From this scientific work:
I quote meticulously from this scientific work :
M. marinum causes minor skin infections, characterised by intracellular bacteria and the granulomatous lesions that are features of infection with many mycobacterial pathogens, notably Mycobacterium tuberculosis[2]. In contrast, M. ulcerans causes Buruli ulcer (BU), a slowly progressing, ulcerative disease characterized by necrosis of subcutaneous tissue. BU has a characteristic histopathology with large numbers of extracellular bacteria during the acute phase of the infection, with a marked lack of inflammatory response in advanced infection."
"This unusual pathology is principally mediated by an immunosuppressive polyketide called mycolactone, which is not produced by M. marinum or M. tuberculosis. In BU patients, mycolactone is present in cutaneous lesions but also diffuses and can be detected in serum [3,4]."
" Two main features differentiate the genomes of M. ulcerans and M. marinum. The first is the pMUM megaplasmid, found in M. ulcerans but absent from M. marinum[5,6]. This plasmid harbours three large genes (mlsA1: 51 kb, mlsA2: 7.2 kb, mlsB: 43 kb) that encode the polyketide synthases (PKSs) required for mycolactone synthesis [2]. The second is the insertion sequence (IS) IS2404 that is absent from M. marinum but present in high copy number (>200) in M. ulcerans genomes. IS2404 expansion in the M. ulcerans genome has led to the inactivation of many genes through disruption of coding and promoter sequences and has mediated the deletion of approximately 1 Mbp of DNA from M. ulcerans compared with M. marinum[1]."
My contribution:
By Gepard Dot plot software:
M.ulcerans versus M.ulcerans
M.marinum versus M.marinum
M.marinum versus M.ulcerans
"Together with loss of DNA, there is also evidence of extensive loss of gene function in M. ulcerans - the genome of M. ulcerans isolate Agy99 harbours 771 pseudogenes (inactivated genes), while the M. marinum genome harbours only 65. Acquisition of foreign DNA, IS expansion, pseudogene accumulation and genome reduction are features in common with bacterial populations that have passed through an evolutionary bottleneck [7-12], suggesting there has been constriction of population size during adaptation to a new, niche environment."
"Analysis of the M. ulcerans Agy99 genome showed deletion or inactivation of genes expressing potent T-cell antigens, and genes required for pigment biosynthesis, anaerobiosis, and intracellular growth [1]. This profile suggested a bacterium that has adapted to a dark, extracellular environment where slow growth, loss of immunogens and production of an immunosuppressive molecule provide a selective advantage [1,13]. In contrast, its progenitor, M. marinum, has the characteristics of both a specialist bacterium that can persist within an intracellular environment as well as a generalist that can survive in extracellular conditions. A niche environment for M. ulcerans has not yet been demonstrated although the recent discovery that Australian native possums inhabiting BU endemic areas appear to harbour the bacteria in their gastrointestinal tracts raises some interesting possibilities [14]."
........After there is the discussion of the results.
My question:
Why these phage are non capable to growth on Mycobacterium marinum?
Growth:
-Photochromogens (Group I)
Produce nonpigmented colonies when grown in the dark and pigmented colonies only after exposure to light and reincubation.
Ex: M. kansasii, M. marinum, M. simiae.
On primary isolation M. marinum grows on LJ slants at 30-33°C in 7–21 days.
-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.
Ex: M. tuberculosis, M. avium-intra-cellulare, M. bovis, M. ulcerans
Ex: M. fortuitum, M. chelonae
M. ulcerans can be cultured from many lesions, either from exudates or tissue fragments, but visible growth often requires 6 to 8 weeks incubation at 33 °C.
