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Standards of Care June 2009 (Vol 11, No 5)

Infective Endocarditis in Dogs

by Kacie E. Schmitt, DVM, Christopher G. Byers, DVM, DACVECC, DACVIM (SAIM)

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    Introduction

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    Endocarditis is inflammation of the endocardial surface of the myocardium. Infective endocarditis is an uncommon, often fatal, systemic disease that results from microorganisms colonizing the endocardium, most commonly the heart valves, leading to myocardial dysfunction and cardiovascular compromise. The causative agent is most often bacterial (Staphylococcus aureus, Streptococcus spp, Pasteurella spp, Pseudomonas spp, Escherichia coli, Corynebacterium spp, Erysipelothrix rhusiopathiae, Actinomyces turicensis), but rickettsial (Bartonella spp) and, rarely, fungal organisms have also been implicated. Permanent or transient bacteremia, as well as disruption of the endocardial surface, must be present for infective endocarditis to develop.

    Although transient bacteremia is common, infective endocarditis is an uncommon sequela because the mononuclear phagocytic system rapidly removes bacteria from the bloodstream in healthy animals. However, in animals with endocardial damage, bacteria adhere to damaged areas of the endocardium and form vegetative lesions consisting of fibrin, platelets, red blood cells, and bacteria; the bacteria are embedded and protected within a fibrin"platelet matrix. The left heart is almost exclusively affected, with nearly equal distribution between the aortic and mitral valves. The lesions cause regurgitation via valvular damage, improper valvular coaptation, or stenosis of the valvular orifice (rare). Valvular damage can be significant and include rupture, perforation, and tears of the valvular leaflets and/or chordae tendinae. Systemic consequences of infective endocarditis are a result of immune complex deposition (glomerulonephritis, myositis, polyarthritis) and septic and aseptic thromboembolization (myocardium, brain, limbs, kidneys, spleen, bowel, iliac artery).

    Diagnostic Criteria

    Historical Information

    Gender Predisposition

    • Male-to-female ratio: 2:1.

    Age Predisposition

    • 4-8 years of age.

    Breed Predisposition

    • Purebred dogs (incidence 0.06% to 6.6%).
    • Medium- and large-breed dogs.
      — German shepherds, German shepherd crossbreeds, golden retrievers, Labrador retrievers, boxers, Doberman pinschers, Newfoundlands, and rottweilers are more commonly affected.

    Owner Observations

    • Lethargy.
    • Depression.
    • Weakness.
    • Shaking or shivering.
    • Gastrointestinal (GI) signs—hyporexia or anorexia, vomiting, diarrhea.
    • Weight loss.
    • Clinical signs of left heart failure (tachypnea, dyspnea, cough, collapse/syncope).
    • Lameness.
    • Abdominal pain.
    • Neurologic abnormalities (altered mentation, generalized seizures, paraparesis).

    Other Historical Considerations/Predispositions

    • Cardiac abnormalities:
      — Subaortic stenosis (the only structural heart disease that significantly predisposes dogs to development of aortic valve infective endocarditis).
      — Prior valvular infection.
      — Pacemaker implantation.
    • Underlying conditions:
      — Recent bacterial infection of the oral cavity, genital tract (especially prostatitis), or skin.
      — Recent surgery or trauma to mucosal surfaces of the oral, GI, or urogenital tracts.
      — Infected wounds or abscesses.
      — Recent dental procedure, although a direct causal relationship has not been documented in the veterinary literature.
      — Diskospondylitis.
      — Pyelonephritis.
      — Pneumonia.
    • Any condition that weakens the immune system or impairs host defenses:
      — Immunosuppressive drug therapy.
      — Neoplasia.
      — Diabetes mellitus.

    Physical Examination Findings

    • Pyrexia (or recent history of a fever): Reportedly occurs in 80%-90% of veterinary patients with infective endocarditis. However, lack of a fever is reportedly more common in aortic valve endocarditis.
    • Heart murmur.
      — Discovery of a new heart murmur in a febrile patient is a classic finding.
      — Systolic murmurs are most common.
      — Murmurs associated with mitral valve endocarditis are caused by regurgitation.
      • Myxomatous valvular degeneration causing a loud systolic murmur is not common in geriatric large-breed dogs. Therefore, recent valvular destruction should be considered in geriatric large-breed dogs with a new systolic murmur, especially if the patient is febrile.
      • In geriatric small-breed dogs, a loud, systolic murmur resulting from myxomatous valvular degeneration is common and, therefore, unlikely to be related to infective endocarditis.
      • Aortic valve endocarditis causes regurgitation and a diastolic ("blowing") murmur best ausculted over the left heart base. Infective endocarditis is the most common cause of a diastolic heart murmur.
    • Evidence of thromboembolism (septic or aseptic).
      — Neurologic signs (posterior paresis, altered mentation, seizures).
      — Arrhythmias.
      — GI signs (abdominal pain, vomiting, diarrhea).
      — Cold extremities.
      — Unequal or absent femoral artery pulses.
      — Skin necrosis.
    • Evidence of immune complex deposition.
      — Glomerulonephritis (hematuria, proteinuria).
      — Polyarthritis (shifting or fixed lameness).
    • Tachycardia.
    • Bounding pulses (associated with aortic regurgitation).
    • Thoracolumbar pain.
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    Laboratory Findings

    • Complete blood cell count. $
      — Mature neutrophilia ± a left shift.
      — Monocytosis.
      — Normocytic, normochromic, nonregenerative anemia.
      — Thrombocytopenia.
    • Chemistry panel. $
      — Hyperglobulinemia.
      — Hypoalbuminemia.
      — Hypoglycemia.
      — Azotemia, prerenal or renal.
      — Elevated alkaline phosphatase.
    • Urinalysis. $
      — Pyuria.
      — Bacteriuria.
      — Proteinuria.
      — Hematuria.
      — Hemoglobinuria.
    • Blood cultures. $$
      — Positive in 50%-90% of cases.
      — Should be obtained in an attempt to identify the infecting organism and subsequently guide antimicrobial therapy.
      — Strict aseptic sampling technique should be used to obtain at least three separate blood samples of 7 to 10 mL each (pediatric vials requiring 1-3 mL of blood may be used for small dogs). The samples should be taken from three separate venipuncture sites at least 30 minutes apart with suction of the sample ceasing before removal of the needle to prevent contamination with skin bacteria. Avoid sampling from indwelling catheters; however, a new, aseptically placed jugular catheter may be used if necessary.
      — If the patient is currently receiving antibiotic therapy, blood samples should be taken during trough periods.
      — Ideally, aerobic and anaerobic cultures should be submitted. For Bartonella spp culture, aseptically collect 2 mL of blood, place in a plastic tube containing EDTA, and freeze at -70oC until plated.
    • Serology ± polymerase chain reaction (PCR) for Bartonella spp.
      — High seroreactivity (>1:1024) may be a minor criterion for the diagnosis of infective endocarditis (Box 1).
      — Comprehensive infectious disease screening, including Ehrlichia canis, Anaplasma spp, Rickettsia rickettsii, Borrelia burgdorferi, and Babesia spp, should be submitted from dogs that are seroactive for Bartonella spp because coinfection is a common finding.

    Box 1: Infective Endocarditis in Dogs

    Other Diagnostic Findings

    • Echocardiography. $$
      — Two-dimensional echocardiography.
      • Vegetative lesions (hyperechoic, oscillating, move independently of valve).
      • Thickened aortic valve leaflets.
      • Increased echogenicity of affected valve.
      — M-mode echocardiography.
      • Changes in cardiac dimensions.
      • Detection of abnormal mitral valve motion (e.g., fluttering from aortic regurgitation).
      — Color-flow Doppler.
      • Mitral valve regurgitation.
      • Aortic valve regurgitation.
    • Electrocardiography. $
      — Ventricular premature complexes.
      — Tachyarrhythmias (atrial/supraventricular and ventricular).
      — Atrial fibrillation.
      — Evidence of chamber enlargement.
      — ST segment deviation suggesting myocardial hypoxia.
      — Heart block from damage to the atrioventricular node or bundle of His.
      — Bundle branch block.
    • Thoracic radiography. $
      — Left-sided cardiac enlargement.
      — Pulmonary edema.
    • Joint fluid analysis and culture. Performed to identify a potential primary bacterial source responsible for valvular colonization.
    • Urine protein:creatinine ratio should be evaluated in any dog with proteinuria. Performed to help document if a concurrent protein-losing nephropathy, specifically glomerulonephritis, may be present.

    Summary of Diagnostic Criteria

    • Diagnosis of infective endocarditis is challenging because of the nonspecific clinical signs and the variety of organ systems that can be involved.
    • Definitive diagnosis of infective endocarditis requires blood cultures and echocardiography.
    • On physical examination, pyrexia, heart murmur (particularly if newly diagnosed), and lameness are considered classic signs consistent with infective endocarditis.
    • Positive blood cultures, with typical microorganisms, are crucial for definitive diagnosis. In the absence of positive blood cultures, laboratory and physical examination findings consistent with systemic infection may be used to make a tentative diagnosis of infective endocarditis.

    Diagnostic Differentials

    • Pyrexia:
      — Infectious.
      • Bacterial: endocarditis, brucellosis, hemobartonellosis, Lyme disease, bartonellosis, abscess (liver, spleen, other), prostatitis, diskospondylitis, pyelonephritis, peritonitis, pyothorax, septic arthritis.
      • Rickettsial: ehrlichiosis, Rocky Mountain spotted fever, salmon poisoning.
      • Mycotic: histoplasmosis, blastomycosis, coccidiomycosis.
      • Protozoal: babesiosis, hepatozoonosis, leishmaniasis.
      — Immune mediated: polyarthritis, vasculitis, meningitis, systemic lupus erythematosus, immune-mediated anemia, steroid-responsive.
      — Neoplastic: leukemia (acute and chronic), lymphoma, necrotic solid tumor.
      • Heart murmur:
        — Systolic: mitral or tricuspid regurgitation, pulmonic or subaortic stenosis, ventricular septal defect.
        — Diastolic: aortic insufficiency.
      • Tachypnea/dyspnea.
        — Physiologic: exercise, fear, pain.
        — Upper airway:
        • Cervical tracheal disease: extramural compression, foreign body, hypoplasia/stenosis, neoplasia, tracheal collapse.
        • Pharyngeal disease: elongated soft palate, nasopharyngeal polyp.
        • Laryngeal disease: everted saccules, laryngeal paralysis, laryngeal collapse, neoplasia, edema.
        • Nasal disease: aspergillosis, foreign body, neoplasia, nasopharyngeal polyp, stenotic nares, rhinitis.
        — Lower airway:
        • Thoracic tracheal disease: extramural compression, foreign body, hypoplasia/stenosis, neoplasia, tracheal collapse.
        • Bronchial disease: bronchiectasis, chronic bronchitis, foreign body, parasitic disease, allergic airway disease, neoplasia.
        • Pulmonary parenchymal disease: foreign body, pneumonia (bacterial, fungal, parasitic, protozoal, rickettsial, viral), pulmonary fibrosis, neoplasia, pulmonary thromboembolism.
        — Restrictive disorders: diaphragmatic hernia, neoplasia, large intraabdominal mass or fluid, pleural effusion, pneumothorax.
      • Collapse/syncope:
        — Cardiac: bradyarrhythmia (second- or third-degree atrioventricular block, sick sinus syndrome, atrial standstill), tachyarrhythmia (atrial or ventricular tachycardia, atrial fibrillation), congenital ventricular outflow obstruction (pulmonic stenosis, subaortic stenosis), acquired ventricular outflow obstruction (heartworm disease, thrombus, tumor), cyanotic heart disease, impaired forward output (valvular insufficiency, dilated cardiomyopathy, myocardial infarction), cardiac tamponade.
        — Pulmonary: hypoxemia, cough syncope, pulmonary hypertension.
        — Metabolic/hematologic: hypoglycemia, hypoadrenocorticism, electrolyte imbalance, anemia.
        — Neurologic: seizures, neuromuscular disease, cerebrovascular accident, narcolepsy.
      • Cough:
        — Infection: canine infectious tracheobronchitis, pneumonia, parasitic disease, fungal disease, heartworm disease.
        — Immune mediated: chronic or allergic bronchitis.
        — Cardiac: left atrial enlargement, heart failure.
        — Neoplasia.
        — Hemorrhage: coagulopathy, neoplasia, trauma.
        — Edema: hypoglycemia, hypoproteinemia, neurologic, electrocution, airway obstruction.
      • Lameness:
        — Infectious: Lyme disease, rickettsial disease, septic arthritis.
        — Immune mediated: systemic lupus erythematosus, polyarthritis.
        — Nutritional/metabolic: hyperparathyroidism, hypervitaminosis A, copper deficiency.
        — Degenerative/congenital: degenerative joint disease, chondrodysplasia, osteochondrosis.
        — Neuromuscular disease.
        — Trauma.

    Treatment Recommendations

    Initial Treatment

    Treatment is directed at eradicating the infecting organism and managing secondary complications of the disease process. Unfortunately, the structure of the vegetative lesions makes eradication difficult because the bacteria reproduce slowly and are protected from being phagocytized by leukocytes. Success depends on early diagnosis and aggressive management with long-term bactericidal antimicrobials.

    Antimicrobial Therapy

    • Ideally, patients should be hospitalized for 1 to 2 weeks for parenteral antibiotic administration (or until stable). If the patient responds well, antibiotic therapy may be continued orally or parenterally at home (teach the owner to administer medications as subcutaneous or intramuscular injections) for a total treatment period of at least 6 weeks. One to 2 weeks of hospitalization for intravenous therapy, followed by several weeks of subcutaneous injections, has been suggested before giving oral medications for a minimum of 1 to 2 months.
    • Antibiotics should be selected based on blood culture minimum inhibitory concentration (MIC) data. Pending results of blood cultures, broad-spectrum antibiotic therapy is indicated because of the wide range of microorganisms that have been implicated in infective endocarditis. The use of bacteriocidal antibiotics is preferred.
    • Initially, treatment with aminoglycosides in combination with β-lactamase-inhibiting antibiotics or penicillins is reasonable. Because of the potential nephrotoxicity of aminoglycosides, some recommend limiting their use to 1 to 2 weeks. However, adequate hydration, concurrent intravenous fluid therapy, monitoring of renal values, once-daily therapy, and adjustment of dosing regimen based on blood culture MIC data may limit nephrotoxicity. Concurrent use of furosemide potentiates nephrotoxicity.
      — Aminoglycosides. $-$$
      • Gentamicin: 6-8 mg/kg q24h IV, SC, or IM.
      • Amikacin: 15-30 mg/kg q24h IV, SC, or IM
      — Penicillins. $-$$
      • Ampicillin: 20-40 mg/kg q8h IV, IM, or PO.
      • Amoxicillin: 20-30 mg/kg q8h IV, IM, or PO.
      — β-Lactamase inhibitors. $-$$
      • Amoxicillin/clavulanate: 13.75 mg/kg q12h PO.
      • Ampicillin/sulbactam: 20-40 mg/kg q8h IV, IM, or PO.
    • Fluoroquinolones may be used as an alternative to aminoglycosides for treatment of suspected or confirmed gram-negative infections. They have been shown to concentrate well in heart valves and myocardium, although high resistance patterns are emerging and may limit their use.
      — Fluoroquinolones. $-$$

      • Enrofloxacin: 5 mg/kg q12h IV, IM, or PO.
      • Marbofloxacin: 2.75-5.5 mg/kg q24h PO.
      • Levofloxacin: 10 mg/kg q24h IV.
    • Cephalosporins may be used as an alternative for treatment of gram-positive infections.
      — Cephalosporins $-$$
      • Cefazolin: 15-33 mg/kg q8h IV.
      • Cephalexin: 20-60 mg/kg q8h PO.
      • Cefovecin: 8 mg/kg q7d SC (not to exceed 2 injections). Studies have shown cefovecin to be effective against some of the common bacterial isolates causing infective endocarditis. However, no prospective study has investigated (1) the efficacy or safety of this medication for treating infective endocarditis or (2) its long-term use.
    • In veterinary medicine, there is no preferred treatment for Bartonella infection, although treatment with azithromycin, enrofloxacin, amoxicillin/clavulanate, and doxycycline (not recommended, bacteriostatic) has been shown to result in clinical recovery and negative posttreatment titers.
    • If a patient is not responding to the current therapy regimen, has negative blood cultures, or is otherwise suspected of having a resistant infection, consider reculturing the blood and initiating treatment with a third-generation cephalosporin or imipenem.

    Heart Failure Therapy

    Congestive heart failure is one of the most common complications of infective endocarditis and is the most common cause of death. Aortic valve endocarditis produces severe heart failure that is often difficult to manage.

    • Furosemide. $-$$
      — 1-4 mg/kg q6-12h prn IV or SC (up to 12 mg/kg/day).
      — 0.1-0.5 mg/kg/hr constant-rate infusion (CRI).
      — Use cautiously in patients with renal disease.
    • Angiotensin-converting enzyme (ACE) inhibitor. $-$$
      — Enalapril: 0.5 mg/kg q12-24h PO.
      — Benazepril: 0.25-0.5 mg/kg q24h PO.
    • Hydralazine. $-$$
      — 0.5 mg/kg q24h PO or IV initially; titrate 1-3 mg/kg q12h prn.
      — May be beneficial in patients refractory to other drugs for managing severe, acute pulmonary edema because it is a potent arteriolar vasodilator. By reducing peripheral vascular resistance, it also reduces the amount of aortic and mitral valve regurgitation.
      — Care must be taken to avoid hypotension, especially when using in combination with an ACE inhibitor.
    • Amlodipine. $-$$
      — 0.1-0.25 mg/kg q12-24h PO.
    • Nitroprusside. $-$$
      — 1-10 µg/kg/min IV CRI. Initiate dose at 1-2 µg/kg/min and increase dose incrementally every 3-5 minutes until a predetermined target blood pressure is attained (mean arterial pressure = 70 mm Hg).
      — Requires continuous intensive care monitoring.
    • Digoxin. $-$$
      — Patients <18 kg: 0.0044-0.011 mg/kg q12h PO.
      — Patients >18 kg: 0.25 mg/m2 q12h PO.
      — Monitor serum levels 3-5 days after initiating therapy (draw sample 6-8 hours after last dose). Suggested therapeutic levels are 0.5-2.0 ng/mL. Adjust dose as needed.
      — Use with caution in patients with glomerulonephritis and heart failure.
      — The narrow therapeutic range of this medication warrants close monitoring for toxicity (vomiting, diarrhea, anorexia, weight loss, increased heart rate, arrhythmias).
    • Oxygen support prn. $-$$$$

    Supportive Treatment

    In addition to antimicrobial treatment and therapy for congestive heart failure, all hydration and nutrition needs, electrolyte derangements, and acid"base imbalances should be addressed appropriately.

    Prophylactic Treatment

    Patients with subaortic stenosis should be given prophylactic antimicrobial therapy 1 hour before and 6 hours after any dental or surgical procedures, especially those involving manipulation of mucosal surfaces. Suggested antibiotics include a β-lactamase inhibitor, cephalosporin, or clindamycin (dental procedures).

    Patient Monitoring

    • Blood cultures should be performed in all patients 2-4 weeks after initiation of antibiotic therapy and 2 weeks after the termination of antibiotic therapy.
    • Echocardiograms should be performed 2 weeks after initiation of antibiotic therapy, then 2 to 4 weeks later, and 2 weeks after termination of antibiotic therapy. Serial echocardiograms allow monitoring of vegetative lesion size and severity of resultant heart disease.
    • Patients infected with Bartonella spp should have repeat serology 4 weeks after initiation of antibiotic therapy. Repeat titers should be reduced. If not reduced, consider using a different antibiotic.

    Home Management

    Postdischarge management relies on owner compliance for medication administration and reevaluations. Owners must be diligent about monitoring for signs of worsening heart disease (e.g., tachypnea, tachycardia, collapse) that may require medication dosage adjustments or hospitalization.

    Treatment Contraindications

    • Corticosteroids have been administered to dogs with infective endocarditis to control pyrexia and to treat signs mistaken for an immune-mediated disease. Although corticosteroids often improve clinical signs for 24-48 hours, they ultimately exacerbate clinical signs and worsen the prognosis.
    • Anticoagulant therapy is controversial and not currently recommended because of the increased risk of bleeding and no benefit in reducing vegetative lesions or the incidence of embolic events.

    Prognosis

    The prognosis for patients with infective endocarditis is guarded, with a survival rate of approximately 20%. Dogs with mitral valve lesions tend to have a better prognosis, depending on the severity of the regurgitation. Large aortic valve lesions commonly cause severe left heart failure and death. In either instance, once severe regurgitation develops, heart failure and death are ultimately expected. Patients may also die of embolic complications, especially renal infarction or sepsis.

    Favorable Criteria

    • Mitral valve endocarditis only.
    • Gram-positive infection.
    • Origin of infection: skin, abscess, cellulitis, wound.
    • Lack of systemic embolization.
    • Negative blood culture results for 3 months after therapy.

    Unfavorable Criteria

    • Aortic valve endocarditis.
    • Gram-negative infection.
    • Vegetative lesion greater than 10 mm (increased risk of septic embolization).
    • Evidence of left ventricular dysfunction.
    • Sustained ventricular tachycardia or atrial fibrillation.
    • Heart or renal failure that does not respond to therapy.
    • Elevated alkaline phosphatase.
    • Hypoalbuminemia.
    • Concurrent treatment with corticosteroids.
    • Treatment with bacteriostatic agents.
    • Premature termination of antimicrobial therapy.

    Costello MF. Endocarditis. In: Silverstein DC, Hopper K, eds. Small Animal Critical Care Medicine. St. Louis: Elsevier Saunders; 2009:486-490.

    Infective endocarditis. In: Ettinger SJ, Feldman EC, eds. Textbook of Veterinary Internal Medicine. St. Louis: Elsevier Saunders; 2005:1036-1039.

    Infective endocarditis. In: Kittleson MD, Kienle RD, eds. Small Animal Cardiovascular Medicine. St. Louis: Mosby; 1998:402-412.

    MacDonald KA. Infective endocarditis. In: Bonagura JD, Twedt DC, eds. Kirk's Current Veterinary Therapy XIV. St. Louis: Elsevier Saunders; 2009:786-791.

    Miller ME. Infectious endocarditis. In: Fox PR, Sisson D, Moise NS, eds. Textbook of Canine and Feline Cardiology. Philadelphia: Saunders; 1999:567-580.

    Peddle G, Sleeper MM. Canine bacterial endocarditis: a review. JAAHA 2007;43:258-263.

    Sykes JE, Kittleson MD, Chomel BB, et al. Clinicopathologic findings and outcome in dogs with infective endocarditis: 71 cases (1992-2005). JAVMA 2006;228(11):1735-1747.

    Sykes JE, Kittleson MD, Pesavento PA, et al. Evaluation of the relationship between causative organisms and clinical characteristics of infective endocarditis: 71 cases (1992-2005). JAVMA 2006;228(11):1723-1733.

    Click here to download this article as a PDF.

    Dr. Byers discloses that he has received financial support from Dechra Pharmaceuticals, Waltham, and Animal Clinical Investigation LLC.

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