Difference between revisions of "Endocarditis"
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==Introduction== | ==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. | |
− | 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 | + | |
+ | [[Image:Bacterial endocarditis.jpg|right|thumb|125px|<small><center>'''Bacterial endocarditis'''. Courtesy of A. Jefferies</center></small>]] | ||
Organisms commonly isolated include: | Organisms commonly isolated include: | ||
− | *Cattle: | + | *Cattle: [[Actinomyces pyogenes]] |
− | *Pigs: [[Erysipelothrix_rhusiopathiae| | + | *Pigs: [[Erysipelothrix_rhusiopathiae|Erysipelothrix spp.]] |
− | *Sheep: [[:Category:Streptococcus species| | + | *Sheep: [[:Category:Streptococcus species|Streptococci.]] |
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==Pathophysiology== | ==Pathophysiology== | ||
===Vegetative Endocarditis=== | ===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. | |
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− | === | + | [[Image:vegetative endocarditis.jpg|right|thumb|125px|<small><center>'''Vegetative endocarditis (dog)'''. Courtesy of T. Scase</center></small>]] |
− | Commonly seen along with renal failure in dogs. | + | |
+ | ===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== | ==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. | |
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==Signalment== | ==Signalment== | ||
− | Endocarditis is rare in dogs but males and large breeds (e.g. | + | 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 | + | 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: |
− | Clinical signs are often vague and rarely referable to congestive heart failure. The | + | * Pyrexia |
− | *Pyrexia | ||
*Lameness | *Lameness | ||
*Neck Pain | *Neck Pain | ||
− | *Lethargy/ | + | *Lethargy/Anoexia |
*Weight loss | *Weight loss | ||
*Epistaxis | *Epistaxis | ||
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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) | 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) | ||
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==Physical examination== | ==Physical examination== | ||
− | A variable murmur depending upon the valve affected. It may be noted that murmur has recently arisen or changed. Other | + | 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== | ==Diagnosis== | ||
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===Laboratory findings=== | ===Laboratory findings=== | ||
'''Blood profiles''': Not all cases will have altered blood changes. Possible changes include: | '''Blood profiles''': Not all cases will have altered blood changes. Possible changes include: | ||
− | ::Haematology - | + | ::Haematology - Neutrophilia, left shift, monocytosis, Thrombocytopaenia and prolonged clotting times if developing D.I.C. |
− | ::Biochemistry - | + | ::Biochemistry - Hypoalbuminaemia and hypoglycaemia. |
− | '''Urinalysis''' : may have proteinuria, casts, pyuria. A | + | '''Urinalysis''' : may have proteinuria, casts, pyuria. A uniary tract infection may be present with the same organism as is responsible for the endocarditis. |
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+ | '''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. | ||
===Echocardiography=== | ===Echocardiography=== | ||
− | Structural abnormalities and vegetations may be visible on the valves although it is difficult to | + | Structural abnormalities and vegetations may be visible on the valves although it is difficult to differentate from [[endocardiosis]]. |
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===Radiography=== | ===Radiography=== | ||
Radiography is often unremarkable. There may be evidence of cardiomegaly or congestive heart failure if valvular damage is chronic or severe. Evidence of a focus of infection such as discospondylitis may be visible. | Radiography is often unremarkable. There may be evidence of cardiomegaly or congestive heart failure if valvular damage is chronic or severe. Evidence of a focus of infection such as discospondylitis may be visible. | ||
− | + | ===Electrogcardiogram (ECG)=== | |
− | === | + | ECG may be normal. Arrhythmias detectected are often ventricular in origin (e.g. ventricular premature complexes) and represent extension fo the inflammatory focus to invlove the moycoardium. 3rd degree heart block may be present if the AV node is affected. |
− | ECG may be normal. Arrhythmias detectected are often ventricular in origin (e.g. ventricular premature complexes) and represent extension | ||
==Treatment== | ==Treatment== | ||
− | Antibiotic treatment with either a broad spectrum antibiotic or an appropriate antibiotic based on | + | Antibiotic treatment with either a broad spectrum antibiotic or an appropriate antibiotic based on cultre and sensitivity results. Antibiotics should be administered intravenously for the first 5 days of therapy followed by a proloned course (>4 weeks) of oral medication. |
− | + | Common Protocols use Ampicillin in combination with fluoroqunilone such as enrofloxacin. | |
− | + | Secondary problems such as septic shock, D.I.C., congestive heart failure and embolisation need to be managed. | |
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==Prognosis== | ==Prognosis== | ||
− | Long term prognosis is guarded to poor. Possible complications include septic shock, | + | Long term prognosis is guarded to poor. Possible complications include septic shock, Disseminated Intravascular coagulation, congestive heart failure and embolisation to other organs. |
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==References== | ==References== | ||
− | Merck & Co (2008) '''The Merck Veterinary Manual (Eighth Edition)''' ''Merial'' | + | * Merck & Co (2008) '''The Merck Veterinary Manual (Eighth Edition)''' ''Merial'' |
− | + | * Nelson, R.W. and Couto, C.G. (2009) '''Small Animal Internal Medicine (Fourth Edition)''' ''Mosby Elsevier''. | |
− | Nelson, R.W. and Couto, C.G. (2009) '''Small Animal Internal Medicine (Fourth Edition)''' ''Mosby Elsevier''. | + | * Tilley,L.P., Smith, F.W.K, Oyama, M., Sleeper, M. (2007) '''Manual of Canine and Feline Cardiology''' ''Saunders''. |
− | + | * Elwood, C.M., Cobb, M.A., Stepien, R.L., (1993) Clinical and echocardiographic findings in 10 dogs with vegetative bacteria endcarditis. '''Journal of small animal practice'''. 34, pp420-427. | |
− | Tilley,L.P., Smith, F.W.K, Oyama, M., Sleeper, M. (2007) '''Manual of Canine and Feline Cardiology''' ''Saunders''. | ||
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− | Elwood, C.M., Cobb, M.A., Stepien, R.L., (1993) Clinical and echocardiographic findings in 10 dogs with vegetative bacteria endcarditis. '''Journal of small animal practice'''. 34, pp420-427. | ||
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− | [[Category:Endocardial_Pathology]][[Category:Cardiovascular_System_-_Inflammatory_Pathology]][[Category: | + | [[Category:Endocardial_Pathology]][[Category:Cardiovascular_System_-_Inflammatory_Pathology]][[Category:Cattle]][[Category:Pig]][[Category:Sheep]] |
− | [[Category: | + | [[Category:To_Do_-_Review]] |
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Revision as of 15:16, 16 November 2010
This article is still under construction. |
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.
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.
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.
Echocardiography
Structural abnormalities and vegetations may be visible on the valves although it is difficult to differentate from endocardiosis.
Radiography
Radiography is often unremarkable. There may be evidence of cardiomegaly or congestive heart failure if valvular damage is chronic or severe. Evidence of a focus of infection such as discospondylitis may be visible.
Electrogcardiogram (ECG)
ECG may be normal. Arrhythmias detectected are often ventricular in origin (e.g. ventricular premature complexes) and represent extension fo the inflammatory focus to invlove the moycoardium. 3rd degree heart block may be present if the AV node is affected.
Treatment
Antibiotic treatment with either a broad spectrum antibiotic or an appropriate antibiotic based on cultre and sensitivity results. Antibiotics should be administered intravenously for the first 5 days of therapy followed by a proloned course (>4 weeks) of oral medication. Common Protocols use Ampicillin in combination with fluoroqunilone such as enrofloxacin. Secondary problems such as septic shock, D.I.C., congestive heart failure and embolisation need to be managed.
Prognosis
Long term prognosis is guarded to poor. Possible complications include septic shock, Disseminated Intravascular coagulation, congestive heart failure and embolisation to other organs.
References
- Merck & Co (2008) The Merck Veterinary Manual (Eighth Edition) Merial
- Nelson, R.W. and Couto, C.G. (2009) Small Animal Internal Medicine (Fourth Edition) Mosby Elsevier.
- Tilley,L.P., Smith, F.W.K, Oyama, M., Sleeper, M. (2007) Manual of Canine and Feline Cardiology Saunders.
- Elwood, C.M., Cobb, M.A., Stepien, R.L., (1993) Clinical and echocardiographic findings in 10 dogs with vegetative bacteria endcarditis. Journal of small animal practice. 34, pp420-427.