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Created page with '===Bovine tuberculosis=== *Epidemiology **World-wide disease caused by ''M. bovis'' **Aerosol transmission between cattle kept in close contact **Transmission to calves via inge…'
===Bovine tuberculosis===
*Epidemiology
**World-wide disease caused by ''M. bovis''
**Aerosol transmission between cattle kept in close contact
**Transmission to calves via ingestion od contaminated milk
**Wildlife reservoirs include badgers and possibly deer in the Europe
*Pathogenesis and pathogenicity
**The ability of mycobacteria to survive and multiply within macrophages determines whether disease will occur within the host
**Survival and multiplication in macrophages at primary site of infection due to prevention of phagosome-lysosome fusion
**Mycobacteria utilize several virulence factors including cord factor or trehalose dimycolate, surface glycolipid, sulfatides, lipoarabinomannan, heteropolysaccharide, heat shock protein, complement, and tubuloprotein
**The types of immune responses that are critical in responding to mycobacterial infection are cell-mediated immunity and the delayed hypersensitivity response
**Pathogenicity of mycobacteria depends on their ability to escape phagocytic killing, mostly imparted by the cell wall consitiutents:
***Cord factor (trehalose dimycolate) – surface glycolipid responsible for serpentine growth in vitro
***Suphatides – surface glycolipid containing sulphur which prevents fusion of phagosome with lysosome. cAMP secreted by the bacteria may also facilitate this.
***LAM – heteropolysaccharide which inhibits macrophage activation by IFNγ and induces macrophages to secrete TNFα which induces fever and IL-10 which suppresses mycobacteria-induced T cell proliferation
***The wax of the cell wall, peptidoglycans and other glycolipids are responsible for the adjuvant activity – attracts antigen presenting cells
***Tubuloprotein – important antigen; purified tubuloprotein is the basis of the tuberculin test
**Mycobacteria are released from macrophages and also migrate within macrophages around the body
**Waxy cell wall contributes to the host immune response to the mycobacteria and the development of lesions
**Cell-mediated immune response with activated macrophages and sensitised T cells
**Delayed-type hypersensitivity response with granuloma formation
**Lesions contain macrophages, multinucleate giant cells and later a central area of caseous necrosis, giving a cheesy appearance
*Clinical signs
**Initially asymptomatic
**Loss of condition
**Cough and intermittent pyrexia with lung pathology
**Tuberculous mastitis with transmission via milk
*Diagnosis
**Tuberculin test - comparative intradermal test
**Avian and bovine tuberculin (purified protein derivative) is injected intradermally into two different clipped sites on the side of the neck
**Skin thickness at these sites is compared before and 72 hours after the injection of tuberculin with calipers
**Increases in skin thickness at the bovine PPD site of more than 4mm greater than the avian PPD site are seen as positive (reactor)
**Blood tests including the gamma interferon assay are being developed
**Laboratory examination of lesions, lymph nodes and milk
**Ziehl-Neelson staining of tissues
**Isolation requires Lowenstein-Jensen medium
*Control
**Eradication programs using a test and slaughter policy
**Reactors positive to the tuberculin test are slaughtered and restrictions applied to the affected herd
[[Category:Mycobacterium species]][[Category:Cattle]]
*Epidemiology
**World-wide disease caused by ''M. bovis''
**Aerosol transmission between cattle kept in close contact
**Transmission to calves via ingestion od contaminated milk
**Wildlife reservoirs include badgers and possibly deer in the Europe
*Pathogenesis and pathogenicity
**The ability of mycobacteria to survive and multiply within macrophages determines whether disease will occur within the host
**Survival and multiplication in macrophages at primary site of infection due to prevention of phagosome-lysosome fusion
**Mycobacteria utilize several virulence factors including cord factor or trehalose dimycolate, surface glycolipid, sulfatides, lipoarabinomannan, heteropolysaccharide, heat shock protein, complement, and tubuloprotein
**The types of immune responses that are critical in responding to mycobacterial infection are cell-mediated immunity and the delayed hypersensitivity response
**Pathogenicity of mycobacteria depends on their ability to escape phagocytic killing, mostly imparted by the cell wall consitiutents:
***Cord factor (trehalose dimycolate) – surface glycolipid responsible for serpentine growth in vitro
***Suphatides – surface glycolipid containing sulphur which prevents fusion of phagosome with lysosome. cAMP secreted by the bacteria may also facilitate this.
***LAM – heteropolysaccharide which inhibits macrophage activation by IFNγ and induces macrophages to secrete TNFα which induces fever and IL-10 which suppresses mycobacteria-induced T cell proliferation
***The wax of the cell wall, peptidoglycans and other glycolipids are responsible for the adjuvant activity – attracts antigen presenting cells
***Tubuloprotein – important antigen; purified tubuloprotein is the basis of the tuberculin test
**Mycobacteria are released from macrophages and also migrate within macrophages around the body
**Waxy cell wall contributes to the host immune response to the mycobacteria and the development of lesions
**Cell-mediated immune response with activated macrophages and sensitised T cells
**Delayed-type hypersensitivity response with granuloma formation
**Lesions contain macrophages, multinucleate giant cells and later a central area of caseous necrosis, giving a cheesy appearance
*Clinical signs
**Initially asymptomatic
**Loss of condition
**Cough and intermittent pyrexia with lung pathology
**Tuberculous mastitis with transmission via milk
*Diagnosis
**Tuberculin test - comparative intradermal test
**Avian and bovine tuberculin (purified protein derivative) is injected intradermally into two different clipped sites on the side of the neck
**Skin thickness at these sites is compared before and 72 hours after the injection of tuberculin with calipers
**Increases in skin thickness at the bovine PPD site of more than 4mm greater than the avian PPD site are seen as positive (reactor)
**Blood tests including the gamma interferon assay are being developed
**Laboratory examination of lesions, lymph nodes and milk
**Ziehl-Neelson staining of tissues
**Isolation requires Lowenstein-Jensen medium
*Control
**Eradication programs using a test and slaughter policy
**Reactors positive to the tuberculin test are slaughtered and restrictions applied to the affected herd
[[Category:Mycobacterium species]][[Category:Cattle]]