Page created on April 9, 2022. Last updated on December 18, 2024 at 16:58

Infective endocarditis

Introduction and epidemiology

Infective endocarditis (IE) is an infection of the endocardium, usually bacterial. It’s mostly a disorder of those with structural heart disease, but it can also occur in those with healthy hearts. It’s characterised by formation of vegetations on the heart valves. The most commonly affected valves are the aortic and mitral valves. IE is usually left-sided.

It’s usually a subacute disease, but it can develop acutely or chronically as well. The clinical features are variable, and so a high index of suspicion is needed. In many cases, correct diagnosis is delayed. It has high morbidity and mortality despite proper treatment. Neither the incidence nor the mortality have decreased in the past 30 years.

Etiology

Risk factors

• Artificial valves or other prosthetic material
• Damaged heart valves
• Congenital heart disease
• IV drug use
• Indwelling vascular catheters or pacemakers
• Dentistry procedures (only together with other risk factors)

Microbes:

• Acute IE – S. aureus
• Subacute IE – Streptococcus viridans
• Blood culture negative IE (BCNIE)
  • Brucella
  • Coxiella
  • Bartonella

In 5 – 10% of cases, blood cultures are negative (blood culture negative IE, BCNIE). This may be due to the causative pathogen not growing in normal blood cultures, or due to prior antibiotic therapy.

Rheumatic heart disease used to be a common cause but is now rare.

Pathomechanism

Intact endothelium is resistant to bacteraemia, and so endothelial damage must be present for bacteria to colonize. Bacterial colonization results in:

• Destruction of the valve
• Embolisation of bacterial vegetations -> microemboli causing infarction in other organs
• Formation of immune complexes -> deposit in organs

IE can also lead to acute regurgitation or valve obstruction, possibly causing acute heart failure or cardiogenic shock.

Classification

• Left sided endocarditis
• Right sided endocarditis – especially in IV drug users, unusual in others
• Native valve infective endocarditis (NVIE)
• Prosthetic valve endocarditis (PVE)

Clinical features

Symptoms are variable, but in most cases the patient is visibly ill. Acute IE presents with marked toxicity and progresses over days or weeks. Subacute IE presents with only moderate toxicity and progresses over weeks to months. General symptoms include:

• Fever
• Shivering
• Night sweat
• Anorexia and weight loss
• Nausea and vomiting
• New or changed murmur

Embolism and deposition of immune complexes can cause the following phenomena (mostly in acute IE):

• Roth spots – retinal haemorrhages with pale middle
• Osler nodes – painful subcutaneous nodules on fingers, toes
• Janeway lesions – non-painful, erythematous macules on palms, soles
• Subuncal haemorrhage – Haemorrhages under fingernails
• Glomerulonephritis – due to deposition of immune complexes
• Neurological symptoms – stroke
  • Due to so-called “mycotic aneurysms” in the brain which rupture
  • Bacterial emboli embolize vasa vasorum of cerebral arteries, causing these aneurysms

Diagnosis and evaluation

Echocardiography and blood culture are essential in the evaluation of IE. Echocardiography may show the vegetations, but if nothing is visible on TTE, TEE should be performed. Blood culture must be taken in 3 separate sets with 30 minutes in-between, preferably before initiation of antibiotics.

In case of blood culture negative IE, PCR and serology may assist in detecting the pathogen. Inflammatory markers are elevated.

Diagnosis is based on the Duke criteria. There are major criteria and minor criteria, and the diagnosis is made when either of the following combinations are present:

• 2 major criteria + 0 minor criteria
• 1 major criteria + 3 minor criteria
• 0 major criteria + 5 minor criteria

These are the criteria:

• Major criteria
  • Blood cultures show typical organism
  • Echocardiographic evidence of endocarditis
  • New murmur
• Minor criteria
  • Predisposing risk factors (especially IV drug use)
  • Fever
  • Vascular abnormalities (emboli, intracerebral haemorrhage, etc.)
  • Immunological abnormalities (glomerulonephritis, Osler nodes, Roth spots, etc.)
  • Blood cultures show atypical organism

Treatment

Empirical antibiotic treatment is initiated after taking blood cultures, followed by specific antibiotics when results arrive. Antibiotic treatment for IE usually lasts 4 – 8 weeks. Penicillin/amoxicillin for streptococci, cloxacillin for staphylococci.

Surgery is often necessary in IE, in as much as 50% of cases. In case of large or embolised vegetations, surgery must be performed urgently. In case of cardiogenic shock, emergency surgery is indicated.

Prophylaxis

Those at high risk (artificial valve, etc.) must practice good oral hygiene and avoid piercing and tattoos, etc. Before high-risk procedures like dental work or procedures involved infected tissues, these patients should take antibiotic prophylaxis.

Rheumatic fever

Introduction and epidemiology

Rheumatic fever is a complication of streptococcus pyogenes (group A streptococci) infection. It typically follows a few weeks after a streptococcal pharyngitis infection, which may be subclinical and therefore go unnoticed.

The condition affects the joints, heart, CNS, and skin. The heart manifestation of rheumatic fever is called rheumatic heart disease.

Rheumatic fever is rare in developed countries nowadays as most cases of streptococcal pharyngitis are diagnosed and treated with antibiotics. However, in developing countries, diagnosis and treatment does not occur as frequently, and rheumatic fever is more common as a result. When it occurs, it mostly affects children.

Pathomechanism

In case of streptococcal infections, antibodies develop against the M protein of streptococcus pyogenes. Due to molecular mimicry, these antibodies cross-react with nerves and myocardium, causing a type II hypersensitivity reaction.

Clinical features

Rheumatic heart disease can affect the mitral or aortic valves, causing regurgitation initially and stenosis later. Rheumatic fever is the most common cause of mitral stenosis. Pancarditis is also typical.

Other features include fever, malaise, fatigue, migratory polyarthritis, Sydenham chorea, subcutaneous nodules, and erythema marginatum.

Diagnosis and evaluation

Inflammatory markers are elevated, and ECG may show 1^st degree AV block. Serology for anti-streptococcal antibodies like ASO and ADB can be used to confirm recent streptococcus pyogenes infection.

The diagnosis is made based on the Jones criteria, which are based on typical clinical features.

Treatment

The treatment for rheumatic heart disease is penicillin. NSAIDs may be used for joint symptoms and pain relief.