Infective Endocarditis

CHAPTER 45 Infective Endocarditis



Sophy A. Jesty


Infective endocarditis is a rare disease in horses and is usually caused by bacterial infection of the cardiac valves. Predisposing factors might or might not be recognized by the clinician. Regardless of treatment, the prognosis is poor. In this chapter, the causes, clinical signs, diagnosis, treatment, and prognosis for horses with infective endocarditis are reviewed.



ETIOLOGY


Most cases of infective endocarditis in horses are caused by bacterial infection, although other pathogens, such as fungi or parasites, are occasionally identified. The two most common bacterial isolates are Actinobacillus and Streptococcus organisms. Numerous case reports in the veterinary literature have recorded other bacterial causes of infective endocarditis in horses, including Escherichia coli, Corynebacterium spp., Klebsiella spp., Pseudomonas spp., Pasteurella spp., Serratia spp., Erysipelothrix spp., and Shigella spp. Species responsible for fungal infective endocarditis include Aspergillus and Candida. In humans and small animals, rickettsial organisms can also be the cause of infective endocarditis, but to my knowledge, this has not been reported in horses.


Although bacteremia is probably a fairly common occurrence in horses, infective endocarditis is rare. The interplay of factors such as the status of the endothelial surface of the valve, hemodynamics, host immune system, adherent properties of the bacteria, and peripheral events that initiate bacteremia is important but usually poorly defined. In humans, infective endocarditis is often preceded by nonbacterial thrombotic endocarditis, which consists of a platelet-fibrin complex that can form on a damaged valve. This matrix is a good medium for bacterial growth, so infective endocarditis often ensues. Although an occasional case of nonbacterial thrombotic endocarditis may be recognized in horses, most cases are infective by the time the horse is examined. Infective lesions consist of platelets, fibrin, bacteria, and inflammatory cells. In horses, the predisposing conditions for infective endocarditis are rarely recognized. This is unlike the situation in humans, in whom predisposing factors for infective endocarditis are commonly identified and include procedures resulting in mucous membrane manipulation such as dental procedures or urinary catheterization, congenital cardiac lesions that cause turbulent blood flow, immunosuppression, and others. Sometimes an infection may be present elsewhere that explains the source of bacteremia, but bacteremia alone is often not sufficient to cause infective endocarditis. Virulent organisms such as Streptococcus spp., however, do not require damaged endothelium to colonize a valve.



CLINICAL SIGNS


Clinical signs associated with infective endocarditis result from three aspects of the disease: damage to the cardiac valves and the resulting pathophysiologic responses, septic embolization of fragments to other organs with resulting dysfunction, and infection of the valves and other sites (metastatic abscess formation).


Most horses with infective endocarditis are less than 3 years old. In some, but not all, case series, males were predominantly affected. The most common concerns that prompt referral are fever and a cardiac murmur. Other presenting concerns include lameness, thrombophlebitis, diarrhea, cough, edema, seizures, depression, colic, poor growth, laminitis, and umbilical infection. Clinical signs have often persisted for longer than 2 weeks before referral. On presentation the most common clinical abnormalities include fever, cardiac murmur, and tachycardia. Heart failure or arrhythmias are sometimes seen in conjunction with infective endocarditis.


In horses, the mitral valve is the most commonly affected, followed in order of prevalence by the aortic, tricuspid, and pulmonic valves. Although vegetative lesions can cause either valvular regurgitation or stenosis, the former is more common. An apical systolic murmur that it loudest on the left is likely mitral valve regurgitation, an apical systolic murmur heard on the right is likely tricuspid valve regurgitation, and a diastolic murmur on either side is likely aortic valve regurgitation. If aortic valve regurgitation is hemodynamically significant, a hyperkinetic pulse should be appreciated as diastolic runoff occurs. Although the pulmonic valve is occasionally involved, murmurs caused by pulmonic valve regurgitation are rare because the pressure gradient across the valve and velocity of regurgitant flow are low. Infective endocarditis can also affect chordae tendineae or the myocardium itself; in those instances, a murmur might not be heard. In horses, however, infection at these sites has not been reported in the absence of valvular lesions. Although this might reflect a selection bias for horses with fevers of unknown origin to undergo echocardiography as part of a diagnostic protocol only if they have a murmur, infection involving those structures alone is unusual even in humans and dogs.


Because infective endocarditis is more commonly left-sided in horses, left-sided congestive heart failure can develop, especially with aortic valve involvement. Clinical signs associated with left-sided heart failure include exercise intolerance, lethargy, increased respiratory rate and effort, nostril flare, cough, and inappetence. Lung sounds may or may not be abnormal on auscultation. Froth at the nostrils or mouth is an indication of fulminant left-sided congestive heart failure and is a grave prognostic indicator.


Infection of the tricuspid valve is often a result of septic jugular thrombophlebitis, which should be considered a risk factor for development of endocarditis. In such cases, signs of right-sided congestive heart failure can develop, including venous (especially jugular) distension, jugular pulses, and abdominomegaly secondary to hepatic congestion and ascites.


If the mitral or aortic valves are affected, systemic thromboembolism can develop. Target organs confirmed at necropsy include the myocardium, kidneys, and central nervous system. Evidence of damage may be clinically obvious or may be evident only on clinicopathologic evaluation. If the tricuspid or pulmonic valves are affected, thromboembolism occurs in the lungs; metastatic pneumonia can be severe. Thromboembolism is usually, but not always, septic in etiology.


In humans and dogs, immune complex disease can arise secondary to infective endocarditis. Immune-mediated glomerulonephritis or polyarthropathy might be appreciated in horses with chronic infective endocarditis.



DIAGNOSIS

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May 28, 2016 | Posted by in EQUINE MEDICINE | Comments Off on Infective Endocarditis

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