Mycobacterium tuberculosis

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Soumya Sachdeva; João André Alves Silva, M.D. [2]

Overview

Mycobacterium tuberculosis is the bacterium that causes most cases of tuberculosis.[1] It was first described on March 24, 1882 by Robert Koch, who subsequently received the Nobel Prize in physiology or medicine for this discovery in 1905; the bacterium is also known as Koch's bacillus. The M. tuberculosis genome was sequenced in 1998.[2][3]

Taxonomy

Cellular organisms; Bacteria; Actinobacteria; Actinobacteria; Actinobacteridae; Actinomycetales; Corynebacterineae; Mycobacteriaceae; Mycobacterium; Mycobacterium tuberculosis complex; M. tuberculosis[4]

Biology

Mycobacterium tuberculosis belongs to the Mycobacterium tuberculosis complex. This complex includes M. tuberculosis, M. bovis, M. africanum, M. canetti, and M. microti.[5]

M. tuberculosis is an obligate aerobe, non-encapsulated, non-motile, acid-fast bacillus. Slender, straight or slightly curved bacillus with rounded ends, occuring singly, in pairs or in small clumps. It does not form spores and its ideal growing environment includes tissues with high levels of oxygen. It cannot be considered gram positive or gram negative due to its high lipid cell wall, that is impermeable to the dyes until combined with an alcohol. On microscopic examination of sputum samples, the bacteria cannot be distinguished from other acid-fast bacteria, such as Nocardia app.[5]

M. tuberculosis has a very slow rate of replication, taking about 15 to 20 hours to divide. This characteristic, added to its ability to remain in latent state for long periods of time, account for the treatment duration required for infected patients.[5]

Genetic variances in the genome of M. tuberculosis lead to important phenotypical changes. There are many different strains of the bacteria, however, 6 of them were noted to be associated with specific geographic areas. This data is important since 3 strains, the Beijing family, strain W and the W-like strains, were noted to be associated with resistance to treatment drugs.[6][7]

Tropism

M. tuberculosis can infect different cells of the human body, however, due to its preference for tissues with high oxygen levels, its cellular tropism is mostly directed towards lung cells.[5]

Natural Reservoir

Human beings are the main natural reservoir for M. tuberculosis, however, the bacteria may infect other species.[5]

Resistance

Mycobacteria are killed at 60 degree celsius in 15-20 minutes. They are sensitive to UV rays and sunlight. They are relatively resistant to 5% phenol, 15% sulphuric acid, 5% oxalic acid, 4% sodium hydroxide. The bacillus are destroyed by tincture of sodium in five minutes and by 80% ethanol in 2-10 minutes.

References

  1. Ryan KJ; Ray CG (editors) (2004). Sherris Medical Microbiology (4th ed. ed.). McGraw Hill. ISBN 0-8385-8529-9.
  2. Cole ST; Brosch R; Parkhill J; et al. (1998). "Deciphering the biology of Mycobacterium tuberculosis from the complete genome sequence". Nature. 393: 537&ndash, 544.
  3. Camus JC; Pryor MJ; Medigue C; Cole ST. (148). "Re-annotation of the genome sequence of Mycobacterium tuberculosis H37Rv". Microbiology. 2002: 2967&ndash, 2973.
  4. "Poliovirus".
  5. 5.0 5.1 5.2 5.3 5.4 Lawn SD, Zumla AI (2011). "Tuberculosis". Lancet. 378 (9785): 57–72. doi:10.1016/S0140-6736(10)62173-3. PMID 21420161.
  6. Smith NH, Hewinson RG, Kremer K, Brosch R, Gordon SV (2009). "Myths and misconceptions: the origin and evolution of Mycobacterium tuberculosis". Nat Rev Microbiol. 7 (7): 537–44. doi:10.1038/nrmicro2165. PMID 19483712.
  7. Gagneux S, Small PM (2007). "Global phylogeography of Mycobacterium tuberculosis and implications for tuberculosis product development". Lancet Infect Dis. 7 (5): 328–37. doi:10.1016/S1473-3099(07)70108-1. PMID 17448936.