Tuberculosis caused by M. bovis (Image sourced from Bristol Biomed Image Archive with permission)


Description

A chronic disease caused by Mycobacterium bovis

Signalment

Diagnosis

Clinical Signs

Laboratory Tests

Radiography

Pathology

Treatment

Prognosis

References

  • Reside primarily within macrophages where they multiply and result in characteristic granulomatous inflammation (macrophages and giant cells, epithelioid cells)
  • Cattle can be infected by inhalation of the organism or through milk
  • The primary complex
    • Describes the initial focus of infection at the portal of entry (lungs) plus involvement of regional lymph nodes
    • 90% of cases exhibit the pulmonary form
    • Grossly:
      • Small tubercles in dorsocaudal subpleural areas which progress to larger confluent areas of caseous necrosis
      • Usually start at bronchio-alveolar junction an progress to the alveoli
      • Caseous lesions, may calcify or be encapsulated
      • Multiple foci may coalesce
      • Ulcers in trachea and bronchi due to coughed up bacteria
      • Spreads into pleura
    • Microscopically:
      • Typical granulomatous inflammation
      • Epitheliod and giant cells at centre of tubercles
        • Macrophages with ingested bacteria, forming epithelioid cells - large vesicular nuclei, abundant pale cytoplasm
        • Giant cells, formed by fusion of macrophages, with multiple nuclei
      • Narrow layer of lymphocytes, mononuclear cells and plasma cells at the periphery of the tubercle
      • With time, peripheral fibroplasia and central necrosis develop
  • If the infection is not contained in the primary complex described above, the mycobacteria can disseminate via lymphatics to other organs and lymph nodes
  • This can allow the development of miliary tuberculosis, i.e. numerous small foci of infection in many organs/ tissues



  • inhalation of Mycobacterium bovis most common via droplets
  • some tubercle bacilli enter the lymph and travel to the bronchial or mediastinal nodes
  • inhaled bacilli reach the alveoli, set up a focus of inflammation
  • phagocytosed by alveolar macrophages
  • two processes may develop if the animal has not encountered the organism before:
- the organism may grow in the phagocytes as intracellular parasites
- produces a nodule of parasitised swollen macrophages known as a tuburculous nodule or a tubercle granuloma
- ultimately, macrophages are killed and infection spreads
- the organism may be broken down and some antigens taken up by the immune system
- cell mediated immune system produces cytotoxic T-lymphocytes
- T-lymphocytes can attack and destroy cells harbouring bacilli
- leads to type IV (delayedd type) hypesensitivity
- 'caseous' or cheesy type of necrosis
- if bacterium destroyed, further infection/disease is prevented

Sequelae

  • chronicity
Tuberculosis pleurisy
  • caseous lymph node ruptures
  • results from extensive tissue necrosis
- if located in lung alveoli, the follicle may rupture into a bronchus, causing spread of the disease to all the other lobules served by that bronchus
- if the ensuing necrosis erodes the wall of a large pulmonary vessel, this ruptures into the lung and a fatal haemoptysis might follow