Intravascular Infections

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Intravascular infections include infective endocarditis, mycotic aneurysm, suppurative thrombophlebitis, and intravenous (IV), catheter-associated bacteremia. Because these infections are within the vascular system, organisms are present in the bloodstream at a fairly constant rate (i.e., a continuous bacteremia). These infections in the cardiovascular system are extremely serious and are considered life-threatening.

Infective Endocarditis. The development of infective endocarditis (infection of the endocardium most commonly caused by bacteria) is believed to involve several independent events. Cardiac abnormalities, such as congenital valvular diseases that lead to turbulence in blood flow or direct trauma from IV catheters, can damage cardiac endothelium. This damage to the endothelial surface results in the deposition of platelets and fibrin. If bacteria transiently gain access to the bloodstream (this can occur after an innocuous procedure such as brushing the teeth) after alteration of the capillary endothelial cells, the organisms may stick to and then colonize the damaged cardiac endothelial cell surface. After colonization, the surface will rapidly be covered with a protective layer of fibrin and platelets. This protective environment is favorable to further bacterial multiplication. This web of platelets, fibrin, inflammatory cells, and entrapped organisms is called a vegetation (Figure 52-1), The resulting vegetations ultimately seed bacteria into the blood at a slow but constant rate.

The primary causes of infective endocarditis are the viridans streptococci, comprising several species (Box 52-2). These organisms are normal inhabitants primarily of the oral cavity, often gaining entrance to the bloodstream as a result of gingivitis, periodontitis, or dental manipulation. Heart valves, especially those that have been previously damaged, present convenient surfaces for attachment of these bacteria. Streptococcus sanguis and Streptococcus mutans are most frequently isolated in streptococcal endocarditis.

With the ever-increasing use of IV catheters, intraarterial lines, and vascular prostheses, organisms found

BOX 52-2 Agents of Infective Endocarditis

Viridans streptococci*

Nutritionally deficient streptococci |Abiotrophie spp. and Granu-

Hcatelia spp.) Enterococci* Streptococcus bovis Staphylococcus aureus* Staphylococci (coagulase-negative) Enterobacteriaceae

Pseudomonas spp. (usually in drug users)

Haemophilus spp., particularly H. aphrophilus

Unusual gram-negative bacilli (e.g„ Actinobacillus, Cardiobacte-

rium, Eikenella, Coxiella burnetii) Yeast

Other (including polymicrobial infectious endocarditis)

*Most common organisms associated with native valve endocarditis In non-drug-using adults.

as normal or hospital-acquired inhabitants-of the human skin are able to gain access to the bloodstream and find a surface on which to grow, including heart valves and vascular endothelium. In such a setting, Staphylococcus epidermidis and other coagulase-negative staphylococci have been increasingly implicated as causes of infection. S. epidermidis is the most common etiologic agent of prosthetic valve endocarditis, with S. aureus being the second most common. S. aureus is an important cause of septicemia without endocarditis and is found in association with other foci, such as abscesses, wound infections, and pneumonia, as well as sepsis related to indwelling intravascular catheters.

Mycotic Aneurysm and Suppurative Thrombophlebitis. TVvo other intravascular infections, mycotic aneurysms and suppurative thrombophlebitis, result from damage to the endothelial cells lining blood vessels. With respect to mycotic aneurysm, an infection causes inflammatory damage and weakening of an arterial wall; this weakening causes a bulging of the arterial wall (le., aneurysm) that can eventually rupture. The etiologic agents are similar to those that cause endocarditis.

Suppurative thrombophlebitis is an inflammation of a vein wall. The pathogenesis of this intravascular infection involves an alteration in a vein's endothelial lining that is followed by clot formation. This site is then seeded with organisms, thereby establishing a primary site of infection. Suppurative thrombophlebitis represents a frequent complication of hospitalized patients that is caused by the increasing use of IV catheters.

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