CRHII Infective Endocarditis Student 2025 PDF

Acquired Valvular Disease: Infective Endocarditis Hillary Hammond, DVM, MS, DACVIM (Cardiology)  Understand the pathophysiology of endocarditis Learning Objectives Review most common etiologic agents Describe clinical signs and...

Acquired Valvular Disease: Infective Endocarditis Hillary Hammond, DVM, MS, DACVIM (Cardiology)  Understand the pathophysiology of endocarditis Learning Objectives Review most common etiologic agents Describe clinical signs and diagnostic findings warranting a high index of suspicion for endocarditis Describe appropriate treatment approach  What is Inflammation of the endocardial surface of the infective heart with invasion by an infectious agent endocarditis? Surface of the valves* Bacterial (BE)* Mural (wall) Rickettsial organisms Edges of septal defects Fungal organisms Chordae tendinae Synonyms: Infective endocarditis (IE): microbial infection (bacteria, fungal, etc) Bacterial endocarditis (BEL): bacterial infection Vegetative endocarditis: vegetations (composed of platelets, fibrin, microorganisms, and inflammatory cells) adherent Andre et al. “Aortic valve endocarditis due to Bartonella clarridgeiae in a dog in Brazil”  EndocardIOSIS EndocardITIS Degenerative/Myxomatous Inflammatory/Infectious Gross lesion: smooth, glistening, nodular Gross lesion: friable, rough, irregular yellowish thickening of the valve margins raised proliferative lesions (vegetative) 4 Incidence/Prevalence Cows - relatively common 0.016 – 0.12 % of cattle populations Important cause of hardware disease Dogs – uncommon diagnosis 0.05 – 0.08% of dogs in referral population Middle- aged to older, medium to large-breed, purebred dogs Horses, pigs, camelids – sporadic Can be mural (wall) in camelids and cattle Cats – rare 0.006 – 0.018% of cats in referral population Avians – few cases documented 5  Pathogenesis 1. Endothelial damage/injury 2. Formation of non-bacterial thrombotic endocarditis (NBTE) 3. Bacteremia 4. Bacterial colonization of NBTE 5. Activation of clotting cascade and lesion extension Macdonald K. Infective endocardit is in dogs: diagnosis and therapy. Vet Cli n North Am Smal l Anim Pract. 2010 6  1. Collagen exposure due to endocardial damage Healthy endothelium is resistant to bacterial colonization (injury is required) Direct trauma Inflammation Turbulent blood flow Underlying cardiac defect NOT present in 87-94% of veterinary cases Of those with lesion, 75% have congenital subaortic stenosis EndocardiOSIS is NOT a predisposing factor Macdonald K. Infective endocardit is in dogs: diagnosis and therapy. Vet Cli n North Am Smal l Anim Pract. 2010 7 2. Formation of non-bacterial thrombotic endocarditis Extracellular matrix proteins, thromboplastin, and tissue factor → coagulation Coagulum (fibrinogen, fibrin, platelet proteins) formation → non-bacterial thrombotic endocarditis (NBTE) Macdonald K. Infective endocardit is in dogs: diagnosis and therapy. Vet Cli n North Am Smal l Anim Pract. 2010 8 3. Presence of Bacteremia*** Transient or persistent Predisposing events: Chronic infections (ex: UTI, diskospondylitis, prostatitis, pneumonia, pyoderma, long-term indwelling catheter) GI/GU tract surgery Sometimes never identified? Immunosuppression Systemic illness: Diabetes mellitus, Cushing’s disease Corticosteroids Macdonald K. Infective endocardit is in dogs: diagnosis and therapy. Vet Cli n North Am Smal l Anim Pract. 2010 9 4. Bacterial colonization to NBTE Circulating bacteria adhere and attach to the thrombus Bacteria that most easily adhere to valves are most commonly involved ie Staphylococcus/Streptococcus spp. Have surface proteins (“microbial surface components recognizing adhesive matrix molecules” or MSCRAMMS) that bind fibrin/fibrinectin Macdonald K. Infective endocardit is in dogs: diagnosis and therapy. Vet Cli n North Am Smal l Anim Pract. 2010 10 5. Lesion extension by activation of clotting cascade Bacteria become embedded and trigger→ Tissue factor production Induce platelet aggregation Forms protected environment for bacterial growth Shielded from host defenses, antimicrobial drug penetration Macdonald K. Infective endocardit is in dogs: diagnosis and therapy. Vet Cli n North Am Smal l Anim Pract. 2010 11  Turbulence Trauma Pathogenesis: Endothelial damage Summary Infection Platelet-fibrin deposition Bacteremia Evasion of host defenses Non-bacterial thrombotic Bacteria secrete enzymes that destroy Endocarditis (NBTE) valve/chordal tissue Adherence bacteria Lesion may fragment, releasing into the bloodstream Colonization Immunologic, thrombotic, Bacterial septicreplication complications Fibrin/platelet deposition Mature vegetation 12 Lesion Pathology: Small Animals Almost exclusively mitral and aortic valves (left sided valves) Lesions most often associated with lower-pressure side of valve/lesion 13 Lesion Pathology: Large Animals Cows Horses, pigs, camelids Right sided valves, esp. the tricuspid Left sided valves >>> right sided, can be mural (wall) as well 14 Etiologic Agents: Small Animals Agent ID in only 60% of case Commonly cultured organisms: Dogs Staphylococcal spp. (aureus, intermedius) Streptococcus spp. (canis, bovis) Escherichia coli Bartonella spp. Cats Pasteurella 15  Bartonella Endocarditis is unique Strong predilection for aortic valve (all reported cases) Associated with poorer outcome (more CHF, earlier death) Affected dogs are usually afebrile (only 20% have fever) Difficult to isolate from blood Responsible for up to 20% of cases that are culture negative with routine methods 16 Etiologic Agents– Large Animal Cattle Trueperella pyogenes (~80% of cultures) Streptococcus spp. Escherichia coli Horses Actinobacillus Streptococcus spp. Staphylococcus spp. Pigs Streptococcus Erysipelothrix 17  Cardiac Consequences of IE (Local Disease) Valve leaflet injury → Insufficiency (most common) Bacterial enzymes destroy affected valve Necrosis/perforation leads to valvular regurgitation Volume overload Left heart enlargement CHF (50% of cases) → Obstruction/stenosis Increase cardiac workload (concentric hypertrophy) 18  Cardiac Consequences of IE (Local Disease) Extension of infection into surrounding tissue Atrioventricular/bundle branch blocks Abscess formation Purulent pericarditis Myocarditis Intracardiac perforation Hsue et al. “Aorta-left atrial fistu la secon dary to infective aortic end ocarditis and endarteritis in a cat with valvu lar aortic stenosis” JVC 2021 19  Systemic Consequences (Metastatic Disease) Embolic disease End-organ infarction/ “metastatic infection” Noted in ~84% cases at necropsy Most common sites: kidney (65%), spleen (45%) Increased risk Larger, mobile vegetations (>10-15 mm) Mitral valve involvement 20  Systemic Consequences (Metastatic Disease) Immune-mediated disease Cell-mediated and humoral immune responses → circulating immune complex deposition→ complement activation → inflammatory tissue damage Most common affected: Joints – polyarthritis (IMPA) 30-75% of cases Kidneys – glomerulonephritis (IMGN) 15- 36% of cases Renal failure (up to 33% of cases) Metastatic infection/infarction Glomerulonephritis Septic Shock Rossi F et al. Immune-complex glomerulonephritis in cats: a retrospective study based on clinico-pathological data, histopathology and ultrastructural features. BMC Vet Res 15, 303 (2019). 21  MR Possible History/Clinical Findings Risk Factor: Prior or current infection Immunosuppressive disease or drug history Fever Constitutionally ill AI Palpable joint effusion New heart murmur Ejection murmur Fever, increased flow Stenotic semilunar valve from large vegetation Regurgitant murmur AoV – diastolic, left base MV – systolic, left apex TV – systolic, right apex 22 Possible History/Clinical Findings Lameness Signs of vasculitis (cutaneous hemorrhage, thrombosis) Other possible cardiac findings Tachycardia Hyperkinetic pulses Arrhythmia Signs of CHF Lethargy, weight loss, inappetence, weakness 23 Diagnosis – Lab Findings Complete Blood Cell Count (CBC): variable Leukocytosis (neutrophils and/or monocytes) Anemia Serum Biochemistry: variable Azotemia Elevated globulins Urinalysis: variable Pyuria 24  Modified Duke Criteria: “What is the probability my patient has IE?” Major Criteria Minor Criteria Positive echocardiogram Fever Oscillating, vegetative lesion Presence of predisposing factors: Erosive lesion Medium to large dog (>15 kg) Abscess Subaortic stenosis New valvular insufficiency Evidence of systemic sequelae Thromboembolic disease Immune-mediated disease Positive blood culture in ≥ 2 Polyarthritis samples Glomerulonephritis Positive blood culture not meeting major criteria Bartonella serology ≥1:1024 25  Modified Duke Criteria: “What What is the probability my patient has IE? IE?” Definite Possible Rejected 2 major criteria OR 1 major + 3 minor criteria OR 5 minor criteria 1 major + 1 minor criteria OR 3 minor criteria Firm alternative diagnosis OR Resolution of signs with