Difference between revisions of "Visna-Maedi Virus"

From WikiVet English
Jump to navigation Jump to search
Line 11: Line 11:
 
**Inflammation results in '''demyelination''' with '''subacute meningitis''' around ventricles and choroid plexus
 
**Inflammation results in '''demyelination''' with '''subacute meningitis''' around ventricles and choroid plexus
 
**'''Posterior paresis''' progresses for up to a year until sheep can no longer stand
 
**'''Posterior paresis''' progresses for up to a year until sheep can no longer stand
**For more on joint pathology, see [[Joints Inflammatory - Pathology#In Sheep|here]]
+
**For more on joint pathology, see [[Infectious Arthritis#In Sheep|here]]
 
*Maedi:
 
*Maedi:
 
**Alveolar septa become infiltrated by lymphocytes and macrophages
 
**Alveolar septa become infiltrated by lymphocytes and macrophages

Revision as of 16:30, 3 March 2011



Maedi-Visna

Pathogenesis

  • Primary replication in lung macrophages
  • These then carry infection to brain, lung, udder and/or joints
  • T cells react: Type IV immune complex disease
  • Target organs become chronically inflamed after 2-6 years
  • Visna:
    • Inflammation results in demyelination with subacute meningitis around ventricles and choroid plexus
    • Posterior paresis progresses for up to a year until sheep can no longer stand
    • For more on joint pathology, see here
  • Maedi:
    • Alveolar septa become infiltrated by lymphocytes and macrophages
    • Smooth muscle hypertrophy
    • PM: lungs are heavy, rubbery and do not collapse
  • All result in loss of condition
  • Infected animals remain antibody and virus positive

Epidemiology

  • Transfer via aerosol, milk or colostrum
  • Increased risk in winter housing

Diagnosis

  • Clinical signs
  • Serology: AGDT/ELISA for antibody

Control

  • Seropositive and progeny must be removed from flock
  • Farm can be re-accredited after 2 years of clear tests



  • Caused by a retrovirus
  • The respiratory from of the disease caused by maedi-visna virus (Maedi) is also called lymphoid interstitial pneumonia
  • Transmitted by close contact and via milk
  • The pulmonary lesions develop very slowly hence this disease is uncommon in sheep < 2 years old
  • Increased respiratory rate upon exertion, loss of weight
  • Remains in Monocytes and macrophages
  • Gross findings
    • Severe interstitial pneumonia
    • Lungs fail to collapse properly on opening the chest and can weigh more than twice the normal weight
    • Impressions of the ribs remain on the visceral pleura
    • Lungs are a mottled grey/ tan colour - the lesions can vary from irregular grey speckling to homogeneous grey consolidation
    • Rubbery in consistence
    • Diaphragmatic lobes most affected
    • Associated bronchial and mediastinal lymph nodes are often enlarged
  • Histologically
    • Major features are extensive lymphoid proliferation around perivascular, peribronchial and peribronchiolar sheaths associated with pulmonary lymphatics
    • Many of these areas contain germinal centres and smooth muscle hyperplasia (in walls of terminal bronchioles and alveoli)