Bacterial endocarditis

By | 2013-08-05

Bacterial endocarditis is an acute or, more commonly, a subacute condition characterized by the formation of septic vegetative thrombi on the valves and / or mural endocardium. Thrombus formation most frequently involves the mitral or aortic valves and the highest incidence occurs in large breed, male dogs older than four years of age. The German shepherd breed appears predisposed. The pathogens most frequently isolated include Streptococcus sp,, Staphylococcus aurecus, Escherichia coli, Pseudomonas aeruginosa, Corynebacterium sp., Aerobacter acrogenes and Erysipelothrix rhusiopathiae.

Pathogenesis

Numerous predisposing factors have been implicated in the pathogenesis of valvular bacterial endocarditis. First, the valve must be damaged, for example by the turbulent blood flow associated with a congenital cardiac defect. Bacterial endocarditis involving the aortic valve has been reported in association with subaortic stenosis. The stenosis leads to ‘jetting’ of blood through the aortic valve which damages the valve leaflets and may eventually result in a degree of aortic regurgitation. Secondly, transient bacteraemiec episodes are presumably necessary to infect the sterile thrombi which form initially. The source of infection in many cases is speculative; infections involving the gastrointestinal tract, skin, lung, urogenital tract, oral cavity, bone and subcutaneous abscesses have been implicated in the pathogenesis as have other factors such as indwelling intravenous catheters, previous surgery and immunosuppressive drug therapy. The vegetations which form on the valves are friable and tend to form emboli. The lesions also alter valve structure and function and may result in mitral and / or aortic regurgitation which may lead ultimately to signs of congestive heart failure.

Clinical signs

The clinical manifestations of bacterial endocarditis reflect (1) altered valve function, (2) bacteraemia, (3) the dissemination of septic emboli with subsequent infarction and localization of infection in joints, kidneys, muscle, myocardium, lungs and central nervous system (CNS) tissue, and (4) the host immune response which may result in immune complex deposition in synovial membranes and glomeruli.

The clinical signs vary depending on which organs are involved. Typically the animal may present with rather non-specific signs (for example anorexia, lethargy, weight loss) in association with a fever. The pyrexie episodes are often intermittent and may last for several days before appearing to resolve spontaneously. Bacterial endocarditis should be considered as a differential diagnosis in an animal which presents with a history of recurrent pyrexia in the absence of more specific localizing signs.

Cardiac signs

A heart murmur may be present although this may develop late in the course of the disease. The murmur may be systolic if the mitral valve is involved or diastolic if due to aortic insufficiency. Embolization of the coronary blood supply leading to myocardial infarction or myocarditis may result in dysrhythmias (particularly ventricular dysrhythmias) or atrioventricular block. Some eases may develop cardiomcgaly and signs of left-sided congestive heart failure.

Extracardiac signs

Extracardiac signs include lethargy, anorexia, pyrexia due to transient, bacteraemic thxomboembolic episodes, lameness, muscle stiffness, petechial or ecchymotic haemorrhages due to thrombocytopenia, dyspnoea and seizures. Direct extension of the infection to one or more joints may result in a septic polyarthritis or prolonged antigenic stimulation may lead to immune complex deposition in the synovial membranes and the development of a non-septic (non-erosive) immune-mediated polyarthropathy.

Many of the clinical signs associated with bacterial endocarditis mimic those of systemic lupus erythematosus or the immune-mediated polyarthropathics since not only may the joints be involved but some animals test positive for anti-red cell, antiplatelet or antinuclcar antibodies.

Diagnosis of Bacterial endocarditis

Ante-mortem diagnosis is often difficult particularly if a cardiac murmur is not present.

Full haematolopical examination and complete biochemical screen.

A mild to moderate non-regenerative anaemia, neutrophilia with or without a left shift, and monocytosis may be evident. The anaemia may be attributed to the chronic inflammatory response; in a few cases there may be an immune-mediated component. Systemic thromboembolism may result in impaired renal function and / or liver damage or dysfunction. Increased alkaline phosphatase (ALP) activity, hypoglycaemia and hypoalbuminaemia are common findings in bacteraemic dogs.

Urine analysis and bacteriology

Urinary tract infections, including those originating in the prostate gland, are a potential source of blood-borne infection. Bacteraemia is often associated with bacteriuria hence a urine sample, preferably one obtained by cystocentesis, should be submitted for routine analysis and bacteriological culture / sensitivity.

Radiographic findings

Thoracic radiographs are often uninformative. Signs of congestive heart failure with left atrial and left ventricular enlargement and possibly pulmonary oedema may be evident in some dogs during the terminal stages of the disease.

Echocardiography

Echocardiography is the most useful and reliable technique for confirming a diagnosis of bacterial endocarditis ante-mortem. Moderate-sized vegetations can be visualized on the heart valves or mural endocardium.

Blood cultures

Bacteraemia in dogs with endocarditis is usually continuous. The timing of the blood cultures is less important and culturing blood during febrile episodes does not increase the frequency of positive results in dogs with endocarditis. Bacterial isolation rates between 50 and 80% have been reported. A negative blood culture does not preclude a diagnosis of bacterial endocarditis and repeated negative results have been reported in confirmed cases. In order to maximize the chances of obtaining a positive culture 2-3 blood samples should be collected, preferably at least one hour apart, over a 24 h period. Each blood sample should be collected from a different vein (jugular or cephalic) using standard aseptic technique. To minimize the risk of contamination a fresh needle should be attached to the syringe before the blood is transferred to the appropriate culture medium. Each sample should be submitted for aerobic and anaerobic culture. If possible, antibiotics should be discontinued at least 2 days beforehand since they may delay bacterial growth.

Synovial aspirates

Multiple joint taps should be obtained from animals with suspected joint involvement, that is those showing signs of shifting lameness. Synovial fluid should be submitted in EDTA for protein concentration and cytology, and in a sterile plain glass tube bacteriology.

Immunological screening tests

Some cases of bacterial endocarditis test positive for anti-red cell, anriplatelct and antinuclear anti-bodies making differentiation from SLH difficult.

Treatment of Bacterial endocarditis

The prognosis for subacute bacterial endocarditis is guarded. Bactericidal antibiotics should be administered for a minimum of 4-6 weeks (parenterally for the first two weeks and thereafter by the oral route) at doses well above the minimum inhibitory concentration. The choice of antibiotic ideally should be based on the blood culture results. Pending these results or in cases where the results are negative but bacterial endocarditis is either suspected or has been diagnosed, a combination of broad spectrum antibiotics should be given. A standard protocol is as follows.

Ampicillin (20-40 mg kg-1 body weight TID) and gentamycin (2 mg kg-1 body weight TID) in combination should be given intravenously for at least the first 5-10 days.

Thereafter, ampillin or cephalexin (20 mg kg-1 bodyweight) can be given orally for a further 2-4 weeks. Additional treatment for congestive heart failure should be given as appropriate.