This site or third-party tools used by this make use of cookies necessary for the operation and useful for the purposes described in the cookie policy. By clicking on "I accept" you consent to the use of cookies.

Infectious endocarditis

  1. Gastroepato
  2. Cardiology
  3. Infectious endocarditis
  4. Practical anatomy of
    the heart and large vessels
  5. The circulatory system
     Cardiac semeiotics
  6. Chest pain

notes by dr Claudio Italiano 

Endocarditis is characterized pathologically by "vegetation", a lesion resulting from the deposition of platelets and fibrin on the endothelial surface of the heart. Infection is the most common cause of the pathogen usually belonging to a variety of bacterial species, including rickettsia and chlamydia, whose microscopic colonies lie beneath the fibrin surface.

However, other types of microorganisms, for example, fungi may be involved, so that the more general term of infectious rather than bacterial endocarditis is preferred. The site of vegetation is usually the heart valve, but in some cases the vegetations may form in other parts of the endocardium. The involvement of extracardiac intravascular sites, which can generate a disease clinically similar to endocarditis, is correctly called endarteritis.

Pathogenesis

Endocarditis is the result of the association between:

(1 host factors that predispose the endothelium to infection,
(2 circumstances that lead to transient bacteraemia
(3 tissue tropism and virulence of circulating bacteria.

GUEST. In population studies, the incidence of age-sex-adjusted endocarditis is 5 per 100,000 people per year.

This variation is probably due to the prevalence of particular risk factors present in the population and probably reflects the high prevalence of intravenous drug use in that particular population examined.

The advancing age is male sex are significant risk factors; the incidence rate for those aged 65 or over is almost 9 times higher than for those under 65 and for boys it is 2 times higher than for females.

The increased frequency in old age is due in part to the increased prevalence of predisposing cardiac lesions (eg, degenerative cardiac lesions and cardiac valvular prosthesis) and to circumstances that may lead to bacteraemia (eg, invasive urological procedures, colon pathologies, and anorectal and intravascular catheterizations.


Local factors

Non-bacterial thrombotic endocarditis. The normal endothelium is not thrombogenic, but when it is damaged or denuded it becomes a powerful inducer of blood coagulation. Some types of congenital or acquired heart disease may produce a high-velocity jet stream from a high-to-low-pressure chamber (aortic or mitral insufficiency, ventricular septal defect or patent arterial duct) or create a pressure gradient along a narrow orifice between two chambers (aortic stenosis or coarctation of the aorta). The high velocity jet can lead to a turbulent blood flow distal to the pressure gradient, which is believed to be damaged according to a predictable model of the valvular and endocardial endothelium distally to the pressure gradient. Damage to the endothelium can be induced in the experimental animal by passing a catheter into the heart via the aortic or tricuspid valve and intracardiac catheters can induce similar lesions in humans. The platelets are deposited on the surface of the damaged endothelium.

Topics of Gastroepato

Cardiology

Dermatology

Diabetology

Hematology

Gastroenterology

Neurology

Nephrology
and Urology


Pneumology

Psychiatry

Oncology
Clinical Sexology

The adherent platelets subsequently degranulate and stimulate the local fibrin deposit. In the development of the lesion, a sterile thrombosis forms on the endothelial surface, the so-called non-bacterial thrombotic endocarditis (ETNB). For unknown reasons, the ETNB is also found in some patients with chronic cachectic diseases (marital endocarditis) and systemic lupus erythematosus (LES) (Libman-Sacks endocarditis). From the ETNB it is possible to detach fibrin, embolize with obstruction of the peripheral arteries and to cause sterile infarcts of distant organs. Clinical manifestations resulting from ETNB in ​​cachectic diseases or SLE may mimic those of infectious endocarditis. ETNB is the point of attack and subsequent proliferation of some organisms once they have gained access to circulation. After induction of bacteraemia in experimental animals in the absence of a pre-existing ETNB, the endothelial surface is resistant to bacterial adhesion and subsequent development of infective endocarditis.

The left side of the heart is apparently more susceptible to infections than the right side. For example, the left side is more readily infected with relatively avirulent microorganisms such as α- hemolytic streptococci, whereas the right side is infected only by virulent pathogens such as Staphylococcus aureus; the bacteria reach higher densities in the left side (eg, 1010-11 colony-forming units than the right side) The lesions on the right tend to respond more appropriately to antimicrobial therapy than the lesions located on the left; The right factors can also heal spontaneously, in contrast to the observation of the persistence of infection on the left.The factors responsible may include differences between the left and right side of the heart in blood PO2 and intracardiac pressure.The spontaneous resolution of an endocarditis Right is probably also a consequence of the bacterial clearance at the right side by polymorphonuclear leukocytes, an ineffective factor with the same entity on the left side for unknown reasons.Preventive cardiac lesions believed to promote ETNB formation are identified in approximately three quarters of patients with infective endocarditis.

Cardiac defects most frequently encountered in patients with endocarditis are mitral valve prolapse, degenerative heart disease, congenital heart disease, rheumatic heart disease and cardiac valvular prostheses. However, the degree of risk to which each type of cardiac lesion exposes for a subsequent endocarditis can not be deduced from their relative frequency since the prevalence of these cardiac defects in the general population varies widely. The absolute risk is indicated by the incidence rate of endocarditis for each cardiac lesion (when the rate of heart defect in the general population is known) and the relative risk from the incidence rate in relation to that of endocarditis in the general population.

Prosthetic heart valves are a major risk factor for endocarditis. Endocarditis occurs in 1-5% of patients with prosthetic valves during the life of the valve, with an incidence rate of approximately 300-600 per 100,000 patient / year. The risk is greater during the first months after the implant. Prosthetic mechanical heart valves probably have about the same risk as bioprosthesis (eg, porcine heteroinnests) and the risk probably does not vary depending on the replacement seat of the prosthetic valve but is larger when the valves are positioned in the presence of endocarditis active. A previous native valve endocarditis represents a significant risk factor for subsequent episodes as a consequence of both the persistence of risk factors that contributed to the initial episode (eg, intravenous drug use or periodontitis) and the risk additional place from the valve damage sustained in the initial episode. The decreasing relative frequency of rheumatic heart disease among patients with endocarditis in the United States reflects the reduction of prevalence of rheumatic heart disease in this nation. Nevertheless, valvular rheumatic heart disease is a major risk factor for endocarditis, with an incidence rate only slightly lower than that of prosthetic valves. Valvular rheumatic heart disease remains a frequent predisposing lesion to endocarditis in developing countries due to its persistence in these populations. Congenital defects at increased risk of endocarditis are shown below:

High risk of endocarditis
Prosthetic heart valves
Previous endocarditis on native valve
Congenital heart disease, e.g. tetralogy of Fallot, single ventricle
Shunts or pulmonary channels


Moderate risk
Valvular rheumatic heart disease
Other acquired cardiopathies
Other congenital heart disease
Hypertrophic heart disease
Prolapse of the mitral valve with regurgitation and / or thickened flaps


As a general rule, cardiac lesions not associated with turbulent blood flow, such as cardiac lesions in a relatively low pressure system (eg, in the right section of the heart) or an abnormal flow through a large orifice (e.g. atrial septal defect of the second type) are less likely to be complicated by endocarditis. Because of its high prevalence in the population, mitral valve prolapse is the most frequent lesion predisposing to endocarditis. Systemic factors of the host. Host system defenses (eg, granulocytes, T lymphocytes, antibodies, complement) most likely play a minor role in the development or maintenance of endocarditis, except perhaps for granulocytes in endocarditis of the right sections. Different immunodeficiency conditions, including HIV infection, do not appear to place the patient in an increased risk of endocarditis, although the rates of morbidity and mortality related to endocarditis in HIV positive patients in AIDS are greater than those of HIV positive patients but not in the established stage.

Causes of bacteremia and endocarditis

Transient bacteraemia is a common occurrence and occurs as a result of skin trauma or mucosal surfaces normally coated by an endogenous flora. Bacteremia is characterized by a low number of organisms per milliliter of blood (usually <10 CFU per milliliter) and a very short duration (15-30 minutes). The intensity of the bacteraemia is directly correlated to the entity of the trauma, to the density of the microbial flora and to the presence of inflammation or infection in the site of cutaneous or mucosal damage. The mucosal sites that have a dense endogenous flora include the gingival fissures, the oropharynx, the terminal ileum and the colon, the distal part of the urethra and the vagina.

Bacteremia can follow certain medical or surgical procedures that traumatize the skin or mucosal surfaces. In fact, cases of endocarditis that occurred early after dental extraction, tonsillectomy and other types of surgery were reported initially in the '30s. A positive history of these procedures in the previous two months was found in 25% of patients with streptococcal viridans endocarditis and in 40% of patients with enterococcal endocarditis. However, these procedures (particularly dental ones) are common practice in the general population, which makes it difficult to evaluate the risk inherent in the procedure. A positive story for a recent dental procedure in a patient with endocarditis does not necessarily mean that it was the next cause of infection. A study of patients with endocarditis divided into population-based control groups and stratified by age and sex attempted to quantify the risk attributable to the different procedures but, with few exceptions, failed to try to demonstrate a relationship between these procedures and endocarditis. . Nevertheless, the interest of preventive strategies has focused on specific procedures because these are predictably followed by episodes of transient bacteraemia with organisms of a type suitable for developing endocarditis.

Minor traumas of the mucous membranes, also routinely, such as the movements of intestinal peristalsis, the washing of the teeth, the chewing of hard candies or even other daily experiences cause transient bacteremia. Although transient bacteraemia is a frequent daily event and each event is associated only with a very small risk of endocarditis, the cumulative risk of these transient episodes of low-grade bacteraemia is sufficient to be largely responsible for 75% of patients with streptococcal viridans endocarditis or 6% of endocarditis by enterococci in which a medical or dental procedure that preceded the onset of their endocarditis is not found. Spontaneous bacteremia is also responsible for some of those cases of patients with a positive history for a previous procedure since the simple temporal association of a rare pathology such as endocarditis with a particularly common procedure such as a dental procedure does not necessarily imply a causal relationship.

It is increasingly evident that spontaneous bacteraemia, especially as a consequence of poor oral hygiene, is responsible for the majority of cases of streptococcal viridans endocarditis. A transient bacteraemia that probably leads to the development of endocarditis can also result from the use of intravenous illicit drugs and nosocomial procedures. The source of bacteraemia can be identified in more than 90% of nosocomial endocarditis cases. However, some of these procedures may be associated with a subsequent endocarditis only in the presence of high risk underlying cardiac lesions such as a prosthetic valve or previous native valve endocarditis. The prosthetic valve is usually infected at the time of valve insertion or following a transient bacteraemia in the postoperative period. The source is rarely a contaminated prosthetic valve before insertion.

Infectious microorganisms

A trauma at the skin or mucosal surfaces that host a prolific endogenous flora allows the release in the bloodstream of many different microbial species. The spectrum of microorganisms entering the circulation varies with the endogenous microflora typical of the particular traumatized site. Staphylococci and diphtheroids are characteristic of the skin; the oral anaerobes and streptococci of the oropharyngeal mucosa; cola anaerobes, gram-negative enterocytic bacilli and enterococci of the urogenital mucosa and distal intestine. However, only a few of these species, for example, more frequently oral streptococci, staphylococci and enterococci, probably cause endocarditis. The frequency with which a particular organism causes endocarditis depends on how frequently it can gain access to the circulation and its ability to survive in the bloodstream and to adhere to the ETNB components, the exposed subendothelial structures or the endothelial surface itself.

A predictable variety of microorganisms cause endocarditis for each of the specific conditions that predispose patients to the development of infectious endocarditis. For example, in community-acquired endocarditis in drug users who do not use the intravenous route, the most common pathogens are a variety of α-hemolytic streptococci (S. mitis, S. sanguis, S. mutans and S. intermedius) and enterococci . Streptococcus bovis, a streptococcal species that contains group D polysaccharide capsular material, such as enterococci, causes endocarditis in patients likely to present an underlying gastrointestinal lesion.

The isolation of S. bovis from blood cultures should suggest a complete evaluation of the gastrointestinal tract, especially of the colon, in that patient. Less frequent are the annoying gram negative bacilli, the so-called HACEK microorganisms (Haemophilus spp., Actinobacillus, Cardiobacterium, Eikenella and Kingella). The species of Haemophilas are usually H. aphrophiIus, H. paraphrophilus or H. parainfluenzae and rarely H. influenzae, S. aureus causes more than 50% of endocarditis cases occurring in intravenous drug users and in many geographical areas. S. aureus strains are resistant to all β-lactam antibiotics (ie, usually designated as methicillin-resistant strains). Streptococci and enterococci are less common pathogens in intravenous drug addicts.

Gram negative bacilli (usually Pseudomonas aeruginosa, Pseudomonas cepacia and Serratia marcescens) and fungi (usually Candida non-albicans species), unusual in native valve endocarditis in non-intravenous drug users, occur in about 8 and 5% of cases of endocarditis in intravenous drug addicts. Although infrequent in patients without valvular prostheses, coagulase-negative staphylococci, usually of the methicillin-resistant variety, are the predominant pathogens of prosthetic valve endocarditis within two months of surgery, defined as early endocarditis of the prosthetic valve. Furthermore, the frequency of methicillin-resistant coagulase-negative staphylococci remains constant for the first 12 months, suggesting that similar pathogenesis may extend up to more than one year after surgery, not just for the first two months. After the first year, the organ spectrum of endocarditis of the prosthetic valve tends to conform to that of endocarditis of the native valve, that is, streptococci. However, fungi, usually C. albicans, and gram-negative enteric aerobic bacilli are more frequently isolated in both early and late prosthetic valve endocarditis than in native valve endocarditis.

Development of vegetation

Microorganisms adhering to the vegetation stimulate further deposition of platelets and fibrin on their surface. Within this isolated focus, included microorganisms then begin to multiply as rapidly as they would in a culture broth, apparently not inhibited by host defenses, for example, phagocytes, antibodies and complement, to reach extremely dense populations of 108-11 CFU per g of vegetation. Over 90% of the microorganisms in these vegetations are metabolically inactive and not growing, that is, in a phase less susceptible to the bactericidal effects of the β-lactam and aminoglycoside antibiotics. The prolonged bacteraemia that is characteristic of endocarditis derives from a balance between the percentage of release of microorganisms as fragments of vegetation, the speed of clearance of the circulating microorganisms by the reticuloendothelial system of the liver, spleen and bone marrow. Vegetation increases in size as the circulating bacteria are redeposited on the surface of the vegetation, which in turn stimulates the further deposition of fibrin on the surface. The resulting vegetation is composed of successive layers of fibrin and clusters of bacteria, with rare red blood cells and leucocytes, almost always covered by a layer of fibrin on the surface of the lumen. The magnification of vegetation tends to be counterbalanced by its continuous fragmentation. The definitive size of the vegetation can range from small sessile granular protuberances to a large pedunculate mass. The size of the vegetation itself and the fragments that are detached depend to some extent on the type of infectious microorganism: for example, H. paraintluenzae and C. albicans tend to form large friable vegetations and large emboli.

 

see >> Endocarditis, therapy and prophylaxis