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Journal of Clinical Microbiology, April 1998, p. 918-925, Vol. 36, No. 4
0095-1137/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.
Differentiation of Mycobacterium
ulcerans, M. marinum, and M. haemophilum:
Mapping of Their Relationships to M. tuberculosis by
Fatty Acid Profile Analysis, DNA-DNA Hybridization, and 16S
rRNA Gene Sequence Analysis
T.
Tønjum,1,*
D. B.
Welty,2
E.
Jantzen,3 and
P.
L.
Small2
Section of Molecular Microbiology, Institute
of Microbiology, University of Oslo, National Hospital, N-0027
Oslo,1 and
Department of Vaccinology,
National Institute of Public Health, N-0403
Oslo,3 Norway, and
Microscopy Section,
Rocky Mountain Laboratory, National Institutes of Health, Hamilton,
Montana2
Received 25 July 1997/Returned for modification 1 October
1997/Accepted 13 November 1997
Although Mycobacterium ulcerans, M. marinum, and M. haemophilum are closely related,
their exact taxonomic placements have not been determined. We performed
gas chromatography of fatty acids and alcohols, as well as DNA-DNA
hybridization and 16S rRNA gene sequence analysis, to clarify their
relationships to each other and to M. tuberculosis. M. ulcerans and M. marinum were most closely related to
one another, and each displayed very strong genetic affinities to
M. tuberculosis; they are actually the two mycobacterial
species outside the M. tuberculosis complex most closely
related to M. tuberculosis. M. haemophilum was
more distinct from M. ulcerans and M. marinum,
and it appeared to be as related to these two species as to M. tuberculosis. These results are important with regard to the
development of diagnostic and epidemiological tools such as
species-specific DNA probes and PCR assays for M. ulcerans,
M. marinum, and M. haemophilum. In addition,
the finding that M. ulcerans and M. marinum are
more closely related to M. tuberculosis than are other
pathogenic mycobacterial species suggests that they may be evaluated as
useful models for studying the pathogenesis of M. tuberculosis. M. marinum may be particularly useful
in this regard since strains of this species grow much more rapidly
than M. tuberculosis and yet can cause systemic disease in
immunocompromised hosts.
*
Corresponding author. Present address: Department of
Microbiology and Immunology, University of Michigan Medical School,
5641 Medical Science Building II, Ann Arbor, MI 48109-0620. Phone: (313) 647 6765. Fax: (313) 764 3562. E-mail:
tone.tonjum{at}rh.uio.no.
Journal of Clinical Microbiology, April 1998, p. 918-925, Vol. 36, No. 4
0095-1137/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.
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