Infective endocarditis

Infective endocarditis is divided into three categories of acute, subacute, and chronic based on the duration of symptoms. Acute infective endocarditis refers to the presence of signs and symptoms of infective endocarditis that are present for days up to six weeks. Culture results Infective endocarditis may also be classified as culture-positive or culture-negative. By far the most common cause of "culture-negative" endocarditis is prior administration of antibiotics and can occur in up to 31% of cases. and the HACEK bacteria group. Some organisms are said to be fastidious because they have demanding growth requirements. Some examples include pathogens like Aspergillus species, Brucella species, Coxiella burnetii, Chlamydia species. Due to delay in growth and identification in these cases, patients may be erroneously classified as "culture-negative" endocarditis. Heart side Endocarditis can also be classified by the side of the heart affected: • People who intravenously inject drugs such as heroin or methamphetamine may introduce infection which can travel to the right side of the heart, classically affecting the tricuspid valve, and most often caused by S. aureus. Valve type Finally, the distinction between native-valve endocarditis and prosthetic-valve endocarditis is clinically important. Prosthetic valve endocarditis can be early (within 1 year of surgery) or late (> 1 year following valvular surgery). Cutibacterium acnes almost exclusively causes endocarditis on prosthetic heart valves. ==Signs and symptoms==

• Fever occurs in 97% of people; malaise and endurance fatigue in 90% of people. • A new or changing heart murmur, weight loss, and coughing occurs in 35% of people. bleeding in the brain, conjunctival hemorrhage, splinter hemorrhages, kidney infarcts, and splenic infarcts. Infective endocarditis can also lead to the formation of mycotic aneurysms. Osler's nodes ("ephemeral spots of a painful nodular erythema, chiefly in the skin of the hands and feet"), Roth's spots on the retina, positive serum rheumatoid factor • Other signs may include night sweats, rigors, anemia, spleen enlargement ==Cause==

Many microorganisms can cause infective endocarditis. These are generally isolated by blood culture, where the patient's blood is drawn and any growth is noted and identified. The term bacterial endocarditis (BE) is commonly used, reflecting the fact that most cases of IE are due to bacteria; however, infective endocarditis (IE) has become the preferred term. Viridans streptococci and Enterococci are the second and third most common organisms responsible for infective endocarditis. The viridans group includes S. oralis, S. mitis, S. sanguis, S. gordonii, and S. parasanguis. The primary habitats for these organisms are the oral cavity and the upper respiratory tract. These bacteria are present in the normal oral flora and enter the bloodstream due to disruption of tissues in the mouth when dental surgical procedures are performed (tooth extractions) or genitourinary manipulation. Similarly, HACEK organisms are a group of bacteria that live on the dental gums and can be seen in people who inject drugs who contaminate their needles with saliva. Patients may also have a history of poor dental hygiene or pre-existing valvular disease. Viridans alpha-hemolytic streptococci, which are present in the mouth, are the most frequently isolated microorganisms when the infection is acquired in a community setting. In contrast, Staphylococcus bloodstream infections are frequently acquired in a health care setting where they can enter the bloodstream through procedures that cause breaks in the integrity of skin, such as surgery, catheterization, or during access of long term indwelling catheters or secondary to intravenous injection of recreational drugs. Enterococcus can enter the bloodstream as a consequence of abnormalities in the gastrointestinal or genitourinary tracts. Some organisms, when isolated, give valuable clues to the cause, as they tend to be specific. • Pseudomonas species, which are very resilient organisms that thrive in water, may contaminate street drugs that have been contaminated with drinking water. P. aeruginosa can infect a child through foot punctures, and can cause both endocarditis and septic arthritis. • S. bovis and Clostridium septicum, which are part of the natural flora of the bowel, are associated with colon cancers. When they present as the causative agent in endocarditis, it usually prompts a colonoscopy to be done immediately due to concerns regarding spread of bacteria from the colon through the bloodstream due to the cancer breaking down the barrier between the inside of the colon (lumen) and the blood vessels which drain the bowel. • Less commonly reported bacteria responsible for so called "culture negative endocarditis" include Bartonella, Chlamydia psittaci, and Coxiella. Such bacteria can be identified by serology, culture of the excised valve tissue, sputum, pleural fluid, and emboli, and by polymerase chain reaction or sequencing of bacterial 16S ribosomal RNA. Multiple case reports of infective endocarditis caused by unusual organisms have been published. Cutibacterium spp., which are normal skin flora, have been responsible for infective endocarditis, preferably in patients with prosthetic heart valves, in rare cases leading to death.Tropheryma whipplei has caused endocarditis without gastrointestinal involvement. Citrobacter koseri was found in an immunocompetent adult. Neisseria bacilliformis was found in a person with a bicuspid aortic valve. Dental operations One in eight cases of infective endocarditis is thought to be caused by viridans streptococci infection associated with dental procedures such as cleaning or tooth extraction and in the UK as of March 2008 due to new NICE guidelines. Fungal Fungal endocarditis (FE) is often fatal and one of the most serious forms of infective endocarditis. The types of fungi most seen associated with this disease are: Candida albicans is found as a spherical or oval budding yeast. It is associated with endocarditis in people who inject drugs, patients with prosthetic valves, and immunocompromised patients. It forms biofilms around thick-walled resting structures like prosthetic heart valves and additionally colonizes and penetrates endothelial walls. Other fungi demonstrated to cause endocarditis are Histoplasma capsulatum and Aspergillus. Risk factors Risk factors for infective endocarditis are based on the premise that in a healthy individual, bacteremia (bacteria entering the bloodstream) is cleared quickly with no adverse consequences. However, if a heart valve is damaged, the bacteria can attach themselves to the valve, resulting in infective endocarditis. Additionally, in individuals with weakened immune systems, the concentration of bacteria in the blood can reach levels high enough to increase the probability that some will attach to the valve. Some significant risk factors are listed here: • Artificial heart valves • Intracardiac devices, such as implantable cardioverter-defibrillators • Unrepaired cyanotic congenital heart defects • History of infective endocarditis • Neoplastic disease • Chronic rheumatic heart disease, which is an autoimmune response to repeated Streptococcus pyogenes infection (mostly in the developing world) • Age-related degenerative valvular lesions • Congenital heart valve abnormalities • Hemodialysis, a medical procedure that filters the blood of individuals with kidney failure • Poor oral hygiene • IVDU (IV drug user) • Co-existing immunosuppressing conditions, such as diabetes mellitus, alcohol use disorder, chronic liver disease, and HIV/AIDS ==Pathogenesis==

Damaged valves and endocardium contribute to the development of infective endocarditis. Specifically, the damaged part of a heart valve forms a local blood clot, a condition known as non-bacterial thrombotic endocarditis (NBTE). The platelet and fibrin deposits that form as part of the blood clotting process allow bacteria to take hold and form vegetations. As previously mentioned, the body has no direct methods of combating valvular vegetations because the valves do not have a dedicated blood supply. This combination of damaged valves, bacterial growth, and lack of a strong immune response results in infective endocarditis. Damage to the valves and endocardium can be caused by: • Altered, turbulent blood flow. The areas that fibrose, clot, or roughen as a result of this altered flow are known as jet lesions. Altered blood flow is more likely in high-pressure areas, so ventricular septal defects or patent ductus arteriosus can create more susceptibility than atrial septal defects. • Catheters, electrodes, and other intracardiac prosthetic devices. • Solid particles from repeated intravenous injections. • Chronic inflammation. Examples include auto-immune mechanisms and degenerative valvular lesions. The risk factors for infective endocarditis provide a more extensive list of conditions that can damage the heart. ==Diagnosis==

by echocardiography. Arrow denotes the vegetation. In general, the Duke criteria should be fulfilled in order to establish the diagnosis of endocarditis. Although the Duke criteria are widely used, they have significant limitations. and among non drug-abusing patients. However, this research is over twenty years old and it is possible that changes in the epidemiology of endocarditis and bacteria such as staphylococci make the following estimates incorrect. The blood tests C reactive protein (CRP) and procalcitonin have not been found to be particularly useful in helping make or rule out the diagnosis. Ultrasound Echocardiography is the main type of diagnostic imaging used to establish the diagnosis of infective endocarditis. However, in endocarditis involving a prosthetic valve, TTE has a sensitivity of approximately 50%, whereas TEE has a sensitivity exceeding 90%. File:UOTW 27 - Ultrasound of the Week 2.webm|Ultrasound showing infectious endocarditis Modified Duke criteria Established in 1994 by the Duke Endocarditis Service and revised in 2000, the Duke criteria are a collection of major and minor criteria used to establish a diagnosis of infective endocarditis. According to the Duke criteria, diagnosis of infective endocarditis can be definite, possible, or rejected. Among people with staphylococcal bacteremia (SAB), one study found a 29% prevalence of endocarditis in community-acquired SAB versus 5% in nosocomial SAB. However, only 2% of strains were resistant to methicillin and so these numbers may be low in areas of higher resistance. ==Prevention==

Not all people with heart disease require antibiotics to prevent infective endocarditis. Heart diseases have been classified into high, medium, and low risk of developing IE. Those falling into the high-risk category require IE prophylaxis before endoscopies and urinary tract procedures. Diseases listed under high risk include: Antibiotics were historically commonly recommended to prevent IE in those with heart problems undergoing dental procedures (known as dental antibiotic prophylaxis). There is, however, insufficient evidence to support whether antibiotics are effective or ineffective at preventing IE when given prior to a dental procedure in people at high risk. They are less commonly recommended for this procedure. In some countries, e.g., the US, high-risk patients may be given prophylactic antibiotics such as penicillin or clindamycin for penicillin-allergic people before dental procedures. Because bacteria are the most common cause of infective endocarditis, antibiotics such as penicillin and amoxicillin (for beta lactamase-producing bacteria) are used in prophylaxis. ==Treatment==

High-dose antibiotics are the cornerstone of treatment for infective endocarditis. These antibiotics are administered by the intravenous (IV) route to maximize diffusion of antibiotic molecules into vegetation(s) from the blood filling the chambers of the heart. This is necessary because neither the heart valves nor the vegetations adhering to them are supplied by blood vessels. Antibiotics are typically continued for two to six weeks, depending on the characteristics of the infection and the causative microorganisms. Antibiotic treatment lowers the risk of embolic complications in people with infective endocarditis. In cases of subacute endocarditis, where the person's hemodynamic status is usually stable, antibiotic treatment can be delayed until the causative microorganism can be identified. Viridans group streptococci and Streptococcus bovis are usually highly susceptible to penicillin and can be treated with penicillin or ceftriaxone. Relatively resistant strains of viridans group streptococci and Streptococcus bovis are treated with penicillin or ceftriaxone along with a shorter two-week course of an aminoglycoside during the initial phase of treatment. and Enterococci are usually treated with a combination therapy consisting of penicillin and an aminoglycoside for the entire duration of 4–6 weeks. Subsequent valve repair can be performed in limited disease. • Patients with significant valve stenosis or regurgitation causing heart failure • Evidence of hemodynamic compromise in the form of elevated end-diastolic left ventricular or left atrial pressure or moderate to severe pulmonary hypertension • Presence of intracardiac complications like paravalvular abscess, conduction defects, or destructive penetrating lesions • Recurrent septic emboli despite appropriate antibiotic treatment • Large vegetations (> 10 mm) • Persistently positive blood cultures despite appropriate antibiotic treatment • Prosthetic valve dehiscence • Relapsing infection in the presence of a prosthetic valve • Abscess formation • Early closure of the mitral valve • Infection caused by fungi or resistant Gram-negative bacteria. The guidelines were recently updated by both the American College of Cardiology and the European Society of Cardiology. There was a recent meta-analysis published that showed surgical intervention at seven days or less is associated with lower mortality. ==Prognosis==

Infective endocarditis is associated with 18% in-hospital mortality. However, adult patients with congenital heart disease can have relatively lower mortality, down to 5% due to younger age, right-sided endocarditis, and management by multidisciplinary teams. As many as 50% of people with infective endocarditis may experience embolic complications. ==Epidemiology==

In developed countries, the annual incidence of infective endocarditis is 3 to 9 cases per 100,000 persons. Infective endocarditis occurs more often in men than in women. There is an increased incidence of infective endocarditis in persons 65 years of age and older, which is probably because people in this age group have a larger number of risk factors for infective endocarditis. In recent years, over one-third of infective endocarditis cases in the United States was healthcare-associated. Another trend observed in developed countries is that chronic rheumatic heart disease accounts for less than 10% of cases. Although a history of valve disease has a significant association with infective endocarditis, 50% of all cases develop in people with no known history of valvular disease. ==History==

Lazare Riviére first described infective endocarditis affecting the aortic valve in 1616. In 1806, Jean-Nicolas Corvisart coined the term vegetation to describe collections of debris found on a mitral valve affected by infective endocarditis. The British physician Joseph Hodgson was the first to describe the embolic complications of infective endocarditis in 1815. It was not until 1878 that Theodor Klebs first suggested that infective endocarditis had a microbial infectious origin. In 1909, William Osler noted that heart valves that experienced degeneration and were sclerotic or poorly functioning had a higher risk of being affected. Later, in 1924, Emanuel Libman and Benjamin Sacks described cases of vegetative endocarditis that lacked a clear microbial origin and were often associated with the autoimmune condition systemic lupus erythematosus. In 1944, physicians reported on the first successful use of penicillin to treat a case of infective endocarditis. == References ==