Graaff-Reinet disease - Maedi-Visna
By Dr Mackie Hobson BSc(Agric),BVSc

Tuesday, 18th April 2017

Maedi-visna or also called Ovine Progressive Pneumonia or Graaff-Reinet disease.

South Africa was thought to be free of the disease until the virus was isolated from sheep in 1986.

Serological survey of sheep after diagnosis in 1986 found a significant prevalence of the virus but it had appeared to have lost its pathogenicity. The virus had not been isolated from Angora goats in South Africa before.


In April 2016 a case of pneumonia in Angora goats was investigated by the SAMGA vet in the Murraysburg district. A diagnosis suggestive of Ovine pneumonia (Maedia or Graaff-Reinet disease) was made by Dr W.Botha by histopathological examination of samples sent to Idexx laboratory.

The Angora goat flock was subsequently serologically tested (n=200) and no positive cases were identified.

There are two most common causes of the disease

  • Dyspnoea (difficult breathing) due to the progressive pneumonia
  • Wasting due to the chronic encephalitic form

The mastitis and arthritis form of the disease is rarely seen.


                               Lungs of the Angora goat Post Mortem in April 2016


How is the virus transmitted?


Transmission occurs under conditions of close contact. Droplet infection via the respiratory route is the most likely route of transmission.

Transmission via the colostrum has also been demonstrated and transmission by blood sucking insects could be possible?

The virus is able to persist latently and infected animals are carriers for life.


What are the clinical signs?


Often the disease has a slow onset (usually seen in animals 3-4 years old)

  • Loss of condition
  • Dyspnoea (difficult breathing) following exercise
  • A dry cough may develop without any nasal discharge
  • Secondary bacterial pneumonia, often associated with Pasteurella is commonly the cause of death. The animal usually dies 6-12 months after the first clinical signs

The nervous form is less common

  • Unsteady gait, especially the hind limbs resulting in stumbling and falling.
  • Trembling of facial muscles
  • Inability to extend the fetlock
  • Gradual progression to paresis and eventual paralysis
  • Swollen joints and mastitis have been reported in sheep.

The clinical signs may last a year and once seen there is no recovery

Post Mortem Findings


  • In advanced cases the lungs do not collapse when the thoracic cavity is opened and impression of the ribs may be maintained.
  • Enlarged (may be 2-4 times their normal weight)
  • Firm rubbery consistency
  • Greyish in colour and the cut surface is dry
  • Secondary bacterial pneumonia may be present
  • Bronchial and mediastinal lymph nodes enlarged (whitish colour on cut surface)



  • Thickening of alveolar septa (infiltration of lymphocytes, monocytes and hyperplasia of smooth muscle). This leads to obliteration of the alveoli.
  • Perivascular, peribronchial lymphoid hyperplasia
  • Transformation of alveolar epithelial cells to cuboidal cells can be confused with jaagsiekte.
  • Intra-alveolar exudate is inconspicuous and consists of macrophages and debris




Diagnosis is based on

  • Clinical signs and serology
  • Confirmation through histopathology


There is no treatment and the condition is fatal. No treatment

How does the virus remain in a carrier state?

The primary target cells for the virus are leukocytes- monocytes. After the initial infection the host mounts an immune response which eliminated cell free virus but can’t destroy infected cells. The virus then remains in infected cells and in this form the virus can spread to all tissues of the body.


Test and slaughter out policy has been followed in the past.

Dr Mackie Hobson



Maedi-visna (D.Verwoerd, R.Tustin and A-l Williamson. Infectious Diseases of Livestock.

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