Infective Endocarditis

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What is infective endocarditis?

Endocarditis is a life-threatening inflammation of the inner lining of your heart’s chambers and valves (endocardium).

Endocarditis is usually caused by an infection. Bacteria, fungi or other germs from another part of your body, such as your mouth, spread through your bloodstream and attach to damaged areas in your heart. If it’s not treated quickly, endocarditis can damage or destroy your heart valves. Treatments for endocarditis include medications and, sometimes, surgery.

People at greatest risk of endocarditis usually have damaged heart valves, artificial heart valves or other heart defects.

Infective endocarditis is an infection in the heart valves or endocardium. The endocardium is the lining of the interior surfaces of the chambers of the heart. This condition is usually caused by bacteria entering the bloodstream and infecting the heart. Bacteria may originate in the:

• mouth
• skin
• intestines
• respiratory system
• urinary tract

When this condition is caused by bacteria, it’s also known as bacterial endocarditis. In rare cases, it can also be caused by fungi or other microorganisms.

Infective endocarditis is a serious condition that requires prompt medical treatment. If left untreated, the infection can damage your heart valves. This can lead to problems including:

• stroke
• damage to other organs
• heart failure
• death

This condition is rare in people with healthy hearts. People who have other heart conditions are at higher risk.

You may need to take antibiotics before certain medical and dental procedures if you’re at high risk for infective endocarditis. Antibiotics help stop bacteria from entering your bloodstream and causing infection. Talk to your surgeon or dentist before any surgical procedure.

Etiology

Endocarditis occurs when germs, usually bacteria, enter your bloodstream, travel to your heart, and attach to abnormal heart valves or damaged heart tissue. Fungi or other germs also may cause endocarditis.

Usually, your immune system destroys any harmful bacteria that enter your bloodstream. However, bacteria that live in your mouth, throat or other parts of your body, such as your skin or your gut, can sometimes cause endocarditis under the right circumstances.

Bacteria, fungi and other germs that cause endocarditis might enter your bloodstream through:

• Improper dental care. Proper toothbrushing and flossing helps prevent gum disease. If you don’t take good care of your teeth and gums, brushing could cause unhealthy gums to bleed, giving bacteria a chance to enter your bloodstream. Some dental procedures that can cut your gums also may allow bacteria to enter your bloodstream.
• Catheters. Bacteria can enter your body through a thin tube that doctors sometimes use to inject or remove fluid from the body (catheter). This is more likely to occur if the catheter is in place for a long period of time. For example, you may have a catheter if you need long-term dialysis.
• Illegal IV drug use. Contaminated needles and syringes are a special concern for people who use illegal IV drugs, such as heroin or cocaine. Often, individuals who use these types of drugs don’t have access to clean, unused needles or syringes

Symptoms-

Endocarditis may develop slowly or suddenly, depending on what germs are causing the infection and whether you have any underlying heart problems. Signs and symptoms of endocarditis can vary from person to person.

Common signs and symptoms of endocarditis include:

• Aching joints and muscles
• Chest pain when you breathe
• Fatigue
• Flu-like symptoms, such as fever and chills
• Night sweats
• Shortness of breath
• Swelling in your feet, legs or abdomen
• A new or changed heart murmur, which is the heart sound made by blood rushing through your heart

Less common signs and symptoms of endocarditis can include:

• Unexplained weight loss
• Blood in your urine, which you might be able to see or that your doctor might see when he or she views your urine under a microscope
• Tenderness in your spleen, which is an infection-fighting organ located just below your left rib cage
• Red spots on the soles of your feet or the palms of your hands (Janeway lesions)
• Red, tender spots under the skin of your fingers or toes (Osler’s nodes)
• Tiny purple or red spots, called petechiae (puh-TEE-kee-ee), on the skin, in the whites of your eyes or inside your mouth

Pathophysiology

Infective endocarditis develops most commonly on the mitral valve, closely followed in descending order of frequency by the aortic valve, the combined mitral and aortic valve, the tricuspid valve, and, rarely, the pulmonic valve. Mechanical prosthetic and bioprosthetic valves exhibit equal rates of infection.

All cases of IE develop from a commonly shared process, as follows:

1. Bacteremia (nosocomial or spontaneous) that delivers the organisms to the surface of the valve
2. Adherence of the organisms
3. Eventual invasion of the valvular leaflets

The common denominator for adherence and invasion is nonbacterial thrombotic endocarditis, a sterile fibrin-platelet vegetation. The development of subacute IE depends on a bacterial inoculum sufficient to allow invasion of the preexistent thrombus. This critical mass is the result of bacterial clumping produced by agglutinating antibodies.

In acute IE, the thrombus may be produced by the invading organism (ie, S aureus) or by valvular trauma from intravenous catheters or pacing wires (ie, NIE/HCIE). Staphylococcus aureus can invade the endothelial cells (endotheliosis) and increase the expression of adhesion molecules and of procoagulant activity on the cellular surface. Nonbacterial thrombotic endocarditis may result from stress, renal failure, malnutrition, systemic lupus erythematosus, or neoplasia.

The Venturi effect also contributes to the development and location of nonbacterial thrombotic endocarditis. This principle explains why bacteria and the fibrin-platelet thrombus are deposited on the sides of the low-pressure sink that lies just beyond a narrowing or stenosis.

In patients with mitral insufficiency, bacteria and the fibrin-platelet thrombus are located on the atrial surface of the valve. In patients with aortic insufficiency, they are located on the ventricular side. In these examples, the atria and ventricles are the low-pressure sinks. In the case of a ventricular septal defect, the low-pressure sink is the right ventricle and the thrombus is found on the right side of the defect.

Nonbacterial thrombotic endocarditis may also form on the endocardium of the right ventricle, opposite the orifice that has been damaged by the jet of blood flowing through the defect (ie, the MacCallum patch).

The microorganisms that most commonly produce endocarditis (ie, S aureus; Streptococcus viridans; groups A, C, and G streptococci; enterococci) resist the bactericidal action of complement and possess fibronectin receptors for the surface of the fibrin-platelet thrombus. Among the many other characteristics of IE-producing bacteria demonstrated in vitro and in vivo, some features include the following:

• Increased adherence to aortic valve leaflet disks by enterococci, S viridans, and S aureus
• Mucoid-producing strains of S aureus
• Dextran-producing strains of S viridans
• Streptococcus viridans and enterococci that possess FimA surface adhesin
• Platelet aggregation by S aureus and S viridans and resistance of S aureus to platelet microbicidal proteins

The pathogenesis of pacemaker IE is similar. Shortly after implantation, the development of a fibrin-platelet thrombus (similar to the nonbacterial thrombotic endocarditis described above) involves the generator box and conducting leads. After 1 week, the connective tissue proliferates, partially embedding the leads in the wall of the vein and endocardium. This layer may offer partial protection against infection during a bacteremia.

Bacteremia (either spontaneous or resulting from an invasive procedure) infects the sterile fibrin-platelet vegetation described above. Bloodstream infections develop from various extracardiac types of infection, such as pneumonias or pyelonephritis, but most commonly from gingival disease. Of those with high-grade gingivitis, 10% have recurrent transient bacteremias (usually streptococcal species). Most cases of subacute disease are secondary to the bacteremias that develop from the activities of daily living (eg, brushing teeth, bowel movements).

The skin is quite resistant to S aureus infection, largely as a result of its production of antimicrobial peptides. Soong et al discovered that, in vitro, the secretion of alpha toxin by S aureus allows the organism to successfully penetrate the keratinocyte layer. This could explain the presence of staphylococcal bacteremia in the absence of any gross damage to the epithelial layer.

Bacteremia can result from various invasive procedures, ranging from oral surgery to sclerotherapy of esophageal varices to genitourinary surgeries to various abdominal operations. The potential for invasive procedures to produce a bacteremia varies greatly. Procedures, rates, and organisms are as follows:

• Endoscopy – Rate of 0% to 20%; coagulase-negative staphylococci (CoNS), streptococci, diphtheroids
• Colonoscopy – Rate of 0% to 20%; Escherichia coli, Bacteroides species
• Barium enema – Rate of 0% to 20%; enterococci, aerobic and anaerobic gram-negative rods
• Dental extractions – Rate of 40% to 100%; S viridans
• Transurethral resection of the prostate – Rate of 20% to 40%; coliforms, enterococci, S aureus
• Transesophageal echocardiography – Rate of 0% to 20%; S viridans, anaerobic organisms, streptococci

The incidence of nosocomial bacteremias, mostly associated with intravascular lines, has more than doubled in the last few years. Up to 90% of BSIs caused by these devices are secondary to the placement of various types of central venous catheters. Hickman and Broviac catheters are associated with the lowest rates, presumably because of their Dacron cuffs. Peripherally placed central venous catheters are associated with similar rates.

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Intravascular catheters are infected from one of the following 4 sources:

• Infection of the insertion site
• Infection of the catheter
• Bacteremia arising from another site
• Contamination of the infused solution

Bacterial adherence to intravascular catheters depends on the response of the host to the presence of this foreign body, the properties of the organism itself, and the position of the catheter. Within a few days of insertion, a sleeve of fibrin and fibronectin is deposited on the catheter. Staphylococcus aureus adheres to the fibrin component.

Staphylococcus aureus also produces an infection of the endothelial cells (endotheliosis), which is important in producing the continuous bacteremia of S aureus BSIs. Endotheliosis may explain many cases of persistent methicillin-susceptible S aureus (MSSA) and MRSA catheter-related BSIs without an identifiable cause.

Staphylococcus aureus catheter-related BSIs occur even after an infected catheter is removed, apparently attributable to specific virulence factors of certain strains of S aureus that invade the adjacent endothelial cells. At some point, the staphylococci re-enter the bloodstream, resulting in bacteremia.

Four days after placement, the risk for infection markedly increases. Lines positioned in the internal jugular vein are more prone to infection than those placed in the subclavian vein. Colonization of the intracutaneous tract is the most likely source of short-term catheter-related BSIs. Among lines in place for more than 2 weeks, infection of the hub is the major source of bacteremia. In some cases, the infusion itself may be a reservoir of infection.

Colonization of heart valves by microorganisms is a complex process. Most transient bacteremias are short-lived, are without consequence, and are often unpreventable. Bacteria rarely adhere to an endocardial nidus before the microorganisms are removed from the circulation by various host defenses.

Once microorganisms do establish themselves on the surface of the vegetation, the process of platelet aggregation and fibrin deposition accelerate at the site. As the bacteria multiply, they are covered by ever-thickening layers of platelets and thrombin, which protect them from neutrophils and other host defenses. Organisms deep in the vegetation hibernate because of the paucity of available nutrients and are therefore less susceptible to bactericidal antimicrobials that interfere with bacterial cell wall synthesis.

Complications of subacute endocarditis result from embolization, slowly progressive valvular destruction, and various immunologic mechanisms. The pathologic picture of subacute IE is marked by valvular vegetations in which bacteria colonies are present both on and below the surface.

The cellular reaction in subacute bacterial endocarditis is primarily that of mononuclear cells and lymphocytes, with few polymorphonuclear cells. The surface of the valve beneath the vegetation shows few organisms. Proliferation of capillaries and fibroblasts is marked. Areas of healing are scattered among areas of destruction. Over time, the healing process falls behind, and valvular insufficiency develops secondary to perforation of the cusps and damage to the chordae tendineae. Compared with acute disease, little extension of the infectious process occurs beyond the valvular leaflets.

Levels of agglutinating and complement-fixing bactericidal antibodies and cryoglobulins are markedly increased in patients with subacute endocarditis. Many of the extracardiac manifestations of this form of the disease result from circulating immune complexes. Among these include glomerulonephritis, peripheral manifestations (eg, Osler nodes, Roth spots, subungual hemorrhages), and, possibly, various musculoskeletal abnormalities. Janeway lesions usually arise from infected microemboli.

The microscopic appearance of acute bacterial endocarditis differs markedly from that of subacute disease. Vegetations that contain no fibroblasts develop rapidly, with no evidence of repair. Large amounts of both polymorphonuclear leukocytes and organisms are present in an ever-expanding area of necrosis. This process rapidly produces spontaneous rupture of the leaflets, of the papillary muscles, and of the chordae tendineae.

The complications of acute bacterial endocarditis result from intracardiac disease and metastatic infection produced by suppurative emboli. Because of their shortened course, immunological phenomena are not a part of acute IE.

When to see a doctor

If you have signs or symptoms of endocarditis, see your doctor as soon as possible — especially if you have risk factors for this serious infection, such as a heart defect or history of endocarditis. Although less serious conditions can cause similar signs and symptoms, you won’t know for sure until you’re evaluated by your doctor.

If you’ve been diagnosed with endocarditis, tell your doctor about any signs or symptoms that may mean your infection is getting worse, such as:

• Chills
• Fever
• Headaches
• Joint pain
• Shortness of breath

If you’re being treated with antibiotics for endocarditis, tell your doctor if you develop diarrhea, a rash, itching or joint pain. These signs and symptoms may mean you’re having a reaction to your prescribed antibiotic.

diagnosis

When you visit your doctor, you will first be asked to describe your symptoms. Your doctor will then perform a physical examination. They will listen to your heart with a stethoscope and check for sounds of a murmur, which may be present with infective endocarditis. Your doctor may also check for a fever and feel for an enlarged spleen by pressing on your left upper abdomen.

If your doctor suspects infective endocarditis, your blood will be tested for bacteria. A complete blood count (CBC) may also be used to check for anemia. A shortage of red blood cells can occur with infective endocarditis.

Your doctor may order an echocardiogram, or an ultrasound of the heart. This procedure uses sound waves to produce an image. The ultrasound wand may be placed on your chest. Alternatively, a smaller device may be threaded down your throat and into your esophagus. This can offer a more detailed image. The echocardiogram looks for damaged tissue, holes, or other structural changes in your heart valve.

Your doctor may also order an electrocardiogram (EKG). An EKG monitors electrical activity in your heart. This painless test can find an irregular heartbeat caused by endocarditis.

Imaging tests can check if your heart has enlarged. They may also be able to detect signs that infection has spread to other areas of your body. Such tests include:

• chest X-ray
• computed tomography (CT) scan
• magnetic resonance imaging (MRI)

If you’re diagnosed with infective endocarditis, you will be immediately admitted to the hospital for treatment.

Risk factors

You’re more likely to develop endocarditis if you have faulty, diseased or damaged heart valves. However, endocarditis does occasionally occur in previously healthy people.

You have an increased risk of endocarditis if you have:

• Older age. Endocarditis occurs most often in older adults over age 60.
• Artificial heart valves. Germs are more likely to attach to an artificial (prosthetic) heart valve than to a normal heart valve.
• Damaged heart valves. Certain medical conditions, such as rheumatic fever or infection, can damage or scar one or more of your heart valves, increasing the risk of infection.
• Congenital heart defects. If you were born with certain types of heart defects, such as an irregular heart or abnormal heart valves, your heart may be more susceptible to infection.
• Implanted heart device. Bacteria can attach to an implanted device, such as a pacemaker, causing an infection of the heart’s lining.
• A history of endocarditis. Endocarditis can damage heart tissue and valves, increasing the risk of a future heart infection.
• A history of illegal IV drug use. People who use illegal drugs by injecting them are at a greater risk of endocarditis. The needles used to inject drugs can be contaminated with the bacteria that can cause endocarditis.
• Poor dental health. A healthy mouth and healthy gums are essential for good health. If you don’t brush and floss regularly, bacteria can grow inside your mouth and may enter your bloodstream through a cut on your gums.
• Long-term catheter use. Having a catheter in place for a long period of time (indwelling catheter) increases your risk of endocarditis.

If you’re at risk of endocarditis, let all of your doctors know. You may want to request an endocarditis wallet card from the American Heart Association. Check with your local chapter or print the card from the association’s website.

Complications

In endocarditis, clumps made of germs and cell pieces form an abnormal mass in your heart. These clumps, called vegetations, can break loose and travel to your brain, lungs, abdominal organs, kidneys, or arms and legs.

As a result, endocarditis can cause several complications, including:

• Heart problems, such as heart murmur, heart valve damage and heart failure
• Stroke
• Pockets of collected pus (abscesses) that develop in the heart, brain, lungs and other organs
• Blood clot in a lung artery (pulmonary embolism)
• Kidney damage
• Enlarged spleen

Prevention

You can take the following steps to help prevent endocarditis:

• Know the signs and symptoms of endocarditis. See your doctor immediately if you develop any signs or symptoms, especially a fever that won’t go away, unexplained fatigue, any type of skin infection, or open cuts or sores that don’t heal properly.
• Take care of your teeth and gums. Brush and floss your teeth and gums often, and have regular dental checkups. Good dental hygiene is an important part of maintaining your overall health.
• Don’t use illegal IV drugs. Dirty needles can send bacteria into your bloodstream, increasing your risk of endocarditis.

Preventive antibiotics

Certain dental and medical procedures may allow bacteria to enter your bloodstream.

If you’re at high risk of endocarditis, the American Heart Association recommends taking antibiotics an hour before having any dental work done.

You’re at high risk of endocarditis and need antibiotics before dental work if you have:

• A history of endocarditis
• A man-made (prosthetic mechanical) heart valve
• A heart transplant, in some cases
• Certain types of congenital heart disease
• Congenital heart disease surgery in the last six months

If you have endocarditis or any type of congenital heart disease, talk to your doctor and dentist about your risks and whether you need preventive antibiotics.

Treating infective endocarditis

Infective endocarditis can cause irreversible damage to the heart. If it’s not caught and treated quickly, it can become life threatening. You will need to be treated in a hospital to prevent the infection from getting worse and causing complications.

Antibiotics and initial treatment

While in the hospital, your vital signs will be monitored. You will be given antibiotics intravenously (IV). Once you go home, you will continue with oral or IV antibiotics for at least four weeks. During this time, you will keep visiting your doctor. Regular blood tests will check that the infection is going away.

Surgery

Surgery may be needed if your heart valves have been damaged. Your surgeon may recommend repairing the heart valve. The valve can also be replaced using a new valve made from either animal tissue or artificial materials.

Surgery may also be necessary if the antibiotics are not working or if the infection is fungal. Antifungal medications are not always effective for infections in the heart.

Recovery and outlook

If left untreated, this condition will be fatal. However, most people are able to recover with antibiotic treatment. The chance of recovery depends on factors including your age and the cause of your infection. In addition, patients who get early treatment have a better chance of making a full recovery.

It may take you longer to recover completely if surgery was necessary.

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