Abstract
Rickettsia australis strain PhillipsT was isolated in Queensland, Australia, in 1950. It is the tick-borne agent of Queensland tick typhus, a disease endemic in Australia. The 1.29-Mb genome sequence of this bacterium is highly similar to that of Rickettsia akari but contains two plasmids.
GENOME ANNOUNCEMENT
The genus Rickettsia is composed of small Gram-negative, obligate intracellular alphaproteobacteria (1) that underwent progressive genomic reduction (2). However, paradoxically, recent genomic studies have suggested that genome reduction was associated with increased virulence in rickettsiae (3). Rickettsia australis was first identified in residents of Northern Queensland, Australia, in 1950 (4). This bacterium is a spotted fever group rickettsia and causes Queensland tick typhus (QTT). QTT is endemic in the eastern part of Australia, where it is transmitted to humans through the bites of Ixodes holocyclus or Ixodes tasmani ticks (6). It is considered to be mostly mild and is characterized by fever, headache, and myalgia followed by the development of a maculopapular or vesicular rash, an inoculation eschar (65% of cases), and lymphadenopathy (71%) (5).
The genome sequencing of R. australis strain PhillipsT was performed by 454 shotgun and 454 paired-end sequencing. Briefly, the shotgun sequencing was performed using a GS-FLX Titanium sequencer (Roche, Meylan, France) with assembly into 1 complete circularized chromosome, 1 complete circularized plasmid, and 1 putative incomplete plasmid. The chromosome has a predicted size of 1,297,390 bp and a G+C content of 31.7%, which is similar to that of other rickettsial genomes. The plasmid (pRau01) has a size of 26,608 bp with a G+C content of 33.7%. The second plasmid is made of 13 contigs, for a total size of 30,176 bp, and has a G+C content of 21.7%. The chromosome contains 1,110 genes (1,426 open reading frames [ORFs]), including 820 complete genes (74%), 139 split genes (12%), and 151 gene fragments (14%). Among these 1,110 genes, 855 genes (77%) encode proteins with putative functions and 255 (23%) encode hypothetical proteins and proteins of unknown function. The R. australis genome contains 3 noncontiguous rRNAs (5S, 16S, and 23S rRNA), 33 tRNAs, and 3 other RNAs. The pRau01 plasmid carries 16 genes (25 ORFs), whereas the second plasmid carries 20 genes (24 ORFs).
R. australis exhibits an almost perfect genomic synteny with Rickettsia akari, its closest phylogenetic neighbor, with the exception of two inversions of 78,519 bp and 36,776 bp. R. australis lacks only 46 genes that are present in R. prowazekii, the agent of epidemic typhus, the most severe human rickettsiosis (7). These genes encode proteins of unknown function (23 genes), transposases (3 genes), ankyrin repeat-containing proteins (2 genes), transferases (6 genes), cell surface antigens (1 gene), synthetases (3 genes), and 1 gene in each of the following categories: BioY family protein, ABC-type transporter related to toluene tolerance protein, dCTP deaminase, putative transcriptional regulator, Sco2 protein precursor, DNA invertase Pin-like protein, VirD4 protein, and beta-glucosidase. None of these genes appears to be related to rickettsial virulence. In contrast, many genes involved in the biosynthesis and regulation of biosynthesis of amino acids and nucleotides present in R. australis are absent from R. prowazekii. Further investigations will be conducted to study the genomic basis of rickettsial virulence and the potential role of plasmids.
Nucleotide sequence accession number.
The whole-genome shotgun project has been deposited in the GenBank database under accession number AKVZ00000000.
ACKNOWLEDGMENT
This work did not benefit from any external funding.
REFERENCES
- 1. Blanc G, et al. 2007. Lateral gene transfer between obligate intracellular bacteria: evidence from the Rickettsia massiliae genome. Genome Res. 17:1657–1664 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 2. Blanc G, et al. 2007. Reductive genome evolution from the mother of Rickettsia. PLoS Genet. 3:e14 doi:10.1371/journal.pgen.0030014 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 3. Fournier PE, et al. 2009. Analysis of the Rickettsia africae genome reveals that virulence acquisition in Rickettsia species may be explained by genome reduction. BMC Genomics 10:166. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 4. Graves S, Stenos J. 1999. Rickettsioses in Australia, p 244–246 In Raoult D, Brouqui P. (ed), Rickettsiae and rickettsial diseases at the turn of the third millenium. Elsevier, Paris, France [Google Scholar]
- 5. McBride WJ, Hanson JP, Miller R, Wenck D. 2007. Severe spotted fever group rickettsiosis, Australia. Emerg. Infect. Dis. 13:1742–1744 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 6. Sexton DJ, Dwyer B, Kemp R, Graves S. 1991. Spotted fever group rickettsial infections in Australia. Rev. Infect. Dis. 13:876–886 [DOI] [PubMed] [Google Scholar]
- 7. Walker DH. 1988. Pathology and pathogenesis of the vasculotropic rickettsioses, p 115–138 In Walker DH. (ed), Biology of rickettsial disease. CRC Press Inc., Boca Raton, FL [Google Scholar]