CURSO CLINICA SAN MIGUEL [Archivo adjunto 1]

---------- Mensaje reenviado ----------
De: LUIS LORO CHERO <lorochero@yahoo.es>
Fecha: 27 de mayo de 2012 23:42
Asunto: [jefaturandolaguardiamedica] CURSO CLINICA SAN MIGUEL [Archivo adjunto 1]
Para: "jefaturandolaguardiamedica@yahoogroups.com" <jefaturandolaguardiamedica@yahoogroups.com>, residente medico PERU interno <interno_residente_medico_PERU@yahoogroups.com>, "sanfernandoperu@yahoogroups.com" <sanfernandoperu@yahoogroups.com>, EMERGENCIA GRUPO <emergencias_y_desastres@yahoogroups.com>, EMERGENCIA DOCENCIA <docenciaemergencia@yahoogroups.com>, DESASTRES EMERGENCIAS <medicinadeemergenciasydesastres@yahoogroups.com>

 

[Más abajo se incluyen archivos adjuntos de LUIS LORO CHERO]

Estimados colegas:

Con las disculpas del caso, les reitero la invitación al Curso de Emergencias y Reanimación Cardiopulmonar que organiza la Clínica San Miguel de San Juan de Lurigancho.

Adjunto esta vez el programa final del curso para su conocimiento y difusión si así lo consideran.

Gracias de antemano.

 

 

 "La Humildad consiste en callar nuestras virtudes y permitirle a los demás descubrirlas; nadie está más vacío, que aquel que está lleno del Yo Mismo"

Med. Emerg. LUIS M. LORO CHERO
Director Médico Clínica San Miguel - SJL
C.M.P. 23627 - R.N.E. 17261
Teléfonos: 3875457 - 994185938 - *753201

 

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Archivos adjuntos de LUIS LORO CHERO

Archivo 1 de 1

CURSO RCP Y EMERGENCIAS.doc

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como el sistema inmune reconoce a los virus

Doherty and Zinkernagel inoculated mice with a virus causing meningitis. They isolated the immune T killer cells and found that these had to recognize two things on the surface of the infected cells in order to kill them: virus antigen, as expected, but also an MHC molecule of the infected mouse strain. MHC molecules are normal components of healthy cells. They were known to differ among individuals and to cause rejection of organ transplants and they are therefore sometimes called transplantation antigens. It came as a surprise that they were also involved in recognition of infected cells. Doherty and Zinkernagel presented two main theoretical models to explain their observations. These models have inspired immunologists and set the stage for research on cell-mediated immunity for at least two decades.
	Wrong combination: the right virus antigen (x) but the wrong MHC molecule (b).
	Wrong combination again: the right MHC molecule (a) but the wrong virus antigen (y).
	The correct combination or virus antigen (x) and MHC molecule (a) leads to killer cell attack.
	A T killer cell (upper right) attaching to and sensing the antigens on a target cell. If the target cell carries the correct antigens fitting the receptor of this particular T cell, the "kiss of death" will follow: the target cell will be destroyed.
The "dual recognition" model assumed that two receptors on the T cell recognized virus antigen and the MHC molecule separately (best illustrated by the previous figure of the "correct combination"). The "altered self" model was based on one T-cell receptor recognizing an MHC molecule modified by virus antigen - or "a little bit of transplantation antigen, a little bit of virus," as Doherty and Zinkernagel have phrased it. (This is illustrated in the "zoom" above, like the previous model based on figures in the original reports.) Through important discoveries made later by other scientists, we are now getting a clearer picture of the scenario. The T-cell receptor, not yet identified at the time of the discovery, recognizes a small part of a virus protein, attached in a cleft formed by the transplantation antigen.

Copyright © Nobel Media AB 2012

oe cunao lee un poquito pes

Overview

The dermatologic manifestations of either toxic epidermal necrolysis or Stevens-Johnson syndrome may constitute a true emergency. Toxic epidermal necrolysis, an acute disorder, is characterized by widespread erythematous macules and targetoid lesions; full-thickness epidermal necrosis, at least focally; and involvement of more than 30% of the cutaneous surface. Commonly, the mucous membranes are also involved. Nearly all cases of toxic epidermal necrolysis are induced by medications, and the mortality rate can approach 40%.^[1]

Manifestations of Stevens-Johnson syndrome include purpuric macules and targetoid lesions; full-thickness epidermal necrosis, although with lesser detachment of the cutaneous surface; and mucous membrane involvement. As with toxic epidermal necrolysis, medications are important inciting agents, although Mycoplasma infections may induce some cases. The mortality rate is much lower than in toxic epidermal necrolysis, approaching 5% of cases.

The prognosis in these diseases is largely a function of the degree of skin sloughing. As the percentage of skin sloughing increases, the mortality rate dramatically worsens. For unknown reasons, however, the disease process in some patients simply stops progressing, and rapid epithelialization ensues. For patients experiencing sloughing over a large area of their skin surface, the mortality rate is much higher. (See the images below.)

Note early cutaneous slough with areas of violaceous erythema. Extensive sloughing on the face. Extensive sloughing on the back.

Together, Stevens-Johnson syndrome and toxic epidermal necrolysis may represent a spectrum of a single disease process. Stevens-Johnson syndrome may also have features of the dermatologic condition erythema multiforme (which has led to confusion in nosology).

Treatment

Only early transfer to and care in a burn unit has been demonstrated to decrease mortality. Coupled with early withdrawal of offending agents, this intervention is the best treatment that can be offered at this time.^{[2, 3]}

Next Section: Patient History and Physical Examination

Patient History and Physical Examination

Constitutional symptoms, such as fever, cough, or sore throat, may appear 1-3 days prior to any cutaneous lesions. Patients may complain of a burning sensation in their eyes, photophobia, and a burning rash that begins symmetrically on the face and the upper part of the torso. Delineation of a drug exposure timeline is essential, especially in the 1-3 weeks preceding the cutaneous eruption.

Primary lesions

The initial skin lesions of Stevens-Johnson syndrome/toxic epidermal necrolysis are poorly defined, erythematous macules with darker, purpuric centers. The lesions differ from classic target lesions of erythema multiforme by having only 2 zones of color: a central, dusky purpura or a central bulla, with a surrounding macular erythema. A classic target lesion has 3 zones of color: a central, dusky purpura or a central bulla; a surrounding pale, edematous zone; and a surrounding macular erythema. (See the image below.)

Note the presence of both 2-zoned atypical targetoid lesions and bullae.

Lesions, with the exception of central bullae, are typically flat. (Lesions of erythema multiforme are more likely to be palpable.) Less frequently, the initial eruption may be scarlatiniform. Flaccid blisters are typically present with full-thickness epidermal necrosis. (See the images below.)

Extensive blistering and sloughing on the back. Low-power view showing full-thickness epidermal necrosis.

Nondenuded areas have a wrinkled paper appearance. A Nikolsky sign is easily demonstrated by applying lateral pressure to a bulla. With regard to the arrangement of lesions, individual macules are found surrounding large areas of confluence. (See the image below.)

Note extensive sloughing.

Distribution

Lesions begin symmetrically on the face and the upper part of the torso and extend rapidly, with maximal extension in 2-3 days. In some cases, maximal extension can occur rapidly over hours. Lesions may predominate in sun-exposed areas.

Full detachment is more likely to occur in areas subjected to pressure, such as the shoulders, the sacrum, or the buttocks. Painful, edematous erythema may appear on the palms and the soles. The hairy scalp typically remains intact, but the entire epidermis, including the nail beds, may be affected. (See the image below.)

Sheetlike desquamation on the foot in a patient with toxic epidermal necrolysis. Courtesy of Robert Schwartz, MD.

A classification proposes that epidermal detachment in Stevens-Johnson syndrome is limited to less than 10% of the body surface area (BSA). Overlapping Stevens-Johnson syndrome/toxic epidermal necrolysis has more extensive confluence of erythematous and purpuric macules, leading to epidermal detachment of 10-30% of the BSA. Classic toxic epidermal necrolysis has epidermal detachment of more than 30%.

An uncommon form of toxic epidermal necrolysis (toxic epidermal necrolysis without spots) lacks targetoid lesions, and blisters form on confluent erythema. Greater than 10% epidermal detachment is required for diagnosis of these cases.

In contrast, bullous erythema multiforme, which was previously grouped with Stevens-Johnson syndrome, may have epidermal detachment of less than 10% of the BSA, but typical target lesions or raised atypical targets are localized primarily in an acral distribution.

Areas of denuded epidermis in Stevens-Johnson syndrome/toxic epidermal necrolysis are dark red with an oozing surface. Mucous membrane involvement is present in nearly all patients and may precede skin lesions, appearing during the prodrome.

Additional findings

Other findings in Stevens-Johnson syndrome/toxic epidermal necrolysis include the following:

• Painful oral erosions cause severe crusting of the lips, increased salivation, and impaired alimentation
• Lesions have been reported in the oropharynx, tracheobronchial tree, esophagus, gastrointestinal tract, genitalia, and anus
• Involvement of the genitalia may lead to painful micturition
• Intact expectorated cylindrical casts of bronchial epithelium have been reported
• Patients may develop a profuse, protein-rich diarrhea
• Internal involvement is not necessarily limited to patients with extensive cutaneous involvement

Ocular lesions are especially problematic because they have a high risk of sequelae. Initially, the conjunctivae are erythematous and painful. The lids are often stuck together, with efforts to loosen them resulting in tearing of the epidermis. Pseudomembranous conjunctival erosions may form synechiae between the eyelids and the conjunctivae. Keratitis, corneal erosions, and a siccalike syndrome may develop.

Previous

Next Section: Patient History and Physical Examination

Pharmacologic Therapy

Corticosteroid therapy

The use of corticosteroids in the management of the Stevens-Johnson syndrome/toxic epidermal necrolysis spectrum is one of the most controversial areas in Dermatology. Administration early in the course of disease has been advocated, but multiple retrospective studies demonstrate no benefit or higher rates of morbidity and mortality related to sepsis. This risk is probably proportional to the area of sloughed skin.

Halebian et al advised against the use of steroids based on 2 open, nonrandomized prospective studies of corticosteroids in 30 patients admitted to a burn unit with Stevens-Johnson syndrome or toxic epidermal necrolysis.^[4] Fifteen patients received corticosteroids and 15 did not. The groups were statistically similar in terms of age, morbid days before burn center admission, and the amount of skin sloughed. Thirty-three percent of the steroid group survived, versus 66% of the nonsteroid group. Sepsis occurred with similar frequency in both groups, but 91% of patients with sepsis in the steroid group died, versus 56% of the infected patients in the nonsteroid group.

Steroids are suggested to predispose patients to gram-negative sepsis by impairing host resistance and by ultimately leading to late clinical recognition of sepsis through suppression of symptoms. Because multiple studies, albeit uncontrolled, have demonstrated a higher morbidity and mortality in patients receiving corticosteroids, most authorities do not recommend their use.

Intravenous immunoglobulin

A number of studies support the use of intravenous immunoglobulin (IVIG) in the treatment of toxic epidermal necrolysis. Viard et al suggested that apoptotic cell death occurs via activation of a cell-surface death receptor.^[5] In vitro, target cell death was blocked by a receptor-ligand blocking antibody and by antibodies present in pooled human IVIG. An open trial of IVIG in 10 patients with toxic epidermal necrolysis resulted in a halt of progression within 24-48 hours, with no mortality.

Since 2000, a number of case reports and 8 noncontrolled, clinical studies containing 9 or more patients have analyzed the efficacy of IVIG in toxic epidermal necrolysis. Some studies did not demonstrate a therapeutic benefit, while others showed decreased mortality.^{[6, 7, 8]} Six of the 8 studies suggested a benefit from IVIG administered at doses above 2g/kg.

Schneck et al published a retrospective study of patients from France and Germany enrolled in EuroSCAR, a case-control study of risk factors, and found that neither IVIG nor corticosteroids decreased mortality in comparison with supportive care alone.^[9]

Given the potentially fatal nature of toxic epidermal necrolysis and the ethical issues involved, a randomized, controlled trial will likely never be performed. Given the suggestion of a therapeutic benefit, many centers are incorporating IVIG into their treatment protocols. At University Hospital at Stony Brook, New York, Stevens-Johnson syndrome/toxic epidermal necrolysis patients are treated with a dosage of 1g/kg/day for 4 consecutive days.

Cyclosporine

An open study from the trauma literature demonstrated the efficacy of cyclosporine in the treatment of toxic epidermal necrolysis. Arevalo et al presented 11 patients admitted consecutively to a burn unit, with toxic epidermal necrolysis involving a large BSA (83% ± 17%).^[10] Each patient received 3mg/kg of cyclosporine daily, with the drug administered enterally every 12 hours. This group was compared to a series of 6 historical control subjects treated with cyclophosphamide and corticosteroids.

In the study, the time from the onset of skin signs to arrest of disease progression and to complete reepithelialization was significantly shorter in the cyclosporine group. All patients in the cyclosporine group survived versus 50% surviving in the cyclophosphamide group. Given a mortality rate of approximately 30% in patients not infected with human immunodeficiency virus (HIV) with toxic epidermal necrolysis, cyclosporine may prove to be a life-saving therapy, but randomized, controlled trials are needed to make definitive recommendations.

Other medications

Cyclophosphamide, N- acetylcysteine, and monoclonal antibodies directed against cytokines have been used in isolated case reports and in small, uncontrolled studies. Thalidomide has been shown to have a deleterious effect on patients' outcomes.^[11]

Previous

 

sangre sin alcohol para armando

el jueves los de su grupo el A vamos  donar sangre para Armando en el Rebagliati. Gil Malca esta coordinando con Manuel para contar con una ambulancia que nos lleve durante la guardia. Tarda un ratito.

Como sabran armando tiene una endocarditis subaguda y va a ser intervenido actualmente esta en la unidad coronaria del Rebagliati

Dia de la Medicina de Emergencias y Desastres

---------- Mensaje reenviado ----------
De: Javier Vasquez Salas <javasa@speedy.com.pe>
Fecha: 22 de mayo de 2012 22:58
Asunto: {emergencias_y_desastres} Dia de la Medicina de Emergencias y Desastres
Para: emergencias_y_desastres@yahoogroups.com, medicinadeemergenciasydesastres@yahoogroups.com

 

Estimados amigos de la SPMED

 

Invitación

 

Nos complace invitar a todos nuestros asociados a la reunion académico y de confraternidad el dia 29 de Mayo en el Auditorio del HCFAP a las 16 horas para conmemorar el aniversario de nuestra especialidad.

Esperamos contar con la presencia de cada uno de Uds.

Ingreso Libre

 

Dr. Javier Vásquez Salas
Medicina de Emergencias y Desastres
Hospital Central de Aeronautica Perú - Clínica San Gabriel (CHSP)
Secretaria General SPMED
Representante IFEM - Perú
webmaster SPMED
www.spmed.org.pe

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a proposito de un caso

Infective endocarditis (IE) is defined as an infection of the endocardial surface of the heart, which may include one or more heart valves, the mural endocardium, or a septal defect. Its intracardiac effects 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.^{[1, 2, 3]}

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.^{[4, 5, 6]}

IE currently can be described as infective endocarditis in the era of intravascular devices, as infection of intravascular lines has been determined to be the primary risk factor for Staphylococcus aureus bloodstream infections (BSIs). S aureus has become the primary pathogen of endocarditis.^[7]

IE generally occurs as a consequence of nonbacterial thrombotic endocarditis, which results from turbulence or trauma to the endothelial surface of the heart. A transient bacteremia then seeds the sterile platelet/fibrin thrombus, with IE as the end result. Pathologic effects due to infection can include local tissue destruction and embolic phenomena. In addition, secondary autoimmune effects, such as immune complex glomerulonephritis and vasculitis, can occur. (See Pathophysiology.)

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. (See Diagnosis.)

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. (See Treatment and Management.)

For other discussions on IE, see Pediatric Bacterial Endocarditis, Infectious Endocarditis, Neurological Sequelae of Infective Endocarditis, and Antibiotic Prophylactic Regimens for Endocarditis.

Types of infective endocarditis

Endocarditis has evolved into several variations, keeping it near the top of the list of diseases that must not be misdiagnosed or overlooked. Endocarditis can be broken down into the following categories:

• Native valve endocarditis (NVE), acute and subacute
• Prosthetic valve endocarditis (PVE),^[8] early and late
• Intravenous drug abuse (IVDA) endocarditis

Other terms commonly used to classify types of IE include pacemaker IE and nosocomial IE (NIE).

The classic clinical presentation and clinical course of IE has been characterized as either acute or subacute. Indiscriminate antibiotic usage and an increase in immunosuppressed patients have blurred the distinction between these 2 major types; however, the classification still has clinical merit.^[9]

Acute NVE frequently involves normal valves and usually has an aggressive course. It is a rapidly progressive illness in persons who are healthy or debilitated. Virulent organisms, such as S aureus and group B streptococci, are typically the causative agents of this type of endocarditis. Underlying structural valve disease may not be present.

Subacute NVE typically affects only abnormal valves. Its course, even in untreated patients, is usually more indolent than that of the acute form and may extend over many months. Alpha-hemolytic streptococci or enterococci, usually in the setting of underlying structural valve disease, typically are the causative agents of this type of endocarditis.

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 areas.^[8]

Early PVE occurs within 60 days of valve implantation. Traditionally, coagulase-negative staphylococci, gram-negative bacilli, and Candida species have been the common infecting organisms. Late PVE occurs 60 days or more after valve implantation. Staphylococci, alpha-hemolytic streptococci, and enterococci are the common causative organisms. Recent data suggest that S aureus may now be the most common infecting organism in both early and late PVE.^[10]

In 75% of cases of IVDA IE, no underlying valvular abnormalities are noted, and 50% of these infections involve the tricuspid valve.^[11] S aureus is the most common causative organism.

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 healthcare-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. An appropriate alternative term would be iatrogenic IE.

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 second most commonly isolated pathogens. These usually arise from a genitourinary source.

Evolution of clinical characteristics of infective 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 NIE, IVDA IE, and 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, and 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 NVE in this age group. IE complicates 5% of cases of asymmetrical septal hypertrophy, usually involving the mitral valve.

Next Section: Pathophysiology

Pathophysiology

IE 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). S 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; group 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
• S 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 due to an invasive procedure) infects the sterile fibrin-platelet vegetation described above. BSIs 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).

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

Intravascular catheters are infected from 1 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. S aureus adheres to the fibrin component.

S 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 methicillin-resistant S aureus (MRSA) catheter-related BSIs without an identifiable cause.

S 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.^[12]

Four days after placement, the risk of infection markedly increases. Lines positioned in the internal jugular 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 not preventable. 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 immunological mechanisms. The pathological 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 SBE 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 are due to 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.

Previous

Next Section: Pathophysiology

Etiology

The different types of IE have varying causes and involve different pathogens.

Native valve endocarditis

The following are the main underlying causes of NVE:

• Rheumatic valvular disease (30% of NVE) - Primarily involves the mitral valve followed by the aortic valve
• Congenital heart disease (15% of NVE) - Underlying etiologies include a patent ductus arteriosus, ventricular septal defect, tetralogy of Fallot, or any native or surgical high-flow lesion.
• Mitral valve prolapse with an associated murmur (20% of NVE)
• Degenerative heart disease - Including calcific aortic stenosis due to a bicuspid valve, Marfan syndrome, or syphilitic disease

Approximately 70% of infections in NVE are caused by Streptococcus species, including S viridans, Streptococcus bovis, and enterococci. Staphylococcus species cause 25% of cases and generally demonstrate a more aggressive acute course (see the images below).

Prosthetic valve endocarditis

Early PVE, which presents shortly after surgery, has a different bacteriology and prognosis than late PVE, which presents in a subacute fashion similar to NVE.

Infection associated with aortic valve prostheses is particularly associated with local abscess and fistula formation, and valvular dehiscence. This may lead to shock, heart failure, heart block, shunting of blood to the right atrium, pericardial tamponade, and peripheral emboli to the central nervous system and elsewhere.

Early PVE may be caused by a variety of pathogens, including S aureus and S epidermidis. These nosocomially acquired organisms are often methicillin-resistant (eg, MRSA).^[13] Late disease is most commonly caused by streptococci. Overall, CoNS are the most frequent cause of PVE (30%).

S aureus causes 17% of early PVE and 12% of late PVE. Corynebacterium, nonenterococcal streptococci, fungi (eg, C albicans, Candida stellatoidea, Aspergillus species), Legionella, and the HACEK (ie, Haemophilus aphrophilus, Actinobacillus actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens, Kingella kingae) organisms cause the remaining cases.

IVDA infective endocarditis

Diagnosis of endocarditis in IV drug users can be difficult and requires a high index of suspicion. Two thirds of patients have no previous history of heart disease or murmur on admission. A murmur may be absent in those with tricuspid disease, owing to the relatively small pressure gradient across this valve. Pulmonary manifestations may be prominent in patients with tricuspid infection: one third have pleuritic chest pain, and three quarters demonstrate chest radiographic abnormalities.

S aureus is the most common (< 50% of cases) etiologic organism in patients with IVDA IE. MRSA accounts for an increasing portion of S aureus infections and has been associated with previous hospitalizations, long-term addiction, and nonprescribed antibiotic use. Groups A, C, and G streptococci and enterococci are also recovered from patients with IVDA IE.

Currently, gram-negative organisms are involved infrequently. P aeruginosa^[14] and the HACEK family are the most common examples.

Nosocomial/healthcare-associated infective endocarditis

Endocarditis may be associated with new therapeutic modalities involving intravascular devices such as central or peripheral intravenous catheters, rhythm control devices such as pacemakers and defibrillators, hemodialysis shunts and catheters, and chemotherapeutic and hyperalimentation lines.^[15] These patients tend to have significant comorbidities, more advanced age, and predominant infection with S aureus. The mortality rate is high in this group.

The organisms that cause NIE/HCIE obviously are related to the type of underlying bacteremia. The gram-positive cocci (ie, S aureus, CoNS, enterococci, nonenterococcal streptococci) are the most common pathogens.

Fungal endocarditis

Fungal endocarditis is found in intravenous drug users and intensive care unit patients who receive broad-spectrum antibiotics.^[16] Blood cultures are often negative, and diagnosis frequently is made after microscopic examination of large emboli.

Clinical features associated with different pathogens

Different causative organisms tend to give rise to varying clinical manifestations of IE, as shown in the Table below.

Table 1. Clinical Features of Infective Endocarditis According to Causative Organism (Open Table in a new window)

Causative Organism(s)	Clinical Features of IE
Staphylococcus 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 CoNS infection. The incidence of 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 MSSA . 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.
Abiotrophia	Approximately 5% of subacute cases of IE are due to infection with Abiotrophia species. They require metabolically active forms of vitamin B-6 for growth. This type of IE 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	The clinical course 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.[17]
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 (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.
Fungal	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	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.
Multiple pathogens (polymicrobial)	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.[18]

Risk factors

The most significant risk factor for IE is residual valvular damage caused by a previous attack of endocarditis.^{[19, 15]}

Many possible risk factors for the development of pacemaker IE have been described, including diabetes mellitus, age, and use of anticoagulants and corticosteroids. The evidence for these is conflicting. The major risk factor is probably surgical intervention to any part of the pacemaker system, especially elective battery replacements. The rate of infection associated with battery replacements is approximately 5 times that of the initial implantation (6.5% vs 1.4%).

Other significant risk factors for pacemaker IE include the development of a postoperative hematoma, the inexperience of the surgeon, and a preceding temporary transvenous pacing.

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Epidemiology

In the United States, the incidence of IE is approximately 2-4 cases per 100,000 persons per year. This rate has not changed in the past 50 years.^[20] The incidence of IE in other countries is similar to that in the United States.

Although endocarditis can occur in a person of any age, the mean age of patients has gradually risen over the past 50 years. Currently, more than 50% of patients are older than 50 years.^[15] Mendiratta et al, in their retrospective study of hospital discharges from 1993-2003 of patients aged 65 years and older with a primary or secondary diagnosis of IE, found that hospitalizations for IE increased 26%, from 3.19 per 10,000 elderly patients in 1993 to 3.95 per 10,000 in 2003.^[21]

IE is 3 times as common in males as in females. It has no racial predilection.

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Prognosis

Prognosis largely depends on whether or not complications develop. If left untreated, IE is generally fatal. Early detection and appropriate treatment of this uncommon disease can be lifesaving.

Cure rates for appropriately managed (including both medical and surgical therapies) NVE are as follows:

• For S viridans and S bovis infection, the rate is 98%.
• For enterococci and S aureus infection in individuals who abuse intravenous drugs, the rate is 90%.
• For community-acquired S aureus infection in individuals who do not abuse intravenous drugs, the rate is 60-70%.
• For infection with aerobic gram-negative organisms, the rate is 40-60%.
• For infection with fungal organisms, the rate is lower than 50%.

For PVE, the cure rates are as follows:

• Rates are 10-15% lower for each of the above categories, for both early and late PVE.
• Surgery is required far more frequently.
• Approximately 60% of early CoNS PVE cases and 70% of late CoNS PVE cases are curable.

Anecdotal reports describe the resolution of right-sided valvular infection caused by S aureus infection in individuals who abuse intravenous drugs after just a few days of oral antibiotics.

The role of valvular surgery in reducing mortality among patients with IE has been unclear. Challenges to resolving this question include the necessity of performing multicentered studies with an apparent difficulty of ensuring that the patients' preoperative assessments and surgical approaches are comparable. The largest study to date indicates that in cases of IE complicated by heart failure, valvular surgery reduces the 1-year mortality rate.^[84]

Mortality rates in NVE range from 16-27%. Mortality rates in patients with PVE are higher. More than 50% of these infections occur within 2 months after surgery. The fatality rate of pacemaker IE ranges up to 34%.^[22]

Increased mortality rates are associated with increased age,^[23] infection involving the aortic valve, development of congestive heart failure, central nervous system (CNS) complications, and underlying disease such as diabetes mellitus. Catastrophic neurological events of all types due to IE are highly predictive of morbidity and mortality.^[24]

Mortality rates also vary with the infecting organism. Acute endocarditis due to S aureus is associated with a high mortality rate (30-40%), except when it is associated with IV drug use.^{[10, 25]} Endocarditis due to streptococci has a mortality rate of approximately 10%.

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Patient Education

Surveys indicate that an appallingly small number of patients who are at risk for developing IE have an understanding of antibiotic and nonpharmacologic (ie, appropriate oral hygiene) principles. Drug rehabilitation for patients who use IV drugs is critical.

The United Kingdom's National Institute for Health and Clinical Excellence (NICE) addresses patient education in its 2008 guideline on prophylaxis against IE in adults and children undergoing interventional procedures. The NICE's guideline recommends that health care professionals teach patients about the symptoms of IE and the risks of nonmedical invasive procedures such as body piercing and tattooing, explain the benefits and risks of antibiotic prophylaxis and the reasons that it is no longer routine, and emphasize the need to maintain good oral health.^[26]

For patient education information, see the Heart Center, as well as Tetralogy of Fallot.

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Proceed to Clinical Presentation

 

 

Contributor Information and Disclosures

Author

John L Brusch, MD, FACP  Assistant Professor of Medicine, Harvard Medical School; Consulting Staff, Department of Medicine and Infectious Disease Service, Cambridge Health Alliance

John L Brusch, MD, FACP is a member of the following medical societies: American College of Physicians and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Coauthor(s)

Steven A Conrad, MD, PhD  Chief, Department of Emergency Medicine; Chief, Multidisciplinary Critical Care Service, Professor, Department of Emergency and Internal Medicine, Louisiana State University Health Sciences Center

Steven A Conrad, MD, PhD is a member of the following medical societies: American College of Chest Physicians, American College of Critical Care Medicine, American College of Emergency Physicians, American College of Physicians, International Society for Heart and Lung Transplantation, Louisiana State Medical Society, Shock Society, Society for Academic Emergency Medicine, and Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Keith A Marill, MD  Faculty, Department of Emergency Medicine, Massachusetts General Hospital; Assistant Professor, Harvard Medical School

Keith A Marill, MD is a member of the following medical societies: American Academy of Emergency Medicine and Society for Academic Emergency Medicine

Disclosure: Medtronic Ownership interest None; Cambridge Heart, Inc. Ownership interest None; General Electric Ownership interest None

Specialty Editor Board

Jon Mark Hirshon, MD, MPH  Associate Professor, Department of Emergency Medicine, University of Maryland School of Medicine

Jon Mark Hirshon, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Public Health Association, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Thomas M Kerkering, MD  Chief of Infectious Diseases, Virginia Tech Carilion School of Medicine

Thomas M Kerkering, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians, American Public Health Association, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, Medical Society of Virginia, and Wilderness Medical Society

Disclosure: Nothing to disclose.

Barry E Brenner, MD, PhD, FACEP  Professor of Emergency Medicine, Professor of Internal Medicine, Program Director, Emergency Medicine, Case Medical Center, University Hospitals, Case Western Reserve University School of Medicine

Barry E Brenner, MD, PhD, FACEP is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Chest Physicians, American College of Emergency Physicians, American College of Physicians, American Heart Association, American Thoracic Society, Arkansas Medical Society, New York Academy of Medicine, New York Academy of Sciences, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Chief Editor

Burke A Cunha, MD  Professor of Medicine, State University of New York School of Medicine at Stony Brook; Chief, Infectious Disease Division, Winthrop-University Hospital

Burke A Cunha, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

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Acute bacterial endocarditis caused by Staphylococcus aureus with perforation of the aortic valve and aortic valve vegetations. Courtesy of Janet Jones, MD, Laboratory Service, Wichita Veterans Administration Medical Center.

Acute bacterial endocarditis caused by Staphylococcus aureus with aortic valve ring abscess extending into myocardium. Courtesy of Janet Jones, MD, Laboratory Service, Wichita Veterans Administration Medical Center.

A middle-aged man with a history of intravenous drug use who presented with severe myalgias and a petechial rash. He was diagnosed with right-sided staphylococcal endocarditis.

This is a magnified portion of a parasternal long axis view from a transthoracic echocardiogram. There is a small curvilinear vegetation on the mitral valve as indicated. The patient presented with a headache and fever, and CT scan of the brain revealed an occipital hemorrhage. The patient had a history of intravenous drug use and multiple blood cultures grew Staphylococcus aureus.

A young adult with a history of intravenous drug use, endocarditis involving the tricuspid valve with Staphylococcus aureus, and multiple septic pulmonary emboli. Pulmonary lesions on chest radiograph are most prominent in the right upper lobe with both solid and cavitary appearance.

A young adult with a history of intravenous drug use diagnosed with right-sided staphylococcal endocarditis and multiple embolic pyogenic abscesses on chest radiograph.

• Table 1. Clinical Features of Infective Endocarditis According to Causative Organism

Table 1. Clinical Features of Infective Endocarditis According to Causative Organism

Causative Organism(s)	Clinical Features of IE
Staphylococcus 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 CoNS infection. The incidence of 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 MSSA . 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.
Abiotrophia	Approximately 5% of subacute cases of IE are due to infection with Abiotrophia species. They require metabolically active forms of vitamin B-6 for growth. This type of IE 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	The clinical course 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.[17]
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 (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.
Fungal	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	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.
Multiple pathogens (polymicrobial)	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.[18]

 

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