ISSN 2398-2993       Transformation '' not found.

Mycobacterium spp


Veronica Fowler

Tammy Hassel




  • Kingdom: bacteria.
  • Phylum: actinobacteria.
  • Order: actinomycetales.
  • Suborder: corynebacterineae.
  • Family: mycobacteriaceae.
  • Genus: mycobacterium.


  • Gk, myco- fungus (alluding to the way mycobacteria have been observed to grow in a mold-like fashion); bakterion, small rod.

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Clinical Effects



  • Found in soils, on vegetation and water. The pathogenic species are shed from infectious animals.
  • Because of lipid-rich walls, mycobacteria are highly resistant to environmental challenges.
  • Tubercle bacilli are obtained from infected individuals: eg humans with M. tuberculosis Mycobacterium tuberculosis, cattle and wildlife with M. bovis Mycobacterium bovis, and birds with M. avium.
  • Non-tuberculous mycobacteria are saprophytic, but some are commensals in various animal species.
  • M. bovis may survive on pasture for ≥2 mo, and M. avium may survive in soil for ≥4 yr.


  • Multiplication occurs both intracellularly in macrophages and extracellularly.
  • The organism is able to survive in phagosomes and inhibit phagosome-lysosome fusion.


  • Infection in cattle is usually contracted from direct contact and via contaminated feed or water.
  • By aerosols or fomites - mainly from respiratory discharges from infected animals. Can also be transmitted by milk, discharging lesions, saliva and urine.
  • M. tuberculosis Mycobacterium tuberculosis can be transmitted from humans to cattle.
  • M. bovis Mycobacterium bovis can be transmitted from cattle to humans.

Pathological effects

  • The organism gains access to the body, usually via the respiratory tract or digestive tract, and avoids initial killing by host phagocytes.
  • The subsequent lesions produced are in part due to the cell-mediated immune response which is generated after the infection has become established.
  • Acquired resistance depends on cell-mediated responses.
  • Role of antibodies in providing natural protection against mycobacterial infections is not fully understood.
  • The virulence of the organism is partly due to the lipids of the cell wall, which protect the bacilli from phagocytosis.
  • Initially, the organism proliferates and lymphatic spread may occur at this stage. Acute or sub acute inflammation occurs with polymorphonuclear infiltration.
  • After delayed hypersensitivity develops, granulomatous inflammation supervenes and the mycobacteri-macrophages become elongated and are concentrically arranged to form a tubercle.
  • Outside these epithelioid cells a fibrous layer builds up and caseous necrosis occurs at the center of the lesion.
  • Liquefaction of the caseous lesion occurs and a cavity develops in which further proliferation of the organism takes place.
  • Further spread may occur via the erosion of bronchi or viscera to new areas or via the bloodstream.

Other Host Effects

  • Some non-tuberculous bacteria are commensals.


Control via animal

  • Routine skin testing (M.bovis Mycobacterium bovis).
  • Slaughter of cattle (M.bovis Mycobacterium bovis; M. paratuberculosis Mycobacterium paratuberculosis).
  • Development of Johne's disease Johne's disease is acquired by calves through ingestion of organisms shed in the feces or colostrum Colostrum of infected animals. Feeding of pooled colostrum is therefore considered a risk factor.
  • Inactivated adjuvanted or live vaccines are available for vaccination against Johnes disease.

Control via chemotherapies

  • Mycobacteria are resistant to most antimicrobials because of the high lipid content and complexity of their cell walls, together with their ability to reside within macrophages.
  • First-line drugs for tuberculosis therapy are isoniazid, pyrazinamide, ethambutol and rifampicin.
  • Second-line drugs include Streptomycin Streptomycin, against which resistance is now common, rifapentine, kanamycin/amikacin, capreomycin and fluoroquinolones.
  • Combinations of drugs are usually used because resistance often develops under a single-drug regime.
  • Long-term therapy is required to effect a cure and eliminate the organism (9-24 months).
  • Short or incomplete courses of therapy are an important cause of the development of resistant M. tuberculosis Mycobacterium tuberculosis.

Control via environment

  • Segregation of cattle from wildlife reservoirs maybe useful.
  • Good farm hygiene and husbandry practices are essential.


  • There are no commercially available vaccines for M.bovis in cattle.
  • There are commercially available vaccines for M. paratuberculosis in cattle.


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Further Reading


Refereed Papers

  • Recent references from PubMed and VetMedResource.
  • Loeffler S H, de Lisle G W, Neill M A, Collins D M, Price-Carter M, Paterson B & Crews K B (2014) The seal tuberculosis agent, Mycobacterium pinnipedii, infects domestic cattle in New Zealand: epidemiologic factors and DNA strain typing. J Wildl Dis 50 (2), 180-7 PubMed.
  • Ameni G, Tadesse K, Hailu E, Deresse Y, Medhin G, Aseffa A et al (2013) Transmission of Mycobacterium tuberculosis between Farmers and Cattle in Central Ethiopia. PLoS ONE 8 (10) PubMed.
  • Rodríguez S, Bezos J, Romero B et al (2011) Mycobacterium caprae Infection in Livestock and Wildlife, SpainEmerg Infect Dis 17 (3), 532-535 PubMed.
  • Romero B, Rodríguez S, Bezos J, Díaz R, Copano M F, Merediz I et al (2011) Humans as Source of Mycobacterium tuberculosis Infection in Cattle, Spain. Emerg Infect Dis 17 (12), 2393-2395 PubMed.
  • Ocepek M, Pate M, Žolnir-Dovč M & Poljak M (2005) Transmission of Mycobacterium tuberculosis from Human to Cattle. J Clin Microbiol 43 (7), 3555-3557.
  • Alfredsen S & Saxegaard F (1992) An outbreak of tuberculosis in pigs and cattle caused by Mycobacterium africanum. Vet Rec 131 (3), 51-53 PubMed.

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