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KEY POINTS

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  • Intravascular infection should be considered in any critically ill patient who has an indwelling intravascular device.

  • Positive blood cultures should always raise the specter of intravascular infection.

  • Intravascular infection should be considered even in a patient with negative blood cultures where there is an unexplained febrile or septic illness.

  • Intravascular infection should especially be considered when there is S aureus bacteremia.

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PATHOGENESIS OF INTRAVASCULAR INFECTIONS

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The pathogenesis of intravascular infections depends on the location of the infection, the organism involved, and the integrity of the underlying vasculature. Native valve endocarditis (NVE) generally results from a cascade of events that begins when mechanical lesions promote microbial adherence to the injured endothelium during transient bacteremia by certain organisms. This initiates a cycle of monocyte activation along with cytokine and tissue factor production that causes enlargement of an infected vegetation, which consists primarily of bacteria, platelets, and fibrin. Local extension, as well as distant metastasis, may result as the primary infection expands.

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NVE is most often due to streptococci of dental origin. Nosocomial NVE in critically ill patients is most often the result of urinary tract infection related to urologic catheterization or bacteremia related to central venous line infection.1

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Intravascular infection involving veins generally results from extension of local microbes or infection into local vasculature by certain pathogens prone to intravascular infection. Intravascular infection involving arteries usually results from bacteremic seeding of arteries at bifurcation sites in the brain or periphery as well as seeding of preexisting aneurysms.2

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Infection involving foreign devices is the result of local spread of bacteria or bacteremic seeding of a vegetation, which has previously formed on the device.

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INFECTIVE ENDOCARDITIS

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ETIOLOGY
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Viridans streptococci remain the most common cause of NVE, accounting for 50% of infections. The other causes of NVE are

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  • Staphylococcus aureus in 25%

  • Enterococci in 7%

  • Coagulase-negative staphylococci in 6%

  • Gram-negative bacilli in 6%

  • Fungi in 1%

  • Culture negative in 7%

  • S aureus accounts for 40% to 50% of infections in patients admitted to the intensive care unit (ICU).3

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Recently there has been a trend toward an increase in the percentage of infections caused by both methicillin-sensitive and methicillin-resistant S aureus (MRSA). This is at least partially related to the increased usage of central venous catheters among both hospitalized and nonhospitalized patients.4 Enterococci and coagulase-negative staphylococci are both twice as common a cause of nosocomial NVE compared to community acquired NVE.5

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The number of infections caused by Streptococcus bovis has also increased and has been attributed to the aging population and related colonic disease.6

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The etiology of prosthetic valve endocarditis (PVE) depends on the onset of infection in relation to the time of valve replacement (Table 67-1).7

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