development of IE. All of these diseases share in common an increased frequency of BSIs
(72,121).
HIV-positive IVDA patients have a two to eight times greater chance of developing IE
than comparable individuals who are HIV-negative. The lower the CD4 count, the greater the
chance of valvular infection developing. A CD4 count less than 200 is associated with
increased morbidity and mortality in these individuals (122).
Clinical Presentation
History
Early in its course, the symptoms of subacute NVIE are marked by a history of quite indolent
process that is marked by fever, fatigue, backache, and weight loss (24,123). Because of the
relative lack of virulence factors of the organisms that are involved in subacute valvular
infections, its manifestations are due primarily to immunological processes, such as focal
glomerulonephritis that is secondary to deposition of circulating immune complexes (124).
Symptoms of arthritis and arthralgias, especially lumbosacral spine pain, are the result of
deposition of immune complexes in the synovium and most likely in the disc space. The
dermal, mucocutaneous, musculoskeletal, central nervous system, and renal presentations are
produced by the embolic phase that occurs later in the course of this disease. A history of
dental or other invasive procedures is found in less than 15% of cases. The incubation time of
the disease is not greater than two weeks (3). Subacute NVIE is a very able mimic of many
infectious and noninfectious diseases. Because of the nonsuppurative nature ofS. viridans, the
emboli of subacute disease are usually sterile. Up to the point of the development of frank heart
failure, the patients symptoms are almost exclusively noncardiac in nature (124) (Table 7).
Acute NVIE begins quite abruptly and dramatically due to the extra and intra-cardiac
suppurative complications produced byS. aureusas well as other pathogens. Accordingly, this
type of IE will most likely be admitted to the CCU. Congestive heart failure is the most
common complication of both acute and subacute disease (15%–65% of patients) The leaflets of
the infected valve are rapidly destroyed as the organisms multiply within the progressively
enlarging, and often quite friable, vegetations. The infected valve may suffer any of the
following insults: tearing and fenestration of the leaflets, detachment from its annulus, and
rupture of the chordae tendineae and/or papillary muscles (125). The regurgitant jetstream of
the incompetent aortic valve can make impact with the mitral and produce erosion of
perforation of this valve’s leaflets or its chordae tendineae. This may dramatically add to the
strain placed on the left ventricle by the insufficient aortic valve (126). Unusually heart failure
may be the result of severe valvular stenosis produced by massive vegetations that occurred in
IE caused byS. aureus, fungi, HACEK organisms, orAbiotrophiaspp (127). The associated
myocarditis of IE may worsen any type of congestive failure. The dyspnea and fatigue of the
result of congestive failure appear well within a week. A wide range of neuropsychiatric
complications frequently occurring in conjunction with those of congestive heart failure
(126,127).
Other intracardiac complications of acute IE include cardiac fistulas, aneurysms of the
sinus of Valsalva, and intraventricular abscesses that may lead to perforation or damage to
Table 7 The Early Nonspecific Signs and Symptoms of Subacute IEa
Low-grade fever (absent in 3%–15% of patients)
Anorexia
Weight loss
Influenza-like syndromes
Polymyaigia-like syndromes with arthralgias, dull sensorium, and headaches resembling typhoid fever
Pleuritic pain
Right upper quadrant pain and right lower quadrant pain
85% of patients present with a detectable murmur; all will eventually develop one
Low-grade fever (absent in 3%–15% of patients)
Anorexia
aThe manifestations of SBE are caused by emboli and/or progressive valvular destruction and/or
immunologic phenomena.
228 Brusch