Pathogeneis

PATHOGENESIS

Lesions

  • Infection is usually by inhalation and ingestion. The mucociliary clearance by mucus and epithelial cilia in the upper respiratory passages provides defense against infection.
  • However, microorganisms on small particles (1-4 μm in size), such as, dust and water droplets reach alveolar spaces.
  • In previously unexposed animals, local multiplication of the mycobacteria occurs and the resistance to phagocytic killing allows continued intra cellular and extra cellular replication.
  • Infected host cells with mycobacteria can reach local lymphnodes and from there may pass to the thoracic duct with general dissemination.
  • After 10-14 days, CMI responses develop and activated macrophages are able to kill some mycobacteria.
  • The aggregation of macrophages contributes to the formation of a tubercle, and a fibrous layer may encompass the lesion.
  • Caseous necrosis due to the cell death and tissue destruction occurs at the center of the lesion and this may proceed to calcification or liquefaction.
  • Once CMI is established, the lymphatic spread is retarded but occurs via the erosion of bronchi or blood vessels to new area.
  • Haematogenous spread may produce miliary tuberculosis (in deer). This involves multifocal tubercle formation in an organ.
Last modified: Monday, 4 June 2012, 5:00 AM