usually due to infarction as a result of emboli. Renal abscesses and acute glomerulonephritis also occur.


Arthritis of the major joints is frequently seen.

Other embolic phenomena

Cerebral emboli can occur, usually to the middle cerebral artery or its branches. Mycotic infected aneurysms are seen and may present after the endocarditis has healed. Peripheral arterial, pulmonary and coronary infarcts may also occur.


BLOOD. A normochromic normocytic anaemia is usual and C-reactive protein and the ESR are increased. A polymorphonuclear leucocytosis is common and thrombocytopenia can occasionally occur.
LIVER BIOCHEMISTRY is often mildly disturbed with, in particular, an increased serum alkaline phosphatase. IMMUNOGLOBULINS AND COMPLEMENT. Serum
immunoglobulins are increased, but total complement and C3 complement are decreased owing to immune complex formation. Circulating immune complexes are present in more than 70% of cases but are not routinely measured.
URINE. Proteinuria may occur and microscopic haematuria is nearly always present.
BLOOD CULTURES are positive in about three-quarters of cases. At least six sets of samples are usually taken  and cultured in aerobic and anaerobic conditions. Special culture techniques may be necessary for unusual microorganisms such as Brucella and Histoplasma. Serological tests are needed to incriminate Coxiella and Chlamydia, and may be helpful for Candida and Brucella.
ECHOCARDIOGRAPHY (particularly using the transoesophageal approach) is used to visualize vegetations, but small vegetations typical of the subacute disease can be missed. Echocardiography is useful to document valvular dysfunction and to identify patients in need of urgent surgery. Vegetations may persist
despite treatment.
CHEST X-RAY may show evidence of heart failure or emboli in right-sided endocarditis. ECGs may show evidence of myocardial infarction (emboli) or conduction defects.

Upper: Two-dimensional echocardiogram

Upper: Two-dimensional echocardiogram


Drug therapy

Any underlying infection should be treated (e.g. a dental abscess should be drained). The endocarditis is treated with bactericidal antibiotics chosen on the basis of the results of the blood culture and antibiotic sensitivity assessment. The treatment should continue for 4-6 weeks. Serum levels are measured and ‘back titration’ is performed to ensure that sufficient bactericidal antibiotic activity is present to inhibit growth of the organism. Strep. viridans is usually treated with i.v. benzylpenicillin 2.4 g 6-hourly daily and low-dose gentamicin 1 mg kg-I 8-hourly for the first 2 weeks because of the additive effects of gentamicin and penicillin against Strep. viridans. Oral amoxycillin 6 g daily can replace intravenous therapy after 2 weeks.
Strep. faecalis (enterococcus) is managed with penicillin and gentamicin (3 mg kg-I in divided 8-hourly doses). The dosage of penicillin should be higher (up to 24 g daily) than for Strep. viridans because Strep. faecalis is relatively insensitive to penicillin and ampicillin 8 g daily is often substituted. The exact dose of gentamicin depends on renal function and efficacy, and blood levels should be measured at least twice each week. It is more difficult to choose antibiotics when the infecting organism has not been isolated. However, in the acute form of the disease this is likely to be Staphylococcus, and treatment should include flucloxacillin and fusidic acid. In the subacute form, unless it is highly likely that the infecting organism is Strep. viridans, it is usual to begin treatment with a broad-spectrum combination of antibiotics such as gentamicin and ampicillin. The treatment is adjusted if it is not successful. The recurrence of fever may suggest that the antibiotic therapy is inadequate, but may also signal a drug reaction.
The antibiotics may be omitted for 24-72 hours to test this.


There are several situations in which surgery is necessary:
• Extensive damage to a valve
• Early infection of prosthetic material
• Worsening renal failure
• Persistent infection but failure to culture an organism
• Embolization
• Large vegetations
• Progressive cardiac failure
The timing of surgery is important. On the one hand the infection should, if possible, be eradicated before surgery is undertaken, but on the other hand the heart should not be left in a badly compromised haemodynamic state. In general, early surgery is preferable.


The prognosis is worse when the organism cannot be isolated, when cardiac failure is present, when infection occurs on a prosthetic valve, and when the microorganisms found are resistant to therapy. In general, 70% of those affected are treated effectively, but greater awareness of the subacute form of the disease will improve the success rate.


Those at risk of developing endocarditis should receive antibiotic therapy before undergoing a procedure likely to result in a bacteraemia. The form of the prophylaxis depends on the procedure and on the likelihood of endocarditis. High-risk patients are those with a prosthetic heart valve or a previous history of endocarditis.

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