Bacterial endocarditis: Serious and Fatal Disease
An infection of either the heart valves or of the inner surface, called the endocardium, of the heart is Bacterial endocarditis. Endocarditis, which forms vegetation by organisms, is a potentially serious condition because the inflammation (swelling) that occurs inside the heart can interrupt the normal blood flow through the heart valves. So this can trigger a range of complications such as: heart failure, stroke, multiple organ damage. It is relatively uncommon compared with other heart diseases; it is associated with significant morbidity and mortality.
Endocarditis is more common in older people, with half of all cases occurring in people who are over 50. However, cases of endocarditis have been recorded in children, particularly those who are born with congenital heart disease. Twice as many men are affected by endocarditis as women. Endocarditis is regarded as a medical emergency and usually requires admission to an intensive care unit (ICU). Intravenous antibiotics are usually used to treat the underlying infection. Just under half of all people with endocarditis will require surgery to repair the damage to their heart.
Bacteria in the mouth, intestinal tract or urinary tract travel to the heart via the bloodstream but usually don’t cause a problem in normal hearts. However, hearts that have defects, often even if the defects have been repaired are vulnerable to infection. As the Once infection occurs, the bacteria continue to grow and may seriously damage the heart. Bacterial endocarditis is most likely to occur in patients who have: Aortic Valve Lesions, Patent Ductus Arteriosus, tetralogy of Fallot, ventricular septal defect, Mitral Valve Prolapse, transposition of the great Arteries.
It is unlikely to occur in patients who have a completely repaired pulmonary valve stenosis, arterial septal defect, ventricular septal defect or patent ductus arteriosus.
Gram positive cocci have always dominated the scene as major etiologic agents. Gram negative bacilli (GNB) other than Hemophilus, Actinobacillus, Cardiobacterium, Eikenella and Kingella (HACEK) are regarded as less frequent cause of endocarditis. They are associated with certain percentage of Endocarditis in Intravenous drug abuser (IVDU) and Prosthetic valve endocarditis (PVE).
The usual signs of bacterial endocarditis are prolonged fever for two to three days in a person with congenital heart disease that occurs after a procedure in the mouth, intestinal tract or urinary tract. However, the infection may occur without a previous procedure. Symptoms may include: Poor appetite, Fatigue, Joint pain, Rash, Weight loss.
Bacterial endocarditis is classified as,
Sub-acute bacterial endocarditis (SBE) is often due to streptococci of low virulence and mild to moderate illness which progresses slowly over weeks and months and has low propensity to hematogenously seed extracardiac sites.
Acute bacterial endocarditis (ABE) is a fulminant illness over days to weeks, and is more likely due to Staphylococcus aureus which has much greater virulence, or disease-producing capacity and frequently causes metastatic infection
It occurs when bacteria spread through the bloodstream and land inside the heart and grow there. Usually, if there are bacteria circulating in the bloodstream, they don’t stick to the inside of the heart: the blood flows smoothly. If the heart is abnormal due to certain types of surgery or other defects, there may be rough surfaces causing turbulent blood flow (known as a murmur) to which bacteria can attach and cause infection.
Although uncertain, it is believed that cardiac valves and other endocardial surfaces become infected after exposure to micro emboli from bacteria circulating in the bloodstream. Dextran-producing bacteria, such as Streptococcus mutans, have a virulence factor that promotes adherence to endovascular surfaces.
Coagulase-negative staphylococci may produce a biofilm on prosthetic surfaces, which also promotes adherence. Beta-hemolytic streptococci and enteric gram-negative bacteria lack recognized adherence factors, and appear less likely to cause endocarditis. Endocardial surfaces previously damaged from valvular heart disease, endocarditis, surgery, or pacemaker wires provide a favorable environment for thrombus formation. Over time, microorganisms proliferate in the thrombus, resulting in classic vegetation. Microorganisms are released into the circulation, usually on a continuous basis, which often results in interesting findings.
Major criteria for probable endocarditis are persistant bacteremia with a new regurgitant heart murmur or valvular heart disease with vesculitis or negative or intermittent bacteremia with fever. Modern blood culture techniques includes three sets suffice for two days, not necessarily beyond this point. CT scan electrocardiogram, echocardiogram, can be done for the diagnosis of disease. New diagnostic approaches like culture of vegetations and infected cardiac valve tissue has shown better result in blood culture negative endocarditis.
When causative microorganisms are cultured or seen histologically in vegetations and valve tissues. In case of streptococcal infection Anti streptolysin O titer can be determined. Latex particle coated with anti-CRP antibodies were used for CRP test by mixing with 50μl of patients’ serum Haematuria and pyuria can be observed by microscopy from urine sample of each patient on same day of blood examination when blood culture is seen negative.
The penicillin, often in combination with gentamicin, remains the cornerstones of therapy for endocarditis caused by penicillin-susceptible streptococci. For penicillin-allergic patients, vancomycin is substituted. For relatively penicillin-insensitive streptococci (minimal inhibitory concentration higher than 0.1 to 0.5 mg/mL), the penicillin dosage is higher and duration of therapy is 2 weeks. Gentamicin is given for the first 2 weeks; treatment for endocarditis caused by enterococci is longer; both penicillin and gentamicin are given for 6 weeks, For vancomycin-resistant enterococci (VRE), streptogramin quinupristin-dalfopristin (Synercid) either alone or in combination with doxycycline and rifampin is administered.
Bacterial endocarditis is one of the most dreaded complications of structural heart disease. Its mortality rate in the pre-antibiotic era was nearly 100% and remains high even today; approaching 20-30 %. This is mainly due to increasing organism resistance to antibiotics and emergence of fungal infections in response to multiple antibiotic treatments. So the prevention is important.
Prophylaxis for Bacterial endocarditis is effective only if appropriate antibiotic is given in a sufficient amount at the right time. Antibiotics should be administered at time only when there is likelihood of bacteremia so as not to give a bacterial resistance. Better the antibiotic administered at a perioperative period. If a procedure involves affected tissue, it is necessary to provide additional doses of antibiotic for treatment of an established infection. The recommended prophylactic regimen for dental and oral procedures is a single dose of oral amoxicillin. If the patient is unable to take oral medication, parenteral administration of antibiotic is required. If parenteral amoxicillin is not available, ampicillin is the alternative.