Gomes, João Paulo

PubMed

João Paulo Gomes

Frontiers - Publisher Connector

CELLULAR AND INFECTION MICROBIOLOGY
is consensual due to the dissimilar genetic 
characteristics or discriminatory power of 
the loci enrolled in each of those.
Although it is assumed that the typing 
schemes should ideally ensure that the cho-
sen loci are stable over the course of evo-
lution, this issue is of difficult assessment. 
Labiran et al. (2012) have now presented a 
study where they have assessed the stability of 
some regions of the C. trachomatis genome 
by using innovate approaches. They have 
used the genetic markers from the described 
typing schemes that provide the highest 
Simpson index of diversity: the multi-
sequence typing (MST) system described by 
Klint et al. (2007) and the multi locus varia-
ble number tandem repeat (VNTR) analysis 
(MLVA-ompA) described by Pedersen et al. 
(2008). Labiran et al. (2012) have initially 
evaluated the stability of those genetic mark-
ers through the first stages of adaptation of 
C. trachomatis to cell culture. This is interest-
ing as the first attempt to study mutational 
patterns over adaptation to cell culture had 
been performed back in 1998 (Stothard 
et al., 1998), by studying solely the stabil-
ity of ompA over 20 in vitro passages. Now, 
by analyzing three VNTR besides ompA, the 
authors undoubtedly increase the chances 
of observing genetic alterations, as these 
loci possess a high discriminatory power. 
Furthermore, as the repeated sequences of 
VNTR loci are generated as a consequence of 
an increased error rate during DNA replica-
tion at these regions, they are hypothetically 
more prone to additional variation. In this 
first approach, the authors found no altera-
tions in those genomic regions by studying 
seven clinical isolates over eight passages. 
The initial inoculations were properly 
done from primary swabs in order to avoid 
previous contact of the strains with the in 
vitro system. Interestingly, the eight passages 
represent about 16 days in culture aiming 
to reflect the in vivo estimated period for 
appearance of symptoms for C. trachomatis 
infection of both genitalia and conjuncti-
vae (Black, 1997). There is no doubt that 
Genomic stability of genotyping markers in  
Chlamydia trachomatis
João Paulo Gomes*
Department of Infectious Diseases, National Institute of Health, Lisbon, Portugal
*Correspondence: j.paulo.gomes@insa.min-saude.pt
A commentary on
Genotyping markers used for multi locus 
VNTR analysis with ompA (MLVA-ompA) 
and multi sequence typing retain stability 
in Chlamydia trachomatis
by Labiran, C., Clarke, I. N., Cutcliffe, L. T., 
Wang, Y., Skilton, R. J., Persson, K., Bjartling, 
C., Herrmann, B., Christerson, L., and Marsh, 
P. (2012). Front. Cell. Infect. Microbiol. 2:68. 
doi: 10.3389/fcimb.2012.00068
Chlamydia trachomatis is an obligate 
intracellular human pathogen that 
infects columnar epithelial cells of ocu-
lar or genital mucosae, and mononuclear 
phagocytes. More than 50 fully sequenced 
genomes are publically available (Harris 
et al., 2012), and despite low polymor-
phic character when compared with most 
bacteria, these data allow a better under-
standing of C. trachomatis chromosomal 
dynamics. Indeed, it revealed not only 
the chromosome regions more prone to 
genetic mutations, but also that recombi-
nation is highly chromosome dispersed, 
although the frequency and relative weight 
of recombination and mutation events 
undoubtedly posits C. trachomatis as a 
low recombining bacterium (Joseph et al., 
2011; Ferreira et al., 2012).
In order to understand the epidemiol-
ogy and pathogenesis of the highly preva-
lent chlamydial diseases, the classification 
of clinical isolates has been a priority of 
researchers for decades. However, the tra-
ditional typing system, which is based on 
the polymorphism of the gene (ompA) 
encoding the major outer membrane pro-
tein (Yuan et al., 1989) has been jeopard-
ized in the last years as it does not group 
the isolated strains according to their cell- 
appetence or virulence. Thus, with the 
progressive release of sequenced genomes, 
several typing systems have been developed 
(Klint et al., 2007; Pannekoek et al., 2008; 
Pedersen et al., 2008; Dean et al., 2009; 
Bom et al., 2011), although none of them 
there is a radical change of environmental 
conditions when transiting from the in vivo 
to the in vitro system, mostly because the 
latter lacks immune system, competing 
flora, pH alterations, hormonal fluctua-
tions, etc. Nevertheless, although the paral-
lelism between these two scenarios remains 
speculative for these reasons, the impossibil-
ity to perform this evaluation in vivo and 
under controlled conditions makes this an 
 interesting approach.
In a second stage, the authors went even 
further by studying the “long-term” genome 
stability under influence of in vitro envi-
ronmental conditions. To achieve this, they 
used the MLVA-ompA and also the five-
locus MST system to monitor the stability of 
the enrolled loci throughout 72 passages in 
tissue culture. The coverage and the runtime 
of this approach make it an unprecedented 
evaluation of genome stability. In this study 
Labiran et al. (2012) used the so called 
“Swedish new variant,” a C.  trachomatis 
isolate that, besides the higher number of 
pseudogenes than most sequenced genital 
isolates (Jeffrey et al., 2010), shows both a 
deletion and duplication within the plas-
mid, which are genomic changes that had 
never been described before (Unemo et al., 
2010). These kind of genomic alterations 
are infrequent as C. trachomatis presents a 
nearly identical core and pan genome and 
a DNA sequence similarity of >98% (Harris 
et al., 2012). So, this isolate could hypotheti-
cally be considered as genomically unstable, 
making this a valuable strain to test stability 
over a long time in vitro passage. Similarly to 
the previous approach, no genetic changes 
were observed throughout the long-term 
in vitro maintenance, suggesting that the 
MLVA-ompA and MST systems are, on a 
genetic stability basis, highly accurate for 
both short-term (such as partner tracing) 
and long-term molecular epidemiology.
Moreover, the results from the Labiran 
et al. (2012) study indirectly bring to light 
a major controversy in the field, which is 
the uncertainty of whether the prototype 
www.frontiersin.org June 2012 | Volume 2 | Article 77 | 1
General Commentary
published: 06 June 2012
doi: 10.3389/fcimb.2012.00077
strains that have been used worldwide lead-
ing to thousands of papers, accurately rep-
resent current circulating clinical strains. In 
fact, the former are laboratory adapted for 
decades but at this stage one cannot know 
the extent of genomic alterations that may 
occur due to laboratory adaptation. On 
one hand, the results from Labiran et al. 
(2012) point to specific genomic stability, 
which, together with the C. trachomatis 
transmission bottlenecks (Andersson and 
Hughes, 1996) and the high doubling time 
of 2.5–4 h (Borges et al., 2010), disfavors 
genetic variability. On the other hand, it is 
known that some loci are prone to generate 
multi-alleles, such as the putative virulence 
factor CT135 (Sturdevant et al., 2010), and 
that Chlamydia undergoes adaptive changes 
when subjected to specific environmental 
alterations (Kutlin et al., 2005; Suchland 
et al., 2005). Ultimately, unless the entire 
genome is analyzed (at the stage of the strain 
isolation and after long-term in vitro pas-
sage), the controversy will certainly remain.
RefeRences
Andersson, D. I., and Hughes, D. (1996). Muller’s ratchet 
decreases fitness of a DNA-based microbe. Proc. Natl. 
Acad. Sci. U.S.A. 93, 906–907.
Black, C. M. (1997). Current methods of laboratory 
diagnosis of Chlamydia trachomatis infections. Clin. 
Microbiol. Rev. 10, 160–184.
Bom, R. J., Christerson, L., Schim Van Der Loeff, M. F., 
Coutinho, R. A., Herrmann, B., and Bruisten, S. M. 
(2011). Evaluation of high-resolution typing methods 
for Chlamydia trachomatis in samples from hetero-
sexual couples. J. Clin. Microbiol. 49, 2844–2853.
Borges, V., Ferreira, R., Nunes, A., Nogueira, P., Borrego, 
M. J., and Gomes, J. P. (2010). Normalization strategies 
for real-time expression data in Chlamydia trachoma-
tis. J. Microbiol. Methods 82, 256–264.
Dean, D., Bruno, W. J., Wan, R., Gomes, J. P., Devignot, 
S., Mehari, T., De Vries, H. J. C., Morre, S. A., Myers, 
A. (2008). Multi locus sequence of Chlamydiales: 
clonal groupings within the obligate intracellular 
bacteria Chlamydia trachomatis. BMC Microbiol. 8, 
42. doi: 10.1186/1471-2180-8-42
Pedersen, L. N., Podenphant, L., and Moller, J. K. (2008). 
Highly discriminative genotyping of Chlamydia tra-
chomatis using omp1 and a set of variable number 
tandem repeats. Clin. Microbiol. Infect. 14, 644–652.
Stothard, D. R., Van Der Pol, B., Smith, N. J., and Jones, 
R. B. (1998). Effect of serial passage in tissue culture 
on sequence of omp1 from Chlamydia trachomatis 
clinical isolates. J. Clin. Microbiol. 36, 3686–3688.
Sturdevant, G. L., Kari, L., Gardner, D. J., Olivares-
Zavaleta, N., Randall, L. B., Whitmire, W. M., Carlson, 
J. H., Goheen, M. M., Selleck, E. M., Martens, C., and 
Caldwell, H. D. (2010). Frameshift mutations in a sin-
gle novel virulence factor alter the in vivo pathogenic-
ity of Chlamydia trachomatis for the female murine 
genital tract. Infect. Immun. 78, 3660–3668.
Suchland, R. J., Bourillon, A., Denamur, E., Stamm, W. 
E., and Rothstein, D. M. (2005). Rifampin-resistant 
RNA polymerase mutants of Chlamydia trachoma-
tis remain susceptible to the ansamycin rifalazil. 
Antimicrob. Agents Chemother. 49, 1120–1126.
Unemo, M., Seth-Smith, H. M., Cutcliffe, L. T., Skilton, 
R. J., Barlow, D., Goulding, D., Persson, K., Harris, 
S. R., Kelly, A., Bjartling, C., Fredlund, H., Olcén, P., 
Thomson, N. R., and Clarke, I. N. (2010). The Swedish 
new variant of Chlamydia trachomatis: genome 
sequence, morphology, cell tropism and phenotypic 
characterization. Microbiology 156, 1394–1404.
Yuan, Y., Zhang, Y. X., Watkins, N. G., and Caldwell, 
H. D. (1989). Nucleotide and deduced amino acid 
sequences for the four variable domains of the major 
outer membrane proteins of the 15 Chlamydia tra-
chomatis serovars. Infect. Immun. 57, 1040–1049.
Received: 14 May 2012; accepted: 18 May 2012; published 
online: 06 June 2012.
Citation: Gomes JP (2012) Genomic stability of genotyp-
ing markers in Chlamydia trachomatis. Front. Cell. Inf. 
Microbio. 2:77. doi: 10.3389/fcimb.2012.00077
Copyright © 2012 Gomes. This is an open-access article 
distributed under the terms of the Creative Commons 
Attribution Non Commercial License, which permits 
non-commercial use, distribution, and reproduction in 
other forums, provided the original authors and source are 
credited.
G., Read, T. D., and Spratt, B. G. (2009). Predicting 
phenotype and emerging strains among Chlamydia 
trachomatis infections. Emerging Infect. Dis. 15, 
1385–1394.
Ferreira, R., Borges, V., Nunes, A., Nogueira, P. J., Borrego, 
M. J., and Gomes, J. P. (2012). Impact of loci nature 
on estimating recombination and mutation rates in 
Chlamydia trachomatis. G3 (Bethesda). 2:761–768. 
doi: 10.1534/g3.112.002923
Harris, S. R., Clarke, I. N., Seth-Smith, H. M., Solomon, 
A. W., Cutcliffe, L. T., Marsh, P., Skilton, R. J., Holland, 
M. J., Mabey, D., Peeling, R. W., Lewis, D. A., Spratt, B. 
G., Unemo, M., Persson, K., Bjartling, C., Brunham, 
R., de Vries, H. J., Morré, S. A., Speksnijder, A., Bébéar, 
C. M., Clerc, M., de Barbeyrac, B., Parkhill, J., and 
Thomson, N. R. (2012). Whole-genome analysis 
of diverse Chlamydia trachomatis strains identifies 
phylogenetic relationships masked by current clinical 
typing. Nat. Genet. 44, 413–419.
Jeffrey, B. M., Suchland, R. J., Quinn, K. L., Davidson, J. 
R., Stamm, W. E., and Rockey, D. D. (2010). Genome 
sequencing of recent clinical Chlamydia trachoma-
tis strains identifies loci associated with tissue tro-
pism and regions of apparent recombination. Infect. 
Immun. 78, 2544–2553.
Joseph, S. J., Didelot, X., Gandhi, K., Dean, D., and Read, 
T. D. (2011). Interplay of recombination and selec-
tion in the genomes of Chlamydia trachomatis. Biol. 
Direct 6, 28.
Klint, M., Fuxelius, H. H., Goldkuhl, R. R., Skarin, H., 
Rutemark, C., Andersson, S. G. E., Persson, K., and 
Herrmann, B. (2007). High-resolution genotyping of 
Chlamydia trachomatis strains by multilocus sequence 
analysis. J. Clin. Microbiol. 45, 1410–1414.
Kutlin, A., Kohlhoff, S., Roblin, P., Hammerschlag, M. 
R., and Riska, P. (2005). Emergence of resistance to 
rifampin and rifalazil in Chlamydophila pneumo-
niae and Chlamydia trachomatis. Antimicrob. Agents 
Chemother. 49, 903–907.
Labiran, C., Clarke, I. N., Cutcliffe, L. T., Wang, Y., 
Skilton, R. J., Persson, K., Bjartling, C., Herrmann, 
B., Christerson, L., and Marsh, P. (2012). Genotyping 
markers used for multi locus VNTR analysis with 
ompA (MLVA-ompA) and multi sequence typing 
retain stability in Chlamydia trachomatis. Front. Cell. 
Infect. Microbiol. 2:68. doi: 10.3389/fcimb.2012.00068
Pannekoek, Y., Morelli, G., Kusecek, B., Morre, S. A., 
Ossewaarde, J. M., Langerak, A. A., and Van Der Ende, 
Gomes Genomic stability in vitro
Frontiers in Cellular and Infection Microbiology  June 2012 | Volume 2 | Article 77 | 2


Genomic Stability of Genotyping Markers in Chlamydia trachomatis

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Frontiers in Cellular and Infection Microbiology

Genomic stability of genotyping markers in Chlamydia trachomatis

Repositório Científico do Instituto Nacional de Saúde

CELLULAR AND INFECTION MICROBIOLOGYis consensual due to the dissimilar genetic characteristics or discriminatory power of the loci enrolled in each of those.Although it is assumed that the typing schemes should ideally ensure that the cho-sen loci are stable over the course of evo-lution, this issue is of difficult assessment. Labiran et al. (2012) have now presented a study where they have assessed the stability of some regions of the C. trachomatis genome by using innovate approaches. They have used the genetic markers from the described typing schemes that provide the highest Simpson index of diversity: the multi-sequence typing (MST) system described by Klint et al. (2007) and the multi locus varia-ble number tandem repeat (VNTR) analysis (MLVA-ompA) described by Pedersen et al. (2008). Labiran et al. (2012) have initially evaluated the stability of those genetic mark-ers through the first stages of adaptation of C. trachomatis to cell culture. This is interest-ing as the first attempt to study mutational patterns over adaptation to cell culture had been performed back in 1998 (Stothard et al., 1998), by studying solely the stabil-ity of ompA over 20 in vitro passages. Now, by analyzing three VNTR besides ompA, the authors undoubtedly increase the chances of observing genetic alterations, as these loci possess a high discriminatory power. Furthermore, as the repeated sequences of VNTR loci are generated as a consequence of an increased error rate during DNA replica-tion at these regions, they are hypothetically more prone to additional variation. In this first approach, the authors found no altera-tions in those genomic regions by studying seven clinical isolates over eight passages. The initial inoculations were properly done from primary swabs in order to avoid previous contact of the strains with the in vitro system. Interestingly, the eight passages represent about 16 days in culture aiming to reflect the in vivo estimated period for appearance of symptoms for C. trachomatis infection of both genitalia and conjuncti-vae (Black, 1997). There is no doubt that Genomic stability of genotyping markers in  Chlamydia trachomatisJoão Paulo Gomes*Department of Infectious Diseases, National Institute of Health, Lisbon, Portugal*Correspondence: j.paulo.gomes@insa.min-saude.ptA commentary onGenotyping markers used for multi locus VNTR analysis with ompA (MLVA-ompA) and multi sequence typing retain stability in Chlamydia trachomatisby Labiran, C., Clarke, I. N., Cutcliffe, L. T., Wang, Y., Skilton, R. J., Persson, K., Bjartling, C., Herrmann, B., Christerson, L., and Marsh, P. (2012). Front. Cell. Infect. Microbiol. 2:68. doi: 10.3389/fcimb.2012.00068Chlamydia trachomatis is an obligate intracellular human pathogen that infects columnar epithelial cells of ocu-lar or genital mucosae, and mononuclear phagocytes. More than 50 fully sequenced genomes are publically available (Harris et al., 2012), and despite low polymor-phic character when compared with most bacteria, these data allow a better under-standing of C. trachomatis chromosomal dynamics. Indeed, it revealed not only the chromosome regions more prone to genetic mutations, but also that recombi-nation is highly chromosome dispersed, although the frequency and relative weight of recombination and mutation events undoubtedly posits C. trachomatis as a low recombining bacterium (Joseph et al., 2011; Ferreira et al., 2012).In order to understand the epidemiol-ogy and pathogenesis of the highly preva-lent chlamydial diseases, the classification of clinical isolates has been a priority of researchers for decades. However, the tra-ditional typing system, which is based on the polymorphism of the gene (ompA) encoding the major outer membrane pro-tein (Yuan et al., 1989) has been jeopard-ized in the last years as it does not group the isolated strains according to their cell- appetence or virulence. Thus, with the progressive release of sequenced genomes, several typing systems have been developed (Klint et al., 2007; Pannekoek et al., 2008; Pedersen et al., 2008; Dean et al., 2009; Bom et al., 2011), although none of them there is a radical change of environmental conditions when transiting from the in vivo to the in vitro system, mostly because the latter lacks immune system, competing flora, pH alterations, hormonal fluctua-tions, etc. Nevertheless, although the paral-lelism between these two scenarios remains speculative for these reasons, the impossibil-ity to perform this evaluation in vivo and under controlled conditions makes this an  interesting approach.In a second stage, the authors went even further by studying the “long-term” genome stability under influence of in vitro envi-ronmental conditions. To achieve this, they used the MLVA-ompA and also the five-locus MST system to monitor the stability of the enrolled loci throughout 72 passages in tissue culture. The coverage and the runtime of this approach make it an unprecedented evaluation of genome stability. In this study Labiran et al. (2012) used the so called “Swedish new variant,” a C.  trachomatis isolate that, besides the higher number of pseudogenes than most sequenced genital isolates (Jeffrey et al., 2010), shows both a deletion and duplication within the plas-mid, which are genomic changes that had never been described before (Unemo et al., 2010). These kind of genomic alterations are infrequent as C. trachomatis presents a nearly identical core and pan genome and a DNA sequence similarity of >98% (Harris et al., 2012). So, this isolate could hypotheti-cally be considered as genomically unstable, making this a valuable strain to test stability over a long time in vitro passage. Similarly to the previous approach, no genetic changes were observed throughout the long-term in vitro maintenance, suggesting that the MLVA-ompA and MST systems are, on a genetic stability basis, highly accurate for both short-term (such as partner tracing) and long-term molecular epidemiology.Moreover, the results from the Labiran et al. (2012) study indirectly bring to light a major controversy in the field, which is the uncertainty of whether the prototype www.frontiersin.org June 2012 | Volume 2 | Article 77 | 1General Commentarypublished: 06 June 2012doi: 10.3389/fcimb.2012.00077strains that have been used worldwide lead-ing to thousands of papers, accurately rep-resent current circulating clinical strains. In fact, the former are laboratory adapted for decades but at this stage one cannot know the extent of genomic alterations that may occur due to laboratory adaptation. On one hand, the results from Labiran et al. (2012) point to specific genomic stability, which, together with the C. trachomatis transmission bottlenecks (Andersson and Hughes, 1996) and the high doubling time of 2.5–4 h (Borges et al., 2010), disfavors genetic variability. On the other hand, it is known that some loci are prone to generate multi-alleles, such as the putative virulence factor CT135 (Sturdevant et al., 2010), and that Chlamydia undergoes adaptive changes when subjected to specific environmental alterations (Kutlin et al., 2005; Suchland et al., 2005). Ultimately, unless the entire genome is analyzed (at the stage of the strain isolation and after long-term in vitro pas-sage), the controversy will certainly remain.RefeRencesAndersson, D. I., and Hughes, D. (1996). Muller’s ratchet decreases fitness of a DNA-based microbe. Proc. Natl. Acad. Sci. U.S.A. 93, 906–907.Black, C. M. (1997). Current methods of laboratory diagnosis of Chlamydia trachomatis infections. Clin. Microbiol. Rev. 10, 160–184.Bom, R. J., Christerson, L., Schim Van Der Loeff, M. F., Coutinho, R. A., Herrmann, B., and Bruisten, S. M. (2011). Evaluation of high-resolution typing methods for Chlamydia trachomatis in samples from hetero-sexual couples. J. Clin. Microbiol. 49, 2844–2853.Borges, V., Ferreira, R., Nunes, A., Nogueira, P., Borrego, M. J., and Gomes, J. P. (2010). Normalization strategies for real-time expression data in Chlamydia trachoma-tis. J. Microbiol. Methods 82, 256–264.Dean, D., Bruno, W. J., Wan, R., Gomes, J. P., Devignot, S., Mehari, T., De Vries, H. J. C., Morre, S. A., Myers, A. (2008). Multi locus sequence of Chlamydiales: clonal groupings within the obligate intracellular bacteria Chlamydia trachomatis. BMC Microbiol. 8, 42. doi: 10.1186/1471-2180-8-42Pedersen, L. N., Podenphant, L., and Moller, J. K. (2008). Highly discriminative genotyping of Chlamydia tra-chomatis using omp1 and a set of variable number tandem repeats. Clin. Microbiol. Infect. 14, 644–652.Stothard, D. R., Van Der Pol, B., Smith, N. J., and Jones, R. B. (1998). Effect of serial passage in tissue culture on sequence of omp1 from Chlamydia trachomatis clinical isolates. J. Clin. Microbiol. 36, 3686–3688.Sturdevant, G. L., Kari, L., Gardner, D. J., Olivares-Zavaleta, N., Randall, L. B., Whitmire, W. M., Carlson, J. H., Goheen, M. M., Selleck, E. M., Martens, C., and Caldwell, H. D. (2010). Frameshift mutations in a sin-gle novel virulence factor alter the in vivo pathogenic-ity of Chlamydia trachomatis for the female murine genital tract. Infect. Immun. 78, 3660–3668.Suchland, R. J., Bourillon, A., Denamur, E., Stamm, W. E., and Rothstein, D. M. (2005). Rifampin-resistant RNA polymerase mutants of Chlamydia trachoma-tis remain susceptible to the ansamycin rifalazil. Antimicrob. Agents Chemother. 49, 1120–1126.Unemo, M., Seth-Smith, H. M., Cutcliffe, L. T., Skilton, R. J., Barlow, D., Goulding, D., Persson, K., Harris, S. R., Kelly, A., Bjartling, C., Fredlund, H., Olcén, P., Thomson, N. R., and Clarke, I. N. (2010). The Swedish new variant of Chlamydia trachomatis: genome sequence, morphology, cell tropism and phenotypic characterization. Microbiology 156, 1394–1404.Yuan, Y., Zhang, Y. X., Watkins, N. G., and Caldwell, H. D. (1989). Nucleotide and deduced amino acid sequences for the four variable domains of the major outer membrane proteins of the 15 Chlamydia tra-chomatis serovars. Infect. Immun. 57, 1040–1049.Received: 14 May 2012; accepted: 18 May 2012; published online: 06 June 2012.Citation: Gomes JP (2012) Genomic stability of genotyp-ing markers in Chlamydia trachomatis. Front. Cell. Inf. Microbio. 2:77. doi: 10.3389/fcimb.2012.00077Copyright © 2012 Gomes. This is an open-access article distributed under the terms of the Creative Commons Attribution Non Commercial License, which permits non-commercial use, distribution, and reproduction in other forums, provided the original authors and source are credited.G., Read, T. D., and Spratt, B. G. (2009). Predicting phenotype and emerging strains among Chlamydia trachomatis infections. Emerging Infect. Dis. 15, 1385–1394.Ferreira, R., Borges, V., Nunes, A., Nogueira, P. J., Borrego, M. J., and Gomes, J. P. (2012). Impact of loci nature on estimating recombination and mutation rates in Chlamydia trachomatis. G3 (Bethesda). 2:1–9. doi: 10.1534/g3.112.002923Harris, S. R., Clarke, I. N., Seth-Smith, H. M., Solomon, A. W., Cutcliffe, L. T., Marsh, P., Skilton, R. J., Holland, M. J., Mabey, D., Peeling, R. W., Lewis, D. A., Spratt, B. G., Unemo, M., Persson, K., Bjartling, C., Brunham, R., de Vries, H. J., Morré, S. A., Speksnijder, A., Bébéar, C. M., Clerc, M., de Barbeyrac, B., Parkhill, J., and Thomson, N. R. (2012). Whole-genome analysis of diverse Chlamydia trachomatis strains identifies phylogenetic relationships masked by current clinical typing. Nat. Genet. 44, 413–419.Jeffrey, B. M., Suchland, R. J., Quinn, K. L., Davidson, J. R., Stamm, W. E., and Rockey, D. D. (2010). Genome sequencing of recent clinical Chlamydia trachoma-tis strains identifies loci associated with tissue tro-pism and regions of apparent recombination. Infect. Immun. 78, 2544–2553.Joseph, S. J., Didelot, X., Gandhi, K., Dean, D., and Read, T. D. (2011). Interplay of recombination and selec-tion in the genomes of Chlamydia trachomatis. Biol. Direct 6, 28.Klint, M., Fuxelius, H. H., Goldkuhl, R. R., Skarin, H., Rutemark, C., Andersson, S. G. E., Persson, K., and Herrmann, B. (2007). High-resolution genotyping of Chlamydia trachomatis strains by multilocus sequence analysis. J. Clin. Microbiol. 45, 1410–1414.Kutlin, A., Kohlhoff, S., Roblin, P., Hammerschlag, M. R., and Riska, P. (2005). Emergence of resistance to rifampin and rifalazil in Chlamydophila pneumo-niae and Chlamydia trachomatis. Antimicrob. Agents Chemother. 49, 903–907.Labiran, C., Clarke, I. N., Cutcliffe, L. T., Wang, Y., Skilton, R. J., Persson, K., Bjartling, C., Herrmann, B., Christerson, L., and Marsh, P. (2012). Genotyping markers used for multi locus VNTR analysis with ompA (MLVA-ompA) and multi sequence typing retain stability in Chlamydia trachomatis. Front. Cell. Infect. Microbiol. 2:68. doi: 10.3389/fcimb.2012.00068Pannekoek, Y., Morelli, G., Kusecek, B., Morre, S. A., Ossewaarde, J. M., Langerak, A. A., and Van Der Ende, Gomes Genomic stability in vitroFrontiers in Cellular and Infection Microbiology  June 2012 | Volume 2 | Article 77 | 2

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Genomic stability of genotyping markers in Chlamydia trachomatis

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