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Heart valves may become infected during transient bacteraemia.
Congenitally abnormal or damaged valves are at greatest risk.
Bacteria may originate from the mouth, urinary tract, intravenous
drug misuse or colonized intravascular lines.
- Malaise, fever and variable heart murmurs.
- Classical stigmata (e.g. splinter haemorrhages, Osler's nodes,
microhaematuria, retinal infarcts, finger clubbing, caf�-au-lait
skin, and Janeway lesions) are only seen in long-standing
- In the later stages, septic emboli may cause a stroke.
- With aggressive organisms (e.g. Staphylococcus aureus) disease
progresses rapidly and valves may rupture.
A diagnosis is made if there are two major Duke criteria present
or one major and three minor criteria.
The major Duke criteria include: positive blood culture with
characteristic organisms (e.g. viridans streptococci); persistently
positive blood cultures with any organism;
evidence of endocardial
involvement demonstrated by echocardiogram; and new valvular
regurgitation. Minor criteria include: predisposition; fever >38 �C;
immunological signs (e.g. septic pulmonary infarcts); and echocardiographic
or microbiological evidence insufficient to be a major
- Local progression may lead to aortic root abscess.
- Valve destruction may lead to cardiac decompensation.
- Cerebral or limb infarction may follow septic embolus.
- Nephritis secondary to immune complex deposition can progress
rapidly if sepsis is uncontrolled or if antibiotics with renal toxicity
are given without care (e.g. aminoglycosides).
Echocardiography, either transthoracic or transoesophageal
(more sensitive), will demonstrate vegetations on the valves; a
plain chest X-ray may show evidence of cardiac failure. At least
three sets of blood cultures should be taken, an hour apart, while
fever is present. Antibiotic therapy should await the results of
blood culture if possible. Serum should be tested for antibodies to
Coxiella, Bartonella and Chlamydia psittaci.
Ideally, antibiotics should not be commenced until the identity and
sensitivities of the infecting organism are known; the prognosis of
empirically treated, culture-negative endocarditis is poorer than
that when the infecting organism is identified. Careful microbiological
monitoring of the markers of inflammation (e.g. CRP) is
associated with an improved outcome.
Therapy is based on the minimum inhibitory concentration
(MIC) and the minimum bactericidal concentration (MBC) of the
antibiotics. If gentamicin is used concentrations must be monitored
closely. Therapy is continued for 2-6 weeks depending on
the organism and its susceptibility. Typical regimens include: benzylpenicillin
and gentamicin for viridans streptococci; flucloxacillin
and gentamicin for staphylococci; vancomycin and gentamicin
for penicillin-allergic patients. National evidence-based guidelines
for management should be followed.
Surgical management may be required to deal with the haemodynamic
consequences of endocarditis (e.g. valve rupture).
Antibiotic prophylaxis is given to patients with damaged valves
when they undergo procedures that give rise to significant bacteraemia,
such as dental work or urogenital surgery. For procedures
that require an anaesthetic, prophylaxis is given at induction followed
by subsequent oral doses. There are alternative regimens
for penicillin allergy and prosthetic valves laid down by national
Most myocarditis is caused by viral infection, with enteroviruses
being the commonest cause; however, it may complicate systemic
viral infections, follow bacteraemia or form part of brucellosis,
rickettsial or chronic Chagas infection.
- Presentation is with influenza-like symptoms associated with
fatigue, exertional dyspnoea, palpitations and precordial pain.
- Tachycardia, dysrhythmia or cardiac failure may be present.
- The electrocardiogram (ECG) may show T-wave inversion, prolongation
of the PR or QRS interval, extrasystoles or heart block.
- Other features include cardiomegaly on chest X-ray and elevated
- The diagnosis is suggested by a temporal relationship between
the viral symptoms and cardiological abnormalities.
- Viruses may be detected in faecal, nasopharyngeal and throat
specimens (see DNA viruses: adenovirus, parvovirus and poxvirus
) by nucleic acid amplification tests
- Treatment is supportive.
Pericarditis is most often secondary to a non-infectious condition,
such as myocardial infarction. It may complicate bacteraemia or
follow spread of pus from an empyema (Streptococcus pneumoniae
or liver abscess (enterococci, Entamoeba histolytica
Tuberculosis can cause sub-acute pericarditis. Viral pericarditis is
a self-limiting condition featuring fever, 'flu-like symptoms and
sharp chest pain. Enteroviruses, especially coxsackie and influenza
viruses, are most commonly implicated. The chest pain may
vary with posture, swallowing or heartbeat. A pericardial rub
may be heard. Cardiographic evidence of pericarditis may be
Patients with suppurative pericarditis present with fever, neutrophilia
and signs of the underlying source of infection. Chest
pain is severe and a fall in blood pressure may indicate developing
tamponade. The ECG shows upward-curving elevated ST segments.
Echocardiography will show pericardial thickening or effusion.
Infection can be complicated by fibrosis and constrictive
pericarditis, leading to congestive cardiac failure. Treatment is
directed against the likely causative organism.