Mycobacterium Explained

Mycobacterium is a genus of Actinobacteria, given its own family, the Mycobacteriaceae. The genus includes pathogens known to cause serious diseases in mammals, including tuberculosis and leprosy.[1] The Latin prefix "myco - " means both fungus and wax; its use here relates to the "waxy" compounds in the cell wall.

Microbiologic characteristics

Mycobacteria are aerobic and nonmotile bacteria (except for the species Mycobacterium marinum which has been shown to be motile within macrophages) that are characteristically acid-alcohol fast.[1] Mycobacteria do not contain endospores or capsules, and are usually considered Gram-positive. While mycobacteria do not seem to fit the Gram-positive category from an empirical standpoint (i.e. they do not retain the crystal violet stain), they are classified as an acid-fast Gram-positive bacterium due to their lack of an outer cell membrane. All Mycobacterium species share a characteristic cell wall, thicker than in many other bacteria, which is hydrophobic, waxy, and rich in mycolic acids/mycolates. The cell wall consists of the hydrophobic mycolate layer and a peptidoglycan layer held together by a polysaccharide, arabinogalactan. The cell wall makes a substantial contribution to the hardiness of this genus. The biosynthetic pathways of cell wall components are potential targets for new drugs for tuberculosis.[2]

Many Mycobacterium species adapt readily to growth on very simple substrates, using ammonia or amino acids as nitrogen sources and glycerol as a carbon source in the presence of mineral salts. Optimum growth temperatures vary widely according to the species and range from 25 °C to over 50 °C.

Some species can be very difficult to culture (i.e. they are fastidious), sometimes taking over two years to develop in culture. Further, some species also have extremely long reproductive cycles - M. leprae, may take more than 20 days to proceed through one division cycle (for comparison, some E. coli strains take only 20 minutes), making laboratory culture a slow process.[1] In addition, the availability of genetic manipulation techniques still lags far behind that of other bacterial species.[3]

A natural division occurs between slowly - and rapidly - growing species. Mycobacteria that form colonies clearly visible to the naked eye within 7 days on subculture are termed rapid growers, while those requiring longer periods are termed slow growers. Mycobacteria are slightly curved or straight rods between 0.2-0.6 µm wide by 1.0-10 µm long.

Pigmentation

Some mycobacteria produce carotenoid pigments without light. Others require photoactivation for pigment production.

Photochromogens (Group I)
  • Produce nonpigmented colonies when grown in the dark and pigmented colonies only after exposure to light and reincubation.
    Scotochromogens (Group II)
  • Produce deep yellow to orange colonies when grown in either the light or dark.
    Non-chromogens (Groups III & IV)
  • Nonpigmented in the light and dark or have only a pale yellow, buff or tan pigment that does not intensify after light exposure.

    Staining characteristics

    Mycobacteria are classical acid-fast organisms.[4] Stains used in evaluation of tissue specimens or microbiological specimens include Fite's stain, Ziehl-Neelsen stain, and Kinyoun stain.

    Mycobacteria appear phenotypically most closely related to members of Nocardia, Rhodococcus and Corynebacterium.

    Ecological characteristics

    Mycobacteria are widespread organisms, typical living in water (including tap water treated with chlorine) and food sources. Some, however, including the tuberculosis and the leprosy organisms, appear to be obligate parasites and are not found as free-living members of the genus.

    Pathogenicity

    Mycobacteria can colonize their hosts without the hosts showing any adverse signs. For example, billions of people around the world are infected with M. tuberculosis but will never know it because they will not develop symptoms.

    Mycobacterial infections are notoriously difficult to treat. The organisms are hardy due to their cell wall, which is neither truly Gram negative nor positive, and unique to the family, they are naturally resistant to a number of antibiotics that work by destroying cell walls, such as penicillin. Also, because of this cell wall, they can survive long exposure to acids, alkalis, detergents, oxidative bursts, lysis by complement and antibiotics which naturally leads to antibiotic resistance. Most mycobacteria are susceptible to the antibiotics clarithromycin and rifamycin, but antibiotic-resistant strains are known to exist.

    As with other bacterial pathogens, surface and secreted proteins of M. tuberculosis contribute significantly to the virulence of this organism. There is an increasing list of extracytoplasmic proteins proven to have a function in the virulence of M. tuberculosis.[5]

    Medical classification

    Mycobacteria can be classified into several major groups for purpose of diagnosis and treatment: M. tuberculosis complex which can cause tuberculosis: M. tuberculosis, M. bovis, M. africanum, and M. microti; M. leprae which causes Hansen's disease or leprosy; Nontuberculous mycobacteria (NTM) are all the other mycobacteria which can cause pulmonary disease resembling tuberculosis, lymphadenitis, skin disease, or disseminated disease.

    Phenotypic testing

    Various phenotypic tests can be used to identify and distinguish different Mycobacteria species and strains.

    Phenotypic testing of Mycobacteria

    Mycosides

    Mycosides are phenolic alcohols (such as phenolphthiocerol) that were shown to be components of mycobacterium glycolipids which are termed glycosides of phenolphthiocerol dimycocerosate (Smith DW et al., Nature 1960, 186, 887) There are 18 and 20 carbon atoms in mycosides A, and B, respectively.[6]

    Species

    M. avium

    M. avium paratuberculosis, which has been implicated in Crohn's disease in humans and Johne's disease in sheep

    M. avium silvaticum

    M. avium "hominissuis"

    M. colombiense

    M. tuberculosis, the major cause of human tuberculosis

    M. bovis

    M. bovis BCG

    M. africanum

    M. canetti

    M. caprae

    M. pinnipedii

    References

    Further reading

    External links

    Notes and References

    1. Book: Ryan KJ, Ray CG (editors). Sherris Medical Microbiology. 4th. McGraw Hill. 2004. 0-8385-8529-9.
    2. Book: Bhamidi S. 2009. Mycobacterial Cell Wall Arabinogalactan. Bacterial Polysaccharides: Current Innovations and Future Trends. Caister Academic Press. 978-1-904455-45-5.
    3. Book: Parish T, Brown A (editors). 2009. Mycobacterium: Genomics and Molecular Biology. Caister Academic Press. 978-1-904455-40-0.
    4. Book: McMurray DN. Baron S et al (eds.). Mycobacteria and Nocardia. Baron's Medical Microbiology. 4th. Univ of Texas Medical Branch. 1996. http://www.ncbi.nlm.nih.gov/books/bv.fcgi?rid=mmed.section.1772. 0-9631172-1-1.
    5. Book: McCann et al. 2009. Secreted and Exported Proteins Important to Mycobacterium tuberculosis Pathogenesis. Bacterial Secreted Proteins: Secretory Mechanisms and Role in Pathogenesis. Caister Academic Press. 978-1-904455-42-4.
    6. http://www.cyberlipid.org/simple/simp0003.htm#10 fatty alcohols and aldehydes