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Journal of Bacteriology, December 2009, p. 7225-7233, Vol. 191, No. 23
0021-9193/09/$08.00+0 doi:10.1128/JB.00746-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.
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Institute for Genome Sciences, University of Maryland, Baltimore, Maryland 21201,1 Institute of Health & Biomedical Innovation, Queensland University of Technology, Kelvin Grove, Queensland 4059, Australia,2 J. Craig Venter Institute, 9712 Medical Center Drive, Rockville, Maryland 20850,3 University of British Columbia Centre for Disease Control, 655 West 12th Avenue, Vancouver, British Columbia V5Z 4R4, Canada,4 Division of Infectious Diseases & Department of Human Genetics, Emory University School of Medicine, 615 Michael Street, Atlanta, Georgia 30322,5 Department of Microbial Pathogenesis, University of Maryland Baltimore, 650 West Baltimore Street, Baltimore, Maryland 212016
Received 9 June 2009/ Accepted 2 September 2009
Zoonotic infections are a growing threat to global health. Chlamydia pneumoniae is a major human pathogen that is widespread in human populations, causing acute respiratory disease, and has been associated with chronic disease. C. pneumoniae was first identified solely in human populations; however, its host range now includes other mammals, marsupials, amphibians, and reptiles. Australian koalas (Phascolarctos cinereus) are widely infected with two species of Chlamydia, C. pecorum and C. pneumoniae. Transmission of C. pneumoniae between animals and humans has not been reported; however, two other chlamydial species, C. psittaci and C. abortus, are known zoonotic pathogens. We have sequenced the 1,241,024-bp chromosome and a 7.5-kb cryptic chlamydial plasmid of the koala strain of C. pneumoniae (LPCoLN) using the whole-genome shotgun method. Comparative genomic analysis, including pseudogene and single-nucleotide polymorphism (SNP) distribution, and phylogenetic analysis of conserved genes and SNPs against the human isolates of C. pneumoniae show that the LPCoLN isolate is basal to human isolates. Thus, we propose based on compelling genomic and phylogenetic evidence that humans were originally infected zoonotically by an animal isolate(s) of C. pneumoniae which adapted to humans primarily through the processes of gene decay and plasmid loss, to the point where the animal reservoir is no longer required for transmission.
Published ahead of print on 11 September 2009.
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