Page 160 - Small Animal Internal Medicine, 6th Edition

132 PART I Cardiovascular System Disorders

enlargement may be the strongest echocardiographic pre- especially B. vinsonii subsp. berkhoffii and B. henselae, have
dictor of reduced survival. However, evidence for reduced been increasingly identified in dogs as well as cats with endo-
VetBooks.ir LV contractility or moderate to severe PH also suggests carditis. Bartonella is an important cause of culture-negative
endocarditis in some geographic areas, where it could be
worse prognosis.
responsible for 20% to 30% of cases. Dogs infected with
Bartonella may harbor more than one species and also may
INFECTIVE ENDOCARDITIS be coinfected with Ehrlichia, Babesia, and/or Rickettsia spp.
Yet in dogs with endocarditis from other more common
Infection of the cardiac valves and other endocardial tissue bacteria, coinfection with Bartonella appears to be rare.
is relatively uncommon; however, it causes severe systemic Besides endocarditis, other consequences of Bartonella
as well as cardiac consequences. Infective endocarditis infection include myocarditis, polyarthritis, meningoen-
occurs more often in dogs than in cats. It can be difficult to cephalitis, and granulomatous inflammation in lymph nodes
diagnose, especially before severe valve damage has occurred. and other tissues. Endocarditis-causing Bartonella spp.
CHF is a common sequela; however, other consequences appear to preferentially affect the aortic valve, although the
include thromboembolic (TE) events, multiorgan infection mitral valve occasionally is involved. Bartonella infection
and abscessation, immune-mediated polyarthritis and glo- appears less likely to cause fever and is often associated with
merulonephritis, arrhythmias, and sometimes sudden death. worse survival. Other organisms less frequently isolated
Because of the widely disparate manifestations, endocarditis from infected valves in dogs include Corynebacterium
has been called the “great imitator.” (Arcanobacterium) spp., Pasteurella spp., Pseudomonas aeru-
ginosa, Erysipelothrix rhusiopathiae (E. tonsillaris), and
Etiology and Pathophysiology others, including anaerobic Propionibacterium and Fusobac-
Multiple factors play a role in the development of infective terium spp. Rarely, fungal organisms (usually associated with
endocarditis, including endothelial damage, disturbed blood a foreign body) are involved. There are only rare reports of
flow, hemostatic and immune responses, bacteremia, and endocarditis in cats; in addition to Bartonella spp., Strepto-
bacterial virulence. Bacteremia, either persistent or tran- coccus spp., Staphylococcus spp., E. coli, Pseudomonas, and
sient, is necessary for endocardial infection to occur. The anaerobic bacteria have been identified in this species.
likelihood of a cardiac infection becoming established is Endothelial disruption stimulates platelet activation and
increased when organisms are highly virulent or the bacte- a local coagulation response, with resulting aggregate of
rial load is heavy. Recurrent bacteremia may occur with fibrin, platelets, red blood cells, and leukocytes. Circulating
infections of the skin, mouth, urinary tract, prostate, lungs, bacteria adhere to and colonize this initially sterile clot. Bac-
or other organs. Dentistry procedures are known to cause a terial clumping caused by the action of an agglutinating anti-
transient bacteremia, although rarely is endocarditis a con- body can facilitate attachment to the valves; some colonizing
sequence. Other procedures presumed to cause transient bacteria secrete enzymes that damage valve tissue. Ulcer-
bacteremia in some cases include endoscopy, urethral cath- ation of the valve endothelium and subendothelial collagen
eterization, anal surgery, and other so-called “dirty” proce- exposure stimulate platelet aggregation and coagulation
dures. Sometimes the predisposing cause of infective cascade activation, leading to the formation of vegetative
endocarditis is never identified. lesions. These vegetations consist mainly of aggregated plate-
The aortic and mitral valves are affected most often. The lets, fibrin, blood cells, and bacteria. Newer vegetations are
endocardial surface of the valve is infected directly from the friable, but with time the lesions become fibrous and may
blood flowing past it. Endothelial damage, with platelet and calcify. As additional fibrin is deposited over bacterial colo-
fibrin aggregation, probably serves as a nidus for circulating nies, they become protected from normal host defenses and
bacterial colonization in most cases. Highly virulent organ- many antibiotics. Some organisms, including S. aureus and
isms or a heavy bacterial load increase the risk of cardiac Bartonella spp., are internalized by endothelial cells, confer-
infection. Virulent bacteria can invade normal valves, but ring more protection from the immune system. Although
previously damaged valves are at greater risk, especially with vegetations usually involve the valve leaflets, lesions may
persistent bacteremia. Such damage may result from extend to the chordae tendineae, sinuses of Valsalva, mural
mechanical trauma (such as jet lesions from turbulent blood endocardium, or adjacent myocardium. Vegetations cause
flow or catheter-induced endocardial injury). For example, valve deformity, including perforations or tearing of the
dogs with subaortic stenosis are at greater risk for aortic leaflet(s), and result in valve insufficiency. Rarely, large veg-
valve endocarditis because the high velocity systolic jet can etations may cause the valve to become stenotic. Streptococ-
damage the endothelium on the underside of the aortic cus spp. appears to more commonly affect the mitral valve.
valve. However, there is no clear evidence linking CMVD Bartonella spp. infects the aortic valve most often, causing
with a higher risk for infective endocarditis of the mitral somewhat different lesions of fibrosis, mineralization, endo-
valve. thelial proliferation, and neovascularization.
The most common organisms identified in dogs with Endothelial damage and mechanical valve trauma also
endocarditis have been Staphylococcus spp., Streptococcus can cause nonbacterial thrombotic endocarditis. This is a
spp., and Escherichia coli. Various Bartonella species, sterile accumulation of platelets and fibrin on the valve