ISSN 2398-2993      

Myocarditis

obovis

Introduction

  • Inflammatory changes/necrosis of myocytes.
  • Can be focal or diffuse.
  • Cause: various: 
    • Idiopathic
    • Viral (eg BVDV, Foot and Mouth Foot and Mouth etc).
    • Bacterial (eg Histophilus Somni, Clostridium chauvoei).
    • Toxic (Ionophores used as growth promoters; drug reactions etc).
    •  Parasitism (eg Neospora Caninum Neospora Caninum can cause myocarditis, along with other pathology, in the fetus). 
    •  Penetrating foreign body: such as a wire from the reticulum leading to bacterial Myocarditis  
  • Signs: vary depending upon underlying etiology: Dysrhythmias Dysrhythmias frequently seen, reduced exercise tolerance, reduced milk yield, poor growth rates , malaise, Congestive heart failure Congestive heart failure, Sudden death.
  • Diagnosis: very difficult - no pathognomic signs; echocardiography.
  • Treatment: in most cases of extensive myocardial damage or necrosis, treatment is ineffectual and cost prohibitive once clinical signs are apparent.
  • Prognosis: guarded.

Pathogenesis

Etiology

  • Possible relationship between parasitism and eosinophillic myocarditis, but definitive link not proven. The exact cause of EM isn't known.
  •  Bacterial myocarditis can originate from hematogenous spread, but a penetrating foreign body (such as a wire) from the reticulum is a commoncause.
  •  Reactions to drugs and ingested toxins can precipitate myocarditis.

Predisposing factors

General 

  • Immunosuppression.
  • Debility.

Specific

  • Exposure to infectious agent or use of myocardiotoxic substances.

Pathophysiology

  • Inflammation of heart muscle caused by infectious/toxic agent(s) affecting pericardium, myocytes, interstitial or vascular tissue of heart.
  • May be acute or chronic if infectious.
  • Results in cardiac dysfunction.
  • Infection may arise locally or be spread from distant sites, e.g. uterus, lung etc.
  • Infection/toxicity → toxin (local or blood borne)/immune-complex/direct invasion → vasculitis/myocyte damage → myocardial inflammation → cardiac dysfunction = dysrhythmias/CHF.
  • Often concurrent signs of sepsis and SIRS.
  • Damage, inflammation +/- necrosis of myocardium and conduction tissues   →   systolic and diastolic dysfunction and dysrhythmias.

Acute 

  • Direct damage to myocytes or ischemia due to coronary artery occlusion   →   myocardial inflammation and reduced myocardial contractile efficiency.
  • Death/inflammation of myocytes   →   increased automaticity and provokes dysrhythmia.

Chronic

  • Replacement fibrosis and loss of contractile tissue cause progressive systolic and diastolic dysfunction of the myocardium resulting in global compromise of cardiac function and signs of low output heart failure.
  • Ultimately the cardiac remodelling results in a hypocontractile dilated ventricle that mimics dilated cardiomyopathy in other species.

Timecourse

  • May have acute (days), or chronic (months) course.
  • Acute disease may progress to a form of cardiomyopathy and eventually heart failure.

Diagnosis

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Treatment

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Prevention

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Outcomes

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Further Reading

Publications

Refereed Papers

  • Recent references from PubMed and VetMedResource.
  • Wouda W, Snoep J J, Dubey J P (2006) Eosinophilic Myositis due to Sarcocystis hominis in a Beef Cow. J Comp Pathol 135 (4), 249–253 PubMed.
  •  Wessels J, Wessels M E (2005) Histophilus somni myocarditis in a beef rearing calf in the United Kingdom. Vet Rec 157 (14) 420-1 PubMed.
  • Dubey J P, Miller S, Lindsay D S & Topper M J (1990) Neospora caninum-associated myocarditis and encephalitis in an aborted calf. J Vet Diagn Invest 2 (1), 66-69.
  •  Jaspers R (1962) Bovine Eosinophillic MyocarditisIowa State University Veterinarian 25 (2), 7.

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