Endocarditis

Introduction

Endocarditis isdefined as an infection and resulting inflammation of one or moreof the cardiac valves. It is usually a result of a bacteraemia or pyaemia, spread from adjaent myocardium is rare. It occurs in all species and is more common in cattle, pigs and sheep than dogs and cats.

Bacterial endocarditis. Courtesy of A. Jefferies

Organisms commonly isolated include:

• Cattle: Actinomyces pyogenes
• Pigs: Erysipelothrix spp.
• Sheep: Streptococci.

Pathophysiology

Vegetative Endocarditis

Predisposed by valvular damage as thrombi occur on the surface of the valves exposed to blood flow. Needs sustained or recurrent bacteraemia. Some bacteria have particular adherence properties and may only need a single episode of bacteraemia to set up an endocarditis.

UlcerativeEndocarditis

Vegetative endocarditis (dog). Courtesy of T. Scase

Pathophysiology:

Loose thrombi of platelets and fibrin form which build up to larger vegetations. Bacterial colonies are found within the mass. Attempts to organise the vegetation occur but complete healing very rarely occurs. The mass may become ulcerated. Progression to rupure of the chordae tendinae is possible, along with spread of the infection to the adjacent mural endocardium. Valves may become stenotic, incompetant or both.

Death usually results from either embolisation of the vegetation or congestive heart failure due to significant valvular damage.

Species differences:

• Cattle: predominantly affects the tricuspid valve, perhaps due to bacteria arising in the GI tract and liver. Congestive right sided failure is manifested as ascites (including bottle jaw) and embolisation to the lungs. Anaemia is often present as the red blood cells are damaged as they pass through the vegetation.
• Pig and dog: Lesions occur particularly on the mitral valve, perhaps due to the higher pressure blood flow on the left side of the heart leading to more valvular damage. Left sided heart failure and pulmonary oedema are seen clinically, as are emboli in various organs, particularly the kidney.

Contributing factors include:

• Trauma: haemodynamic turbulence.
• Valve tissue ageing.
• Avascularity of valves; poor healing capacity.
• Tissue exposure; constant contact with blood-borne pathogens.

References

Vegetative endocarditis

Predisposed by valvular damage as thrombi occur on the surface of the valves exposed to blood flow. Needs sustained or recurrent bacteraemia. Some bacteria have particular adherence properties and may only need a single episode of bacteraemia to set up an endocarditis.

Vegetative endocarditis (dog). Courtesy of T. Scase

Pathophysiology:

Loose thrombi of platelets and fibrin form which build up to larger vegetations. Bacterial colonies are found within the mass. Attempts to organise the vegetation occur but complete healing very rarely occurs. The mass may become ulcerated. Progression to rupure of the chordae tendinae is possible, along with spread of the infection to the adjacent mural endocardium. Valves may become stenotic, incompetant or both.

Death usually results from either embolisation of the vegetation or congestive heart failure due to significant valvular damage.

Species differences:

• Cattle: predominantly affects the tricuspid valve, perhaps due to bacteria arising in the GI tract and liver. Congestive right sided failure is manifested as ascites (including bottle jaw) and embolisation to the lungs. Anaemia is often present as the red blood cells are damaged as they pass through the vegetation.
• Pig and dog: Lesions occur particularly on the mitral valve, perhaps due to the higher pressure blood flow on the left side of the heart leading to more valvular damage. Left sided heart failure and pulmonary oedema are seen clinically, as are emboli in various organs, particularly the kidney.

Ulcerative endocarditis

Commonly seen along with renal failure in dogs. Uraemia irritates and damages the endocarium, particularly in the left atrium. Oedema is seen in the sunendocardial tissue with deposition of glycosaminoglycans.

Healing may occur by fibrosis or the lesion may progress to a necrotising endcarditis and, in extreme cases, left atrial rupture. If renal sufficieny is re-established then healing of the endocardial lesion is possible.

from clinical

Infective Endocarditis

Bacterial endocarditis. Courtesy of A. Jefferies

Signalment

Present in small animals:

Dogs: (uncommon); Males & Large Breeds (e.g. German Shepherd) most affected

Cats: (rare)

Present in large animals:

Cattle: (common); Adult cattle

Swine: (very common); Young pigs

Horse: (uncommon); Males more affected

Description

• Infective endocarditis is a bacterial infection of the cardiac endocardium. The infection can affect the valves (valvular endocarditis) and then spread to the heart wall (mural endocarditis).

• Bacteremia is essential for the development of endocarditis. Once bacteria colonize the valvular endocardium, vegetative lesions composed of platelets and fibrin are formed on the valves. Pieces of the vegetative lesions can detach as emboli. Most often these emboli travel to the kidneys and spleen.

Diagnosis

History & Clinical Signs

-Sings of Embolization:

• sudden death
• lameness
• seizure
• arrhythmias
• cold extremities

-Signs of Sepsis:

• Pyrexia
• Neck Pain
• Joint Pain
• Muscle Pain
• Anorexia
• Lethargy

-Signs of Cardiac Involvement:

• Syncope
• Weakness
• Exercise Intolerance
• Heart Failure
• Pulmonary edema
• Pulse deficits

Physical Exam

-Systolic Murmur (Mitral Valve Affected)

-Diastolic Murmur (Aortic Valve Affected)

-Pulmonary crackles (If edema is present)

Laboratory Findings

-Urine analysis

• If UTI is present, could be (+/-) for the same bacteria that caused endocarditis

• Proteinuria

• Casts

• Pyuria

• Hematuria

-Blood Culture

• collect blood from the jugular vein

• 3-4 sterile samples taken 1 hour apart over 24 hours and grown in enhancement media

• Positive culture (Rare)

• Negative culture is not diagnostic

-Blood Profiles:

• Hematology=leukocytosis, neutrophilia, monocytosis, nonregenerative anemia, thrombocytopenia (See with development of: disseminated intravascular coagulation); clotting times may be prolonged

• Biochemistry=hypoalbumenemia, hypoglycemia (if septic), signs of complications from emboli

Radiography

-Usually normal unless severe damage is present

-Left atrial and ventricular enlargement (Mitral Valve Incompetence)

-Right atrial and ventricular enlargement (Aortic Valve Incompetence)

-Signs of congestive heart failure with chronic/severe valve damage

Electrocardiography (ECG)

-Usually normal

-Arrhythmias (especially ventricular premature complexes; AV node damage causes 3rd degree AV block)

Echocardiography

-Vegetative lesions on valves and/ mural surfaces

Treatment

-Antibiotic given I/V for at least five days and then given orally for at least six weeks (Broad Spectrum or Culture/Sensitivity)

-Manage secondary problems:

(e.g. septic shock, congestive heart failure, embolization, D.I.C.)

Prognosis

-Guarded

(Possibility of recurrent infections, embolic complications, congestive heart failure)