cells but are eventually released back into the circulation.S. aureusalso induces production of
tissue factor (TF) by both monocytes and endothelial cells. TF then leads to thrombus on the
surface of the endothelial cell by means of the extrinsic clotting system. Once this pathogen is
in the bloodstream, it makes effective use of its unique abilities to invade the endothelium and
propagate the platelet fibrin thrombus (27–30). When it returns back into the circulation,
S. aureusis able to infect the valvular endothelium and produce a thrombus de novo in the
same fashion as described for the venular endothelium. One should never forget thatS. aureus
is ubiquitous. It resides on the skin of both the healthy and the ill as well as being colonizer of
the nares.
S. aureushas several defense mechanisms that shield it from the defenses host’s
phagocytic system. Among these are protein A; catalase; alpha, beta, and gamma toxins;
leukocidins and its capsule. After the phagocytes dies, 5% ofS. aureusremain viable for several
minutes within the white cell. It makes use of these circulating cells to travel throughout the
body (28). Upon the death of the white cell, the viable staphylococci are deposited into the
surrounding tissue or return to the intravascular space. At least 30% of isolates ofS. aureus
from cases of IE are resistant to theb-lactams. The morbidity and mortality for these isolates
are significantly greater than the corresponding values for MSSA—63% versus 45% and 55%
versus 25%, respectively. (31). The choice of the most appropriate antibiotic in a given patient
with MRSA IE can be a daily challenge for the clinician who cares for patients in CCUs.
The term “CoNS” represents at least 15 species of coagulase-negative staphylococci.
Similar toS. aureus, it is a constant part of our environment. It also possesses a superb ability to
infect prosthetic devices of all kinds including intravascular devices/catheters by means of its
production of the glycocalix biofilm. This environment protects the organisms from the host’s
defenses as well as from most antimicrobial agents (32). CoNS currently accounts for 30% of
PVE.
There has been in a significant increase in CoNS infections of native valves in recent
years. Currently 7.8% of non-IVDA IE of native valves is caused by these organisms, 50% are
acquired in the hospital or in other health-care associated venues, and 45% arise from the
community. The risk factors are the same as forS. aureusIE— hemodialysis fistulas, long-term
indwelling central catheters, and pacemakers in implantable defibrillators. Because of its high
rate of complications (60% of cases require surgery and 20% die), these patients are often cared
for in CCUs (33).
Not all CoNS are species ofStaphylococcus epidermidis,Staphylococcus lugdunensisis much
more aggressive than other CoNS with a mortality rate of 70% despite being sensitive to a large
variety of antibiotics. It is quite difficult for the clinical laboratory to differentiate them from
other coagulase-negative organisms. BecauseS. lugdunensisproduces clumping factor and its
colonies have a golden hue, it may be confused withS. aureus(34).
Gram-negative aerobic organisms account for approximately 5% of cases of IE (23).
Although quite commonly involved in spontaneous BSIs, they are unable to adhere as
efficiently to valvular endothelium as do the gram-positive cocci. Cirrhotics are particularly at
risk of developing gram-negative IE.Pseudomonas aeruginosaadheres to the endothelium the
most effectively of any of the gram-negative rods. It elaborates several virulence factors,
extracellular proteases, elastase alkaline proteases. These produce necrosis in a range of tissues
especially in the elastic layer of the lamina propria of all caliber is the blood vessels. Ecthyma
gangrenosum is the classic dermatological manifestation of this process. These toxins also
disrupt the function of polymorphonuclear leukocytes, K- and T-cells, as well as the structure
of complement and immunoglobulins. Exotoxin A disrupts protein synthesis and is the factor
that is best correlated with systemic toxicity and mortality. Unlike most gram-negative bacilli,
P. aeruginosais resistant to the bactericidal activity of human serum. Its polysaccharide capsule
interferes with phagocytosis and the antibacterial effect of the aminoglycosides (35,36). This
pathogen is responsible for 4% of IVDA IE (37,38).
The non-HACEK gram-negative rods seldom produce valvular infection. Fifty-seven
percent of such cases are acquired in health care facilities (39).Haemophilusspp.,Actinobacillus
actinomycetemcomitans,Cardiobacteriumhominis,Eikenella corrodensandKingellaspp. constitute
the HACEK group. These are genetically unrelated gram-negative bacilli/cocobacilli that share
the oropharynx as the primary site of residence. All require incubation in CO2 for growth. This
Infective Endocarditis and Its Mimics in Critical Care 221