 Infective Endocarditis
Infective Endocarditis Quote: Introduction
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Infective endocarditis (IE) is an infection of the endocardial surface of the heart. The intracardiac effects of this infection include severe valvular insufficiency, which may lead to intractable congestive heart failure and myocardial abscesses. IE also produces a wide variety of systemic signs and symptoms through several mechanisms, including both sterile and infected emboli and various immunological phenomena.
Endocarditis has evolved into several variations, keeping it near the top of the list of diseases that must not be misdiagnosed or overlooked. The history of IE can be divided into several eras. Lazaire Riviere first described gross autopsy findings of the disease in 1723. In 1885, William Osler presented the first comprehensive description of endocarditis in English. Lerner and Weinstein presented a thorough discussion of this disease in modern times in their landmark series of articles, "Infective Endocarditis in the Antibiotic Era," published in 1966 in the New England Journal of Medicine.
Since the 1980s, IE could be described as infective endocarditis in the era of intravascular devices because infection of intravascular lines has been determined to be the primary risk factor for Staphylococcus aureus bloodstream infections (BSIs). S aureus is currently the primary pathogen of endocarditis.
Since the 1960s, the clinical characteristics of IE have changed significantly. The dramatic "graying" of the disease and the increase in recreational drug use and proliferation of invasive vascular procedures underlie this phenomenon. Varieties of IE that were uncommon in the early antibiotic era have become prominent. Cases of nosocomial infective endocarditis (NIE), intravenous drug abuse (IVDA) IE, and prosthetic valve endocarditis (PVE) have markedly increased. Valvular infections have entered the era of IE caused by intravascular devices and procedures.
The underlying valvular pathology has also changed. Rheumatic heart disease currently accounts for less than 20% of cases, but 6% of patients with rheumatic heart disease eventually develop IE. Approximately 50% of elderly patients have calcific aortic stenosis as the underlying pathology. Congenital heart disease accounts for 15% of cases, with the bicuspid aortic valve being the most common example.
Other contributing congenital abnormalities include ventricular septal defects, patent ductus arteriosus, and tetralogy of Fallot. Atrial septal defect (secundum variety) is rarely associated with IE. Mitral valve prolapse is the most common predisposing condition found in young adults and is the predisposing condition in 30% of cases of native valve endocarditis (NVE) in this age group.
Calcific aortic stenosis is the underlying defect in 50% of cases of IE among elderly individuals. IE complicates 5% of cases of asymmetrical septal hypertrophy, usually involving the mitral valve.
The most significant risk factor for IE is residual valvular damage caused by a previous attack of endocarditis.
In 75% of cases of IVDA IE, no underlying valvular abnormalities are noted, and 50% of these infections involve the tricuspid valve.
PVE accounts for 10-20% of cases of IE. Eventually, 5% of mechanical and bioprosthetic valves become infected. Mechanical valves are more likely to be infected within the first 3 months of implantation, and, after 1 year, bioprosthetic valves are more likely to be infected. The valves in the mitral valve position are more susceptible than those in the aortic area.
Analogous to PVE are infections of implantable pacemakers and cardioverter-defibrillators. Usually, these devices are infected within a few months of implantation.
Infection of pacemakers includes that of the generator pocket (the most common), infection of the proximal leads, and infection of the portions of the leads in direct contact with the endocardium. This last category represents true pacemaker IE, is the least common infectious complication of pacemakers (0.5% of implanted pacemakers), and is the most challenging to treat. Of pacemaker infections, 75% are produced by staphylococci, both coagulase-negative and coagulase-positive.
NIE is defined as an infection that manifests 48 hours after the patient is hospitalized or that is associated with a hospital, based on a procedure performed within 4 weeks of clinical disease onset. The term health care–associated infective endocarditis (HCIE) is preferable to NIE, since it is inclusive of all sites that deliver patient care, such as hemodialysis centers. The term NIE should be applied to cases of IE acquired in the hospital.
Two types of NIE have been described. The right-sided variety affects a valve that has been injured by placement of an intravascular line (eg, Swan-Ganz catheter). Subsequently, the valve is infected by a nosocomial bacteremia. The second type develops in a previously damaged valve and is more likely to occur on the left side. S aureus has been the predominant pathogen of NIE/HCIE since the recent prevalence of intravascular devices. Enterococci are more frequently isolated in these cases.
The classic clinical presentation and clinical course of IE has been characterized as either acute or subacute. Acute IE frequently involves normal valves. It is a rapidly progressive illness in persons who are healthy or debilitated. Subacute IE typically affects only abnormal valves. Its course, even in untreated patients, may extend over many months. Indiscriminate antibiotic usage and an increase in immunosuppressed patients have blurred the distinction between these 2 major types of IE . However, the classification still has clinical merit.
| | Quote: Organism clinical features
•S aureus
◦Overall, S aureus infection is the most common cause of IE, including PVE, acute IE, and IVDA IE.
◦Approximately 35-60.5% of staphylococcal bacteremias are complicated by IE.
◦More than half the cases are not associated with underlying valvular disease.
◦The mortality rate of S aureus IE is 40-50%.
◦S aureus infection is the second most common cause of nosocomial BSIs, second only to coagulase-negative staphylococci (CONS) infection.
◦The incidence of methicillin-resistant S aureus (MRSA) infections, both the hospital- and community-acquired varieties, has dramatically increased (50% of isolates). Sixty percent of individuals are intermittent carriers of MRSA or methicillin-sensitive S aureus.
◦The primary risk factor for S aureus BSI is the presence of intravascular lines. Other risk factors include cancer, diabetes, corticosteroid use, IVDA, alcoholism, and renal failure.
◦The realization that approximately 50% of hospital- and community-acquired staphylococcal bacteremias arise from infected vascular catheters has led to the reclassification of staphylococcal BSIs. BSIs are acquired not only in the hospital but also in any type of health care facility (eg, nursing home, dialysis center).
◦Of S aureus bacteremia cases in the United States, 7.8% (200,000) per year are associated with intravascular catheters.
•Streptococcus viridans◦This organism accounts for approximately 50-60% of cases of subacute disease.
◦Most clinical signs and symptoms are mediated immunologically.
•Streptococcus intermedius group
◦These infections may be acute or subacute.
◦S intermedius infection accounts for 15% of streptococcal IE cases.
◦S intermedius is unique among the streptococci; it can actively invade tissue and can cause abscesses.
•Nutritionally variant streptococci◦Approximately 5% of subacute cases of IE are due to infection with nutritionally variant streptococci.
◦They require active nutritionally variant streptococci forms of vitamin B-6 for growth.
◦The condition is associated with large vegetations that lead to embolization and a high rate of posttreatment relapse.
•Group D streptococci◦Most cases are subacute.
◦The source is the gastrointestinal or genitourinary tract.
◦It is the third most common cause of IE.
◦They pose major resistance problems for antibiotics.
•Nonenterococcal group D organisms◦The condition is subacute.
◦Infection often reflects underlying abnormalities of the large bowel (eg, ulcerative colitis, polyps, cancer).
◦The organisms are sensitive to penicillin.
•Group B streptococci◦Acute disease develops in pregnant patients and older patients with underlying diseases (eg, cancer, diabetes, alcoholism).
◦The mortality rate is 40%.
◦Complications include metastatic infection, arterial thrombi, and congestive heart failure.
◦It often requires valve replacement for cure.
•Group A, C, and G streptococci◦Acute disease resembles that of S aureus IE (30-70% mortality rate), with suppurative complications.
◦Group A organisms respond to penicillin alone.
◦Group C and G organisms require a combination of synergistic antibiotics (as with enterococci).
•Coagulase-negative S aureus
◦This causes subacute disease.
◦It behaves similarly to S viridans infection.
◦It accounts for approximately 30% of PVE cases and less than 5% of NVE cases.
•Pseudomonas aeruginosa
◦This is usually acute, except when it involves the right side of the heart in IVDA IE.
◦Surgery is commonly required for cure.
•HACEK organisms (ie, Haemophilus aphrophilus, Actinobacillus actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, Kingella kingae)
◦These organisms usually cause subacute disease.
◦They account for approximately 5% of IE cases.
◦They are the most common gram-negative organisms isolated from patients with IE.
◦Complications may include massive arterial emboli and congestive heart failure.
◦Cure requires ampicillin, gentamicin, and surgery.
•Fungi◦These usually cause subacute disease.
◦The most common organism of both fungal NVE and fungal PVE is Candida albicans.
◦Fungal IVDA IE is usually caused by Candida parapsilosis or Candida tropicalis.
◦Aspergillus species are observed in fungal PVE and NIE.
•Bartonella species◦The most commonly involved species is Bartonella quintana.
◦IE typically develops in homeless males who have extremely substandard hygiene. Bartonella must be considered in cases of culture-negative endocarditis among homeless individuals.
•Polymicrobial infective endocarditis◦Pseudomonas and enterococci are the most common combination of organisms.
◦It is observed in cases of IVDA IE.
◦The cardiac surgery mortality rate is twice that associated with single-agent IE.
| Quote: Approximately 5% of cases of possible IE yield negative blood culture results (ie, culture-negative IE). These may have noninfectious causes (eg, vasculitis) or may be caused by fastidious organisms, such as nutritionally variant streptococci. Overall, the most common cause of culture-negative IE is the prior use of antibiotics. In certain populations, infections with Coxiella burnetii (in southern France and Israel) and Bartonella species (among homeless persons) have become more significant causes of culture-negative IE. The blood culture results in fungal valvular infections are often sterile. S aureus may burrow deep within the thrombus, becoming sequestered from the vascular space.
IE remains a diagnostic and therapeutic challenge. Its manifestations may be muted by the indiscriminate use of antimicrobial agents or by underlying conditions in frail and elderly individuals or immunosuppressed persons. Effective therapy has become progressively more difficult to achieve because of the proliferation of implanted biomechanical devices and the rise in the number of resistant organisms. Antibiotic prophylaxis has probably had little effect in decreasing the incidence of IE. | --------------- Full Details:
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Last edited by trimurtulu; 02-02-2009 at 08:41 PM.
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02-02-2009, 08:36 PM
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