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The louse-borne human pathogen
Bartonella quintana is a genomic derivative of the zoonotic
agent Bartonella henselae
Cecilia M. Alsmark *   ,
A. Carolin Frank * ,
E. Olof Karlberg * ,
Boris-Antoine Legault *, David H.
Ardell *  ,
Björn Canbäck * ¶, Ann-Sofie
Eriksson *, A. Kristina Näslund *,
Scott A. Handley * ||, Maxime Huvet *,
Bernard La Scola * **, Martin
Holmberg
and Siv G. E. Andersson *,
*Department of Molecular Evolution, Evolutionary
Biology Center, Uppsala University, 752 36 Uppsala, Sweden; and
Department
of Medical Sciences, Section for Infectious Diseases, Uppsala
University Hospital, 752 85 Uppsala, Sweden
Edited by Stanley Falkow, Stanford University, Stanford, CA,
and approved February 19, 2004 (received for review September 4,
2003)
We present the complete genomes of two human
pathogens, Bartonella quintana (1,581,384 bp)
and Bartonella henselae (1,931,047 bp). The two
pathogens maintain several similarities in being transmitted
by insect vectors, using mammalian reservoirs, infecting
similar cell types (endothelial cells and erythrocytes)
and causing vasculoproliferative changes in
immunocompromised hosts. A primary difference between
the two pathogens is their reservoir ecology. Whereas
B. quintana is a specialist, using only the human as
a reservoir, B. henselae is more promiscuous and is
frequently isolated from both cats and humans. Genome
comparison elucidated a high degree of overall
similarity with major differences being B. henselae
specific genomic islands coding for filamentous
hemagglutinin, and evidence of extensive genome reduction in
B. quintana, reminiscent of that found in
Rickettsia prowazekii. Both genomes are reduced
versions of chromosome I from the highly related
pathogen Brucella melitensis. Flanked by two rRNA operons
is a segment with similarity to genes located on chromosome
II of B. melitensis, suggesting that it was acquired
by integration of megareplicon DNA in a common ancestor
of the two Bartonella species. Comparisons of
the vector-host ecology of these organisms suggest that
the utilization of host-restricted vectors is associated
with accelerated rates of genome degradation and may explain
why human pathogens transmitted by specialist vectors are
outnumbered by zoonotic agents, which use vectors of
broad host ranges.
This paper was submitted directly (Track II)
to the PNAS office.
Data deposition: The sequences
reported in this paper have been deposited in the
GenBank database [accession nos. BX897699
(B. henselae) and BX897700 (B. quintana)].
C.M.A., A.C.F., and E.O.K. contributed equally to this work.
Present address: Department of Zoology, Natural History Museum,
London SW7 5BD, United Kingdom.
Present
address: Linnaeus Centre for Bioinformatics, Biomedical
Center, Uppsala University, 752 36 Uppsala, Sweden.
¶ Present address:
Department of Microbial Ecology, Lund University, 223
62 Lund, Sweden.
|| Present address:
Department of Molecular Microbiology, Washington
University School of Medicine, St. Louis, MO 63110.
** Present address:
Unité des Rickettsies, Faculté de Médecine, 133 85
Marseille, France.
To whom correspondence should be addressed. E-mail:
siv.andersson@ebc.uu.se
.
© 2004 by The
National Academy of Sciences of the USA
Full Article:
http://www.pnas.org/cgi/content/full/101/26/9716
Dr Cecilia Alsmark
University Research Fellow
Email:
cecilia.alsmark"at"ncl.ac.uk
Telephone: 0191 246 4812
Address: School of Biology
Institute for Research on Environment and Sustainability,
Devonshire Building,
University of Newcastle,
Newcastle upon Tyne
NE1 7RU
http://www.ncl.ac.uk/biol/staff/profile/cecilia.alsmark
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