**4.** *S. aureus* **virulence factors leading to bacteremia**

infections, from a simple skin infection to more dangerous situations such as bacteremia, endocarditis, pneumonia, bone and joint infections, and many others that may jeopardize the life of the patient. Bacteremia is one major cause of morbidity in both the inpatient and outpatient setting, and *S. aureus* is notorious for causing invasive infections that lead

Patients with *S. aureus* bacteremia can be at risk for many complications that may increase morbidity, with mortality rates of 20–40% that have been described. The higher the level of resistance, the higher the mortality rates. This is why methicillin‐resistant *S. aureus* (MRSA) is expected to have a higher morbidity/morality, longer hospital stays, and higher health care costs when compared with methicillin‐sensitive *S. aureus* (MSSA) bacteremia [1]. Also, in cases of infection with MRSA, there is a higher rate of treatment failure that may include death within 30 days of receiving therapy, persistent positive blood cultures for more than 10 days after therapy, or recurrence of septicemia within 60 days after finishing therapy.

*S. aureus* is a part of the normal human flora; up to 50% of healthy individuals may be persis‐ tently colonized with it. Colonization with *S. aureus* can be persistent in up to 20% of cases, intermittent in 60%, and always absent in up to 20% of people. In a study performed on the general US population that looked at colonization rates in the nares with *S. Aureus*, it was found that the prevalence of MRSA colonization was 0.8% between 2001 and 2002, and went up to 1.5% between 2003 and 2004. The anterior nares is felt to be the major site of *S. aureus* colonization, but some people can be colonized with *S. aureus* outside the nares in areas such as the throat, axilla, inguinal region, and perirectal area. Several conditions may increase the rate of colonization such as diabetes mellitus, HIV infection, underlying skin diseases, and end stage renal disease requiring hemodialysis. Colonization typically precedes *S. aureus* infection. These conditions can place the subject at a higher risk of invasive staphylococcal infections such as bacteremia, which is why much of infection control and prevention efforts

Nasal carriage of *S. aureus* colonization has been associated with the development of infec‐ tions. A substantial proportion of cases of *S. aureus* bacteremia appear to be of endog‐ enous origin as they originate from colonies in the nasal mucosa. This is one reason why strategies to prevent systemic *S. aureus* infections by eliminating nasal carriage need to

Since methicillin‐resistant *S. aureus* constitutes a major burden on health care systems we will focus mainly on it. There are several terms for classifying MRSA infections, namely bacteremia. The first category is the health care–associated MRSA (also called nosocomial)

to bacteremia.

118 Frontiers in Frontiers in Staphylococcus Aureus *Staphylococcus aureus*

**2.** *S. aureus* **colonization**

target colonization with *S. aureus.*

be supported.

**3. Epidemiology**

In observing individual responses to MRSA infection, some hosts become severely ill while others have only mild symptoms. It is unclear why certain factors are directly linked to this discrepancy in response. There are several virulence factors of *S. aureus* that may be struc‐ tural and secreted products that could cause the pathogenesis of the disease with *S. aureus*. Microbial surface components recognizing adhesive matrix molecules (MSCRAMMs) are surface proteins that mediate adherence of *S. aureus* to host tissues. These molecules bind molecules belonging to different surfaces such as fibronectin, collagen, and fibrinogen. The MSCRAMMs help establish invasive and serious infections like endovascular infections, bone and joint infections, and prosthetic‐device infections. **Figure 1** represents a schema of the structural and secreted products that *S. aureus* uses in order to achieve a high viru‐ lence level, and serious infections like blood stream infection. **Table 1** listed a few selected virulence factors [2].

**Figure 1.** Pathogenic factors of *Staphylococcus aureus* with structural and secreted products both playing roles as virulence factors. (A) Surface and secreted proteins. (B and C) Cross sections of the cell envelope. TSST‐1, toxic shock syndrome toxin‐1. Source: With permission from the Massachusetts Medical Society. Copyright 1998 Massachusetts Medical Society.


**Table 1.** Selected *Staphylococcus aureus* virulence factors.
