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Antimicrobial Agents and Chemotherapy, July 2005, p. 2865-2873, Vol. 49, No. 7
0066-4804/05/$08.00+0     doi:10.1128/AAC.49.7.2865-2873.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.

Frequency of Spontaneous Mutations That Confer Antibiotic Resistance in Chlamydia spp.

Rachel Binet and Anthony T. Maurelli*

Department of Microbiology and Immunology, F. Edward Hébert School of Medicine, Uniformed Services University of the Health Sciences, 4301 Jones Bridge Road, Bethesda, Maryland 20814-4799

Received 1 December 2004/ Returned for modification 30 December 2004/ Accepted 18 March 2005

Mutations in rRNA genes (rrn) that confer resistance to ribosomal inhibitors are typically recessive or weakly codominant and have been mostly reported for clinical strains of pathogens possessing only one or two rrn operons, such as Helicobacter pylori and Mycobacterium spp. An analysis of the genome sequences of several members of the Chlamydiaceae revealed that these obligate intracellular bacteria harbor only one or two sets of rRNA genes. To study the contribution of rRNA mutations to the emergence of drug resistance in the Chlamydiaceae, we used the sensitivities of Chlamydia trachomatis L2 (two rrn operons) and Chlamydophila psittaci 6BC (one rrn operon) to the aminoglycoside spectinomycin as a model. Confluent cell monolayers were infected in a plaque assay with about 108 wild-type infectious particles and then treated with the antibiotic. After a 2-week incubation time, plaques formed by spontaneous spectinomycin-resistant (Spcr) mutants appeared with a frequency of 5 x 10–5 for C. psittaci 6BC. No Spcr mutants were isolated for C. trachomatis L2, although the frequencies of rifampin resistance were in the same range for both strains (i.e., 10–7). The risk of emergence of Chlamydia strains resistant to tetracyclines and macrolides, the ribosomal drugs currently used to treat chlamydial infections, is discussed.

* Corresponding author. Mailing address: Department of Microbiology and Immunology, Uniformed Services University of the Health Sciences, 4301 Jones Bridge Road, Bethesda, MD 20814-4799. Phone: (301) 295-3415. Fax: (301) 295-1545. E-mail: amaurelli{at}usuhs.mil.

Antimicrobial Agents and Chemotherapy, July 2005, p. 2865-2873, Vol. 49, No. 7
0066-4804/05/$08.00+0     doi:10.1128/AAC.49.7.2865-2873.2005
Copyright © 2005, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Binet, R., Maurelli, A. T. (2009). Transformation and isolation of allelic exchange mutants of Chlamydia psittaci using recombinant DNA introduced by electroporation. Proc. Natl. Acad. Sci. USA 106: 292-297 [Abstract] [Full Text]  
  • DeMars, R., Weinfurter, J. (2008). Interstrain Gene Transfer in Chlamydia trachomatis In Vitro: Mechanism and Significance. J. Bacteriol. 190: 1605-1614 [Abstract] [Full Text]  
  • Rupp, J., Solbach, W., Gieffers, J. (2008). Variation in the mutation frequency determining quinolone resistance in Chlamydia trachomatis serovars L2 and D. J Antimicrob Chemother 61: 91-94 [Abstract] [Full Text]  
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