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MRSA Staphylococcus aureus is a leading cause of both community-acquired and hospital-acquired bacteremia. Several important underlying conditions predispose patients to the development of S. aureus bacteremia (SAB). The morbidity and mortality of SAB is high and the presence of individual risk factors substantially affects clinical management. Nosocomial SAB — MRSA has predominantly become a nosocomial infection in the United States over the last decade. This trend is due largely to increasing use of intravascular catheters and subsequent catheter-associated staphylococcal bacteremia. In one prospective case-control study of hospitalized Danish patients, the presence of a central venous catheter was the single greatest risk factor for the development of SAB. Patients with hospital-acquired SAB tend to be older, frequently have one or more comorbid illnesses, and typically have one or more of the following risk factors: 1) Intravascular catheter 2) Respiratory illness 3) Surgical wound The seriousness of hospital-acquired MRSA is demonstrated by the following observations:Approximately 20 percent of patients develop metastatic complications, including osteomyelitis. and Approximately 20 to 30 percent die from their bacteremia In those with health care-associated and nosocomial bacteremia, S. aureus was the most common organism isolated and intravascular catheters were the most frequent source of bacteremia. Intravascular catheters — Intravascular catheters serve as a direct conduit into the intravascular space, allowing easy access for pathogens such as S. aureus to enter the bloodstream. As previously mentioned, intravascular catheters are both the most common etiology of SAB in hospitalized patients and an increasingly important cause of community-acquired infection. At Emory University Medical Center, for example, the number of cases of nosocomial intravascular catheter-associated SAB increased eightfold to 56 percent during the period 1980 to 1993; the rate of community-acquired intravascular catheter- associated SAB increased from no cases to 22 percent during the same interval . The mortality of intravascular catheter-associated SAB exceeds 20 percent [28 Metastatic complications (osteomyelitis, endocarditis, septic arthritis) range in frequency from 3.2 to 50 percent, with most studies quoting an average of 25 percent, depending upon the type of vascular access and the organism involved [3,12,18]. The increased use of cuffed catheters has led to an increasing incidence of metastatic infections . The risk is higher (41 percent in one study) with Staphylococcus aureus infection . Vertebrae osteomyelitis — The mechanism by which bacteria in the bloodstream cause vertebral osteomyelitis is complex. Unlike long bones, whose metaphyseal marrow cavity is composed of relatively avascular adipose tissue, vertebral bone in adults has abundant, highly vascular marrow with a sluggish but high-volume blood flow via nutrient vessels of the posterior spinal artery. In addition, these vessels progressively develop a characteristic "corkscrew" anatomy with aging that may predispose to bacterial hematogenous seeding . (See "Vertebral osteomyelitis"). Blood-borne organisms that randomly percolate through the marrow cavity of the vertebrae can spontaneously produce a local suppurative infection. Initiation of infection may be facilitated by recent or prior bone trauma with disruption of the normal architecture. The segmental arteries supplying the vertebrae usually bifurcate to supply two adjacent bony segments. Thus, hematogenous vertebral osteomyelitis usually causes bone destruction in two adjacent vertebral bodies and their intervertebral disc. Spread to adjacent vertebral bodies may occur rapidly through the rich venous networks in the spine. Extension of infection is facilitated by the absence of a circumferential cartilage plate or a layer of subchondral compact bone . Bacterial factors — The pathogenesis of hematogenous osteomyelitis is also dependent upon the ability of specific bacteria to bind to host tissue, a critical first step that is required to initiate infection. S. aureus can adhere to tissue by binding host proteins, including fibronectin, fibrinogen, and collagen . This ability may well account for the predominance of S. aureus in hematogenous osteomyelitis. (See "Pathogenesis of osteomyelitis"). The importance of binding to collagen for the development of osteomyelitis was illustrated in a murine model of acute hematogenous osteomyelitis . Mice infected with a S. aureus collagen-binding adhesin (cna) mutant were less likely to develop osteomyelitis compared to mice infected with a S. aureus strain wild type for this gene (1 of 20 [5 percent] infected with the cna mutant compared to 14 of 20 [70 percent] the wild type strain). These adhesion factors may account for the predominance of S. aureus in bone infections. C reactive protein: This blood test measures the amount of C-reactive protein (CRP) produced by your liver when you have inflammation somewhere in your body. Higher-than-normal levels of CRP may indicate inflammation or a bacterial infection, such as rheumatic fever. CRP levels do not always change with a viral infection. However, a CRP test cannot indicate where the inflammation is located or what is causing it. Other tests are needed to determine the cause and location of the inflammation. A CRP test is most commonly done to monitor the activity of a range of inflammatory conditions. Some of these conditions are polymyalgia rheumatica, inflammatory bowel disease, temporal arteritis, and rheumatoid arthritis. This test can also be used to monitor your response to cancer treatment. It may be used to monitor your risk for infection after a major surgery. A special type of CRP test, the high-sensitivity CRP test (hs-CRP), may be done to evaluate your risk for having a sudden heart problem, such as a heart attack. However, the connection between high CRP levels and heart attack risk is not yet fully known A C-reactive protein (CRP) test is more sensitive than an erythrocyte sedimentation rate (ESR) test, but ESR may be used more frequently to help detect inflammation in the body. Neither CRP nor ESR indicates the cause of inflammation. However, CRP can detect inflammation sooner than ESR because CRP levels become elevated within 6 hours of the start of inflammation. ESR levels increase about a week after the start of inflammation. For more information about ESR, see the medical test Sedimentation Rate. Since CRP testing may help detect inflammation sooner than an ESR, a CRP test may be more helpful in detecting severe inflammation, such as inflammation caused by appendicitis or pelvic inflammatory disease. High-sensitivity C-reactive protein (hs-CRP) is a new test that measures very low amounts of CRP in the blood. This test may be helpful in predicting your risk for heart problems, especially when it is combined with total cholesterol and HDL cholesterol tests. However, hs-CRP is not widely available. High CRP levels before a major surgery may indicate that you are at risk for developing an infection after surgery. CRP testing can be used to monitor your response to cancer treatment or treatment of an infection. Your CRP levels will elevate quickly and then quickly return to normal if you are responding to treatment measures The norm values for CRP is 0–1.0 milligrams per deciliter (mg/dL) or less than 10 mg/L (SI units) Some medications may decrease the CRP values.
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