The principal MSCRAMM ofS. viridansis dextran. This carbohydrate promotes its attachment
to the fibrin platelet clot. Other MSCSRAMMs interact with fibrin and platelets.
Abiotrophia spp. (formerly known as nutritionally variant streptococci) requires the
presence of cystine or pyridoxine for growth. This type of IE is usually subacute in nature. The
organisms may produce massive valvular vegetations that often embolize. Many isolates of
Abiotrophiaare relatively resistant to penicillin. These properties contribute to the greater rate
of mortality than that ofS. viridans, 15% versus less than 5%, (11,12). Accordingly, a greater
percentage of these cases would be cared for in a CCU than those due toS. viridans.
S. anginosus,S. intermediusandStreptococcus constellatuscomprise theAnginosusgroup of
S. viridans. They are very invasive and abscess producing in both myocardium and valvular
structures. Clinically they behave very similar toS. aureus. Although they comprise only about
6% of total cases of IE, they are becoming a more frequent cause of health-care associated
bloodstream infections (HCBSI) especially among neutropenic cancer patients (13).
Group B. streptococci) (GBS are increasingly the cause of acute valvular infection in the
elderly suffering from a multiplicity of chronic diseases such as diabetes, renal failure, and
cancer. Its mortality rate may be as high as 40% due to metastatic infection, severe valvular
damage, and congestive heart failure. The recurrence rate is as high as 4%. The silaic acid
component of its capsule is a major virulence factor that inhibits the activation of the
alternative complement pathway (14–16, 16a).
Enterococci have classically been classified as group D streptococci. They are now
categorized as members of the genusEnterococcus.Enetroccocus faeciumandEnterococcus faecalis
account for 10% to 20% of cases of IE, which is usually subacute in nature. Of these,E. faecalisis
responsible for 90% of cases. Enterococcal BSI/IE arise from infections of urinary tract,
abdominal and pelvic infections, wound infections, biliary tract infections, and intravascular
catheters. Up to 40% of these BSI have no definable source. Such a situation is more commonly
seen in the immunosuppressed (17,18). Enterococcal BSI are a health-care associated
phenomena. Many are polymicrobial. Patients with enterococcal IE are usually debilitated
and aged, more often than not male (17).
Enterococci have always been a therapeutic challenge to the clinician. It was recognized
early on antibiotic era that enterococcal IE required a synergistic combination of the cell wall
antibiotic with an aminoglycoside were. Vancomycin-resistant enterococcal (VRE) bacteremia
is on the increase. However, the true incidence of VRE IE is difficult to arrive at because of
methodological differences between the criteria used to differentiate VRE BSI from VRE IE.
Most of the isolates of VRE representE. faecium; few belong toE. faecalis. It appears that the
outcome of VRE IE is determined by the overall condition of the patient as much as by the
course of the valvular infection itself (19,20).
IE, due to infection withS. bovis, clinically is very similar to that produced byS. viridans.
There is a striking association betweenS. bovisBSI and lesions of and/or manipulation of the
gastrointestinal tract. Its connection with chronic liver disease has been more recently
appreciated (21) Most isolates are quite sensitive to penicillin (22).
S. aureusis overall the most common cause of IE (50% of cases) (5,23). It is especially
prominent in acute cases of IE, in prosthetic valve endocarditis (PVE) and intravenous drug
abuser (IVDA) IE. More than 50 % of the cases have no known prior valvular disease. The
mortality rate ofS. aureusIE is 40%. In the United States, 78% ofS. aureusBSI (250,000 cases per
year) are associated with intravascular catheters (24). At least, 30% ofS. aureusBSI progress to
IE (25). The ability ofS. aureusto adhere to the fibrin sheaths of intravascular catheters is its
major virulence factor in producing HCBSI (26).S. aureuspossesses a variety of pathogenic
mechanisms. The teichoic acid component of the cell wall facilitates its attachment to the nasal
mucosa from which it may set up a “beachhead” on the skin of the patient. Any break in the
dermis promotes the entry for the staphylococcus into the microcirculation. Prostatitis and
pneumonia are other common portals of entry into the bloodstream. The organisms reach the
microcirculation by means of the lymphatic route. They then attach to the venous endothelium,
without the need for a preformed thrombus, by means of their MSCRAMMs. Most notable
among these are fibronectin-binding proteins and various clumping factors. MSCRAMMs
trigger the ingestion of these pathogens by the endothelium (endotheliosis) as well as
promoting bacterial aggregation. Staphylococci may remain dormant within the endothelial
220 Brusch