The Hydropericardium Syndrome and Inclusion Body Hepatitis in Domestic Fowl SpringerLink

hydropericardium

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Hydropericardium

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Contents

  • 1 Introduction
  • 2 Clinical Signs
  • 3 Diagnosis
  • 4 Treatment
  • 5 Prognosis
  • 6 References

Introduction

This is a condition where excessive fluid accumulates in the pericardial cavity.

Fluid accumulation within the pericardial sac may lead to fibrous thickening and opacity of the pericardium if prolonged. Villous proliferation of the serosa will occur due to the irritation caused by the presence of the fluid.

Large volumes of fluid within the pericardial sac may cause cardiac tamponade, a compression of the heart. Side effects associated with the build up of fluid, such as degrees of embarrassment of the function of the heart, depend on the length of time build up of the fluid occurs.

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Serous transudate can be seen in the pericardial sac due to congestive heart failure. This will cause a low cellular and high protein content in the fluid. Other conditions producing transudate in the pericardial sac of this consistency include neoplasia such as heart base tumours or secondary metastasis to the pericardium. Other debilitating diseases can also contribute to this.

A serous transudate with a high cell and protein count may be caused by an acute toxaemia or by Mulberry Heart disease and Gut Oedema of pigs. As these disease cause damage to the endothelium, the fluid containing cells of the endothelium demonstrates just how severe the disease has been. There may also be fibrinous clots within the pericardial sac.

Clinical Signs

If fluid build up is slow, then signs will include gradually worsening right sided heart failure, due to compression of the heart, the right ventricle will compress causing right sided failure. Signs will include ascites, hepatomegaly, jugular distension, jugular pulses and lethargy. If fluid build up is sudden e.g. in toxaemias, then the only clinical sign may be sudden death.

Diagnosis

History and clinical signs can be characteristic of the disease and may lead to a presumptive diagnosis.

Diagnostic imaging can be performed. An ultrasound can show fluid surrounding the heart and the presence of fibrinous clots if any exist. It can also show compression of the right ventricle. Radiography may show an enlarged cardiac silhouette, which is suggestive of a pericardial disease and fluid lines may be seen within the pericardial sac.

Pericardiocentesis can be performed to demonstrate the type of fluid in the pericardium so as to aid diagnosis.

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Treatment

The only effective way to treat animals with pericardial effusions is pericardiocentesis. This will relieve clinical signs even when only one third of the fluid is drained. This requires ECG monitoring throughout and for it to be ultrasound guided if possible.

In cases of recurrent pericardial effusion, a pericardectomy can be performed as a palliative measure to reduce the amount of recurrence.

Prognosis

This is dependent on the cause of the hydropericardium. If neoplastic then prognosis is guarded. If due to heart failure, medical treatment of this is important.

Hydropericardium syndrome: current state and future developments

Affiliation

  • 1 Department of Molecular Biology and Genetic Engineering, G. B.P.U.A. & T., Pantnagar, Uttarakhand, India. manubt07@gmail.com
  • PMID: 23242777
  • DOI: 10.1007/s00705-012-1570-x

Hydropericardium syndrome: current state and future developments

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Authors

Affiliation

  • 1 Department of Molecular Biology and Genetic Engineering, G. B.P.U.A. & T., Pantnagar, Uttarakhand, India. manubt07@gmail.com
  • PMID: 23242777
  • DOI: 10.1007/s00705-012-1570-x

Abstract

Hydropericardium syndrome (HPS) is a highly infectious disease caused by fowl adenovirus serotype 4 (FAV-4) affecting poultry, especially broiler birds. The disease was initially reported from Angara Goth, Pakistan, and then from India during 1994, in the poultry belt of Jammu and Kashmir, and thereafter, from almost all parts of the country, causing heavy economic losses to the poultry industry. The disease occurs predominantly in broilers of the age group of 3-5 weeks, characterized by sudden onset of high mortality up to 80 %. The causative agent of HPS is fowl adenovirus 4, which is a member of the species Fowl Adenovirus C, genus Aviadenovirus, family Adenoviridae [60]. FAV-4 is non-enveloped and icosahedral in shape, measuring 70-90 nm in size and containing a linear dsDNA of approximately 45 kb in size as its genome. The livers of affected birds show necrotic foci and basophilic intranuclear inclusion bodies in the hepatocytes. The disease can be diagnosed from its gross and microscopic changes in the liver and by various serological tests, such as agar gel immunodiffusion, counterimmunoelectrophoresis, indirect haemagglutination, fluorescent antibody techniques, and ELISA. In the past few years, PCR has been used as a rapid diagnostic tool for the detection of fowl adenoviruses. The disease has been brought under control by the use of formalin-inactivated, attenuated or live vaccines in experimentally infected birds. Advancement in the field of computational immunology accelerates knowledge acquisition and simultaneously reduces the time and effort involved in screening potential epitopes, leading toward the development of epitope-based vaccines.

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