Infectious Endocarditis and Chylothorax in a Cat

Introduction

Bacterial endocarditis is a rare diagnosis in cats.¹ This is partly due to vague clinical signs, such as lethargy, inappetance, dyspnea, and lameness. Routine diagnostic tests such as the complete blood count, biochemical profile, and urine analysis do not frequently help to discern or distinguish the underlying disease process. In this case, the presence of pleural effusion and a concurrent heart murmur created suspicion for underlying cardiac disease. The purpose of this case report is to describe a documented case of feline bacterial endocarditis and the importance of echocardiographic evaluation to identify suspicious lesions of valvular structure.

Case Report

A 6 yr old, indoor only, male, castrated domestic longhair cat weighing 4.9 kg presented to the referring veterinarian for evaluation of hyporexia, weight loss, and weakness of 3 wk duration and dyspnea of 2 day duration. A heart murmur was auscultated on physical examination, and thoracic radiographs were obtained. Pleural effusion was diagnosed based on increased soft tissue opacity throughout the thorax, retraction of the lung lobes from the thoracic wall, and multiple pleural fissure lines that widened toward the periphery. The pleural fluid caused partial border effacement of the cardiac silhouette, precluding a thorough radiographic evaluation of the heart. The referring veterinarian suspected an underlying cardiac cause for the pleural effusion. Neoplastic and idiopathic etiologies were also considered. Thoracocentesis was performed to further evaluate the underlying cause, and 200 mL of white-tinged fluid compatible with chylous effusion were obtained. The cat was hospitalized and placed on enalapril 0.5 mg/kg per os (PO) q 12 hr, furosemide 2.5 mg/kg PO q 12 hr, aspirin 81 mg PO twice weekly, and amoxicillin/clavulanic acid^a 12.75 mg/kg PO q 12 hr. Multiple thoracocenteses were repeated over the 3 days of hospitalization before the cat was referred to our hospital for further evaluation to rule out cardiomyopathy as the cause of the recurrent pleural effusion.

Upon presentation to the referral institution, the cat was bright and alert with a respiratory rate of 32 breaths/min. A grade IV/VI left parasternal systolic murmur and gallop rhythm were auscultated. The femoral arterial pulses were strong and symmetric. Inspection of the neck did not reveal jugular venous distension or pulsation, and hepatojugular reflux could not be elicited. The remainder of the physical examination was within normal limits. A six-lead electrocardiogram displayed a normal sinus rhythm, a heart rate of 200 beats/min, and a mean electrical axis of +90°. Evidence of left ventricular enlargement was present and included increased R-wave amplitude in lead II (1.4 mV) and in the left precordial leads. ST-segment coving was also present and thought to be a consequence of the patient's elevated heart rate, myocardial ischemia, electrolyte disturbances, or cardiac trauma (Figure 1).

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An echocardiogram was performed, and severe left atrial enlargement and moderate left ventricular eccentric hypertrophy were evident. The right atrium appeared subjectively severely enlarged. The ratio of the left atrial to aortic root dimension was 2.58:1, with measurements obtained on static two-dimensional examination (reference range <1.6:1) (Table 1).² No spontaneous contrast (“smoke”) was evident within the left atrium. The left ventricular end diastolic diameter was 2.3 cm (reference range 1.48±0.26).³

Table 1 M-mode and Doppler Values of the Cat Described in the Case Report with Reference Ranges

AR Vmax, maximum regurgitant aortic flow velocity; AV Vmax, maximum forward aortic flow velocity; FS, fractional shortening; IVSd, interventricular septum diastole; LA/Ao, left atrium to aortic root ratio; LA diameter, left atrium diameter; LVIDd, left ventricular internal dimension diastole; LVIDs, left ventricular internal dimension systole; LVPWd, left ventricular posterior wall diastole.

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The fractional shortening, which is a measurement of left ventricular systolic function, was within normal limits at 34% (reference range 42.7±8.1%).⁴ The thickness of the left ventricular posterior wall at end diastole was within the upper limits of normal at 0.6 cm (0.25–0.60 cm) and the interventricular septum at end diastole was normal at 0.4 cm (0.30–0.60 cm).⁵ A large mobile hyperechoic pedunculated lesion was visible on the noncoronary aortic valve cusp (Figure 2). Color-flow Doppler echocardiography showed a mildly elevated left ventricular outflow tract velocity and aortic insufficiency (Figure 3). The maximum aortic velocity measured from a left apical four-chamber view continuous-wave Doppler tracing was 2.25 m/s (reference range <1.0 m/s), and the forward aortic flow profile exhibited a shape consistent with a fixed outflow tract obstruction.^6,7 The elevated left ventricular outflow tract velocity was hypothesized to represent either a relative stenosis resulting from either left ventricular volume overload caused by the aortic insufficiency or aortic stenosis caused by the presence of a valvular vegetative lesion. Echocardiography could not completely rule out the presence of an underlying congenital stenosis. The peak aortic regurgitant velocity recorded was 2.06 m/s, with a pressure half time of 18 m/s (no reference range available; Figure 4). The deceleration slope was steep, suggesting rapid equilibration between aortic and left ventricular pressures and a large regurgitant orifice area.

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Based on the echocardiographic findings, aortic insufficiency secondary to infectious endocarditis was tentatively diagnosed. Performing a complete blood count, blood chemistry, urinalysis, urine culture and sensitivity, and blood cultures was recommended, but declined by the owner. The cat was subsequently discharged with the plan of instituting broad-spectrum antibiotic therapy and continuing palliative cardiac medication under the care of the referring veterinarian. The cat became dyspneic again 2 days after discharge and died suddenly during transport to the referring hospital. Postmortem examination and histopathologic analysis were performed.

Aortic valve endocarditis and chylothorax with associated pulmonary atelectasis were found at necropsy. The noncoronary aortic valve cusp contained fusiform shaped, white, rough, irregular, nodular proliferations that were approximately 1×1×0.2 cm (Figure 5). The left coronary cusp also displayed smaller proliferative lesions. The right coronary cusp did not have any nodular lesions, but all aortic valve leaflets were grossly thickened. On gross examination, there was no evidence of thromboembolism within either the myocardium or in the other organ systems. Histologically, the valvular proliferative masses consisted of eosinophilic coagulated serum admixed with fibrin, low numbers of degenerate neutrophils and macrophages, and large areas of mineralization. Distinguishing histopathologic findings of hypertrophic cardiomyopathy, such as myofiber disarray or intramural coronary artery abnormalities, were absent, although myofibrillar disarray is only present in approximately 30% of cats with hypertrophic cardiomyopathy.⁸ No evidence of endocardial fibrosis and only minimal myocardial interstitial fibrosis were present, which decreased the possibility of coexisting restrictive or unclassified cardiomyopathy.⁹ Corresponding to visual assessment, the kidneys, liver, spleen, brain, and heart showed no histologic evidence of emboli. Preexisting congenital malformations of the aortic valve, such as subaortic stenosis, have been linked in the dog to the development of endocarditis.¹⁰ The absence of fibrous tissue encircling the aortic subvalvular area and lack of histopathologic changes consistent with aortic stenosis confirmed that congenital subaortic stenosis was not present in this case. No evidence of other congenital heart disease was present by gross examination or by histopathology of sections of the myocardium. Aerobic culture of the aortic valve grew a Pseudomonas species.

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Discussion

Infectious endocarditis is considered uncommon in dogs, with an occurrence rate of 0.05–6.6%.¹¹ The disease is considered rare in cats, with an incidence best estimated to be between 0.006% and 0.018%.¹ There is extrapolation of the pathogenesis and clinical signs from dogs and humans to the cat population within several case reports.^12–16 The disease can be difficult to diagnose antemortem due to nonspecific clinical signs, such as weakness, lethargy, anorexia, dyspnea, and lameness. The aortic and mitral valves are most commonly affected in the dog and cat.¹⁷ Therefore, signs of left-sided congestive heart failure frequently occur and are more likely when the aortic valve is affected.¹³ A published case series suggests that, in contrast to acute bacterial endocarditis of dogs, cats may experience clinically undetected, extended disease that causes valvular dystrophic calcification, as was documented in this case.¹⁶ Valvular mechanics are altered by the presence of the vegetative lesion and local leaflet disruption, with valvular insufficiency being more common than valvular stenosis.¹⁸ On physical examination, the cat discussed in this report did not have a diastolic murmur, although aortic regurgitation was present on echocardiographic evaluation. The loud systolic murmur was consistent with the diagnosed aortic outflow tract obstruction. Mitral regurgitation was not present.

The pathogenesis of infectious endocarditis is most likely multifactorial and not completely known. Bacteremia must be present for the bacteria to reach, localize, and proliferate on a heart valve.¹⁹ Key interactions between the infecting organism and the patient include the host immune system response and the virulence of the organism. Decreased or ineffective immune responses due to infection with feline leukemia virus, feline immunodeficiency virus, or prolonged steroid administration have been postulated to play a part in bacterial adherence to valvular structures in the heart.²⁰ Other risk factors that raise the clinical suspicion of endocarditis include history of an indwelling catheter and recent surgery, trauma, or infection of the alimentary and urinary systems.¹⁷ In this case, the cat had no known history of any risk factors. Dental extractions, chewing hard food, tooth brushing, and defecating all create frequent transient bacteremic events; however, endocarditis is rare, indicating intact, healthy endothelium has protective properties.²¹ Platelet-fibrin deposition on heart valves is hypothesized to be the scaffolding on which microorganisms can adhere and infiltrate. These vegetations are thought to form through endothelial injury and hypercoagulable states. The endothelium can be injured through elevated shear stress caused by abnormal hemodynamics (e.g., high flow, high velocity, turbulence). It has been theorized that bacteria can be marginalized in focal areas of decreased pressure and eddy currents due to the Venturi effect. The Venturi effect causes pressure to decrease when fluid moves through a constricted area, which occurs as blood moves from the left ventricle into the aorta; however, up to 50% of human patients with endocarditis do not have lesions that can be associated with high velocity jets.^21,22 Therefore, the precise mechanism of bacterial attachment to vegetative lesions is not yet completely understood.

There is a direct correlation between increased intraluminal pressure exerting additional force upon the valve and the incidence of endocarditis.²³ Additional risk factors for humans include congenital heart disease and degenerative valve disease. With the exception of subaortic stenosis, dogs do not appear to have the same risk factors.¹⁹ Further, based on the limited number of feline case reports available, neither congenital heart disease nor dynamic left ventricular outflow tract obstruction due to systolic motion of the mitral valve appears to be a predisposing factor for endocarditis.

Diagnosis of infectious endocarditis in humans utilizes the Modified Duke Criteria.²¹ Physical examination findings, diagnostics, and anamneses are categorized as major or minor criteria. Combinations of major and minor criteria help to differentiate definitive from probable endocarditis or reject the diagnosis. This algorithm has also been proposed for veterinary patients.²⁴ Typical etiological agents cultured from dogs included Staphylococcus spp., Streptococcus spp., Escherichia coli, Pseudomonas aeruginosa, Corynebacterium spp., and Erysipelothrix rhusiopathiae.¹⁸ Recent evidence suggested that Bartonella spp. could be a cause of canine endocarditis, especially in culture negative cases.²⁵ Bacterial isolates from feline endocarditis case reports included Staphylococcus aureus, Escherichia coli, Streptococcus sp., Bartonella, and Pasteurella haemolytica from a tiger.^13,14,16,26

Echocardiography remains the primary way to diagnose infectious endocarditis; however, false-positive and false-negative results can occur.²² Vegetative lesions appear hyperechoic and oscillate on two-dimensional echocardiography. Differentiation from severe myxomatous valvular degeneration can be difficult when the mitral valve is affected.²⁷ Sequelae to vegetative lesions include fixed or dynamic obstruction at the level of the valve and valvular regurgitation due to poor valve coaptation. Sudden valvular damage or tearing can cause acute cardiac decompensation, resulting in heart failure. Extension of the inflammatory and/or infectious process to contiguous tissues has been described as well.¹¹ In these instances, abscess formation and subsequent rupture can create an open communication between heart chambers or a heart chamber and great vessel.²²

Treatment of endocarditis consists of antibiotics to sterilize the vegetative thrombus, managing congestive heart failure and arrhythmias, and supporting the systemic disorders created by embolic events. Long-term antimicrobial therapy is ideally based upon culture and sensitivity results. If cultures are not available, empirical treatment with broad-spectrum antibiotics can be initiated. Initial intravenous drug therapy is recommended before oral therapy. Treatment of congestive heart failure should begin concomitant to antibiotic therapy and may include diuretics and angiotensin-converting enzyme inhibitors. The development of heart failure secondary to infectious endocarditis commonly carries a grave prognosis.¹¹

Infectious endocarditis is an uncommon disease of both cats and dogs. Clinical signs associated with this disease in dogs, such as lameness, kidney failure, and fever, have not been frequently reported in cats.^13–16 The presence of a diastolic murmur at the left heart base, the onset of a new murmur, or a murmur that changes in intensity or characteristics have been considered classic clinical features of valvular endocarditis.¹¹ In 8 of 11 reported cases of feline endocarditis, cardiac auscultation revealed either no murmur or the presence of only a systolic murmur.^12–16,28 Similarly, the cat in this case did not have a diastolic murmur associated with aortic insufficiency. Therefore, when appropriate, feline infectious endocarditis should be considered even in the absence of a diastolic murmur. In many of the isolated feline cases, the primary presenting complaints were signs related to fulminant congestive heart failure, such as tachypnea, dyspnea, weakness, and anorexia. Many of the aforementioned signs are similar to those expected for feline cardiomyopathies; therefore, the true incidence of endocarditis may be higher than reported. Echocardiographic evaluation remains the most reliable way to identify suspicious lesions and determine if further diagnostics should be performed.

Treatment of congestive heart failure should begin concomitant to antibiotic therapy and may include diuretics and angiotensin-converting enzyme inhibitors. Congestive heart failure is a common cause of chylothorax in the cat due to high systemic venous pressures. If present, thoracocentesis may be warranted to increase cardiac output and decrease venous pressures.²⁹

Conclusion

This was an uncommon case report of bacterial endocarditis and chylothorax in the cat. Although endocarditis is rare, it should be considered as a differential diagnosis for cats presenting with congestive heart failure. Advanced imaging and blood cultures are often required to confirm the diagnosis antemortem. Due to the grave prognosis, aggressive medical treatment is required when congestive heart failure occurs secondary to infective endocarditis.