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Journal of Clinical Microbiology, May 2005, p. 2546-2547, Vol. 43, No. 5
0095-1137/05/$08.00+0 doi:10.1128/JCM.43.5.2546-2547.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.
Chlamydia trachomatis Serovars Causing Urogenital Infections in Women in Melbourne, Australia

LETTER
Studies on the prevalence of
Chlamydia trachomatis serovars
and genotypes could improve our understanding of
C. trachomatis epidemiology and transmission. There have been few studies characterizing
C. trachomatis detected in clinical specimens in Australia (
4,
7). In one study of
C. trachomatis among men who have sex with
men (MSM) in Melbourne, Australia, it was reported that serovar
D was predominant (54%), followed by G and J (
4). For comparison
with the serovar distribution among MSM in Melbourne (
4), we
used
omp1 sequencing to determine the serovars of
C. trachomatis consecutively detected in specimens from 56 women attending
gynecological clinics in Melbourne (May to July and October
to December 2003). This project was sanctioned by the Royal
Women's Hospital Human Research Ethics Committee and the Victorian
Department of Human Services Human Research Ethics Committee.
(All of the information in this letter has been presented at the 13th International Union against Sexually Transmitted Infections (IUSTI) Asia Pacific Conference 2004, 6 to 9 July 2004, Chiang Mai, Thailand.)
From these women, 60 C. trachomatis-positive specimens were stored after COBAS Amplicor PCR testing performed by the Royal Women's Hospital Molecular Microbiology Unit, Melbourne, Australia (urine = 30, cervical swab = 19, high-vaginal swab = 9, urethral swab = 1, throat swab = 1).
omp1 PCR has a lower sensitivity in comparison to the plasmid-directed COBAS Amplicor PCR (5, 6), and past work has shown a higher yield of confirmation for COBAS Amplicor PCR with a nested protocol (5). Hence, for this study a nested omp1 PCR was used to achieve a higher amplicon yield for sequencing. DNA extraction, nested omp1 PCR with primers NL-f and NL-r (4), and DNA sequencing of PCR products were performed as described previously (4).
Of the 60 specimens, 47 (78%) were positive by the nested omp1 PCR. Despite a second round of PCR, one NLf/r-positive sample was not included for sequencing as the estimated concentration of DNA was below the threshold for the sequencing reaction. Future work should seek to perform multiple PCRs on samples with low amplicon yields.
A total of 46 samples from 42 women underwent sequencing of the NLf/r omp1 fragment, and the sequencing results were compared to known omp1 nucleotide sequences in the GenBank databases (http://www.ncbi.nlm.nih.gov/BLAST/) to determine the corresponding serovars. No mixed infections of more than one serovar were observed for this sample of women, and only one sample per patient was used in the analysis (Table 1). Sequence analysis showed that the most prevalent omp1 sequences corresponded to serovar E (17, 40%), followed by F (8, 19%), G (7, 17%), J (4, 10%), D (3, 7%), and K (3, 7%). These findings are consistent with serovar distributions reported for other developed countries where serovar E has been identified as the most prevalent (3, 8).
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TABLE 1. C. trachomatis serovar distribution among 42 women tested at Royal Women's Hospital clinics and serovar distribution among 39 MSM tested in male-only saunas in Melbourne, Australia
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The serovar distribution of chlamydia among this sample of women
is significantly different from the distribution of serovars
causing urogenital infections among MSM in Melbourne (Table
1), in particular the differences in the most successful serovars
(as measured by the most prevalent serovars). Different serovars
identified from heterosexually acquired chlamydia and MSM-acquired
chlamydia have also been reported by Barnes and colleagues (
1)
and Geisler and colleagues (
2). Although it is difficult to
interpret these findings using a small and relatively uncharacterized
population of women, this study has highlighted several areas
for future research on
C. trachomatis epidemiology and transmission.
Future research could investigate the possible explanations for this phenomenon, such as transmission pathways or sexual networks (heterosexual versus MSM), tissue tropism, or perhaps other confounding ligands that may be responsible for directing colonization of various tissues. It is also likely that patient characteristics are a key component to understanding the different serovar distributions in women and MSM, such as age, history of chlamydial infections, sexualbehavior, and presence or absence of symptoms. A comprehensive study with a large and diverse study population may offer fresh insight into chlamydial infections in Australia.

ACKNOWLEDGMENTS
We gratefully acknowledge the assistance of Gemma Eldridge,
Shujun Chen, and Elice Rudland at the Royal Women's Hospital,
Melbourne, Australia, in DNA extraction of
C. trachomatis-positive
specimens. This work was supported by funding from the
Royal Women's Hospital 2004 Postgraduate Research Degree Scholarship
(awarded to Nichole Lister) and funding from the Victorian Department
of Human Services (Public Health Research Projects 2002-03 in
Communicable Diseases). Anthony Smith is supported by a senior
research fellowship from the Victorian Health Promotion Foundation,
Australia. We do not have a commercial or other association
that might pose a conflict of interest.

REFERENCES
1 - Barnes, R. C., A. M. Rompalo, and W. E. Stamm. 1987. Comparison of Chlamydia trachomatis serovars causing rectal and cervical infections. J. Infect. Dis. 156:953-958.[Medline]
2 - Geisler, W. M., W. L. Whittington, R. J. Suchland, and W. E. Stamm. 2002. Epidemiology of anorectal chlamydia and gonococcal infections among men having sex with men in Seattle: utilizing serovar and auxotype strain typing. Sex. Transm. Dis. 29:189-195.[Medline]
3 - Jonsdottir, K., M. Kristjansson, J. Hjaltalin Olafsson, and O. Steingrimsson. 2003. The molecular epidemiology of genital Chlamydia trachomatis in the greater Reykjavik area, Iceland. Sex. Transm. Dis. 30:249-256.[Medline]
4 - Lister, N. A., S. N. Tabrizi, C. K. Fairley, P. Janssen, and S. Garland. 2004. Chlamydia trachomatis omp1 variability among men tested in male-only saunas in Melbourne, Australia. J. Clin. Microbiol. 42:2596-2601.[Abstract/Free Full Text]
5 - Lister, N. A., S. N. Tabrizi, C. K. Fairley, and S. Garland. 2004. Validation of Roche COBAS Amplicor assay for detection of Chlamydia trachomatis in rectal and pharyngeal specimens by an omp1 PCR assay. J. Clin. Microbiol. 42:239-241.[Abstract/Free Full Text]
6 - Pedersen, L. N., H. O. Kjaer, J. K. Moller, T. F. Orntoft, and L. Ostergaard. 2000. High-resolution genotyping of Chlamydia trachomatis from recurrent urogenital infections. J. Clin. Microbiol. 38:3068-3071.[Abstract/Free Full Text]
7 - Stevens, M. P., S. N. Tabrizi, R. Muller, V. Krause, S. M. Garland. 2004. Characterization of Chlamydia trachomatis omp1 genotypes detected in eye swab samples from remote Australian communities. J. Clin. Microbiol. 42:2501-2507.[Abstract/Free Full Text]
8 - Suchland, R. J., L. O. Eckert, S. E. Hawes, and W. E. Stamm. 2003. Longitudinal assessment of infecting serovars of Chlamydia trachomatis in Seattle public health clinics: 1988-1996. Sex. Transm. Dis. 30:357-361.[Medline]
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Nichole A. Lister*
Christopher K. Fairley
Department of Public Health Sexual Health Unit Melbourne Sexual Health Centre 580 Swanston Street Carlton 3053 Victoria, Australia
Sepehr N. Tabrizi
Suzanne Garland
Department of Microbiology and Infectious Diseases Royal Women's Hospital Melbourne, Australia
Anthony Smith
Australian Research Centre in Sex, Health and Society La Trobe University Melbourne, Australia
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* Phone: 61 3 9341 6260, Fax: 61 3 9347 6757, E-mail: nicholel{at}pgrad.unimelb.edu.au |
Journal of Clinical Microbiology, May 2005, p. 2546-2547, Vol. 43, No. 5
0095-1137/05/$08.00+0 doi:10.1128/JCM.43.5.2546-2547.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.
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