Equis ISSN 2398-2977

Mycobacterium spp

Contributor(s): Sarah Binns, Susan Dawson, Richard Walker

Introduction

Classification

Taxonomy

  • Order:Actinomycetales.
  • Family:Mycobacteriaceae.
  • Genus:Mycobacterium- closely related toCorynebacterium,NocardiaandRhodococcus.
  • Mycobacteria can be classified into three groups:
    • Strict pathogens, egM. bovis.
    • Opportunistic, egM. avium.
    • Rare pathogens or saprophytes, egM. smegmatis.

Etymology

  • Gr:myces- a fungus;bakterion- a small rod.

Active Forms

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Clinical Effects

Epidemiology

Habitat

  • Tubercle bacteria are obtained from infected individuals: humans withM. tuberculosis, cattle and wildlife withM. bovis,and birds withM. avium.
  • Non-tuberculous mycobacteria are saprophytic, but some are commensals in various animal species.

Lifecycle

  • Multiplication occurs both intracellularly in macrophages and extracellularly.
  • The organism is able to survive in phagosomes and phagolysosomes.

Transmission

  • Infection in horses usually contracted from contaminated feed or water.
  • By aerosols or fomites - mainly from respiratory discharges from infected animals.

Pathological effects

  • The organism gains access to the body, usually via the respiratory tract or digestive tract (horses), 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.
  • Antibodies are not protective.
  • The virulence of the organism is 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 subacute inflammation occurs with polymorphonuclear infiltration.
  • After delayed hypersensitivity develops, granulomatous inflammation supervenes and the 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.

Equine cases

  • Horses are rarely affected, but more often byM. avium  Mycobacteriosis  thanM. bovis.
  • Usually infected via the gastrointestinal tract, primary lesions occur in the pharynx and intestine.
  • Lesions in horses often do not exhibit caseation or calcification.
  • Cutaneous forms, arthritis/synovitis, abortion, guttural pouch infection   Guttural pouch: mycosis  and ocular lesions have also been reported.

Other Host Effects

  • Some non-tuberculous bacteria are commensals.

Control

Control via animal

  • Most equine cases diagnosed at necropsy.
  • Treatment rarely attempted because of the zoonotic risk.
  • Treatment has been successfully attempted in non-human primate colonies.

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    Rifampicin  .
  • Second-line drugs include streptomycin    Streptomycin  , against which resistance is now common, rifapentine, kanamycin   Kanamycin  /amikacin   Amikacin  , capreomycin and fluoroquinolones   Therapeutics: nitrofurans / nitroimidazoles / quinolones  .
  • 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 resistantM. tuberculosis.
  • Prophylactic treatment with isoniazid may be considered for pets exposed to tuberculosis.
  • Genomic and proteomic technologies can be used in drug development to analyze the metabolic patterns of mycobacteria and predict the activity of drugs.

Diagnosis

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Further Reading

Publications

Refereed papers

  • Recent references from PubMed and VetMedResource.
  • Monreal L, Segura D, Segales J, Garrido J M & Prades M (2001) Diagnosis of Mycobacterium bovis infection in a mare. Vet Rec 149 (23), 712-714 PubMed
  • Booth T M & Wattret A (2000) Stifle abscess in a pony associated with Mycobacterium smegmatis.Vet Rec 147 (16), 452-454 PubMed
  • Leifsson P S, Olsen S N & Larsen S (1997) Ocular tuberculosis in a horse. Vet Rec 141 (25), 651-654 PubMed
  • Thorel M F, Huchzermeyer H, Weiss R & Fontaine J J (1997) Mycobacterium avium infections in animals. Literature review. Vet Res 28 (5), 439-447 PubMed
  • Hart C A, Becking N J & Duerden B I (1996) Tuberculosis into the next century. J Med Microbiol 44, 1-34 PubMed
  • Helie P & Higgins R (1996) Mycobacterium avium complex abortion in a mare. J Vet Diagn Invest (2), 257-258 PubMed.
  • Gunnes G, Nord K, Vatn S & Saxegaard F (1995) A case of generalized avian tuberculosis in a horse. Vet Rec 136 (22), 565-566 PubMed
  • Cline J M, Schlafer D W, Callihan D R et al (1991) Abortion and granulomatous colitis due to Mycobacterium avium complex infection in a horse. Vet Pathol 28 (1), 89-91 PubMed.
  • Flores J M, Sanchez J & Casta M (1991) Avian tuberculosis dermatitis in a young horse. Vet Rec 12 8(17), 407-408 PubMed.

Other sources of information

  • Manning E J B & Collins M T (2001) Mycobacterial infections in domestic and wild animals. Rev Sci Tech 20 (1), 331. ISBN: 929044519X.
  • Biberstein E L (1990) Mycobacterium species: The Agents of Animal Tuberculosis. In: Review of Veterinary Microbiology. Eds: Biberstein E L & Zee Y C. Blackwell Scientific, USA. pp 202-212. ISBN: 0865420858.

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