13
Infective Endocarditis and Its Mimics
in Critical Care
John L. Brusch
Department of Medicine, Harvard Medical School, Cambridge, Massachusetts, U.S.A.INTRODUCTION
Since Osler’s landmark clinical description in the 1880s, infective endocarditis (IE) has
undergone significant changes as regards its epidemiology, clinical manifestations, and
treatment. The availability of antibiotics and the decrease in the prevalence of rheumatic fever
in the developed world has significantly altered the profile of IE (1); however, antibiotics have
failed to lessen the frequency of embolic complications and mycotic aneurysms in those with
subacute IE (2). This is most likely due to the six-week gap between onset of infection and its
recognition (3). In this age of intravascular devices, critical care units (CCUs) have become a
focal point of concern, both for the treatment and prevention of infective endocarditis. For
decades, CCUs have cared for those individuals suffering from the serious effects of IE. The
surgical and medical modalities that have been developed to treat these infections actually
contribute to both the number and types of cardiac and extracardiac complications of IE. The
various intravascular devices that are mainstays of treatment in CCUs have become the most
prominent offenders in this regard. The replacement of a damaged valve by a prosthetic one
presents a lifetime of infectious risks to the patient. The challenge of IE in the CCU lies with not
only treating its life-threatening complications but also preventing its development in this site
of care. In many respects, the latter is the much more formidable task. Discussion will focus
upon those pathogens that are most frequently encountered in the CCU as well as on the risks
of catheter-related bloodstream infections (CRBSI). In addition, the most effective mimics of IE
will be discussed.
MICROBIOLOGY
There is a close association between the type of endocarditis and the infecting organism (Table 1)
(4). Gram-positive cocci are clearly the predominant pathogens for all forms of the disease.
Staphylococcus aureus, both methicillin sensitive (MSSA) and methicillin-resistant (MRSA), cause
32% of cases overall; coagulase-negative staphylococci (CoNS) 10.5%; theStreptococcus viridans
group 18%;Streptococcus bovis6.5%; other streptococci (Abiotrophiaspp, formerly known as
nutritionally various streptococci) 5.1%;Enterococcusspp. 10.6%; other gram-negative anaerobic
organisms 2%; fungi 1.8%; polymicrobial 1.3%; other isolates 3.1%, and culture negative 8.1% (5).
The data, collected internationally between June 2000 and January 2004,are reflective of cases
acquired both in the in community and in health-care facilities (see ‘Epidemiology’).
The percent of cases of IE caused by theS. viridansgroup has decreased by 35% (Table 2).
Overall, these streptococci produce less than 50% of all types of endocarditis compared with
greater than 75% in the pre-antibiotic era (6,6a).S. viridansremains as the classic organism of
subacute IE. It is the major pathogen in cases of IE that are associated with mitral valve
prolapse (MVP) (7). For the purposes of this chapter, the term “S. viridans” applies to all non-
pneumococcal streptococci excluding groups A, B, C and G.Streptococcus salivarius,Strepto-
coccus sanguis I and II,Streptococcus mitis,Streptococcus intermedius,Streptococcus milleriand
Streptococcus mutansbelong to theS. viridansgroup. These streptococci are commensals of the
respiratory and gastrointestinal tracts. With the exception of theStreptococcus anginosusgroup,
they generally possess little invasive potential (8). Instead, they are able to adhere to and
promote the growth of the fibrin/platelet thrombus. They do so by their ability to stimulate
local production of tissue factor by monocytes and to promote platelet aggregation. These
bacteria possess microbial surface components recognizing adhesive matrix molecules
(MSCRAMMS) on the extracellular matrix molecules of the fibrin platelet thrombus (9,10).