Endocarditis

Introduction

Endocarditis is defined as an inflammation of the cardiac endocardium. The infection can affect the valves (valvular endocarditis) and then spread to the heart wall (mural endocarditis). 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. 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. Progression to rupture 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 vegetative material or congestive heart failure due to significant valvular damage.

Vegetative endocarditis (dog). Courtesy of T. Scase

UlcerativeEndocarditis

Commonly seen along with renal failure in dogs.Uraemia irritates and damages the endocarium, particularly in the left atrium. Oedema is seen in the subendocardial tissue with deposition of glycosaminoglycans. This may progress to a necrotising endocarditis and, in extreme cases, left atrial rupture. If renal sufficieny is re-established then healing of the endocardial lesion is possible.

Species differences

• Cattle: predominantly affects the tricuspid valve, perhaps due to bacteria arising in the GI tract and liver. COmmon underlying causes include Liver abcesses, traumatic reticulitis, metritis, mastitis, navel ancesses and 'joint ill'. 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.
• Horse: Lesions occur mainly on the mitral valve. The site of sepsis is often not identified but may be a sequale to septic jugular thrombophlembitis.
• Pig and dog: Lesions occur particularly on the mitral valve (71% of cases in dogs), 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.

Signalment

Endocarditis is rare in dogs but males and large breeds (e.g. german Shepherds) are most affected. Very rare in cats. The disease mainly affects adult cattle and young pigs. In Horses, males are more comonly affected than females.

Histroy & Clinical Signs

Clinical signs are often vague and rarely referable to congestive heart failure. The folowing clinical signs are seen related to sepsis:

• Pyrexia
• Lameness
• Neck Pain
• Lethargy/Anoexia
• Weight loss
• Epistaxis

Signs of embolisation to other organs may also be seen and those of congestive heart failure (dyspnoea, poor pulses, pale mucous membranes, tacchycardia, pulmonary crackles)

Physical examination

A variable murmur depending upon the valve affected. It may be noted that murmur has recently arisen or changed. Other clincial examination findings include joint effusions, lymphadenopathy, pyrexia and in advanced cases signs associated with disseinated intravascular coagulopathy (D.I.C) such as bleeding diathesis and petichiation.

Diagnosis

Laboratory findings

Blood profiles: Not all cases will have altered blood changes. Possible changes include:

Haematology - Neutrophilia, left shift, monocytosis, Thrombocytopaenia and prolonged clotting times if developing D.I.C.

Biochemistry - Hypoalbuminaemia and hypoglycaemia.

Urinalysis : may have proteinuria, casts, pyuria. A uniary tract infection may be present with the same organism as is responsible for the endocarditis. Blood cultures : Requires 3-4 sterile samples colected from the jugular vein at least 1 hour apart over a 24 hour period. Negative cultures do not rule out the possibility of bacerial endocarditis.

from clinical

Bacterial endocarditis. Courtesy of A. Jefferies

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)